sports medicine Volume 40 Issue 5 May 2010

Sports Med 2010; 40 (5): 361-366 0112-1642/10/0005-0361/$49.95/0

CURRENT OPINION

ª 2010 Adis Data Information BV. All rights reserved.

First Aid for Dental Trauma Caused by Sports Activities State of Knowledge, Treatment and Prevention Katarzyna Emerich1 and Jan Kaczmarek2 1 Department of Paediatric Dentistry, Medical University of Gdansk, Gdansk, Poland 2 Department of Technology, Gdansk University of Technology, Gdansk, Poland

Abstract

In view of the widespread lack of knowledge of first aid procedures in cases of dental trauma, this article describes the current state of knowledge and highlights the need for education of those likely to witness or be victims of dental trauma while practising sports. Dental and oral injuries, the commonest type of orofacial injuries, are often sustained by athletes playing contact sports; indeed, they represent the most frequent type of sporting injury. Studies of a large group of children and adults have shown that as many as 31% of all orofacial injuries are caused by sporting activities. Furthermore, current literature on the subject emphasizes that awareness of appropriate triage procedures following dental trauma is unsatisfactory. Delay in treatment is the single most influential factor affecting prognosis. What should we know and, more importantly, what should we do? Immediate replantation of an avulsed tooth is the best treatment option at the site of the accident. If replantation is impossible, milk is the preferred transport medium for the avulsed tooth. There is a general low level of awareness about the need for prompt triage of traumatic dental injuries sustained in sports, despite their relative frequency. When a cohort of Swiss basketball players was interviewed, only half were aware that an avulsed tooth could be replanted. Cheap, commercially available tooth storage devices containing an isotonic transport medium (socalled ‘Save-a-Tooth boxes’), can maintain the viability of an avulsed tooth for up to 72 hours, prior to replantation. More readily available storage media such as milk, sterile saline or even saliva may be used, but knowledge of this information is rare among sports participants. For example, just 6.6% of the Swiss basketball players interviewed were aware of the ‘Tooth Rescue box’ products. Sporting organizations seem to offer very little information about sports-related risks or preventive strategies for orodental trauma. Having an attending dentist at sports events – amateur or professional – is clearly a luxury that is neither practical nor affordable. The solution must lie in extending the knowledge of management of orodental trauma beyond the dental profession. Educational posters, when displayed prominently in sports clubs, gym halls and dressing rooms of swimming pools, are a clear, accessible and low cost method of presenting the appropriate procedures to follow after

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orodental injury. When the potentially avoidable financial burden and discomfort of protracted restorative or cosmetic dentistry are taken into account, rarely can such significant morbidity be so easily prevented.

Our general health and well-being are among the most appreciated benefits of modern society. Few of us still need to be convinced that sports can sustain and improve our physical condition and, subsequently, our psychological state. Active participation in sport opens up new ways of reaching our ambitions and satisfies our primary need for competition. Thanks to sports, society is becoming and staying healthier. That is why in developed countries and societies, the practice of sports is on the rise, stimulated by governments who, well aware of the multiple benefits, are putting all their energy into opening up all kinds of sports to children and adults. This sponsorship has resulted in a growing percentage of children and adults taking an active part in organized sports events and competitions. Frequently, however, we forget that practising sports can have negative consequences. Even during moderate sport practice, not to mention high level competition, accidents do happen, with some leading to traumas that can handicap a person for life. Sport-related injuries are a growing concern worldwide. For example, in children aged 5–18 years the commonest injury location is the wrist/hand (28%), followed by the head/face (22%) and the ankle/foot (18%).[1] In view of the widespread lack of knowledge of first aid procedures in cases of dental trauma, we would like to report the current state of knowledge and highlight the need for education of individuals who are likely to witness or be a victim of sports-related dental trauma. Participants in fast sport activities with close body contact are prone to orofacial injuries.[2] Dental injuries are the commonest type of orofacial injuries,[3] and are often sustained by athletes playing contact sports. Contact sports are defined as those in which players physically interact with each other, trying to prevent the opposing team or person from winning.[4,5] Sports activities using bats and/ or rackets present a particular danger of causing ª 2010 Adis Data Information BV. All rights reserved.

dental injuries,[5,6] which occur more frequently than is commonly recognized.[1,7] Studies of a large cohort of children and adults have shown that as many as 31% of all orofacial injuries are sports-related.[3,8-11] One of the most remarkable and relevant problems regarding dental traumatology is the wide range of existing diagnostic classification systems. Over 50 distinct classification systems have been identified in the literature.[12] In light of this discrepancy, some clinical and epidemiological studies have shown vast differences regarding the prevalence and incidence of dental injuries. The consequences of dental trauma can vary from simple tooth fractures to complicated tooth avulsion. However, in the literature the most frequently described consequences are crown fractures, representing up to 79% of all dental injuries,[7] or 14% of sports-related dental trauma.[13] The most complex injury is the complete dislocation of the tooth from its alveolus. Tooth avulsion, which should be considered the real emergency in dentistry, represents up to 21% of all dental injuries,[7,14,15] and 10% of sportsrelated dental injuries.[16,17] What should we know and, more importantly, what should we do to minimize the effects of orodental injuries? 1. Awareness To cope with such a large number of orodental injuries in a modern and effective manner, there is a pressing need to promote better education on the subject to coaches, athletes, players and parents – those who can provide immediate help on the sports field to minimize long-lasting consequences. Prevention of oral and dental trauma during sport is an area where there is an almost total lack of information.[18] Education should be provided as early as possible in schools and within sporting clubs, primarily targeting instructors, coaches Sports Med 2010; 40 (5)

First Aid for Dental Trauma

and managers of sports facilities. This knowledge and awareness could then be passed on to athletes and their families.[18] Compared with other outpatient injuries, traumatic dental injuries are more time consuming and costly to treat.[19] If every sports club, gym, sports hall, swimming pool or pitch displayed dental trauma first aid explanatory posters, costly long-term consequences of complications arising from the delayed treatment of teeth injuries could be prevented. A campaign by the International Association of Dental Traumatology provided a good example, creating a multi-language poster entitled ‘Save Your Tooth’.[20] Most available literature emphasizes that awareness of the correct procedure following dental trauma is unsatisfactory.[21-23] It is recognized that the prognosis of traumatic dental injuries depends on the time between the accident and initiation of treatment.[24,25] Paradoxically, the literature highlights the tendency to delay presentation for dental treatment. One study showed that only 17% of children sought treatment the same day or the day after the injury occurred, while 40% delayed treatment for more than a month.[26] In other studies, the time between the accident and presentation for medical care was 24 hours for almost half the studied population.[7] It has been commonly accepted that all injuries should be treated on an emergency basis for the comfort of the patient and to reduce wound healing complications. Thus, a general rule for all sports participants is that earlier treatment is always preferable to delayed treatment.[27] 2. Managing Tooth Avulsion Tooth avulsion is a complex injury affecting multiple tissues with the complete displacement of a tooth from its alveolar support, and should be considered a genuine emergency requiring prompt and appropriate management to significantly improve prognosis.[28] Immediate replantation or maintenance of the avulsed tooth in storage media compatible for the survival of periodontal ligament cells before replantation is fundamental to a successful replantation procedure.[28-30] The longer the time elapsed between ª 2010 Adis Data Information BV. All rights reserved.

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tooth avulsion and replantation, the greater the risk of replacement resorption and inflammatory root resorption.[27,30] Although all participants in sports activities should know that avulsed teeth can be replanted with relative ease, the literature shows that this is not common knowledge.[21-23] According to Perunski et al.,[21] just 51.9% of interviewees from Swiss basketball teams were aware of the possibility of tooth replantation. It must be stressed that the most important factor in the treatment of injured teeth is time. The best way to preserve the vitality of periodontal ligament cells is immediate replantation at the site of the accident, ideally within the first 30 minutes.[31] If the root surface is contaminated, it should be gently cleaned with a stream of saline or even cold tap water before replantation. Under no circumstances should the tooth be held by the root, to avoid periodontal ligament damage.[20,27] A temporary splint comprising aluminium foil, available in every kitchen or by unwrapping a chocolate bar, can be applied before attending an emergency dental surgery.[32,33] Alternatively, if there is no one brave enough to replant and stabilize the tooth, an avulsed tooth can be placed in milk, which is the preferred transport medium, or in saliva (between the cheek and the lower molars). Mori et al.[34] found that only 7% of sports participants knew that milk is the ideal storage medium for an avulsed tooth. Other possible transport media – if available at the site of the accident – are Viaspan, Hank’s Balanced Salt Solution and physiological saline.[30,35] Products such as the ‘Save-a-Tooth box’ or ‘Tooth Rescue box’ are the best options for preserving the vitality of periodontal ligament cells for up to 72 hours.[36] However, only 6% of interviewees from the Swiss basketball teams knew about such products.[21] When the tooth is maintained in a wet storage medium (i.e. milk), replantation can be performed later and the chance of success is subsequently increased.[37-39] However, people often allow the tooth to dry by keeping it wrapped in plastic or immersed in solutions inappropriate for cell survival (e.g. hydrogen peroxide).[40,41] This can lead to ankylosis and root resorption, which are both undesirable consequences of tooth replantation.[30] Sports Med 2010; 40 (5)

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The best way to preserve the vitality of periodontal ligament cells is immediate replantation. In a hospital scenario, where first aid is given by medical staff, fixation of an avulsed tooth can be made by a suture using an easy-to-perform temporary fixation method.[42] All sports participants should be aware of the first aid procedure to avoid extra-oral dry time of a tooth. For the future outcome of tooth avulsion treatment, the extra-oral dry time is far more important than the time when the patient was able to obtain a dentist’s help. Based on 400 cases of replantation, 20 minutes of both dry and wet storage only resulted in up to 15% of correct periodontal ligament healing and pulp healing.[35] It would seem obvious that an orofacial injury requires the attention of a dentist, but some studies show that many individuals fail to seek any treatment or advice after an accident.[7,26,43] If everyone would keep in mind six simple rules for managing traumatic dental injury, the costs of treatment of tooth avulsion will drop significantly.[44] Those rules are: 1. locate the tooth as quickly as possible; 2. handle the tooth only by the crown (the white part); 3. replace the tooth in its socket immediately (see the adjacent teeth as a guide); 4. immobilize any loosened teeth (e.g. with aluminium foil); 5. if the tooth cannot be replanted, immediately place it into a physiological medium, keeping it wet at all times (e.g. use milk, saline or even saliva – place the tooth between the cheek and the lower molars); and 6. attend a dentist as soon as possible. These rules could be presented in a simple leaflet and distributed to schools and sporting clubs. As shown by Al-Asfour and Andersson,[45] such a leaflet could be a valuable tool for conveying the basic information to enhance the knowledge of how people should act if a tooth avulsion occurs. 3. Prevention Knowledge of aetiological factors that contribute to an increased risk of sport injury should ª 2010 Adis Data Information BV. All rights reserved.

form the basis for preventive action.[46] Malocclusion or early stage orthodontic treatment should be considered predisposing factors to traumatic dental injury.[47] Thus, dentists should identify and target patients who are at risk of dental trauma, especially active sports participants. Dental practitioners should also promote the use of mouth guards as a prevention measure to all patients involved in sport.[16,48] Mouth guards have been proven to greatly reduce the number and severity of traumatic oral injuries,[49] but studies have found that most people turn to prevention only after an accident has already happened.[21] Fakhruddin et al.[50] found that only 5.5% of school children wore mouth guards for school sports. The lack of awareness about the benefits of wearing mouth guards and lack of parental or coaching advice on mouth guard usage, as well as peer beliefs about aesthetics and function, were the main reasons for noncompliance.[50,51] The low level of knowledge and lack of interest for the problem of prevention and treatment of dental injuries in all sports-related environments makes it vital to introduce and continue education on a wide-ranging scale, targeted at both active and passive participants of all kinds of sports. Instruction for the caregivers and onlookers in all sports-related environments should be short and comprehensible. The message should be ‘‘once the tooth is out of the mouth, replant immediately, otherwise immediately place the tooth into a physiological medium, keeping it wet at all times, and see a dentist as soon as possible.’’ 4. Conclusion In the face of large numbers of dental injuries, there is an urgent need to promote better education on the subject of sports-related orofacial injuries to coaches, athletes, players and parents – people who could provide instant help at the site of an accident and minimize long-lasting consequences. The extensive consequences of injury could be prevented with such simple knowledge and action. Furthermore, efforts should be made to train general medical practitioners and other Sports Med 2010; 40 (5)

First Aid for Dental Trauma

emergency room staff to perform appropriate first aid procedures for dental trauma. This would result in an improved outcome for many thousands of sports participants worldwide who injure their teeth during play. Acknowledgements The authors wish to thank Dr Mike Harrison, Consultant in Paediatric Dentistry from Cardiff University Dental Hospital, for his enthusiastic and untiring help and encouragement. No sources of funding were used to assist in the preparation of this article. The authors have no conflicts of interest that are directly relevant to the content of this article.

References 1. Taylor BI, Attia MW. Sports-related injuries in children. Acad Emerg Med 2000; 7: 1376-82 2. Flanders RA, Bhat M. The incidence of orofacial injuries in sports: a pilot study in Illinois. J Am Dent Assoc 1995; 126: 491-6 3. Gassner R, Bosch R, Tuli T, et al. Prevalence of dental trauma in 6000 patients with facial injuries: implications for prevention. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1999; 87: 27-33 4. Dorney B. Dental screening for rugby players in New South Wales, Australia. FDI World 1998; 7: 10-3 5. American Academy of Pediatrics, Committee on Sports Medicine and Fitness. Medical conditions affecting sports participation. Pediatrics 2001; 107: 1205-9 6. Bolhuis JH, Leurs JM, Flogel GE. Dental and facial injuries in international field hockey. Br J Sports Med 1987; 21: 174-7 7. Gabris K, Tarjan I, Rozsa N. Dental trauma in children presenting for treatment at the Department of Dentistry for Children and Orthodontics, Budapest, 1985-1999. Dent Traumatol 2001; 17: 103-8 8. Bemelmanns P, Pfeiffer P. Haufigkeit von Zahn- Mund- und Kieferverletzungen und bewahrung von Mundschutzen bei Spitzensportlern. Sportverletz Sportschaden 2000; 14: 139-43 9. Gassner R, Tuli T, Hachl O, et al. Cranio-maxillofacial trauma: a 10 year review of 9543 cases with 21,067 injuries. J Craniomaxillofac Surg 2003; 31: 51-61 10. Gassner R, Tuli T, Hachl O, et al. Craniomaxillofacial trauma in children: a review of 3385 cases with 6060 injuries in 10 years. J Oral Maxillofac Surg 2004; 62: 399-407 11. Huang B, Marcenes W, Croucher R, et al. Activities related to the occurrence of traumatic dental injuries in 15- to 18-year-olds. Dent Traumatol 2009; 25: 64-8 12. Feliciano KMPC, de Franca Caldas Jr A. A systematic review of the diagnostic classifications of traumatic dental injuries. Dent Traumatol 2006; 22: 71-6 13. Cetinbas T, Yildirim G, Sonmez H. The relationship between sports activities and permanent incisor crown fractures in a group of school children aged 7-9 and 11-13 in Ankara, Turkey. Dent Traumatol 2008; 24: 532-6

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14. Marcenes W, Alessi ON, Traebert J. Causes and prevalence of traumatic injuries to the permanent incisors of school children aged 12 years in Jaragua do Sul, Brazil. Int Dent J 2000; 50: 87-92 15. Andreasen JO. Etiology and pathogenesis of traumatic dental injuries: a clinical study of 1298 cases. Scand J Dent Res 1970; 78: 329-42 16. Ma W. Basketball players’ experience of dental injury and awareness about mouthguards in China. Dent Traumatol 2008; 24: 430-4 17. Kececi AD, Eroglu E, Baydar ML. Dental trauma incidence and mouthguard use in elite athletes in Turkey. Dent Traumatol 2005; 21: 76-9 18. Spinas E, Savasta A. Prevention of traumatic dental lesions: cognitive research on the role of mouthguards during sport activities in paediatric age. Eur J Paediatr Dent 2007; 8 (4): 193-8 19. Glendor U. Aetiology and risk factors related to traumatic dental injuries: a review of the literature. Dent Traumatol 2009; 25: 19-31 20. International Association of Dental Traumatology. Save your tooth [online]. Available from URL: http://www.iadtdentaltrauma.org/web/index.php?option=com_content&task= view&id=28&Itemid=43 [Accessed 2009 Mar 1] 21. Perunski S, Lang B, Pohl Y, et al. Level of information concerning dental injuries and their prevention in Swiss basketball: a survey among players and coaches. Dent Traumatol 2005; 21: 195-200 22. Lang B, Pohl Y, Filippi A. Knowledge and prevention of dental trauma in team handball in Switzerland and Germany. Dent Traumatol 2002; 18: 329-34 23. Hamilton FA, Hill FJ, Mackie IC. Investigation of lay knowledge of the management of avulsed permanent incisors. Dent Traumatol 1997; 13: 19-23 24. Adair SM, Durr DP. Practical clinical applications of sports dentistry in private practice. Dent Clin North Am 1991; 35: 757-70 25. Kumomoto DP, Winters JE. Private practice and community activities in sports dentistry. Dent Clin North Am 2000; 44: 209-20 26. Rajab LD. Traumatic dental injuries in children presenting for treatment at the Department of Pediatric Dentistry, University of Jordan, 1997-2000. Dent Traumatol 2003; 19: 6-11 27. Andreasen JO, Andreasen FM, Bakland LK, et al. Traumatic dental injuries: a manual. 2nd ed. Odder: Blackwell Munksgaard, 2003; 50-3, 68-69 28. Andreasen JO, Andreasen FM, Skeie A, et al. Effect of treatment delay upon pulp and periodontal healing of traumatic dental injuries [review article]. Dent Traumatol 2002; 18: 116-28 29. Andersson L, Bodin I. Avulsed human teeth replanted within 15 minutes: a long-term clinical follow-up study. Endod Dent Traumatol 1990; 6: 37-42 30. Andreasen JO, Andreasen FM, Andersson L. Textbook and color atlas of traumatic injuries to the teeth: avulsion. 4th ed. Odder: Blackwell Munksgaard, 2007; 444-79 31. Glendor U. Has the education of professional caregivers and lay people in dental trauma care failed? Dent Traumatol 2009; 25: 12-8

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32. Fuss Z. Successful self-replantation of avulsed tooth with 42-year follow-up. Dent Traumatol 1985; 1: 120-2 33. Emerich K, Wyszkowski J. Clinical practice: dental trauma. Eur J Pediatr. Epub 2010 Jan 8 34. Mori GG, de Mendonca Janjacomo DM, Castilho LR, et al. Evaluating the knowledge of sports participants regarding dental emergency procedures. Dent Traumatol 2009; 25: 305-8 35. Chamorro MM, Regan JD, Opperman LA, et al. Effect of storage media on human periodontal ligament cell apoptosis. Dent Traumatol 2008; 24: 11-6 36. Andreasen JO, Borum MK, Jacobsen HL et al. Replantation of 400 avulsed permanent incisors: 4, factors related to periodontal ligament healing. Endod Dent Traumatol 1995; 11 (2): 76-89 37. Vendrame dos Santos CL, Sonoda CK, Poi WR, et al. Delayed replantation of rat teeth after use of reconstituted powdered milk as a storage medium. Dent Traumatol 2009; 25: 51-7 38. Blomlof L, Andersson L, Lindskog S, et al. Periodontal healing of replanted monkey teeth prevented from drying. Acta Odont Scand 1983; 41: 117-23 39. Lindskog S, Blomlof L. Influence of osmolality and composition of some storage media on human periodontal ligament cells. Acta Odont Scand 1982; 40: 435-41 40. Kivttem B, Hardie NA, Roettger M, et al. Incidence of orofacial injuries in high school sports. J Public Health Dent 1998; 58: 288-93 41. Ranalli DN. Prevention of sport-related traumatic dental injuries. Dent Clin North Am 2000; 44: 35-51 42. Lin S, Emodi O, El-Naaj IA. Splinting of an injured tooth as part of emergency treatment. Dent Traumatol 2008; 24: 370-2

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43. Soriano EP, Caldas AF, Carvalho MVD, et al. Prevalence and risk factors related to traumatic dental injuries in Brazilian schoolchildren. Dent Traumatol 2007; 23 (4): 232-40 44. Andersson L, Al-Asfour A, Al-Jame Q. Knowledge of firstaid measures of avulsion and replantation of teeth: an interview of 221 Kuwaiti school children. Dent Traumatol 2006; 22: 57-65 45. Al-Asfour A, Andersson L. The effect of a leaflet given to parents for first aid measures after tooth avulsion. Dent Traumatol 2008; 24: 515-221 46. Van Mechelen W, Twisk J, Molendijk A, et al. Subjectrelated risk factors for sport injuries. Med Sci Sports Exerc 1996; 28: 1171-9 47. Bauss O, Rohling J, Schwestka-Polly R. Prevalence of traumatic injuries to the permanent incisors in candidates for orthodontic treatment. Dent Traumatol 2004; 20: 61-6 48. Ranalli DN. Sports dentistry and dental traumatology. Dent Traumatol 2002; 18: 231-6 49. Yamada T, Sawaki Y, Tomida S, et al. Oral injury and mouthguard usage by athletes in Japan. Endod Dent Traumatol 1998; 14: 84-7 50. Fakhruddin KS, Lawrence HP, Kennz DJ, et al. Use of mouthguards among 12- and 14-year-old Ontario schoolchildren. J Can Dent Assoc 2007; 73: 505-505e 51. Holmes C. Mouth protection in sports in Scotland: a review. Br Dent J 2000; 188: 473-4

Correspondence: Dr Katarzyna Emerich, Assistant Professor, Department of Paediatric Dentistry, Medical University of Gdansk, ul. Orzeszkowej 18, 80-208 Gdansk, Poland. E-mail: [email protected]

Sports Med 2010; 40 (5)

Sports Med 2010; 40 (5): 367-376 0112-1642/10/0005-0367/$49.95/0

CURRENT OPINION

ª 2010 Adis Data Information BV. All rights reserved.

Young Women’s Anterior Cruciate Ligament Injuries An Expanded Model and Prevention Paradigm Diane L. Elliot, Linn Goldberg and Kerry S. Kuehl Division of Health Promotion & Sports Medicine, Department of Medicine, Oregon Health & Science University, Portland, Oregon, USA

Abstract

Anterior cruciate ligament (ACL) injuries among young female athletes occur at rates three- to eight-times greater than in male competitors and, in general, females experience more sports injuries than males, when balanced for activity and playing time. ACL injuries are a particular concern, as they result in immediate morbidity, high economic costs and may have long-term adverse effects. While several closely monitored ACL injury preventive programmes have been effective, those efforts have not been uniformly protective nor have they achieved widespread use. To date, ACL injury prevention has focused on neuromuscular and anatomical factors without including issues relating more broadly to the athlete. Coincident with greater female sport participation are other influences that may heighten their injury risk. We review those factors, including early single sport specialization, unhealthy dietary behaviours, chronic sleep deprivation and higher levels of fatigue, substance use and abuse, and psychological issues. We augment existing models of ACL injury with these additional dimensions. The proposed expanded injury model has implications for designing injury prevention programmes. High school athletic teams are natural settings for bonded youth and influential coaches to promote healthy lifestyles, as decisions that result in better athletes also promote healthy lifestyles. As an example of how sport teams could be vehicles to address an expanded injury model, we present an existing evidenced-based sport team-centered health promotion and harm reduction programme for female athletes. Widening the lens on factors influencing ACL injury expands the prevention paradigm to combine existing training with activities to promote psychological well-being and a healthy lifestyle. If developed and shown to be effective, those programmes might better reduce injuries and, in addition, provide life skills that would benefit young female athletes both on and off the playing field.

Athletic injuries in young women are a growing concern. Data from the National Athletic Trainers’ Association indicate that during a sport season more than one-third of female high school athletes experience an injury.[1] Non-contact

anterior cruciate ligament (ACL) injuries are a particular interest, as they occur at rates three- to eight-times higher than in male competitors.[2] The problem has captured the attention of both the medical profession[3,4] and the public.[5]

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Changes in the demographics of sport participation and gender-specific factors contribute to the increase in young women’s knee injuries. First, since enacting the Title IX provision of the Education Amendments in 1972,[6] female sport participation has risen almost 10-fold, so that currently more than half of female adolescents are in school or club sports.[7] Second, in addition to greater athletic involvement, young women experience more knee injuries than males, even when playing time and conditions are factored into that figure.[8,9] Knee injuries are the largest single problem in orthopaedic sports medicine.[4] Among female collegiate athletes, 1 in 20 sustains a knee injury, and for high school players, estimates are 1 in 50.[10] These devastating injuries cause immediate morbidity and expense, and long-term consequences are also concerning. Despite ACL repair and correction of instability, young women demonstrate an early onset of degenerative osteoarthritic changes.[11-13] 1. Existing Thinking about ACL Injuries in Females As the marked increase of knee injuries in young women was appreciated, efforts were made to understand the phenomenon. Analysing videotapes affords the opportunity to identify the mechanisms of injury. For example, videotape review was used to recognize that certain football tackling techniques resulted in cervical spine injuries, which led to rule change and improved instruction, with a resultant marked reduction in those problems.[14,15] Accordingly, when the gender disparity in knee injuries was identified, videotapes of female athletes experiencing noncontact ACL tears were examined to identify their mechanism. Non-contact ACL injuries appeared to reflect two patterns: (i) deceleration of a planted foot with an internally rotated hip plus valgus knee; and (ii) anterior tibial shear related to quadriceps contraction near full knee extension.[16-19] In addition, researchers looked for differences in female hormonal milieu, anatomy and biomechanics in an attempt to understand their ª 2010 Adis Data Information BV. All rights reserved.

greater incidence of knee injuries.[3] Female estrogen levels may result in greater joint laxity,[20,21] and because of the differences in the ratio of pelvic width to femoral length, limb alignment differs for females.[18,22] Recent studies have also shown that gender-specific dynamic differences in patterns of neuromuscular activation may add to females predisposing to injury.[8,23] However, those factors and their combination do not completely predict or explain who sustains an ACL injury. 2. Widening the Lens on Contributing Factors While gender-related biomechanical differences may be relevant, they may not provide a complete model of ACL injuries. By analogy, acute rupture of an atherosclerotic plaque causes myocardial infarction. However, focusing just on the blood vessel wall would omit the importance of lifestyle issues, such as smoking, dietary indiscretions and lack of physical activity, as more proximal risk factors contributing to atherosclerosis. In a similar way, upstream aspects, such as psychosocial influences and personal habits, may contribute to knee injuries in young women. Concurrent with the proliferation of knee injuries in females are lifestyle changes in the domains of training characteristics, sleeping habits, nutrition, and substance use or abuse. In addition, gender-specific psychological influences may be contributing to the already identified factors influencing injury risk. Incorporating these variables into models for knee injuries in females may lead to more effective programmes to identify those at risk and prevent ACL injuries. 2.1 Sport Specialization, Overuse and Burnout

Today, many girls and boys in the US begin athletics in elementary school, and by middle school they focus on a single sport, participating year round in that activity in school and club teams.[24] The greatest male sport involvement in the US is with football, which is a seasonal activity, and although some players may have personal coaches and attend offseason camps, most Sports Med 2010; 40 (5)

Expanded Model of ACL Injuries

American football players do not compete year round. Accordingly, the pattern of sport specialization often differs for boys and girls. Unlike single-sport youth, even most professional athletes do not have year-round competitions. Sport specialization can lead to both physical and mental adverse effects and females may be more prone to those consequences. In 2007, the American Academy of Pediatrics Council on Sports Medicine and Fitness issued a document warning that a single-sport focus and resultant overtraining may lead to injuries.[25] They recommend limiting a single-sport activity to 5 days a week, with at least 2 months off per year from the sport. A correlation between training volume and overuse injuries is well recognized,[26] and longer duration of play may be a greater injury risk for females.[27] Overtraining also can lead to the psychophysiological state of ‘burnout’. The syndrome is characterized by chronic fatigue, sleep disturbance, irritability, musculoskeletal complaints, lack of training motivation and under performance.[28] Burnout is not limited to adults, and occurs in children and adolescents.[29] Although the occurrence of the disorder correlates with training volume, its pathogenesis is not well understood. Certain psychological traits, such as maladaptive perfectionism, more prevalent in females, may predispose to the condition.[30,31] 2.2 Dietary Habits

Nutritional deficiencies related to injuries are more common among young females. Unhealthy dietary practices among adolescents are well documented[32,33] and those habits are only marginally better among athletes than their non-athletic classmates.[34] For example, survey findings indicate that 80% of adolescent females do not eat the recommended daily servings of fruits and vegetables.[35] In addition, a high percentage of young women practice food restriction, with more than half of normal-weight girls skipping meals.[36] Dietary habits might affect injury rates through direct central mechanisms relating to blood glucose and alertness as well as peripheral effects on muscle glycogen levels. Carbohydrate intake relates to mental functioning, as evidenced by superior ª 2010 Adis Data Information BV. All rights reserved.

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test scores among students who eat breakfast,[37] which might be extrapolated to concentration and focus during athletic events. Adequate carbohydrate intake is also needed to optimize glycogen stores,[38] and during prolonged exercise reduced glycogen might lead to muscular weakness and reduced joint stability. Importantly, females appear more susceptible to the injurypromoting effects of fatigue on both muscular balance and landing mechanics.[39-42] Those observations suggest that improved nutrition might reduce ACL injury rates by improving mental alertness and reducing the muscle fatigue, imbalance and joint instability that can lead to knee injury. We and others have identified that calcium intake in young females is often inadequate.[43] Calcium is needed for the integrity of bones and supporting structures. Ligament injuries, in addition to stress fractures, are increased with calcium deficiency,[44] and appropriate calcium intake would strengthen bones and other connective tissue. Thus, in addition to its importance in bone health, calcium intake may be important for injury prevention. Finally, the gender-related issue of disordered eating is well recognized. A recent survey of female high school athletes identified that almost 20% had disordered eating habits.[45] The sociocultural pressures toward being thin may be compounded by similar influences in sports, resulting in a greater prevalence of unhealthy eating habits among high school athletes.[46,47] The female athlete triad of disordered eating, menstrual irregularities and reduced bone mass is a consequence of the extreme adverse effects that can accompany sport participation.[48,49] Although there is case series evidence that the triad may be linked with ACL injuries, it is more commonly related to stress fractures and other overuse injuries.[48,49] 2.3 Sleep and Fatigue

Chronic sleep deprivation is common among teenagers, especially females.[50,51] In a large US survey, sleep disorders were twice as common among adolescent girls compared with boys, with almost one-third of females experiencing Sports Med 2010; 40 (5)

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problems initiating or maintaining sleep.[52] Those differences do not represent females needing less sleep, as the consequences of inadequate sleep are also increased. A recent report indicated that 20% of young women complained of excessive daytime fatigue, a rate three-times greater than male counterparts.[53] The adverse performance effects of chronic sleep deprivation are well recognized.[54-56] For example, the National Highway Traffic Safety Administration estimates that drowsiness is the primary cause of more than 100 000 policereported motor vehicle crashes each year.[57] Repeated failure to obtain sufficient sleep has a cumulative detrimental effect on alertness and performance, which increases linearly with sleep loss.[58-61] Even modest increases in fatigue can have performance effects. For example, the fatigue that accumulates during an 8-hour shift results in an increase in on-the-job accidents during its later hours.[62] Fatigue effects have been compared with the performance effects of alcohol, and studies show that being awake for 24 hours or missing 1 hour of sleep a night for a week result in impairment equal to a blood alcohol concentration of 0.10.[63,64] While competing when intoxicated would never be allowed, a similar risk of athletic injury might apply to fatigued athletes. Sleep deprivation has been related to decreased athletic abilities.[65] The connection was established when win-loss records on the road were examined. Athletes travelling west to east, with its greater circadian disruption and resultant fatigue, are known to lose more games than do teams travelling east to west.[66] Professional teams have begun to consult sleep experts for advice on how to adjust their sleep schedules when travelling, with anecdotal improvement in performance.[67] To date, the impact of sleep loss and fatigue on sport injury rates has not been studied. Nevertheless, the greater disordered sleep and heightened fatigue in young women would be predicted to increase their injury risk. 2.4 Substance Use

Despite the public’s perception of the ‘allAmerican’ athlete, those in sports are not proª 2010 Adis Data Information BV. All rights reserved.

tected from substance use and abuse. Objective assessment of high school athletes reveals that their rates of alcohol and other drug use (other than tobacco use, which is reduced among female athletes) are comparable to non-athletic classmates.[68-70] Recent national surveys indicate that 45% of high school students drank alcohol in the previous month, and 24% of females had an episode of heavy drinking during that interval. In addition, more than one-third of female high school students had used marijuana, with 17% using it within the last 30 days.[71] Alcohol and other drug use may predispose young athletes to injury, as they impair coordination and the ability to perceive and respond to hazards.[72-74] The association of substance use, in particular alcohol, and adult work-related injury is clear, and that relationship is also present for adolescent workers.[75-78] Females appear more susceptible to the CNS effects of alcohol,[79] and for both alcohol[74] and marijuana[80] those adverse effects can persist beyond acute intoxication.[81] In addition, the toxic effects of alcohol can accentuate muscle damage,[82] which may be especially harmful for females – as a result of the potential neuromuscular contribution to ACL injuries. Perhaps because athletes are inappropriately assumed to not use drugs, the relationship between substance use and sport injuries has not been explored. 2.5 Stress and Psychological Issues

There is a recognized connection between ‘stress’ and injuries,[83-85] presumably due to stress causing alterations in attention, decision making and muscular tension. However, clarifying that connection is problematic because of the multiple components of stress, imprecision in its indexing and the necessary time lag between its assessment and subsequent injuries.[86] Among adolescents, stress has been deconstructed as primarily relating to the emotional states of anxiety, depression and self-esteem, with lesser contributions due to home life, school and peer relationships.[87] That relationship also holds for athletes.[88] In general, girls appear more vulnerable to stress than boys.[87,89] Sports Med 2010; 40 (5)

Expanded Model of ACL Injuries

Throughout adolescence and adulthood, females experience more psychological distress than males. Females have double the male rate of depression.[47,90] As a single factor, depression has been related to a greater likelihood of sport trauma.[91] Young females also have higher levels of anxiety[53] and their self-esteem decreases more than among their male classmates.[92,93] Lower selfesteem appears to increases sport injury risk.[94,95] Only a few studies have examined stress reduction and injury prevention, and then only in select groups of athletes using relatively intense interventions. Johnson et al.[96] reviewed existing stress reduction and injury trials in gymnasts,[97] elite alpine skiers,[98] marathoners,[99] collegiate swimmers and NCAA football players[100] and presented their own findings in male competitive soccer players. In general, beneficial effects are inconsistent and modest, and no studies have focused on female high school student athletes. 3. An Expanded Injury Model and Prevention Paradigm 3.1 Limitations in the Existing Model

Current ACL injury models include factors in the domains of intrinsic risk factors (e.g. age, gender, anatomy, postural stability and mechanics) and extrinsic or external factors (e.g. protective sport equipment and weather conditions).[3,101] That model has been used to design and assess ACL injury prevention programmes. Several comprehensive reviews and meta-analyses have been published summarizing the results of those trials.[4,8,102-108] In general, well-designed multicomponent programmes have demonstrated a reduction in injuries. Training components typically involve strength and neuromuscular conditioning, plyometrics and agility training; programmes with efficacy usually begin before and continue throughout the season. The number needed to treat to prevent an ACL injury is estimated at 65,[106] which is a favourable ratio and would argue for widespread use of these efforts. However, to date, the translation of smaller scale efficacy to more widespread effectiveness has been limited, and the programmes have limited reach among collegiate ª 2010 Adis Data Information BV. All rights reserved.

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athletes and even less in high school athletes;[107,108] they also require high compliance for efficacy,[109] and a potential deterrent for implementation is that, despite the time required, they may not result in general sport performance improvements.[110] Despite extensive efforts to understand and prevent knee injuries, neither their overall rate nor the gender disparity has diminished.[111,112] 3.2 Factors in an Expanded Model

We propose expending the injury model to incorporate additional determinants that extend beyond knee injury in the female athletes to include her lifestyle and psychological state. The hypothetical model is presented in figure 1. The items traditionally included in ACL injury models are included in the ellipses.[3,101,106] This expanded model provides new avenues for identification of those at risk and potentially benefits athletes in addition to injury prevention. 3.3 A Paradigm to Prevent Injuries and Improve Health

Widening the lens on knee injuries allows adding components that focus on lifestyle habits and psychological well-being, with the potential to provide a skill set that will also have utility off the playing field. School sport teams are natural settings where bonded peers and an influential coach interact, and they can be effective vehicles for altering attitudes and habits in adolescents. The ATLAS (Athletes Training & Learning to Avoid Steroids) and ATHENA (Athletes Targeting Healthy Exercise & Nutrition Alternatives) programmes are genderspecific sport team-centered harm reduction/health promotion curricula, which are integrated into a team’s usual practice activities. Both programmes were developed and studied with the National Institutes of Health funding, and their efficacy in deterring performance enhancing drug use and other health-harming behaviours were proven in randomized controlled trials.[113-117] Subsequent longterm study of ATHENA programme participants indicated durable positive changes. One to three years following high school graduation, compared with control athletes, intervention-ATHENA graduates reported significantly less lifetime use of Sports Med 2010; 40 (5)

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Age Physical fitness Anatomy (alignment) Prior injury Skill levels

Restrictive dietary habits Carbohydrate intake Calcium intake Disordered eating

Inadequate sleep Fatigue

Biomechanical influences and coordination

Sport specialization Overtraining Burnout

ACL injury Alertness

Stress (depression, anxiety, low self-esteem) Performance climate Sport factors (rules, coaching) Equipment (shoes) Environment (weather, surface)

Substance use, alcohol, marijuana

Fig. 1. An expanded hypothetical model of injury. Injury-promoting factors discussed in the text are enclosed in rectangles, and their potential interactions are indicated by the double-headed arrows. Items in traditional models of anterior cruciate ligament (ACL) injuries are represented in the ellipses.

ª 2010 Adis Data Information BV. All rights reserved.

4. Conclusion Each year, high school athletes experience more than two million injuries; findings from the Injury Cost Model of the US Consumers Product Control Intervention 0.38 Rate self-reported injury in last 3 mo

cigarettes, marijuana and alcohol (odds ratios [95% CI] of 0.52 [0.28, 0.94], 0.38 [0.18, 0.79], 0.55 [0.36, 0.84], respectively).[117] The ATHENA programme was designed to reduce disordered eating and body shaping drug use, and its curriculum included healthy eating habits for sport performance, cognitive restructuring to prevent depression and peer communication abilities to enhance self-esteem.[116] Neuromuscular conditioning or sport-specific skills were not an ATHENA component, yet we observed that intervention participants experienced half the self-reported injuries of control student athletes (figure 2).[115] Our findings alerted us to how secular trends in injury-promoting influences, amenable to preventive interventions, may be contributing to the injury epidemic among young female athletes. Sport team-centered injury reduction programmes could be enhanced with components related to nutrition, sleep, substance use and sport psychology, all of which are aspects relevant to athletic performance (and potentially injury reduction), but also providing life skills that could benefit student athletes after their sport seasons.

* p < 0.05

0.36 0.34 0.32 0.30 0.28 0.26 0.24 Pre-season injury rate

Post-season injury rate

Fig. 2. Mean number of self-reported injuries in the last 3 months by control and ATHENA (Athletes Targeting Healthy Exercise & Nutrition Alternatives) curriculum participants prior to the season and immediately following the sport season. Post-season injuries differed at p < 0.05,[115] using an ANCOVA-based approach within the Generalized Estimating Equations random effects model framework.

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Expanded Model of ACL Injuries

Safety Commission in 2003 indicated that annually almost $600 million in direct medical expenses resulted from injuries in the top five school sports alone.[105] Certain problems, such as ACL tears, are more frequent among young female athletes.[2] Current models of prevention and the aetiology of ACL injuries are focused on biomechanical factors relating to the knee, proprioception and neuromuscular conditioning. However, female equality in sport participation has occurred coincident with social pressures and lifestyle trends that may predispose to injury: sport specialization, unhealthy dietary behaviours, lack of sleep, and increases in substance use and abuse. Young women may be particularly at risk for those influences. In addition, females have a higher prevalence of low self-esteem, anxiety and depression, each of which relate to greater injury risk. Broadening the model of ACL injury to include those latter components, in addition to the training components of the current knee protection programmes, adds the potential of addressing factors besides landing mechanics and muscle balance. Typical health class curricula for high school health promotion have limited efficacy, as teacher authority diminishes, peer influences increase and gender differences emerge.[118] However, sport teams are natural same-sex settings where bonded youth meet longitudinally with an influential adult. We propose a paradigm shift in thinking about knee injuries, with greater recognition of the athlete’s lifestyle and psychological state as injury aetiological factors. An expanded injury model provides new prevention directions. Developing and evaluating the efficacy of a curriculum with a wider focus might achieve greater traction among coaches and provide young women with abilities that would continue to serve them off the playing field. Acknowledgements Funding for this review was supported in part by the Research Center for Gender-Based Medicine at Oregon Health & Science University. ATLAS and ATHENA are programmes on the Substance Abuse and Mental Health Services Administration’s National Registry of Evidence-

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based Programs and Practices, and they are distributed through the Center for Health Promotion Research at Oregon Health & Science University (OHSU). OHSU and Drs Elliot and Goldberg have a financial interest from the sale of those technologies. This potential conflict of interest has been reviewed and managed by the OHSU Conflict of Interest in Research Committee. Dr Kuehl has reported no conflicts of interest that are directly relevant to the content of this review.

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Correspondence: Dr Diane L. Elliot, Division of Health Promotion & Sports Medicine, Oregon Health & Science University CR110, 3181 SW Sam Jackson Park Road, Portland, OR 97239-3098, USA. E-mail: [email protected]

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REVIEW ARTICLE

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The Efficacy of Foot Orthoses in the Treatment of Individuals with Patellofemoral Pain Syndrome A Systematic Review Christian J. Barton,1,2 Shannon E. Munteanu,2,3 Hylton B. Menz2 and Kay M. Crossley4,5 1 School of Physiotherapy, Faculty of Health Sciences, La Trobe University, Bundoora, Victoria, Australia 2 Musculoskeletal Research Centre, Faculty of Health Sciences, La Trobe University, Bundoora, Victoria, Australia 3 Department of Podiatry, Faculty of Health Sciences, La Trobe University, Bundoora, Victoria, Australia 4 Mechanical Engineering, University of Melbourne, Parkville, Victoria, Australia 5 School of Physiotherapy, University of Melbourne, Parkville, Victoria, Australia

Contents Abstract. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 377 1. Methods. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 379 1.1 Inclusion and Exclusion Criteria. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 379 1.2 Search Strategy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 379 1.3 Review Process . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 379 1.4 Quality Assessment of Reviews . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 380 1.5 Data Extraction and Analysis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 381 2. Results . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 381 3. Discussion. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 385 3.1 Quality Assessment and Considerations for Interpretation of Findings . . . . . . . . . . . . . . . . . . . . . . 386 3.2 Current Evidence . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 389 3.3 Possible Mechanisms for Foot Orthoses Efficacy in Individuals with Patellofemoral Pain Syndrome 389 3.4 Prescription Considerations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 391 3.5 Clinical Implications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 391 3.5.1 Foot Orthoses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 391 3.5.2 Foot Orthoses or Physiotherapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 391 3.5.3 Combining Foot Orthoses and Physiotherapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 392 3.6 Future Research Directions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 392 4. Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 392

Abstract

Patellofemoral pain syndrome (PFPS) is a highly prevalent condition, often reducing functional performance and being linked to osteoarthritis development later in life. Prescribing foot orthoses is often advocated, although the link between foot mechanics and PFPS development remains unclear. This systematic review was conducted to summarize and critique the existing evidence for the efficacy of foot orthoses in individuals with PFPS and to provide guidance for future research evaluating foot orthoses in

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individuals with PFPS. A comprehensive search of MEDLINE, EMBASE, CINAHL and Current Contents revealed 138 citations for review. Two of the authors independently reviewed and assessed each citation for inclusion and quality using a modified version of the quality assessment scale for randomized controlled trials in PFPS designed by Bizzini and colleagues. A total of seven studies were included in the final review. The review found limited evidence that prefabricated foot orthoses may reduce the range of transverse plane knee rotation and provide greater short-term improvements in individuals with PFPS compared with flat inserts. Findings also indicated that combining physiotherapy with prefabricated foot orthoses may be superior to prefabricated foot orthoses alone. Further research is now needed to establish the mechanisms behind the efficacy of foot orthoses and to identify individuals with PFPS who are most likely to benefit from prescription of foot orthoses. A comparison of the efficacy between prefabricated and customized foot orthoses is also needed.

Patellofemoral pain syndrome (PFPS) is the most common diagnosis of knee pain found in orthopaedic[1,2] and sports medicine clinics.[3-5] It is defined by the presence of pain in the retropatellar or peripatellar region during tasks that increase patellofemoral joint (PFJ) loading.[6] Aggravating tasks include walking, running, ascending/descending stairs/slopes, squatting, prolonged sitting and kneeling.[7,8] PFPS commonly develops insidiously[8,9] and is frequently observed in adolescents and young adults.[8,10,11] The condition has been reported to reduce functional performance[12,13] and result in persistent symptoms for one in four individuals at a mean of 16 years following initial presentation.[14] Because of the impact of PFPS on functional performance, its potential to contribute to osteoarthritis development later in life[15,16] and its high prevalence rate, the availability of effective management strategies is important to all healthcare practitioners. The aetiology of PFPS is considered multifactorial, with both intrinsic and extrinsic factors thought to contribute. Extrinsic factors may include excessive training load and/or inappropriate footwear.[8] Intrinsic factors can be divided into local (around the knee), proximal (thigh, hip, pelvis and trunk) and distal (foot and lower leg) components.[8] One long-standing, intrinsic aetiological consideration in PFPS has been abnormal motion of the foot. Tiberio[17] hypothesized that excessive or prolonged pronation of the foot may ª 2010 Adis Data Information BV. All rights reserved.

lead to increased tibial and femoral internal rotation, subsequently resulting in greater lateral PFJ stress due to an increased knee valgus and quadriceps (Q) angle. However, evidence from studies assessing the association of foot structure and mechanics with PFPS is equivocal. While some case-control studies have reported increased foot mobility[18] and a more valgus rear foot in relaxed stance[19] in individuals with PFPS, others have reported no significant difference in foot posture.[20-22] Dynamically, increased rear foot eversion at heel strike and delayed timing of peak rear foot eversion in individuals with PFPS has been observed during walking[23-25] and running.[20,26] In contrast, prospective studies investigating the relationship of the foot with PFPS development have failed to confirm posture or function of the foot as an independent risk factor.[27,28] The equivocal nature of previous research evaluating the association of the foot with PFPS development may be due to the multifactorial nature of the condition. It may be that there are subgroups of people in whom foot and ankle characteristics have contributed to PFPS development. However, other subgroups may have greater contributions from more proximal characteristics such as alignment and/or functional deficiencies of the hip and PFJ itself.[7,29] Based on the belief that foot orthoses may correct more proximal alignment and functional deficiencies Sports Med 2010; 40 (5)

Foot Orthoses in Patellofemoral Pain Syndrome

(i.e. increased tibial/femoral internal rotation and associated Q angle) in the presence of abnormal foot motion, their provision continues to be advocated in journal literature[7,29] and sports medicine texts.[8] Although correction of abnormal lower limb internal rotation in the presence of excessive pronation is the long-standing hypothesis for the mechanism of foot orthoses effectiveness,[7,29] the validity of this hypothesis remains unclear.[30,31] More recently, alternative hypotheses for the efficacy of foot orthoses in PFPS treatment have been proposed, including enhanced activation of the vasti and gluteal musculature as a result of improved plantar cutaneous afferent feedback,[32] and reduced lower limb muscle activity and joint moments through to enhanced footwear comfort and facilitation of preferred movement pathways.[33] We recently identified the need for an up-todate systematic review evaluating the efficacy of foot orthoses in the treatment of PFPS.[34] Therefore, the aim of this systematic review was to: (i) summarize and critique the existing evidence for the use of foot orthoses in the treatment of PFPS; (ii) summarize and discuss evidence for proposed mechanisms that may contribute to the effectiveness of foot orthoses in individuals with PFPS; and (iii) provide guidance for future research evaluating the efficacy of foot orthoses in the treatment of PFPS. 1. Methods 1.1 Inclusion and Exclusion Criteria

Studies evaluating foot orthoses in the treatment of individuals with PFPS without language restriction were considered for inclusion. The inclusion criteria required participants to be described as experiencing: retropatellar, peripatellar, or patellofemoral pain; anterior knee pain; patella or patello-femoral dysfunction; chondropathy; or chondromalacia patellae. Studies that reported inclusion of participants with concomitant injury or pain from structures other than the PFJ were excluded. This included internal derangement, knee ligament insufficiency, previous knee surgery, patellar tendinopathy, Osgood Schlatª 2010 Adis Data Information BV. All rights reserved.

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ter’s disease, fat pad inflammation or PFJ instability. Non-peer-reviewed and single-participant design publications were also excluded. Outcome measures of interest included: (i) symptom reduction including pain and stiffness; (ii) function including functional outcome measures, disability and ability to complete functional tasks (e.g. ascend/descend stairs, run, squat, etc.); (iii) patient satisfaction; and (iv) lower limb alignment, kinematics, kinetics, muscle activity, ease of functional tasks and footwear comfort. 1.2 Search Strategy

MEDLINE, EMBASE, CINAHL and Current Contents electronic databases were searched without language restriction in December 2008. A search strategy with keywords related to diagnosis was taken and modified from the Cochrane systematic review on exercise therapy for PFPS.[35] This was used in all databases. To narrow the search, the following keywords were explored in database search tools: ‘orthotic’, ‘orthoses’ and ‘orthosis’. The search strategy and results are reported in table I. The Cochrane Musculoskeletal Injuries Group register, Cochrane Database of Systematic Reviews and PEDro were searched following the initial database search using the keywords ‘patella’, ‘patellofemoral’, ‘anterior knee pain’ and ‘chondromalacia patellae’. Following electronic searches, references of included studies were screened for additional relevant studies. A cited reference search in PubMed for each of the authors’ studies found was conducted and the terms ‘patellofemoral pain syndrome’, ‘anterior knee pain’ and ‘chondromalacia patellae’ were searched in the Web of Science. 1.3 Review Process

All titles and abstracts found were downloaded into Endnote version 9 (Thomson Reuters, Philadelphia, PA). The set was cross-referenced and any duplicates were deleted. Each title and abstract was evaluated and reviewed independently for potential inclusion by two of the authors (CJB and SEM) using a checklist developed from the inclusion/exclusion criteria. If insufficient information was contained in the title Sports Med 2010; 40 (5)

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Table I. Search strategy and results from each included database Keywords

MEDLINE

EMBASE

Current contents

CINAHL

Arthralgia/ or pain, mp

317 517

313 234

170 210

75 714

40 800

10 719

0

15 051

5 724

1 676

0

3 565

581

541

524

200

{(patell$ or femoropatell$ or femoro-patell$ or retropatell$) adj [pain or syndrome or dysfunction]}, mp

1 160

1 150

802

970

{(lateral compression or lateral facet or lateral pressure or odd facet) adj [pain or syndrome or dysfunction]}, mp

17

17

8

378

839

251

Knee joint/ or knee/ or patella/ 1 and 2 Anterior knee pain, mp

{(chondromalac$ or chondropath$) adj [knee$ or patell$ or femoropatell$ or femoro-patell$ or retropatell$]}, mp or/3–7

6 734

3 642

1 339

87 200

Orthotica

1 203

1 310

619

3 592

Orthosesa

1 490

3 261

899

3 636

Orthosisa

5 115

3 351

1 050

3 620

or/9–11

1 490

4 505

1 980

3 865

77

57

37

68

8 and 12 a

Keywords explored using the search tools for each database.

mp = title, original title, abstract, name of substance word, subject heading word.

and abstract to make a decision on a study, it was retained until the full text could be obtained for evaluation. Any disagreements regarding the studies were resolved by a consensus meeting between the two authors. If this failed to resolve the issue, the third author (HBM) was consulted to evaluate the study of concern. 1.4 Quality Assessment of Reviews

Criteria for the quality assessment scale were taken and modified from Bizzini et al.,[36] who developed a quality assessment scale for randomized clinical trials (RCTs) for PFPS (please see the appendix, Supplemental Digital Content 1, at http://links.adisonline.com/SMZ/A3). The original scale was modified by simplifying the scoring system from a 100-point scale to a 40point scale and applying more strict definitions to scoring allocations. These modifications were made to decrease the ambiguity of scoring allocations in an attempt to improve reliability of individual items that scored only moderate inter-rater reliability (i.e. intraclass correlation coefficients [ICCs] 0.50–0.75) in the original scale (particiª 2010 Adis Data Information BV. All rights reserved.

pant inclusion criteria, homogeneity between groups and description of interventions).[36] The item relating to the adequate number of participants was also modified to improve its validity. The original scale required at least 25 participants in each group to score full points.[36] However, the authors of this review felt that the inclusion of a sample size calculation was more valid. Similar item weightings were retained from the original publication.[36] The modified scale consisted of 14 items divided into four components. The four components included: participants, interventions, outcome measures and data presentation and analysis, with each containing a maximum allocation of 10 points. Whilst the original purpose of the scale was to assess the quality of RCTs, it was applied to all identified studies with the omission of irrelevant items for the various study designs (e.g. homogeneity between groups was not applied to studies containing only one group). This meant that RCTs were scored out of 40, case series studies out of 36, clinical prediction rule studies out of 26 and studies relating to effects on theoretical mechanisms of efficacy out of 32. The modified Sports Med 2010; 40 (5)

Foot Orthoses in Patellofemoral Pain Syndrome

scale was applied by two of the authors (CJB and SEM) independently to each included study. Any score differences were discussed until consensus could be reached. If consensus could not be reached, the third author was consulted to resolve the issue (HBM). The inter-rater reliability of the quality assessment scale was evaluated using percentage agreement statistics for each individual item. These data would normally be more suited to a weighted kappa statistic. However, not all items were applicable to all included studies, meaning some items contained an inadequate number of comparisons to validate the use of a weighted kappa statistic (i.e. as low as two comparisons).[37] To evaluate the inter-reliability of each of the four components and the overall score, ICC2,1 and percentage agreements were calculated.[37] 1.5 Data Extraction and Analysis

Study types (e.g. RCT), groups/comparisons and sample sizes, population sources, primary outcome measures, participant inclusion/exclusion criteria and participant age and sex were extracted from each included study to assist the interpretation of included findings. Means and standard deviations for all baseline and follow-up (i.e. immediate, short, medium and/or long term) continuous data from each study were extracted to allow effect size calculations (with 95% confidence intervals [CIs] and significance using two-tailed t-tests without correction). If included studies had made corrections of their statistical significance levels to account for multiple comparisons, effect size CIs were adjusted accordingly (e.g. 99% CIs were used for p < 0.01). Effect sizes and CIs were then entered into forest plots to allow easy visual comparison. Categorical data (i.e. success rate comparisons between different interventions) were presented and compared between studies using relative risk reductions (RRR) and number needed to treat (NNT) calculations. RRR calculations were also entered into forest plots to allow visual comparison. If inadequate data were available from the original studies to complete effect size or RRR calculations, attempts were made via email and/ ª 2010 Adis Data Information BV. All rights reserved.

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or post to contact the authors of the studies for additional data. Determining the level of evidence available from the current literature was based on a predetermined rating system, which has been used in a previous PFPS systematic review.[35] The rating system is outlined below (note that the definition of an RCT included randomized clinical trials that contained an alternative treatment rather than a control group):  Strong evidence: provided by generally consistent findings in multiple high quality RCTs.  Moderate evidence: provided by generally consistent findings in one high quality RCT and one or more low quality RCTs, or by generally consistent findings in controlled clinical trials (CCTs – studies that contain a control group but group allocation is not randomized, e.g. use of a waiting list control).  Limited evidence: provided by only one RCT (either high or low quality) or generally consistent findings in CCTs.  Conflicting evidence: inconsistent findings in multiple RCTs and CCTs.  No evidence: no CCTs or RCTs. 2. Results The initial search yielded 138 citations. Following application of the inclusion/exclusion criteria to each citation, the number was reduced to 11,[38-48] and after viewing full texts, the final yield was seven.[38-44] Two studies by Saxena and Haddad[45,46] were omitted because they contained participants with degenerative joint disease, iliotibial band syndrome and plica pathology; Neptune et al.[47] was omitted because it contained only asymptomatic participants; and MacLean et al.[48] was omitted because it did not contain an adequate case definition of PFPS. Consensus was reached on all decisions independently by the two authors without the need for a review by the third author. The final yield included two randomized clinical trials (i.e. contained an alternative comparison treatment as a control group),[38,44] three case series studies,[40-42] one clinical prediction rule study,[43] and one study on the effects of foot orthoses on lower limb kinematics.[39] The quality Sports Med 2010; 40 (5)

Study

1.1 IC (/2)

1.2 EC (/2)

1.3 Ad. no. (/4)

1.4 Hom (/2)

1 Pop

2.1 S/D (/4)

2.2 C/PlA (/4)

2.3 CA (/2)

2 Int

3.1 RO (/4)

3.2 BOA (/4)

3.3 F/uA (/2)

3 OM

4.1 RD (/2)

4.2 Dropouts (/2)

4.3 ITT (/2)

4.4 SP (/4)

4 DP/A

Total score

TPS (%)

382

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Table II. Quality assessment score allocations for each included study, including subsequent inter-rater reliability for each item, component and overall score. A complete description of the scoring system related to the quality assessment scale can be found in the appendix (please see the Supplemental Digital Content)

Randomized clinical trials (/40) Collins et al.[38]

2

2

4

2

10

4

4

2

10

4

4

2

10

2

2

2

4

9

40

100

Eng and Pierrynowski[44]

2

0

2

2

6

2

4

0

6

4

0

0

4

0

2

2

3

7

23

58

Johnston and Gross[40]

1

1

2

NA

4

4

0

0

4

3

0

1

4

NA

2

2

3

7

19

53

Pitman and Jack[41]

2

0

2

NA

4

2

0

0

2

2

0

1

3

NA

0

0

0

0

9

25

Amell et al.[42]

0

0

0

NA

0

2

0

0

2

2

0

1

3

NA

0

0

0

0

5

14

2

0

NA

4

4

NA

0

4

4

NA

0

4

NA

2

NA

4

6

18

69

0

NA

NA

3

3

11

42

100

80

100

86

71

57

0.99

0.99

Case series (/36)

Clinical prediction rules (/26)

Sutlive et al.[43]

2

Effects on theoretical mechanisms of efficacy (/28)

Eng and Pierrynowski[39]

Reliability ICC2,1

0

0

NA

0

4

NA

NA

4

4

0

NA

4

86

71

100

50

57

86

80

67

86

71

100

100

71

0.94

0.96

0.98

Ad. no. = adequate number; BOA = blinded outcome assessment; CA = co-intervention avoided; C/PlA = control and placebo adequate; DP/A = data presentation and analysis; EC = exclusion criteria; F/uA = follow-up adequate; Hom = homogeneity; IC = inclusion criteria; ICC = intraclass correlation coefficient; Int = interventions; ITT = intention to treat; NA = not applicable; OM = outcome measures; Pop = population; RD = randomization described; RO = relevant outcome; S/D = standardized and described; SP = statistical procedures; TPS = total possible score.

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% agreement

0

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Table III. Participant characteristics for each included study Study

Age (y) [mean]

M/F (%)

Inclusion criteria

Exclusion criteria

Collins et al.[38]

18–40 [27.9]

44/56

18–40 y; anterior knee or retropatellar pain >6 wk duration; pain of insidious onset; pain provoked by at least two of prolonged sitting or kneeling, squatting, running, hopping or stair walking; tenderness on palpation of the patella, or pain with step down or double legged squat; worst pain in previous wk of at least 30 mm on a 100 mm VAS

Concomitant injury or pain from the hip, lumbar spine or other knee structures; previous knee surgery; patellofemoral instability; knee joint effusion; any foot condition precluding the use of foot orthoses; allergy to strapping tape; use of physiotherapy or foot orthoses within the previous y; use of anti-inflammatory drugs

Eng and Pierrynowski[44]

13–17 [14.4]

Bilateral PFPS; adolescents F; duration of signs and symptoms >6 wk; insidious onset unrelated to trauma; retropatellar tenderness on palpation, pain of patellar compression or patellar crepitus; calcaneal valgus or forefoot varus >6 in prone STJN

Previous physical therapy or orthotic treatment; leg length discrepancies >1 cm; known pathological or neurological disorders that could affect gait pattern

Johnston and Gross[40]

14–50 [25.4]

19/81

14–50 y; non-traumatic onset of anterior knee pain of at least 2 mo duration; composite score ‡200/2400 on the WOMAC osteoarthritis index; patellar facet tender on palpation; able to walk without an assistive device for at least 10 m; able to perform an unsupported unilateral squat to 45 knee flexion; active knee range of motion of 0 extension and 60 flexion; excessive foot pronation (>9 calcaneal valgus and <141 longitudinal arch angle in bilateral weight bearing)

NR

Pitman and Jack[41]

11–64 [NR]

29/71

Anterior knee pain significantly affecting athletic, vocational or avocational performance; pain associated with or preventing exercise; pain during running, hiking, stair negotiation or prolonged sitting; pain on medial patellar facet palpation; ‘miserable malalignment’ or excessive ‘Q’ angle (>10 in M or >15 in F); determination of significant foot pronation at rest and/or during a treadmill running evaluation

History of acute injury; other knee abnormalities

Amell et al.[42]

NR [28.4]

Bilateral PFPS; orthotics prescribed as treatment; F

NR

Sutlive et al.[43]

18–40 [28.1]

18–40 y; retropatellar pain provoked by either a partial squat or stair descent

Recent knee trauma; knee ligament laxity; previous surgery; history of systemic or neurological disease; reporting of stress fractures or shin splints

Eng and Pierrynowski[39]

13–17 [14.4]

Bilateral PFPS; adolescent F; duration of signs and symptoms >6 wk; insidious onset unrelated to trauma; retropetellar tenderness on palpation, pain of patellar compression or patellar crepitus; calcaneal valgus or forefoot varus >6 in prone STJN

Previous physical therapy or orthotic treatment; leg length discrepancies >1 cm; known pathological or neurological disorders that could affect gait pattern

0/100

0/100

70/30

0/100

F = female; M = male; NR = not reported; PFPS = patellofemoral pain syndrome; Q = quadriceps; STJN = subtalar joint neutral; VAS = visual analogue scale; WOMAC = Western Ontario and McMaster Universities Arthritis Index.

ª 2010 Adis Data Information BV. All rights reserved.

Sports Med 2010; 40 (5)

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assessment of each included study, along with the reliability analysis of the quality assessment scale, is given in table II. Participant characteristics from each included study are outlined in table III. Heterogeneity between study designs, participant inclusion/exclusion criteria, type of foot orthoses interventions, primary outcome measures and timepoints used, and statistical reporting made meta-analysis and statistical pooling inappropriate. Of the studies evaluating the medium to long term (‡6 weeks) effectiveness of foot orthoses, the RCT by Collins et al.[38] was the only study with adequate data to complete effect size calculations. Their study investigated a general adult PFPS population and contained flat insert (n = 44), prefabricated foot orthoses moulded and posted to optimize comfort (n = 46), 6-week multimodal physiotherapy (n = 45), and combined foot orthoses/6-week multimodal physiotherapy (n = 44) groups. Effect size, RRR and NNT calculations indicated greater patient-perceived global success in the foot orthoses group compared with the flat insert group at 6 weeks (figure 1), with the NNT calculated as four (table IV). This finding was supported by greater improvement in the

‘global improvement’ visual analogue scale in the foot orthoses group at 6 weeks (figure 2). Although trends for all outcome measures and timepoints indicated physiotherapy produced superior outcomes to foot orthoses, no significant between-group differences were identified (figure 3). Likewise, no significant differences in outcomes were identified between the foot orthoses/physiotherapy and the foot orthoses groups (figure 4). Combining physiotherapy with foot orthoses indicated significantly greater improvements compared with foot orthoses alone on the ‘Functional Index Questionnaire’ at 6 and 12 weeks and the ‘Anterior Knee Pain Scale’ at 52 weeks (figure 5). The RCT by Eng and Pierrynowski[44] investigated an adolescent female PFPS population, comparing a group completing exercise rehabilitation versus a group combining prefabricated foot orthoses prescription (posted to subtalar joint neutral) and exercise rehabilitation over 8 weeks. They reported significantly greater pain reduction during functional tasks in the foot orthoses group; however, inadequate data were available to confirm this via effect size calculations. Studies by Johnston and Gross,[40] Pitman and Jack,[41]

FO + PT vs FO (wk) 52 12 6 FO + PT vs PT (wk) 52 12 6 FO vs PT (wk) 52 12 6 FO vs FI (wk) 52 12 6 0.2

0.5 Favours alternative or stand alone treatment

1.0

2.0 Favours FO or combined treatment

4.0

Fig. 1. Between-group comparisons for patient-perceived global success (relative risk reductions calculated using number with moderate or marked improvement) results from Collins et al.[38] Effect sizes are presented with 99% confidence intervals. Black plots indicate significant findings and grey plots indicate non-significant findings. FO = foot orthoses; FI = flat inserts; PT = physiotherapy; FO + PT = foot orthoses plus physiotherapy.

ª 2010 Adis Data Information BV. All rights reserved.

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385

Table IV. Number needed to treat calculations based on the patient-perceived global success outcome measure for each group comparison and timepoint[38] Timepoint (wk)

FO vs FI 4a,b

6 12

50

b

FO vs FO + PT

14c

20c

c

b

7c

226b

33b

51

9b

52

FO + PT vs PT

FO vs PT

8

29b

a

Significant RRR calculation between groups.

b

Favours first listed intervention.

c

Favours second listed intervention.

20c

FI = flat inserts; FO = foot orthoses; PT = physiotherapy; RRR = relative risk reduction.

and Amell et al.[42] were all case series designs evaluating the effectiveness of prescribed customized foot orthoses. Each reported significant benefits to participants; however, none provided adequate data and/or appropriate outcome measures to complete statistical analysis in this systematic review. The clinical prediction rule study by Sutlive et al.[43] reported a successful outcome rate of 60% following the provision of firm prefabricated foot orthoses and activity modification in their group of 50 military recruits. Predictors reported in this study included forefoot valgus ‡2 in non-weightbearing subtalar joint neutral position, navicular drop £3 mm and relaxed calcaneal stance angle £5. These cut-off scores all produced high specificities (0.80–0.97), but low sensitivities (0.13–0.47) and poor reliability (ICCs 0.25–0.55).

The study of Eng and Pierrynowski,[39] was the only study that evaluated theoretical mechanisms of foot orthoses effectiveness. They investigated the effects of prefabricated foot orthoses posted to subtalar joint neutral on foot/ankle and knee kinematics during walking and running in a group of ten adolescent females who were successfully treated with the same prescription. Although they reported statistically significant reductions to frontal and transverse plane foot/ankle kinematics during walking and running, reduced frontal plane knee motion during walking, and greater frontal plane knee motion during running with the foot orthoses condition, effect size calculations from their data did not find differences for these variables (figure 6). However, effect size calculations did indicate a significant reduction in transverse plane motion of the knee during the contact phase of walking (figure 6d). 3. Discussion The aims of this systematic review were to summarize and critique the existing evidence for the use of foot orthoses in individuals with PFPS, discuss evidence for proposed mechanisms that may contribute to the effectiveness of foot orthoses in individuals with PFPS and provide guidance for future research relating to PFPS. A total of seven studies were found in the current systematic review. Of these studies, only two were randomized

a

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Fig. 2. (a) Functional outcome measures; and (b) visual analogue scales, for foot orthoses (FO) vs flat inserts (FI). Results from Collins et al.[38] Effect sizes are presented with 99% confidence intervals. Black plots indicate significant findings and grey plots indicate non-significant findings. AKPS = Anterior Knee Pain Scale; FIQ = Functional Index Questionnaire.

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a

b Global improvement (wk) 52 12 6 Worst pain (wk) 52 12 6 Usual pain (wk) 52 12 6

AKPS (wk) 52 12 6 FIQ (wk) 52 12 6

0 0.6 1.2 −0.6 −1.2 Less improvement Greater improvement for FO group for FO group

0 0.6 1.2 −1.2 −0.6 Less improvement Greater improvement for FO group for FO group

Fig. 3. (a) Functional outcome measures; and (b) visual analogue scales, for foot orthoses (FO) vs physiotherapy. Results from Collins et al.[38] Effect sizes are presented with 99% confidence intervals. Grey plots indicate non-significant findings. AKPS = Anterior Knee Pain Scale; FIQ = Functional Index Questionnaire.

clinical trials,[38,44] with just one scoring highly on the quality assessment scale (full points) and presenting adequate data to complete effect size and RRR/NNT calculations.[38] Of the remaining studies, three were single-group case series,[40-42] one was a clinical prediction rule study,[43] and one examined the effects of foot orthoses on lower limb kinematics.[39] 3.1 Quality Assessment and Considerations for Interpretation of Findings

The quality assessment scale was found to have excellent inter-rater reliability for each component and the total score, validating its use in the current systematic review. Compared with the original scale developed by Bizzini et al.,[36] almost

identical reliability was indicated for the modified version used in the current review (ICC = 0.99 compared with 0.97[36]). The percentage agreements for all items were ‡67% with the exception of the item relating to homogeneity between groups (item 1.4), which scored 50%. However, this value needs to be considered in the context that it was only applicable and assessed in two studies, and is still comparable with the moderate reliability (ICC < 0.75) reported in the original version of the scale.[36] Reliability of the other two items reported to have only moderate reliability in the original scale (inclusion criteria [1.1] and description of interventions [2.1])[36] appeared to be enhanced by the modified version of the scale, with high percentage agreements obtained (both 86%). The superior inter-rater

b Global improvement (wk) 52 12 6 Worst pain (wk) 52 12 6 Usual pain (wk) 52 12 6

a AKPS (wk) 52 12 6 FIQ (wk) 52 12 6 −1.2

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0

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Less improvement Greater improvement for FO + PT group for FO + PT group

−1.2

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0

0.6

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Greater improvement for FO + PT group

Fig. 4. (a) Functional outcome measures; and (b) visual analogue scales, for foot orthoses plus physiotherapy (FO + PT) vs PT. Results from Collins et al.[38] Effect sizes are presented with 99% confidence intervals. Grey plots indicate non-significant findings. AKPS = Anterior Knee Pain Scale; FIQ = Functional Index Questionnaire.

ª 2010 Adis Data Information BV. All rights reserved.

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a

b

AKPS (wk)

Global improvement (wk) 52 12 6 Worst pain (wk) 52 12 6 Usual pain (wk) 52 12 6

52 12 6 FIQ (wk) 52 12 6 1.2 0 0.6 −1.2 −0.6 Less improvement Greater improvement for FO + PT group for FO + PT group

0.6 1.2 −1.2 −0.6 0 Less improvement Greater improvement for FO + PT group for FO + PT group

Fig. 5. (a) Functional outcome measures, and (b) visual analogue scales for foot orthoses plus physiotherapy (FO + PT) vs FO. Results from Collins et al.[38] Effect sizes are presented with 99% confidence intervals. Black plots indicate significant findings and grey plots indicate nonsignificant findings. AKPS = Anterior Knee Pain Scale; FIQ = Functional Index Questionnaire.

reliability of these two items and the total score justifies the modifications made in the current review to simplify, provide greater scoring guidance and improve the validity of the original scale.[36] With the exception of the randomized clinical trial by Collins et al.,[38] which scored full points, the quality assessment scale highlighted various methodological weaknesses among the included studies. Only one[43] of the remaining six studies scored full points for the adequacy of both participant inclusion and exclusion criteria, limiting the external applicability for the conclusions in the remaining studies to a PFPS population. The varying inclusion/exclusion criteria used (table III) also made comparisons between studies difficult. Five[39-42,44] of the seven studies contained only participants with signs of excessive pronation. This is problematic, as the current review found no evidence that excessively pronated foot posture or correction of abnormal foot alignment is required to produce a successful foot orthoses prescription in individuals with PFPS. In fact, the only included clinical prediction rule study reported that a less pronated foot posture was more likely to benefit from foot orthoses intervention.[43] However, these findings need to be considered cautiously as a result of a number of methodological issues identified, including poor reliability of foot posture assessment techniques.[43] Another problem with attempting to exclude individuals who do not display signs of ª 2010 Adis Data Information BV. All rights reserved.

excessive pronation is that there is currently no consensus approach to identifying individuals with excessively pronated foot structure or function[49] and each study used a different definition or method to do so (table III). Therefore, applicability of findings from these studies is limited to a population demonstrating excessively pronated foot structure or function as measured by the chosen assessment technique for each study. Two of the studies reported included participants >40 years of age.[40,41] This may be problematic since these older individuals may possess degenerative changes in the PFJ or tibiofemoral joint and hence form a different clinical population to individuals with PFPS. With the exception of the study by Collins et al.,[38] none of the included studies completed an a priori power calculation to determine sample size; or in the case of the clinical prediction rule study,[43] it did not contain an adequate number of participants for the number of variables evaluated. All six studies scored at least ‘in part’ for the standardization and description of their interventions; however, of the five lower quality clinical trial studies,[40-44] only one possessed a control group,[44] and none adequately addressed possible co-intervention contamination. One study included a co-intervention of exercise modification and acknowledged that this may have affected the results.[43] These methodological weaknesses limit the confidence that any clinical improvements were the direct result of foot orthoses intervention Sports Med 2010; 40 (5)

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b

a Walking

Walking

Contact*

Contact

Midstance*

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Propulsion

Propulsion

Running

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Propulsion* −1.8

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Propulsion −1.8

0 0.6 1.2 1.8 −1.2 −0.6 Reduced with FO Increased with FO

1.9°

0 0.6 1.2 1.8 −1.8 −1.2 −0.6 Reduced with FO Increased with FO

Fig. 6. Results of differences in knee and ankle ranges of motion during walking and running between foot orthoses (FO) and flat inserts in the study by Eng and Pierrynowski:[39] (a) frontal plane talocrural/subtalar joint (TC/STJ) kinematics; (b) transverse plane TC/STJ kinematics; (c) frontal plane knee kinematics; and (d) transverse plane knee kinematics. Effect sizes are presented with 99% confidence intervals. Black plots indicate significant findings; grey plots indicate non-significant findings. 1.9 indicates the difference between the two groups in degrees as denoted by  – this is reported as it is a significant finding; * indicates variables reported to have statistically significant differences between groups in original study.

alone and not natural history, placebo or additional treatment either administered or sought by participants. Primary outcome measures varied greatly in type and assessment timepoints across the included studies. With the exception of Collins et al.,[38] items related to outcome measures scored poorly on the quality assessment scale. Some studies used outcome measures that have not been validated for use in a PFPS population,[40-42] and all studies either failed to complete a blinded outcome assessment or adequate follow-up. This made comparison between studies difficult and the use of meta-analysis inappropriate. Addressing these issues in future clinical trials is essential to ensuring the validity of results to clinical practice is optimized. The use of multiple (six) primary outcome measures in the RCT by Collins ª 2010 Adis Data Information BV. All rights reserved.

et al.[38] made interpretation of findings difficult, as some outcomes indicated significant group differences whilst others did not. Statistical correction in the Collins et al.[38] paper to account for potential type I errors may have also inadvertently produced some type II errors for some between-group comparisons. Randomization of intervention/condition allocation was applicable in the two randomized clinical trials[38,44] and the kinematic evaluation study,[39] but was only adequately described by the high quality randomized clinical trial.[38] The two randomized clinical trials,[38,44] the prospective case series clinical trial[40] and the clinical prediction rule study[43] scored well for dropouts, intention to treat and statistical procedures items. However, the two retrospective case series studies[41,42] scored poorly for these items because of Sports Med 2010; 40 (5)

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low questionnaire response rates and a lack of well defined outcome measures that were able to provide adequate data for statistical analysis. These weaknesses were one of the major contributors to the lower overall quality scores found for retrospective study designs when compared with prospective study designs (table II), highlighting the importance of prospective designs in future research. 3.2 Current Evidence

Evidence for the efficacy of foot orthoses in the treatment of PFPS is limited by a paucity of high quality randomized controlled (clinical) trials, with just one[38] identified in this review. Whilst there was one other randomized clinical trial,[44] this was of lower quality and failed to provide adequate data for effect size calculations. The remaining studies evaluating clinical outcomes were low quality case series study designs. A paucity of studies evaluating parameters that have been hypothesized to be associated with clinical success was identified in this review. This evidence was limited to just one study, which evaluated the effects of prefabricated foot orthoses on lower limb kinematics. Based on current literature, there is limited evidence in a PFPS population indicating that:  prefabricated foot orthoses provide greater short to medium term (6 weeks) improvements in function measured by the patient-perceived success rates and global improvement scores compared with flat inserts;[38]  adding foot orthoses intervention to physiotherapy in all individuals who present with PFPS may not significantly enhance overall clinical success;[38]  adding physiotherapy treatment to foot orthoses intervention may enhance overall clinical success, with limited evidence indicating significantly greater improvements in the Functional Index Questionnaire at 6 and 12 weeks and the Anterior Knee Pain Scale at 52 weeks;[38]  limited evidence indicates that foot orthoses may reduce transverse plane knee rotation during the contact phase of walking in individuals with PFPS.[43] ª 2010 Adis Data Information BV. All rights reserved.

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A number of gaps in the literature were identified in this review. There are no high quality randomized clinical trials that have included a group being treated with customized foot orthoses. Whilst current evidence indicates prefabricated foot orthoses may be effective, it is not clear whether the use of customized foot orthoses would have equal, lesser or greater effectiveness. The three studies included in this review that used customized foot orthoses prescription methods reported beneficial patient outcomes.[40-42] Unfortunately, none of these studies included either a control or alternative treatment group for comparison. An important consideration when using foot orthoses for the treatment of individuals with PFPS is identifying those most likely to benefit from them. Only one clinical prediction rule study[43] was identified in the current review. However, this failed to identify any cluster of predictor variables, and variables that were retained following logistic regression were reported to possess poor reliability.[43] Unfortunately, this leaves healthcare practitioners with a lack of guidance to assist clinical decision making when determining which PFPS patients are likely to benefit from foot orthoses. 3.3 Possible Mechanisms for Foot Orthoses Efficacy in Individuals with Patellofemoral Pain Syndrome

The current review identified a paucity of research explaining the mechanism(s) behind the efficacy of foot orthoses treatment in a PFPS population. Previous advocacy of foot orthoses for the treatment of PFPS has been based on the belief that they control excessive foot pronation.[7,29] In this paradigm, it is considered that reducing excessive pronation in individuals with PFPS will result in reduced internal rotation of the lower limb and hence the Q angle. Therefore, laterally directed PFJ forces and altered PFJ contact pressures that may have resulted from these abnormal alignment profiles would be reduced.[7] In their review, Fox and Grossworth[7] also hypothesized that foot orthoses may be beneficial to individuals without excessive Sports Med 2010; 40 (5)

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pronation if correction of abnormal lower extremity alignment (e.g. excessive lower limb internal rotation) is still achieved.[7] Only one study was found in the current review that examined the effects of foot orthoses on alignment or kinematics in individuals with PFPS. Eng and Pierrynowski[39] evaluated the effects of soft prefabricated foot orthoses posted to the subtalar joint neutral position on foot/ ankle and knee kinematics in ten adolescent females[39] who were successfully treated with this prescription.[44] Interestingly, effect size calculations using data from the study indicated no significant differences in range of motion at the talocrural/subtalar joints in either the frontal or transverse planes during walking or running between the orthoses and flat inserts conditions (figures 6a and 6b). However, the methodological approach used by Eng and Pierrynowski[39] may have been inadequate to evaluate and detect subtle changes in the complex kinematics of the foot and ankle. Therefore, the significance of these findings must be considered with caution. Results from the same kinematic study[39] indicated that prefabricated foot orthoses reduced transverse plane knee rotation during the contact phase of walking (figure 6d). Since there is some evidence that greater knee external rotation may be a feature of PFPS pathology, reduction of this motion may provide some partial explanation for foot orthoses effectiveness in these individuals. Considering evaluation of alignment and kinematic changes associated with successful foot orthoses intervention is limited to this single study, further research in this area is required. This should include evaluation of the effects of foot orthoses in individuals with PFPS on not only distal kinematics, but also proximal and local kinematics. Current research evaluating orthotic effects is further limited by difficulties in measuring PFJ kinematics and resultant contact forces. With the advent of newer imaging techniques (e.g. fluoroscopy, weight-bearing MRI), it may be possible to evaluate the effects of foot orthoses on PFJ kinematics and contact forces. Another possible explanation for the efficacy of foot orthoses intervention in individuals with ª 2010 Adis Data Information BV. All rights reserved.

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PFPS is that they may alter undesirable lower limb muscle activity. Previous studies have reported decreased hip musculature strength,[1,50,51] gluteus medius timing deficits[52,53] and vastus medialis oblique muscle activity timing deficits[54,55] in individuals with PFPS. Correction of vastus medialis oblique timing deficits during stair negotiation,[56] increased gluteus medius muscle activity during maximal isometric contraction,[57] and hip muscle strength training[58] have been associated with positive clinical outcomes in individuals with PFPS. Although no studies evaluating alterations to muscle activity with the addition of foot orthoses in individuals with PFPS were identified in this review, reported findings relating to asymptomatic populations are worthy of consideration. Hertel et al.[32] reported an increase in vastus medialis and gluteus medius muscle activity during single-leg squat and lateral step-down tasks with the addition of prefabricated foot orthoses in 30 young healthy adults. These changes were reported to occur regardless of posting (i.e. medial or lateral) and of participant foot type (i.e. pes planus, pes cavus and pes rectus). Therefore, the alterations observed may not have been caused by changes in foot posture or function but may have been due to changes in afferent feedback from the cutaneous plantar receptors of the foot influencing muscle activity.[32] Nigg et al.[33] have suggested that foot orthoses may reduce muscle activity and joint moments, thereby enhancing the ease of performance during functional tasks. These changes are proposed to be produced by optimizing footwear comfort, tuning muscles to dampen impact forces, and supporting a preferred movement path with the addition of a foot orthosis or insert.[33] The current review did not find any studies evaluating the effects of foot orthoses on the variables associated with this theoretical paradigm in individuals with PFPS. However, findings reported by Stefanyshyn and Hettinga[59] support the concept that reductions in joint moments using foot orthoses in individuals with PFPS may be a desirable effect. In a prospective study, they reported greater internal knee abduction moments were associated with PFPS development.[60] Sports Med 2010; 40 (5)

Foot Orthoses in Patellofemoral Pain Syndrome

Although no study has evaluated the relationship between changes in knee joint moments and treatment success in PFPS, a recent study on individuals with knee osteoarthritis reported that reductions to abnormal knee joint moments with foot orthoses were predictive of clinical success after 3 months of orthosis use.[61] Therefore, it is plausible to hypothesise that a similar effect when using foot orthoses to treat individuals with PFPS may occur.

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prescription is currently limited. Therefore, further studies using valid and reliable clinical measures are required to establish what specific features of an individual (e.g. foot posture or alignment) can predict successful outcomes with foot orthoses prescription. With this information, clinical trials can then be undertaken to evaluate the efficacy of foot orthoses for the appropriate subgroup of people with PFPS. 3.5 Clinical Implications

3.4 Prescription Considerations

Whilst Collins et al.[38] and Sutlive et al.[43] prescribed foot orthoses to all included participants regardless of foot structure and function, the remaining studies used some measure to determine the presence of a pronated foot prior to including participants. This inclusion criterion was presumably based on the assumption that the efficacy of foot orthoses is related to the control of excessive or abnormal pronation of the foot. However, the current systematic review indicates evidence to support this theoretical paradigm in a PFPS population is limited. The variable assessment approaches to categorize foot posture from the included studies highlights the lack of consensus on choice of a reliable and valid approach for foot structure and function assessment when considering foot orthoses prescription. Contrary to previous hypotheses,[17] the clinical prediction rule study by Sutlive et al.[43] indicated that military recruits with a less pronated foot posture may be more likely to benefit from prefabricated foot orthoses, possibly due to the orthoses offering some degree of enhanced shock absorption. However, low sensitivities (0.13–0.47) and poor reliability (ICC 0.25–0.55) for the identified predictor variables combined with methodological weaknesses (table II) including the provision of concurrent treatment (activity modification), means the use of these prediction rules in clinical practice may not be valid. Considering the heterogeneous presentation of individuals with PFPS, it is likely that there are subgroups of people who are more likely to respond favourably to foot orthoses. However, research to identify these subgroups and guide ª 2010 Adis Data Information BV. All rights reserved.

3.5.1 Foot Orthoses

Based on limited evidence that prefabricated foot orthoses produce positive patient outcomes as a stand-alone treatment or when combined with physiotherapy treatment, clinicians should consider their use when treating individuals with PFPS. Results from the current review indicate superior outcomes with prefabricated foot orthoses compared with flat inserts. Importantly, the NNT was low, calculated as four and nine at the 6- and 52-week time intervals, respectively (table IV). 3.5.2 Foot Orthoses or Physiotherapy

Trends for superior outcomes with physiotherapy treatment compared with foot orthoses were indicated by effect size calculations using data from Collins et al.,[38] with the functional outcome measures in particular approaching significance across all timepoints (figure 3). Obtaining significant differences between groups for improvements in function may have been limited due to the use of a more conservative p-value or inadequate power for functional outcome measures, since power calculations for this study were based on the outcome measure ‘usual pain in the previous week’. It must also be considered that estimates of both foot orthoses and physiotherapy effectiveness may be improved through identification of individuals most likely to benefit from either treatment choice. Comparing foot orthoses prescription versus physiotherapy treatment also needs to be considered in the context of cost and resource availability. The physiotherapy treatment administered in the study by Collins et al.[38] entailed weekly treatment sessions for 6 weeks with an estimated cost of $A495.[38] Sports Med 2010; 40 (5)

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In comparison, the cost of three pairs of prefabricated foot orthoses (prescription used in Collins et al.[38]) was reported to be substantially less (approximately $A174),[38] and could conceivably be administered in one session. Future clinical trials should consider cost-effectiveness evaluations of treatments administered. 3.5.3 Combining Foot Orthoses and Physiotherapy

Adding prefabricated foot orthoses to physiotherapy treatment did not appear to enhance clinical outcomes. However, as with comparing foot orthoses and physiotherapy as stand-alone treatments, identification of those most likely to benefit from foot orthoses and consideration of costs and resource availability are important in the clinical decision-making process. Adding physiotherapy treatment to foot orthoses provided greater functional improvements, with significantly greater improvements for the Functional Index Questionnaire at 6 and 12 weeks, and the Anterior Knee Pain Scale at 52 weeks.[38] Trends towards greater improvements when combining treatments were also indicated for all other outcome measures and timepoints (figure 5). This would indicate that non-physiotherapy healthcare practitioners providing prefabricated foot orthoses for the treatment of individuals with PFPS should consider referral to a physiotherapist to optimize treatment outcomes. 3.6 Future Research Directions

The current review identified a paucity of evidence to guide clinical decision making when prescribing foot orthoses for individuals with PFPS. Results from the only identified high quality RCT[38] are based on a heterogeneous PFPS population. In reality, not all patients are going to benefit equally from foot orthoses and/or physiotherapy, and some will improve regardless of the presence or absence of intervention. The efficacy of using foot orthoses may be enhanced by identifying a more specific group of individuals with PFPS who are most likely to obtain the greatest benefit. This will require the use of adequately powered clinical prediction rule studies that evaluate well developed and reliª 2010 Adis Data Information BV. All rights reserved.

able clinical measures. Consideration and evaluation of theoretical mechanisms associated with the aetiology of PFPS and foot orthoses success should be used to assist the development of clinical predictors. Variables of interest should include alterations to foot posture, lower limb alignment, lower limb kinematics and kinetics, lower limb muscle activity, pain, ease of task completion, quality of movement and footwear comfort. A lack of guidance with the large range of foot orthoses choices confronting healthcare practitioners also needs to be addressed. These choices include material density, orthotic length, provision of posting and deciding between a customized and a prefabricated device. The current review did not identify any studies that evaluated clinical outcomes with different types of foot orthoses. Due to large differences in costs and levels of expertise required to prescribe foot orthoses, a comparison of outcomes between prefabricated and customized foot orthoses in individuals with PFPS in future trials will be of considerable clinical value to healthcare practitioners who prescribe foot orthoses. To avoid identified methodological weaknesses from previous studies, it is recommended where possible that future clinical trials adhere to methodological design standards reflected in the Delphi list of criteria for the quality assessment of RCTs,[62] and report findings according to the CONSORT statement.[63] Of particular emphasis should be prospective studies using consensus inclusion and exclusion criteria for the diagnosis of PFPS during participant recruitment,[38,64] and development of valid, reliable and sensitive clinical measures to predict patient outcomes. 4. Conclusions Limited evidence exists that prefabricated foot orthoses provide greater short-term improvements in patient-perceived success in individuals with PFPS compared with flat inserts. Although limited evidence indicates prefabricated foot orthoses may reduce transverse plane knee rotation in individuals with PFPS, the mechanism Sports Med 2010; 40 (5)

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behind their effectiveness remains unclear. Limited evidence also indicates that combining physiotherapy with prefabricated foot orthoses may be superior to prefabricated foot orthoses used alone. To optimize the efficacy of foot orthoses prescription for individuals with PFPS, patient characteristics that are associated with successful outcomes and the efficacy of various prescriptive approaches need to be identified. This will require development and evaluation of potential clinical prediction rules. Research investigating the importance of modifying variables associated with theoretical foot orthosis efficacy paradigms (e.g. foot posture and function, muscle activity, comfort) and comparing different prescription approaches (e.g. prefabricated vs customized orthoses) is also needed. Acknowledgements H.B. Menz is currently a National Health and Medical Research Council of Australia fellow (Clinical Career Development Award, ID: 433049). No sources of funding were used to assist in the preparation of this review. The authors have no conflicts of interest that are directly relevant to the content of this review.

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pronation and the incidence of anterior knee pain among military recruits. J Bone Joint Surg 2006; 88-B (7): 905-8 Witvrouw E, Lysens R, Bellemans J, et al. Intrinsic risk factors for the development of anterior knee pain in an athletic population: a two-year prospective study. Am J Sports Med 2000; 28 (4): 480-9 McConnell J. The physical therapist’s approach to patellofemoral disorders. Clin Sports Med 2002 Jul; 21 (3): 363-87 Zammit GV, Payne CB. Relationship between positive clinical outcomes of foot orthotic treatment and changes in rearfoot kinematics. J Am Podiatr Med Assoc 2007 May-Jun; 97 (3): 207-12 Payne CB. The past, present, and future of podiatric biomechanics. J Am Podiatr Med Assoc 1998 Feb; 88 (2): 53-63 Hertel J, Sloss BR, Earl JE. Effect of foot orthotics on quadriceps and gluteus medius electromyographic activity during selected exercises. Arch Phys Med Rehabil 2005 Jan; 86 (1): 26-30 Nigg BM, Nurse MA, Stefanyshyn DJ. Shoe inserts and orthotics for sport and physical activities. Med Sci Sports Exerc 1999 Jul; 31 (7 Suppl.): S421-8 Barton CJ, Webster KE, Menz HB. Evaluation of the scope and quality of systematic reviews on nonpharmacological conservative treatment for patellofemoral pain syndrome. J Orthop Sports Phys Ther 2008 Sep; 38 (9): 529-41 Heintjes E, Berger M, Bierma-Zeinstra S, et al. Exercise therapy for patellofemoral pain syndrome. Cochrane Database Syst Rev 2003; (4): CD003472 Bizzini M, Childs JD, Piva SR, et al. Systematic review of the quality of randomized controlled trials for patellofemoral pain syndrome. J Orthop Sports Phys Ther 2003; 33 (1): 4-20 Portney L, Watkins C. Foundations of clinical research: applications to practice. 2nd ed. Upper Saddle River (NJ): Prentice-Hall, 2000 Collins N, Crossley K, Beller E, et al. Foot orthoses and physiotherapy in the treatment of patellofemoral pain syndrome: randomised clinical trial. Br Med J 2008; 337: a1735 Eng JJ, Pierrynowski MR. The effect of soft foot orthotics on three-dimensional lower-limb kinematics during walking and running. Phys Ther 1994 Sep; 74 (9): 836-44 Johnston LB, Gross MT. Effects of foot orthoses on quality of life for individuals with patellofemoral pain syndrome. J Orthop Sports Phys Ther 2004 Aug; 34 (8): 440-8 Pitman D, Jack D. A clinical investigation to determine the effectiveness of biomechanical foot orthoses as initial treatment for patellofemoral pain syndrome. J Prosthet Orthot 2000; 12 (4): 110-6 Amell TK, Stothart JP, Kumar S. The effectiveness of functional foot orthoses as a treatment for patellofemoral stress syndrome: the clients’ perspective. Physiother Can 2000; 52 (2): 153-7 Sutlive TG, Mitchell SD, Maxfield SN, et al. Identification of individuals with patellofemoral pain whose symptoms improved after a combined program of foot orthosis use and modified activity: a preliminary investigation. Phys Ther 2004 Jan; 84 (1): 49-61 Eng JJ, Pierrynowski MR. Evaluation of soft foot orthotics in the treatment of patellofemoral pain syndrome, includ-

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ing commentary by Maffulli N with author response. Phys Ther 1993; 73 (2): 62-70 Saxena A, Haddad J. The effect of foot orthoses on patellofemoral pain syndrome. Lower Extremity 1998; 5 (2): 95-102 Saxena A, Haddad J. The effect of foot orthoses on patellofemoral pain syndrome. J Am Podiatr Med Assoc 2003 Jul-Aug; 93 (4): 264-71 Neptune RR, Wright IC, van den Bogert AJ. The influence of orthotic devices and vastus medialis strength and timing on patellofemoral loads during running. Clin Biomech 2000 Oct; 15 (8): 611-8 MacLean CL, Davis IS, Hamill J. Short- and long-term influences of a custom foot orthotic intervention on lower extremity dynamics. Clin J Sport Med 2008 Jul; 18 (4): 338-43 Razeghi M, Batt ME. Foot type classification: a critical review of current methods. Gait Posture 2002 Jun; 15 (3): 282-91 Robinson RL, Nee RJ. Analysis of hip strength in females seeking physical therapy treatment for unilateral patellofemoral pain syndrome. J Orthop Sports Phys Ther 2007; 37 (5): 232-8 Bolgla LA, Malone TR, Umberger BR, et al. Hip strength and hip and knee kinematics during stair descent in females with and without patellofemoral pain syndrome. J Orthop Sports Phys Ther 2008 Jan; 38 (1): 12-8 Cowan SM, Crossley KM, Bennell KL. Altered hip and trunk muscle function in individuals with patellofemoral pain. Br J Sports Med 2008 Oct 9; 43 (8): 584-8 Brindle TJ, Mattacola C, McCrory J. Electromyographic changes in the gluteus medius during stair ascent and descent in subjects with anterior knee pain. Knee Surg Sports Traumatol Arthrosc 2003 Jul; 11 (4): 244-51 Cowan SM, Bennell KL, Hodges PW, et al. Delayed onset of electromyographic activity of vastus medialis obliquus relative to vastus lateralis in subjects with patellofemoral pain syndrome. Arch Phys Med Rehabil 2001 Feb; 82 (2): 183-9 Cowan SM, Hodges PW, Bennell KL, et al. Altered vastii recruitment when people with patellofemoral pain syndrome complete a postural task. Arch Phys Med Rehabil 2002 Jul; 83 (7): 989-95 Cowan SM, Bennell KL, Crossley KM, et al. Physical therapy alters recruitment of the vasti in patellofemoral pain syndrome. Med Sci Sports Exerc 2002 Dec; 34 (12): 1879-85 Nakagawa TH, Muniz TB, Baldon M, et al. The effect of additional strengthening of hip abductor and lateral rotator muscles in patellofemoral pain syndrome: a randomized controlled pilot study. Clin Rehabil 2008 Dec; 22 (12): 1051-60 Mascal CL, Landel R, Powers C. Management of patellofemoral pain targeting hip, pelvis, and trunk muscle function: 2 case reports. J Orthop Sports Phys Ther 2003 Nov; 33 (11): 647-60 Stefanyshyn DJ, Hettinga BA. Running injuries and orthotics. Int Sport Med J 2006; 7 (2): 109-19 Stefanyshyn DJ, Stergiou P, Lun VMY, et al. Knee angular impulse as a predictor of patellofemoral pain in runners. Am J Sports Med 2006 Nov; 34 (11): 1844-51

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61. Hinman RS, Payne C, Metcalf BR, et al. Lateral wedges in knee osteoarthritis: what are their immediate clinical and biomechanical effects and can these predict a three-month clinical outcome? Arthritis Rheum 2008 Mar 15; 59 (3): 408-15 62. Verhagen AP, de Vet HC, de Bie RA, et al. The Delphi list: a criteria list for quality assessment of randomized clinical trials for conducting systematic reviews developed by Delphi consensus. J Clin Epidemiol 1998 Dec; 51 (12): 1235-41 63. Altman DG, Schulz KF, Moher D, et al. The revised CONSORT statement for reporting randomized trials:

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explanation and elaboration. Ann Intern Med 2001 Apr 17; 134 (8): 663-94 64. Crossley K, Bennell K, Green S, et al. Physical therapy for patellofemoral pain: a randomized, double-blinded, placebo-controlled trial. Am J Sports Med 2002 Nov-Dec; 30 (6): 857-65

Correspondence: Mr Christian J. Barton, Musculoskeletal Research Centre, Faculty of Health Sciences, La Trobe University, Bundoora, Victoria 3086, Australia. E-mail: [email protected]

Sports Med 2010; 40 (5)

REVIEW ARTICLE

Sports Med 2010; 40 (5): 397-415 0112-1642/10/0005-0397/$49.95/0

ª 2010 Adis Data Information BV. All rights reserved.

Resistance Training in the Treatment of the Metabolic Syndrome A Systematic Review and Meta-Analysis of the Effect of Resistance Training on Metabolic Clustering in Patients with Abnormal Glucose Metabolism Barbara Strasser,1 Uwe Siebert2,3,4 and Wolfgang Schobersberger1 1 University for Health Sciences, Medical Informatics and Technology, Institute for Sport Medicine, Alpine Medicine and Health Tourism, Hall i. T., Austria 2 Department of Public Health, Medical Decision Making and Health Technology Assessment, UMIT-University for Health Sciences, Medical Informatics and Technology, Hall i. T., Austria 3 Cardiovascular Research Program, Institute for Technology Assessment and Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA 4 Program in Health Decision Science, Department of Health Policy and Management, Harvard School of Public Health, Boston, Massachusetts, USA

Contents Abstract. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1. The Metabolic Syndrome (MS) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2. Epidemiology of the MS. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3. Overview: Resistance Training (RT) and Metabolic Risk. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4. Impaired Glucose Regulation and Type 2 Diabetes Mellitus: A Meta-Analysis . . . . . . . . . . . . . . . . . . . 4.1 Methods of the Meta-Analysis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.1.1 Literature Search . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.1.2 Inclusion Criteria. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.1.3 Assessed Outcomes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.1.4 Data Extraction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.1.5 Statistical Analysis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.2 Results of the Meta-Analysis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.2.1 Included Studies and Study Characteristics. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.2.2 Study Quality . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.2.3 Pooled Effects of RT . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.2.4 Heterogeneity and Dose-Response Relationship . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.2.5 Publication Bias . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.3 Discussion of the Meta-Analysis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.3.1 Using RT as a Treatment for Glycaemic Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.3.2 Impact on MS Risk Modification. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.3.3 Dose Response: How Much RT is Needed? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5. Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

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Abstract

Over the last decade, investigators have given increased attention to the effects of resistance training (RT) on several metabolic syndrome variables. The metabolic consequences of reduced muscle mass, as a result of normal aging or decreased physical activity, lead to a high prevalence of metabolic disorders. The purpose of this review is: (i) to perform a meta-analysis of randomized controlled trials (RCTs) regarding the effect of RT on obesityrelated impaired glucose tolerance and type 2 diabetes mellitus; and (ii) to investigate the existence of a dose-response relationship between intensity, duration and frequency of RT and the metabolic clustering. Thirteen RCTs were identified through a systematic literature search in MEDLINE ranging from January 1990 to September 2007. We included all RCTs comparing RT with a control group in patients with abnormal glucose regulation. For data analysis, we performed random effects meta-analyses to determine weighted mean differences (WMD) with 95% confidence intervals (CIs) for each endpoint. All data were analysed with the software package Review Manager 4.2.10 of the Cochrane Collaboration. In the 13 RCTs included in our analysis, RT reduced glycosylated haemoglobin (HbA1c) by 0.48% (95% CI -0.76, -0.21; p = 0.0005), fat mass by 2.33 kg (95% CI -4.71, 0.04; p = 0.05) and systolic blood pressure by 6.19 mmHg (95% CI 1.00, 11.38; p = 0.02). There was no statistically significant effect of RT on total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, triglyceride and diastolic blood pressure. Based on our meta-analysis, RT has a clinically and statistically significant effect on metabolic syndrome risk factors such as obesity, HbA1c levels and systolic blood pressure, and therefore should be recommended in the management of type 2 diabetes and metabolic disorders.

The inclusion of resistance training (RT) as an integral part of an exercise programme has been endorsed by the American Heart Association,[1] the American College of Sports Medicine[2] and the American Diabetes Association.[3] Crosssectional studies have shown that muscular strength is inversely associated with all-cause mortality[4] and the prevalence of the metabolic syndrome (MS),[5] independent of cardiorespiratory fitness levels. However, at present, the evidence that RT reduces cardiovascular disease (CVD) risk factors remains equivocal.[6] The purpose of this review is: (i) to perform a meta-analysis of randomized controlled trials (RCTs) regarding the effect of RT on obesityrelated impaired glucose tolerance (IGT) and type 2 diabetes mellitus (T2D); and (ii) to assess the potential of a dose-response relationship between intensity, duration and frequency of RT exercise and the metabolic clustering. There are discrepancies in findings as to whether RT 3 days per week elicits superior strength gains when ª 2010 Adis Data Information BV. All rights reserved.

compared with training regimens of lower frequency.[7,8] The question is whether progressively higher volumes of RT and subsequent increases in muscle mass may reduce multiple CVD risk factors as hypothesized by other investigators.[9] 1. The Metabolic Syndrome (MS) The pathogenesis of the MS is multifactorial and progressive. The risk factors of the MS are of metabolic origin and consist of abdominal adipose tissue accumulation, atherogenic dyslipidaemia, elevated plasma glucose, elevated blood pressure and a prothrombotic and proinflammatory state. The major risk factors are obesity and insulin resistance (IR) accompanied by increased risk for CVD and T2D. Furthermore, aging, physical inactivity and endocrine, and genetic factors exacerbate the MS.[10] There is no standard definition of the MS, but three definitions, two proposed by the WHO and the other one by the National Cholesterol Sports Med 2010; 40 (5)

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Education Program Adult Treatment Panel III (NCEP ATP III), are well known. The WHO definitions include IGT, T2D and/or IR together with two more of the following risk factors: (i) arterial BP ‡140/90 mmHg; dyslipidaemia, defined as plasma triglyceride (TG) concentration ‡150 mg/dL and/or high-density lipoprotein cholesterol (HDL-C) £35 mg/dL in men, £39 mg/dL in women; and (ii) central obesity, defined as waist-to-hip ratio >0.90 in men, >0.85 in women and/or body mass index (BMI) >30 kg/m2; microalbuminuria, defined as urinary albumin excretion rate ‡20 mg/min or albumin-to-creatinine ratio ‡30 mg/g.[11] The NCEP ATP III definition includes the presence of any three of the following risk factors: (i) abdominal obesity, defined as a waist circumference of >102 cm in men, >88 cm in women; (ii) plasma TG ‡150 mg/dL; HDL-C <40 mg/dL in men, <50 mg/dL in women; and (iii) BP ‡130/85 mmHg; fasting glucose ‡110 mg/dL.[12] Recently, the International Diabetes Federation replaced WHO criteria with those closer to ATP III. Waist circumference thresholds are ethnic-specific and abdominal adiposity was required for diagnosis.[13] The prevalence of MS has been shown to vary, depending on which medical society definition is adopted (e.g. in the US adult population between 21.2% and 38.9%). Thus, direct comparisons of prevalence values across MS studies are not valid.[14] 2. Epidemiology of the MS Being overweight, especially in the presence of environmental and genetic risk factors, leads to abdominal obesity and ectopic fat deposition with consequent IR. Genetic factors[15] and environmental factors including a sedentary lifestyle and poor physical fitness,[16] a diet rich in saturated fat and low in fibre[17] and a low socioeconomic status[18] contribute to the development of both overweight and IR.[19] Furthermore, adipose tissue is a major endocrine organ, secreting substances such as adiponectin, leptin, resistin, tumour necrosis factor-a, interleukin-6 and plasminogen activator inhibitor-1 that may play a critical role in the pathogenesis of the MS.[20] The manifestations of cardiovascular risk ª 2010 Adis Data Information BV. All rights reserved.

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factors such as abnormal insulin and glucose metabolism, dyslipidaemia, obesity, hypertension, endothelial dysfunction, inflammation and impaired fibrinolysis predispose persons with the MS to another end-stage consequence of the MS, namely CVD.[21-23] Published evidence indicates that the risk for CVD associated with the MS is greater than the sum of its individual risk factors.[24] Epidemiological studies show a strong association for obesity with CVD[25] and T2D.[26] Obesity-induced risk factors such as plasma cholesterol, elevated plasma glucose and elevated BP increase the risk for CVD and have thus been called the metabolic complications of obesity.[27] IR is an underlying risk factor in MS and contributes to prediabetes and, ultimately, to T2D. Approximately 75% of people with prediabetes and 86% of people with T2D have the MS. Both MS and T2D are known to predict CVD. In many patients, the MS culminates in T2D, which further increases the risk of CVD.[10] Most patients with the MS have lipid abnormalities, namely raised TG levels, low HDLC levels and a greater preponderance of small low-density lipoprotein (LDL) particles.[28] Abdominal obesity is positively correlated with fasting plasma TG and insulin levels and negatively correlated with HDL-C levels.[29] The atherogenic lipoprotein profile associated with obesity and IR has been found to be largely attributable to intra-abdominal fat.[30] The combination of abdominal obesity and high plasma TG is a strong marker for the MS. Physical activity is considered to reduce the risk of CVD, T2D and the MS and is an important component of CVD prevention. This concept is supported by prospective epidemiological studies demonstrating that low cardiorespiratory fitness is a strong and independent predictor of all-cause and CVD mortality in adults.[31-39] Although many investigators have documented that cardiorespiratory fitness reduced T2D and MS risk independent of bodyweight,[40,41] some found that obesity was more strongly linked with CVD risk factors.[42-44] Several reports demonstrate that cardiorespiratory fitness is an independent predictor of all-cause or CVD mortality in patients with T2D or the MS and that this association is Sports Med 2010; 40 (5)

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independent of BMI.[45-48] In contrast, a recent report demonstrated that T2D and diabetesrelated cardiovascular co-morbidities increased with BMI, regardless of physical activity, and increased with physical inactivity regardless of BMI.[49] These findings suggest that both physical inactivity and obesity are strongly and independently associated with T2D, cardiovascular risk factors and the MS. 3. Overview: Resistance Training (RT) and Metabolic Risk Aging is associated with a loss in both muscle mass and the metabolic quality of skeletal muscle. Sarcopenia, the loss of muscle mass associated with aging, is a main cause of muscle weakness in old age and consequently leads to an increased risk for development of IR and T2D.[50] The aetiology of sarcopenia involves multiple factors such as loss of motoneurons and muscle cell apoptosis and, as a result, the number of muscle fibres considerably decreases with aging.[51] A major part of these changes is associated with an age-related decrease in the physical activity level and can be counteracted by RT. There is concurring research evidence that RT prevents the age-related decline in skeletal muscle mass which is approximately 0.46 kg of muscle per annum from the 5th decade on and the best available evidence suggests that muscle maintains its plasticity and capacity to hypertrophy even into the 10th decade of life.[52-54] Skeletal muscle is the primary metabolic target organ for glucose and triglyceride disposal and is an important determinant of resting metabolic rate. The potential consequences of age-related reduction in skeletal muscle mass are diverse, including reduced muscle strength and power, reduced resting metabolic rate, reduced capacity for lipid oxidation and increased abdominal adiposity. With increasing adiposity in aging, the insulin-mediated glucose uptake in the skeletal muscle of elderly patients is reduced. The maintenance of a large muscle mass can contribute to the prevention of metabolic risk factors – namely obesity, dyslipidaemia and T2D – associated with CVD.[55] ª 2010 Adis Data Information BV. All rights reserved.

Both resting and activity-related energy expenditure decline with age,[56] and decreased energy expenditure can have a major adverse effect on weight maintenance.[57] Although it is clear that aerobic exercise is associated with much greater energy expenditure during the exercise session than RT, studies have shown that regular RT is effective in promoting weight loss in obese persons.[58] Many studies have shown that RT is associated with a decrease in fat mass (FM) and a concomitant increase in lean body mass (LBM) and thus little or no change in total bodyweight.[59-67] Because of this, it has been assumed that the main effect of RT on body composition is a shift from fat to muscle mass. RT increases resting metabolic rate as a result of a greater muscle protein turnover. A difference of 10 kg in LBM translates to a difference in energy expenditure of 100 kcal/day, equivalent to 4.7 kg FM per year.[68] However, a number of studies have shown that RT will increase resting metabolic rate at least if the training is intense enough to induce an increase in LBM.[69-71] Several studies have demonstrated decreases in visceral adipose tissue after RT programmes.[64,66,67,72-74] Excessive central obesity and especially visceral adipose tissue have been linked with the development of dyslipidaemia, hypertension, IR, IGT, T2D and CVD.[53,75,76] A relative increase in body fat is linked with a decline in insulin sensitivity in both obese and elderly individuals. RT has been shown to improve muscle strength in both healthy elderly individuals and individuals with chronic disease and to improve insulinstimulated glucose uptake in patients with IGT or manifest T2D.[77] RT and subsequent increases in muscle mass, may improve glucose and insulin responses to a glucose load in healthy[78,79] and diabetic men and women[60,80,81] and improve insulin sensitivity in diabetic or insulin-resistant middleaged and elderly men and women.[81-85] Highintensity RT decreases glycosylated haemoglobin (HbA1c) levels in diabetic men and women, regardless of age.[59-62,82,86-90] Apart from the positive effect on glycaemic control, it is unclear whether RT also has therapeutic effects on other conditions associated with the MS, namely dyslipidaemia and hypertension. At Sports Med 2010; 40 (5)

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present, there is little evidence that RT improves lipoprotein-lipid profiles.[59,61,91] Most studies show no improvement in lipid profiles after RT.[60,62,72,89,92,93] In some studies this may be due to the fact that lipid values were normal at study entry.[67,79,94] Although there is general agreement that endurance training lowers resting BP in patients with mild to severe hypertension,[95] there is only some evidence that both isometric[96,97] and dynamic[59,61] RT elicit reductions of both resting systolic and diastolic blood pressure (SBP; DBP) in individuals with hypertension. This is in agreement with two meta-analyses.[98,99] RT, when performed regularly and with sufficient intensity, stimulates skeletal muscle to synthesize new muscle proteins (hypertrophy). The effective amount of RT to promote muscle growth in relatively sedentary diseased or aged individuals is an understudied area. It is believed that one to two sets of eight to twelve repetitions per set with an intensity >60% of an individual’s one repitition maximum (1 RM) [the maximum load that can be lifted once only throughout a complete range of motion], with eight to ten exercises per session, two to three sessions per week, are likely to have beneficial for health effects with the increase in skeletal muscle mass.[100] A recent study examining the effects of systematic RT in the elderly (76.2 – 3.2 years) demonstrated that RT consisting of two training sessions per week was at least as efficient as RT that included three training sessions per week, provided that the number of sets performed was equal.[8] These findings contradict the results of another study that reported performing RT 3 days per week elicits superior strength gains when compared with RT performed 2 days per week.[7] However, the latter study was for low volume RT; therefore, a higher RT frequency produced better results. A recent review demonstrated that there was no difference in mean rates of increase in the whole muscle cross-sectional area between two and three sessions per week for longer periods of training.[101] Systematic reviews comparing RT frequencies in patients with metabolic or CVD risk revealed no apparent association between RT frequencies and changes in risk factors for MS.[102,103] However, limitations still exist, since ª 2010 Adis Data Information BV. All rights reserved.

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only a few studies were conducted in subjects with risk factors for MS, and most of the included RT studies had a training frequency of 3 days per week. 4. Impaired Glucose Regulation and Type 2 Diabetes Mellitus: A Meta-Analysis Impaired fasting glucose and IGT refer to the conditions in which blood glucose levels are higher than normal but do not meet the diagnostic criteria for T2D. Both disorders are associated with a significantly increased risk of developing T2D, with the highest risk among individuals exhibiting both conditions.[104] IGT is associated with IR and is also a risk factor for all-cause mortality.[105] According to the criteria of the WHO, IGT is defined as 2-hour glucose levels of 140–199 mg/dL (7.8–11.0 mmol) on the 75 g oral glucose tolerance test.[106] T2D is a metabolic disorder that is primarily characterized by IR, relative insulin deficiency and hyperglycaemia. Furthermore, T2D is often associated with obesity, hypertension, elevated cholesterol and the MS. The WHO definition of T2D is fasting plasma glucose ‡7.0 mmol/L (126 mg/dL) or plasma glucose ‡11.1 mmol/L (200 mg/dL) 2 hours after a 75 g oral dose of glucose measured with a glucose tolerance test.[106] The beneficial effect of physical activity in patients with abnormal glucose regulation is very well documented, and there is international consensus that physical training comprises one of the three cornerstones of the treatment, together with diet and medicine.[107,108] Two RCTs including persons with IGT have found that lifestyle modification protects against the development of T2D.[34,35] Large observational cohort studies have found that higher levels of aerobic fitness and physical activity are associated with significantly lower cardiovascular and overall mortality, to a much greater extent than could be explained by glucose lowering alone.[46,109,110] Most of the information available concerns aerobic endurance training (AET) in the treatment of IR and T2D. Recent systematic reviews focused on the relationship between exercise and/or physical activity and glycaemic control Sports Med 2010; 40 (5)

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in patients with T2D.[3,111,112] Results indicate that physical training significantly improves glycaemic control and reduces visceral adipose tissue and plasma TG in people with T2D, even without weight loss. One further meta-analysis, including 27 RCTs, examined the effects of different modes of exercise training on glucose control and risk factors for complications in patients with T2D.[113] Differences among the effects of AET, RT and combined training on HbA1c were minor. For training lasting ‡12 weeks, the overall effect was a small beneficial reduction (HbA1c 0.8% – 0.3%). Aerobic and combined exercise had small or moderate effects on BP. All three modes of exercise produced trivial or unclear effects on blood lipids. The effects of RT on glycaemic control and risk factors associated with CVD in T2D were small (HbA1c), unclear (BP) or trivial (blood lipids), and combined training was generally superior to RT alone. Of the 27 studies in the meta-analysis of Snowling and Hopkins,[113] six used RT and five combined AET and RT. Since then, there have been some new studies of RT although, so far, limited and unclear data are available concerning the effects of RT on the metabolic clustering among individuals with abnormal glucose metabolism. For the purposes of this review, we have evaluated the RCT data on the effects of RT on obesity-related metabolic risk factors in adult men and women with IGT or T2D. 4.1 Methods of the Meta-Analysis 4.1.1 Literature Search

We performed a systematic literature review. An English language literature search from 1990 to September 2007 was conducted via MEDLINE. The following key words were used alone or in various combinations in computer searches: ‘resistance training’, ‘metabolic syndrome’, ‘impaired glucose tolerance’, ‘type 2 diabetes’, ‘obesity’, ‘blood pressure’ and ‘lipids’. The reference lists from original and review articles were also reviewed to identify other relevant studies. 4.1.2 Inclusion Criteria

We considered all RCTs comparing RT with an exercise or non-exercise control group in ª 2010 Adis Data Information BV. All rights reserved.

patients with impaired glucose metabolism or T2D. We included trials of 6 weeks or longer, because we wanted to evaluate the effect of ongoing RT rather than acute single bouts of RT. A training period of <6 weeks would be too short to expect alterations in glycaemic control and body composition. The exclusion criteria for this review were as follows:  studies with single-bout RT interventions;  studies with mere recommendations as intervention, without further detail;  studies where the RT was not either directly supervised or well documented;  studies with a dietary co-intervention in the experimental group that was not also applied to the control group. However, we did not exclude studies with the same diet applied to both the intervention group and the control group and hence the RT in the intervention group was the only difference between the two groups. The participants were males and females with impaired glucose regulation or T2D. All patients fulfilled the diagnosis criteria for IGT or T2D according to the WHO or the American Diabetes Association standards.[11,108] We considered RCTs where RT prescriptions included specific recommendations for the type, intensity, frequency and duration of RT with a specific objective. This systematic review included studies involving the following four types of intervention:  RT versus non-exercise control;  RT plus AET versus non-exercise control;  RT versus AET;  RT plus diet versus diet alone. 4.1.3 Assessed Outcomes

The primary outcomes of our systematic review were glycaemic control measured in percent HbA1c and FM (kg). Secondary outcomes included blood lipids (mg/dL), i.e. total cholesterol (CHOL), HDL-C, LDL cholesterol (LDL-C), TG, and BP (mmHg) measures, both SBP and DBP. 4.1.4 Data Extraction

We used a standardized data extraction form to extract data on study population, intervention and outcome in each study. This form included the following items: (i) general information Sports Med 2010; 40 (5)

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including title, authors, source, setting and year of publication; (ii) trial characteristics including design and randomization; (iii) characteristics of participants such as inclusion criteria, exclusion criteria, total number in intervention/control groups, sex, age, diagnostic criteria, baseline characteristics and dropouts; (iv) intervention type, intensity, and frequency as well as duration of trial and outcomes specified in the methods; and (v) results. For continuous variables we extracted the number of participants, baseline and post-intervention means with standard deviation for the intervention and control groups. There were no dichotomous variable outcomes. Study characteristics were reported in evidence tables. 4.1.5 Statistical Analysis

For each outcome of interest, we performed a meta-analysis to determine the pooled effect of the intervention in terms of weighted mean differences (WMD) between the post-intervention values of the intervention and control groups. All data were analysed with a software program (Review Manager 4.2.10) from the Cochrane Collaboration (www.cochrane.org/software/revman. htm). Heterogeneity between trial results was tested with a standard Chi-squared (w2) test. The I2 parameter was used to quantify any inconsistency (I2 = [(Q-df)] · 100%, where Q is the w2 statistic and df are the degrees of freedom). A value for I2 >50% has been considered to be substantial heterogeneity.[114] To consider heterogeneity, we used the random-effects model to estimate WMD and 95% confidence intervals. We used the funnel plot method to assess the potential of a publication bias (i.e. the tendency for studies that yield statistically significant results that are more likely to be submitted and accepted for publication). 4.2 Results of the Meta-Analysis 4.2.1 Included Studies and Study Characteristics

Out of 25 potentially appropriate papers selected for closer examination,[59-62,72,79-90,92,115-121] 13 studies finally met the inclusion criteria.[59-62,72,79,83,84,87,88,92,115,117] The main reasons for exclusion were as follows: studies did not compare similar groups (e.g. abnormal ª 2010 Adis Data Information BV. All rights reserved.

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glucose tolerance versus normal glucose tolerance);[80,85,119-121] the study had no control group;[81,86,89,90] the study was a follow-up;[116] studies were home-based;[118] and multiple publications of studies.[82] The characteristics of the included studies are presented in table I. All of the final 13 studies selected for the review were RCTs. They were conducted in Australia,[62,117] Austria,[61] Canada,[72] Finland,[83,87,88] Italy,[59] Japan,[84] New Zealand[92] and the US.[60,79,115] The studies included involved 513 participants. The number of participants in a single study ranged from 17 to 120, with a pooled total of 425 participants in studies reporting HbA1c; of these, 219 participants received the RT intervention. The mean age of the groups was between 46.8 and 67.6 years. Detailed descriptions of the exact RT regimens are provided in table I. This systematic review included studies involving the following four types of RT interventions: RT versus nonexercise control;[60,79,83,84,87,92,115,117] RT plus AET versus AET or non-exercise control;[59,72,88] RT versus AET;[61,79,83] and RT plus diet versus diet alone.[62] The duration of the interventions ranged from 6 weeks in one study,[84] 8 to 10 weeks in three studies,[83,92,117] 4 months in three studies,[60,61,72] 5 months in two studies,[79,87] 6 months in one study,[62] 12 months in two studies,[59,88] to 2 years in one study.[115] Most interventions involved three training sessions per week with RT occurring on non-consecutive days. Two studies involved two sessions per week[87,88] and one short study, five sessions per week.[84] Interventions were either progressive RT[60-62,79,83,84,87,92,115,117] or combinations of RT and AET.[59,72,88] The percentage of the 1 RM or 10–15 repetition maximum (10–15 RM) were scales used to define the intensity of RT. One set consisted of 10–15 repetitions without interruption, until severe fatigue occurred and completion of further repetitions was impossible. The training load was systematically adapted to keep the maximum possible repetition per set between 10 and 15. A 10–15 RM is equivalent to 70–80% 1 RM for most exercises[122] but may not be accurate for selected exercises.[123] The intensity of the Sports Med 2010; 40 (5)

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ª 2010 Adis Data Information BV. All rights reserved.

Table I. Characteristics of included randomized controlled resistance training (RT) intervention trials Sample size

Study design

Study length

RT prescription

Primary findings

Secondary findings

Baldi and Snowling[92]

18 T2D men 9 RT, 9 control

RT vs control

3 d/wk for 10 wk

10 exercises; intensity: 10–15 RM; dose: 6 S/MG/W

fl HbA1c with RT (p = 0.057) › LBM with RT (p < 0.05)

fl fasting insulin fl fasting glucose (p < 0.05) 2 2 h glucose or insulin with RT

Balducci et al.[59]

120 T2D 62 RT, 58 control

Combined RT + AET vs control

3 d/wk for 1 y

RT: 6 exercises 40–60% 1 RM; dose: 9 S/MG/W; AET: 40–80% HRR; dose: 90 min/wk

fl HbA1c with RT + AET (p < 0.0001) fl BMI (p < 0.0001) › LBM (p < 0.0001)

› fl fl fl

Brandon et al.[115]

31 T2D 16 RT, 15 control

RT vs control

2.6 d/wk for 2 y

50–70% 1 RM 6–9 S/MG/W

fl FM

Castaneda et al.[60]

62 T2D 31 RT, 31 control

RT vs control

3 d/wk for 16 wk

5 exercises 60–80% 1 RM 9 S/MG/W

fl HbA1c, FM with RT (p < 0.01) › LBM (p < 0.05)

fl SBP 2 HDL, LDL, TG, fasting glucose

Cauza et al.[61]

39 T2D 22 RT, 17 AET

RT vs AET

3 d/wk for 16 wk

RT: 8 exercises; intensity: 10–15 RM; dose: 3–6 S/MG/W; . AET: 60% VO2max 45–90 min/wk

fl HbA1c with RT (p < 0.01) fl FM with RT › LBM with RT

fl fl › fl

Cuff et al.[72]

28 T2D women 10 RT + AET, 9 AET, 9 control

Combined RT + AET vs AET vs control

3 d/wk for 16 wk

RT: 5 exercises; intensity: 12 RM; dose: 6 S/MG/W; AET: 60–75% HRR; dose: 60 min/wk

2 HbA1c › glucose disposal rate with RT + AET

fl abdominal visceral and subcutaneous tissue (p < 0.05) in both groups 2 blood lipids

Dunstan et al.[62]

36 T2D 19 RT + WL, 17 WL control

Combined RT + WL vs WL only

3 d/wk for 6 mo

RT: 9 exercises intensity: 75–85% 1 RM; dose: 9 S/MG/W

fl HbA1c with RT + WL (p < 0.01) fl FM in both groups (p < 0.01)

2 HDL, LDL, TG, fasting glucose 2 SBP, DBP in both groups

Dunstan et al.[117]

27 T2D 15 RT, 12 control

RT (CWT) vs control

3 d/wk for 8 wk

RT: 10 exercises; intensity: 50–55% 1 RM; dose: 6–9 S/MG/W

2 HbA1c fl 2 h glucose fl 2 h insulin

2 fasting glucose, fasting insulin 2 SBP, DBP

Eriksson et al.[83]

22 IGT 8 RT, 7 AET, 7 control

RT (CWT) vs AET vs control

3 d/wk for 10 wk RT, for 6 mo AET

RT: 50–60% 1 RM; dose: 9 S/MG/W; AET: 60% HRR 120–150 min/wk

2 FM for RT

2 fasting glucose, fasting insulin › HDL with RT 2 SBP, DBP

HDL (p < 0.0001) LDL, TG SBP (p < 0.04) DBP (p < 0.0001)

fasting glucose fasting insulin HDL, fl LDL, fl TG SBP, fl DBP with RT

Continued next page

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AET = aerobic endurance training; BMI = body mass index; CHOL = total cholesterol; CWT = circuit weight training; DBP = diastolic blood pressure; FM = fat mass; HbA1c = glycosylated haemoglobin; HDL = high-density lipoprotein; HRR = heart rate reserve; IGR = impaired glucose regulation; IGT = impaired glucose tolerance; LBM = lean body mass; LDL = low-density lipoprotein; RM = repetition maximum; SBP = systolic blood pressure; S/MG/W = sets for each muscle group per week; T2D = type 2 diabetes; TG = triglycerides; . VO2max = maximum oxygen uptake; WL = weight loss; › indicates higher/more, fl indicates lower/less; 2 indicates unchanged.

fl 2 h glucose fl 2 h insulin 2 FM, LBM with RT 3 d/wk for 5 mo RT vs AET vs control 18 IGR 8 RT, 8 AET, 10 control Smutok et al.[79]

RT: 12–15 RM 6 S/MG/W; AET: 75–85% HRR 90 min/wk

fl SBP with RT + AET fl HbA1c with RT (p < 0.05) 2 d/wk for 1 y Combined RT + AET vs control 49 T2D men 24 RT + AET, 25 control Loimaala et al.[88]

RT: 70–80% 1 RM 6 S/MG/W; AET: . 65–75% VO2max 60 min/wk

› glucose disposal rate with RT 2 HbA1c with RT 2 FM, LBM with RT 5 d/wk for 4–6 wk RT vs control 17 T2D 9 RT, 8 control Ishii et al.[84]

RT: 9 exercises; intensity: 50–50% 1 RM; dose: 10 S/MG/W

fl CHOL, LDL, TG with RT (p < 0.05) 2 SBP, fl DBP fl HbA1c with RT (p < 0.05)

Primary findings RT prescription Study length

Honkola et al.[87]

2 d/wk for 5 mo

Study design

RT (CWT) vs control

Sample size

38 T2D 18 RT, 20 control

Study

Table I. Contd

RT: 8–10 exercises; intensity: 12–15 RM; dose: 4 S/MG/W

Secondary findings

Resistance Training and Metabolic Risk

interventions ranged from 40% 1 RM[84] to 85% 1 RM.[62] The maximum numbers of sets for each muscle group per week (S/MG/W) at the end of the intervention programme ranged from four S/MG/W[87] to ten S/MG/W.[84] The most common dose of RT at the end of the intervention was six S/MG/W or nine S/MG/W. 4.2.2 Study Quality

The methodological quality of RCTs included in this review was not assessed by assigning a formal scoring system. Rather, key components of methodological quality such as blinding, randomization, compliance and dropouts, are described for each of the studies. Blinding of the people administering the intervention and of the participants performing the exercise is not possible in exercise intervention trials, so blinding of these was not assessed as a quality criterion. Although blinding of the outcome assessment is feasible, no trial reported blinding of the outcome assessors. All selected trials were described as randomized. All studies included in the review reported no significant differences in the main characteristics of the participants at baseline. Compliance with exercise was between 85%[115] and 90%[62,83,92] and in some trials more than 90%.[60,61,72] Compliance with exercise was not mentioned in some studies.[59,79,84,87,88,117] Dropouts in the intervention group ranged from zero in seven studies,[72,79,83,84,87,88,92] to two,[60] four[61] and six[117] in one study each, 17–19% in two studies[59,62] and 45% in one study.[115] In this review, HbA1c was used as the principal measure for glycaemic control. Ten of 13 studies measured HbA1c, involving a total of 425 participants[59-62,72,84,87,88,92,117] of these: 219 participants received the RT intervention; seven of 13 studies measured fasting plasma glucose concentration;[59-62,83,92,117] four studies reported results of oral glucose tolerance tests;[61,62,79,117] eight of 13 studies reported results for FM in percentage of body mass[59,79,84,115] or absolute in kilograms;[60-62,92] one study reported visceral and subcutaneous adipose tissue;[72] TG and CHOL were reported in seven studies;[59-62,83,87,92] six of these also reported HDL-C[59-62,83,87] and four LDL-C;[60-62,87] and eight studies provided Sports Med 2010; 40 (5)

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data on BP, seven recording both SBP and DBP[59-62,83,87,117] and one recording only SBP.[88] 4.2.3 Pooled Effects of RT

Our meta-analysis showed that the pooled effect of RT on HbA1c was a reduction of 0.48% (95% CI -0.76, -0.21). This is both clinically and statistically significant (p < 0.0005). FM was reduced by a statistically significant 2.33 kg with RT (95% CI -4.71, 0.04; p = 0.05). There was a significant decrease in visceral adipose tissue reported in one study (-119.8 cm2, 95% CI -154.8, -84.8; p < 0.05). There were no significant differences between the RT group and the control group in CHOL (WMD -7.75 mg/dL, 95% CI -17.02, 1.51; p = 0.10), HDL-C (WMD -0.68 mg/dL, 95% CI -3.68, 2.31; p = 0.66), LDL-C (WMD -7.72 mg/dL, 95% CI -17.92, 2.48; p = 0.14), TG (WMD -18.53 mg/dL, 95% CI -38.43, 1.36; p = 0.07) and in DBP (WMD 0.86 mmHg, 95% CI -1.73, 3.45; p = 0.51). The change in SBP with RT was statistically significant (WMD -6.19 mmHg, 95% CI -11.38, -1.00; p = 0.02). Table II summarizes the pooled results for the intervention effects. Figure 1 shows the results from each study group for HbA1c change (WMD point estimate and 95% CI) in response to RT graphically displayed as a forest plot. 4.2.4 Heterogeneity and Dose-Response Relationship

Of the outcomes tested, there was substantial heterogeneity in the results of trials for the outcomes of HbA1c (I2 = 87.1%), FM (I2 = 88.6%), TG (I2 = 84.8%), CHOL (I2 = 90.8%), LDL-C (I2 = 92.2%), HDL-C (I2 = 82.0%), SBP (I2 = 94.9%) and DBP (I2 = 94.4%). The different RT interventions and protocols employed (concerning frequency, duration, intensity and dose), different exercise equipment used and diversity in the initial strength status of the participants in the studies may explain the heterogeneity. Heterogeneity in the results of trials for the outcomes and insufficient data from reviewed RCTs made it difficult to establish dose-response relationships between intensity and volume of RT and the metabolic clustering in patients with abnormal glucose regulation. Regression-based analyses revealed ª 2010 Adis Data Information BV. All rights reserved.

Table II. Pooled estimates of effect size (95% confidence intervals [CIs]) expressed as weighted mean difference (WMD) for the effect of resistance training on glycaemic control (glycosylated haemoglobin [HbA1c]), fat mass (FM), blood lipids (total cholesterol [CHOL], high-density lipoprotein cholesterol [HDL-C], low-density lipoprotein cholesterol [LDL-C], triglycerides [TG]) and systolic and diastolic blood pressure (SBP; DBP) in overweight/obese adults with type 2 diabetes mellitus Risk factor

Effect size

95% CI

p-Value

I2 87.1

HbA1c (%)

-0.48

-0.76, -0.21

0.0005

FM (mg/dL)

-2.33

-4.71, 0.04

0.05

88.6

CHOL (mg/dL)

-7.75

-17.02, 1.51

0.10

90.8

HDL-C (mg/dL)

-0.68

-3.68, 2.31

0.66

82.0

LDL-C (mg/dL)

-7.72

-17.92, 2.48

0.14

92.2

-18.53

-38.43, 1.36

0.07

84.8

SBP (mg/dL)

-6.19

-11.38, -1.00

0.02

94.9

DBP (mg/dL)

0.86

-1.73, 3.45

0.51

94.4

TG (mg/dL)

I2 = inconsistency.

no statistically significant dose-response relationships between volume of RT and the metabolic clustering in patients with abnormal glucose regulation; however, there was a tendency towards a greater reduction of SBP and DBP with increasing volume of RT. The only factor that explained part of the heterogeneity was duration of intervention period with a moderate positive impact on HbA1c and DBP with increasing study duration. 4.2.5 Publication Bias

The funnel plot with respect to effect size changes for HbA1c, FM, CHOL, HDL-C, LDLC, TG, and SBP and DBP responses to RT indicates no asymmetry, suggesting no potential publication bias (figure 2). However, interpretative caution is urged in that the above analyses are based on the context of a limited number of study groups. 4.3 Discussion of the Meta-Analysis 4.3.1 Using RT as a Treatment for Glycaemic Control

An RT intervention resulted in a clinically significant improvement in glycaemic control compared with controls. The decrease of 0.48% HbA1c (ten trials) was achieved over relatively short periods of time, since the shortest studies in the review were of 6- to 8-weeks’ duration. Most Sports Med 2010; 40 (5)

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studies had a duration of 10 to 20 weeks, and there were three studies with an intervention of 6 months or more. The mean reduction of 0.48% HbA1c achieved compares well with reported reductions achieved through medications. Metaanalysis has shown that metformin can lower HbA1c levels by 0.9% compared with placebo. The clinical significance of a 0.5% decrease in HbA1c can be gauged by studying large prospective intervention studies examining morbidity and mortality outcomes in people with T2D.[124] Data suggest that a 1% rise in HbA1c represents a 21% increase in risk for any diabetesrelated death, a 14% increased risk for myocardial infarction and a 37% increased risk for microvascular complications. The impact of a decrease of 0.5% HbA1c equates to a 50% improvement towards a target value of 7% HbA1c and a 25% improvement towards a normal value of 6% HbA1c, for a person diagnosed with 8% HbA1c. It is unclear whether the improvement in glycaemic control can be maintained in the longer term. In the 6-month post-intervention follow-up reported by one author,[116] the participants Review: Comparison: Outcome: Study (y)

continuing with supervised RT maintained the improvement in glycaemic control, while in one other 6-month home-based follow-up, the improvements were lost.[118] The reason could result from the difficulty in motivating people to maintain RT prescriptions as part of a regular lifestyle. The major finding from one study was that completing RT and AET over extended durations will result in similar improvements to glycaemic control.[61] However, this finding requires further validation, as the RT group appeared to spend a larger volume of time training than the AET group. Another limitation of this study was that participants randomized for the RT group had higher baseline levels for HbA1c than participants randomized for the AET group. Based on this meta-analysis, the greatest improvements to glycaemic control occurred when HbA1c was poor (>8.0%) at baseline. Clinically relevant improvements of 0.5% were generally seen with moderate-high intensity RT or where the duration of training was 10 weeks or longer. The exception to this was a 4- to 6-week application of low intensity RT 5 days per week

A systematic review and meta-analysis of the relationship between RT and metabolic risk 01 RT vs KO 01 HbA1c (%) No. of RT No. of Control subjects mean (SD) subjects mean (SD)

Balducci et al. (2004) Castaneda et al. (2002) Loimaala et al. (2003) Honkola et al. (1997) Dunstan et al. (1998) Cauza et al. (2005) Dunstan et al. (2002) Cuff et al. (2003) Ishii et al. (1998) Baldi and Snowling (2003)

62 31 24 18 15 22 19 10 9 9

7.10 (1.16) 7.30 (0.20) 7.60 (1.40) 7.40 (0.20) 8.00 (0.50) 7.10 (0.20) 6.90 (1.00) 6.80 (0.22) 7.60 (1.30) 8.40 (0.60)

58 31 25 20 12 17 17 9 8 9

WMD (random) [95% CI]

Weight (%)

WMD (random) [95% CI]

9.29 13.39 6.56 13.64 10.05 13.60 8.59 13.40 2.50 9.00

−1.18 [−1.71, −0.65] −1.00 [−1.19, −0.81] −0.70 [−1.48, 0.08] −0.70 [−0.86, −0.54] −0.30 [−0.77, 0.17] −0.30 [−0.47, −0.13] −0.20 [−0.79, 0.39] −0.07 [−0.26, 0.12] 0.00 [−1.57, 1.57] 0.00 [−0.55, 0.55]

100.00

−0.48 [−0.76, −0.21]

8.28 (1.73) 8.30 (0.50) 8.30 (1.40) 8.10 (0.30) 8.30 (0.70) 7.40 (0.30) 7.10 (0.80) 6.87 (0.20) 7.60 (1.90) 8.40 (0.60)

219 206 Total (95% CI) Test for heterogeneity: χ2 = 69.93, df = 9 (p < 0.00001), I2 = 87.1% Test for overall effect: Z = 3.47 (p = 0.0005) −4 −2 0 2 4 Favours treatment Favours control

Fig. 1. Forest plot showing the results of a meta-analysis as pooled weighted mean difference (WMD) with 95% confidence intervals (CIs) in glycosylated haemoglobin (HbA1c), for the ten included randomized controlled resistance training (RT) studies. For each RT study, the shaded square represents the point estimate of the intervention effect. The horizontal line joins the lower and upper limits of the 95% CI of this effect. The area of the shaded square reflects the relative weight of the study in the meta-analysis. The diamond at the bottom of the graph represents the pooled WMD with the 95% CI for the ten study groups. Included studies: Honkola et al.,[87] Dunstan et al.,[117] Ishii et al.,[84] Castaneda et al.,[60] Dunstan et al.,[62] Baldi and Snowling,[92] Cuff et al.,[72] Loimaala et al.,[88] Balducci et al.,[59] Cauza et al.[61] v2 = Chi squared; df = degrees of freedom; I2 = inconsistency; KO = control; RT = resistance training; Z = overall effect.

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Overall effect estimate 95% CI Studies Review: Comparison: Outcome:

A systematic review and meta-analysis of the relationship between RT and metabolic risk 01 RT versus KO 01 HbA1c (%)

4.3.2 Impact on MS Risk Modification

0 0.2 SE (WMD)

changes in HbA1c have been inversely correlated with changes in the quadriceps cross-sectional area.[86] It has been proposed that hyperglycaemia has a direct adverse effect on muscle contractile function and force generation.[126]

0.4 0.6 0.8

−4

−2

0 WMD

2

4

Fig. 2. Funnel plot showing study precision, against the weighted mean difference (WMD) effect estimate with 95% confidence intervals (CIs) for glycosylated haemoglobin (HbA1c). KO = control; RT = resistance training; SE = standard error.

resulting in a 2.0% improvement of HbA1c.[84] However, participants of the referenced study were of remarkable light weight and had a low BMI, reducing the generalizability of this study. The effect of combining RT with AET on glycaemic control remains unclear, with only one study that made a direct comparison between combined training and isolated AET intervention reporting no effect.[72] In one study,[62] the combination of RT and moderate dietary restriction was associated with a 3-fold greater decrease in HbA1c levels after 6 months compared with moderate weight loss without RT, and this was not mediated by concomitant reductions in bodyweight, waist circumference and FM. It is possible that an increase in LBM after RT may be an important mediator of the improved glycaemic control. An increase in the number of GLUT4 transporters is discussed specifically,[77] because the transporter protein GLUT4 expression at the plasma membrane is related to fibre volume in human skeletal muscle fibres.[125] One study found the improvement in LBM after a 10-week RT programme had a greater impact on HbA1c levels than the reduction in FM, suggesting that increases in muscle mass improved glycaemic control.[92] Furthermore, RT-induced ª 2010 Adis Data Information BV. All rights reserved.

In addition to the decrease in HbA1c, there was a significant overall decrease of 2.3 kg in FM (eight trials) and in visceral adipose tissue.[72] Thus, RT is contributing to the decrease of one of the major risk factors for the MS. Despite the decrease in fat, there was no decrease in body mass and this probably reflects an increase in muscle mass, which is heavier than adipose tissue. Data show that RT may be an effective alternative to improve body composition and maintain the reduced FM in obese patients after exercise training or energy intake restriction.[65] The implementation of RT within a dietary intake restriction programme has been studied intensively.[74,127-130] The addition of RT prevents the loss of LBM, secondary to dietary restriction.[131,132] RT twice a week increases LBM by 1–2 kg per 6 months and could prevent age-associated loss of LBM.[54] As a result, RT could prevent age-related decline of resting metabolic rate, which is closely correlated to losses in LBM.[133] RT contributes to elevations of resting metabolic rate as a result of a greater muscle protein turnover.[134] Studies of the usefulness of RT in the context of weight loss have had mixed results. Although it is clear that AET is associated with much greater energy expenditure during the exercise session than RT, several studies have shown that regular RT is effective in promoting weight loss in obese persons.[58,65,135-137] RT appears to provide a unique stimulus to spare catabolism of body protein and thus alter the relationship between the LBM and FM.[136] An RT intervention did not result in any significant weight loss but could prevent age-associated fat gains over a period of years.[65] In a recent study, RT (8 weeks, 3 times weekly at 60% 1 RM) significantly changed body mass (+0.58%), percentage of body fat (-13.05%), LBM (+5.05%) and FM (-12.11%) when compared with the control group.[137] It appears that there is a relationship between RT and BMI, as Sports Med 2010; 40 (5)

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indicated in this study, which demonstrated an increase in BMI. Therefore, the use of BMI in ascribing CHD risk should be undertaken with caution in individuals with increased LBM, as would be expected, following RT. Recently, exercise-induced oxidative stress and homocysteine and cholesterol were analysed in normal-weight and overweight elderly adults after a 6-month RT programme.[138] Oxidative stress is suggested to be a potential contributor to early and advanced stages of CVD.[139] Lipid hydroperoxides and homocysteine levels were lower in both the overweight and normal-weight RT groups compared with control groups. The change in muscle strength was associated with homocysteine at 6 months, whereas the change in lipid hydroperoxides was associated with the change in body fat. The present study showed that RT reduces exercise-induced oxidative stress and homocysteine regardless of adiposity, indicating that this protection can be afforded in an older, overweight/obese population as effectively as in healthy elderly adults, which might indicate protection against oxidative insults (i.e. ischaemia). A potential mechanism for RT-induced reduction of oxidative stress could include contractioninduced antioxidant enzyme upregulation.[140] An RT intervention resulted in a significant lowering of SBP by 6.2 mmHg (eight trials) compared with the controls, but there was no significant difference between groups in total CHOL (seven trials), HDL-C (six trials), LDL-C (four trials), TG (seven trials) and DBP (seven trials). These results are in conflict with the results of one study that found positive effects of RT on blood lipid levels in elderly women,[91] while in one other trial,[93] no significant alterations in blood lipid profiles were documented after 8 weeks of RT (five exercises, three sets at 80% of 10 RM) in healthy, sedentary postmenopausal women. At present, there are few and conflicting data on the effects of RT on blood lipid levels in healthy elderly people and patients with dyslipidaemia.[141-146] The principal finding of one study was that RT can reduce coronary risk factors without changes in bodyweight or body composition.[9] Unfortunately, no information is available about the effect of RT on individuals with dyslipidaemia. ª 2010 Adis Data Information BV. All rights reserved.

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Only one of the above-mentioned studies included patients with abnormal lipoprotein-lipid levels.[144] The RT programme resulted in no significant changes in plasma concentrations of TG, total CHOL and HDL–C. This meta-analysis confirms that RT does not increase resting BP, as was once thought, and might even have potential benefits on resting SBP. The BP-lowering effect of RT seems to be independent of weight loss and is believed to be mediated via reduced sympathetically induced vasoconstriction in the trained state and decreased catecholamine levels.[147,148] A decrease of approximately 6.2 mmHg for resting SBP is not insubstantial, since a reduction of as little as 3 mmHg in SBP has been estimated to reduce CHD by 5–9%, stroke by 8–14% and all-cause mortality by 4%.[149] RCTs examining the effects of RT on resting BP in adults have resulted in mixed findings. A meta-analysis of nine RCTs on mostly dynamic RT revealed a net weight reduction in BP of 3.2/3.5 mmHg associated with RT.[147] These results are in agreement with two further meta-analyses that also examined the effects of long-term RT on resting SBP and DBP in normotensive and hypertensive adults;[98,99] however, limitations still exist. No information is available about the effect of RT on hypertensive subjects alone. Only three of the included studies were conducted with hypertensive individuals. Additional studies about the effect of RT in the hypertensive population are needed, as it has been shown that the reduction in BP is more pronounced in patients who are hypertensive at baseline.[147,150,151] 4.3.3 Dose Response: How Much RT is Needed?

Considering the benefits of RT for major risk factors of the MS, an important question is: how much RT (intensity, duration, frequency and volume) is needed to confer such benefits? Insufficient data from reviewed RCTs and, furthermore, substantial heterogeneity in the results of trials for the outcomes, made it difficult to establish dose-response relationships between intensity and volume of RT and metabolic clustering in patients with abnormal glucose regulation. Improvements in glycaemic control were achieved Sports Med 2010; 40 (5)

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over a range of exercise intensities and volumes. For example, improvements in HbA1c were observed following low intensity at 50% 1 RM,[59,117] moderate intensity at 60–70% 1 RM[60,61] and high intensity at 75–85% 1 RM.[62,88] Furthermore, improvements in glycaemic control were observed following low volume (four sets per muscle group per week),[87] moderate volume (six sets per muscle group per week)[61,88] and high volume (nine sets per muscle group per week)[59] of RT. However, we found a small positive correlation between the total duration of RT and changes in HbA1c. Most studies of longer duration (>10 weeks),[59,60,87,88] but not all studies,[62] revealed more beneficial effects on glycaemic control than short-term studies (£10 weeks).[84,92,117] We found no dose-response relationship between intensity of RT and glycaemic control in patients with IGT and T2D, but there was a tendency towards a low negative impact of intensity on HDL-C. One study of low intensity (50% 1 RM) observed a greater improvement in HDL-C,[59] while other studies of high intensities (70–80% 1 RM) revealed no improvements or even diminished HDL-C levels.[60-62] Regressionbased analyses suggest no apparent association between RT frequency and glycaemic control but indicate a trend to a negative correlation for some outcomes of lipid profile in patients with abnormal glucose regulation. One study found LDL-C and TG were more strongly affected when exercising twice a week compared with studies exercising three times per week.[87] The effect of RT on resting SBP and DBP appears to be dose dependent, since decreases in resting BP were more pronounced when the RT programme was of high volume. Studies of high volume (nine sets per muscle group per week)[59,60] revealed more beneficial effects on resting SBP and DBP than studies of low volume (four to six sets per muscle group per week).[61,87] Relatively modest increases in RT frequency had hypotensive effects, since resting SBP and DBP were further reduced when exercising three times per week compared with twice a week.[59,60,87,88] However, the referenced studies of low frequency RT were also of low volume and therefore higher frequency RT was superior. Furthermore, we ª 2010 Adis Data Information BV. All rights reserved.

found a small positive correlation between the total duration of RT and reductions in DBP. In summary, RT is at least as effective as AET in improving glycaemic control. The skeletal muscle is responsible for up to 40% of total weight and may induce beneficial changes in glycaemic control via muscle mass development. Possible mechanisms could include enhanced muscle contraction-induced glucose uptake in the muscle, increased GLUT4 content and insulin signalling in skeletal muscle in patients with IGT and T2D. Longer intervention duration of RT appears most beneficial, while higher intensity is more likely to have a harmful effect on glycaemic control. This meta-analysis confirms that RT might also have potential benefits on resting BP. The antihypertensive effect of RT is believed to be mediated via decreased sympathetic and increased vagal activity in the trained state. It seems that there is some tendency towards a doseresponse relationship between volume of RT and risk factors associated with CVD in patients with abnormal glucose regulation. Progressively higher volumes of RT may reduce resting SBP and DBP more significantly. However, interpretative caution is urged on the fact, that the analyses in this review are based on the context of a limited number of study groups. 5. Conclusions Although our meta-analysis has several limitations such as the limited number of study groups and the heterogeneity in the results of trials for the outcomes, this systematic review found that RT significantly decreases HbA1c levels in people with abnormal glucose metabolism. Furthermore, there is now good evidence that RT reduces total body FM and visceral adipose tissue independently from dietary restriction. There is now clear evidence that RT elicits significant reductions in resting SBP and tends to improve lipoprotein-lipid profiles. Improved glycaemic control, decreased FM, improved blood lipid profiles and decreased BP are important for reducing microvascular and macrovascular complications in people with metabolic risk. As with increasing adiposity in aging and loss of muscle Sports Med 2010; 40 (5)

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mass, the insulin-mediated glucose uptake and TG disposal in the skeletal muscle of elderly persons is reduced and the maintenance of a large muscle mass can contribute to the prevention of T2D, which is associated with CVD. Thus, RT is contributing to the decrease of major risk factors for the MS and should be recommended for the management of T2D and metabolic disorders. Furthermore, although the number of studies on the effects of RT on BP is small, this metaanalysis confirms that RT does not increase BP, as was once thought, and may even have potential benefits on resting SBP. As it is unclear whether the improvement in glycaemic control with RT can be maintained in the longer term, further studies with post-intervention follow-ups of at least 6 months are required to assess whether RT prescriptions can be maintained as part of a regular lifestyle and whether the improved metabolic clustering can be maintained over longer periods. Acknowledgements The authors are grateful to David Pamphlett for carefully reading our manuscript. We thank Bjoern Stollenwerk, PhD, for his advice regarding the statistical analysis. No sources of funding were used to assist in the preparation of this systematic review. The authors have no conflicts of interest that are directly relevant to the content of this review.

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139. Stocker R, Keaney JF. Role of oxidative modifications in atherosclerosis. Physiol Rev 2004; 84: 1381-478 140. Parise G, Phillips SM, Kaezor JJ, et al. Antioxidant enzyme activity is up-regulated after unilateral resistance exercise training in older adults. Free Radic Biol Med 2005; 39: 289-95 141. Boardley D, Fahlman M, McNevin N, et al. The impact of exercise training on blood lipids in older adults. Am J Geriatr Cardiol 2007; 16 (1): 30-5 142. Fenkci S, Sarsan A, Ardic F, et al. Effects of resistance or aerobic exercises on metabolic parameters in obese women who are not on a diet. Adv Ther 2006; 23 (3): 404-13 143. Boyden TW, Pamenter RW, Aickin M, et al. Resistance exercise training is associated with decreases in serum lowdensity lipoprotein cholesterol levels in premenopausal women. Arch Intern Med 1993; 153 (1): 97-100 144. Kokkinos PF, Hurley BF, Smutok MA, et al. Strength training does not improve lipoprotein-lipid profiles in men at risk for CHD. Med Sci Sports Exerc 1991; 23 (10): 1134-9 145. Manning JM, Dooly-Manning CR, Ruoff M, et al. Effects of a resistive training program on lipoprotein-lipid levels in obese women. Med Sci Sports Exerc 1991; 23 (11): 1222-6 146. Goldberg L, Elliot DL, Schutz RW, et al. Changes in lipid and lipoprotein levels after weight training. JAMA 1984; 252 (4): 504-6 147. Fagard RH, Cornelissen VA. Effect of exercise on blood pressure control in hypertensive patients. Eur J Cardiovasc Prev Rehabil 2007; 14 (1): 12-7 148. Padilla J, Wallace JP, Park S. Accumulation of physical activity reduces blood pressure in pre- and hypertension. Med Sci Sports Exerc 2005; 37: 1264-75 149. Whelton PK, He J, Appel LJ, et al. Primary prevention of hypertension: clinical and public health advisory from the National High Blood Pressure Education Program. JAMA 2002; 299: 1882-8 150. Martel GF, Hurlbut DE, Hurley BF, et al. Strength training normalizes resting blood pressure in 65- to 73-year-old men and women with high normal blood pressure. J Am Geriatr Soc 1999; 47 (10): 1215-21 151. Cononie CC, Graves JE, Hagberg JM, et al. Effect of exercise training on blood pressure in 70- to 79-yr-old men and women. Med Sci Sports Exerc 1991; 23 (4): 505-11

Correspondence: Dr Barbara Strasser, University for Health Sciences, Medical Informatics and Technology, Institute for Sport Medicine, Alpine Medicine and Health Tourism, A-6060 Hall i. T, Eduard Wallno¨fer-Zentrum 1, Austria. E-mail: [email protected]

Sports Med 2010; 40 (5)

Sports Med 2010; 40 (5): 417-431 0112-1642/10/0005-0417/$49.95/0

REVIEW ARTICLE

ª 2010 Adis Data Information BV. All rights reserved.

The Rodeo Athlete Sport Science: Part I Michael C. Meyers1 and C. Matthew Laurent Jr2 1 Department of Health and Human Development, Montana State University, Bozeman, Montana, USA 2 Department of Kinesiology, St Ambrose University, Davenport, Iowa, USA

Contents Abstract. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1. The History of Rodeo . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2. Physiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.1 Anthropometry and Body Composition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.2 Oxygen Uptake and Energy Expenditure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.3 Blood Chemistry . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.4 Coronary Risk. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.5 Muscular Strength and Power. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.6 Flexibility, Agility and Balance. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3. Kinesiology and Biomechanics. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4. Nutrition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5. Psychology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5.1 Personality Traits . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5.2 Precompetitive Mindset. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5.3 Injury Incidence and Mood States . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5.4 Athletic and Pain Coping Skills . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6. Training. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7. Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Abstract

417 418 420 420 421 422 422 422 423 423 424 424 424 425 426 426 427 427

Based on the tradition, history and lore of the American West, as well as the individualistic nature and lifestyle of the sport of rodeo, the rodeo athlete has achieved iconic status in sport, literature, art and entertainment. For over half a century, rodeo has become a staple of organized sport programmes in high schools, universities and international competitions. The origins of rodeo grew from ranch work dating back to the Spanish vaqueros in the 1700s. The sport was officially organized in 1929 and, by the 1930s, championships were determined and the sport of rodeo surpassed baseball and auto racing in spectator attendance. Since then, sponsorship has grown, resulting in extensive worldwide popularity through major media outlets. Despite growing popularity, few investigations exist regarding the scientific aspects of the sport. Rodeo competition is an activity that is basically intermittent in nature, with short periods of highly intense activity. When considering that experience and, thus, improvement in rodeo is achieved solely through constant and punishing practices involving actual and repetitive, human versus livestock competition, the practices closely imitate a sport-specific form of interval

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training. Studies, which address the anthropometric and performance characteristics of rodeo competitors, reveal that they are comparable to athletes in more traditional sports. The psychological constructs conducive to performance in rodeo have been varied and limited, with most research efforts focused on personality characteristics, sensation seeking and competitive anxiety. Nevertheless, when evaluated relative to higher levels of traditional sport performance, rodeo participants closely resemble their mainstream counterparts. Although efforts to quantify this non-traditional sport are still in the initial stages, information concerning what the optimal fitness level of rodeo athletes should be for maximal performance levels, in a basically anaerobic sport, remains to be determined and is an area for future study. Rodeo performance, as with all sports, is based on a multifactorial array of variables and, therefore, interdisciplinary efforts encompassing expertise across medicine, science and coaching are encouraged. Taking a comprehensive approach in the assessment of athletes, as well as the development and quantification of event-specific training protocols, may ultimately enhance athletic potential, minimize opportunity for injury and possibly provide information to coaches and allied health professionals for the appropriate development and optimal medical care of these athletes.

Rodeo is comparable in skill level, and often has an inherently higher risk of injury, when compared with traditional sports.[1-6] An extensive amount of skill and agility is required to oppose the tremendous power generated by livestock, overshadowed by an awareness of the constant potential for a debilitating injury on a daily basis. Unfortunately for the rodeo athlete, the sport science knowledge and facilities conducive for optimal performance that have existed for traditional sports over the years, still remain elusive for rodeo activities. Although researchers have extensively determined the physical, physiological and psychological aspects of various team and individual sports,[5,7-11] currently, there is still limited quantitative research directed toward this sport.[12-18] Rodeo competition encompasses the elements of skill, technique, strength, power and agility observed among traditional athletes, while also revealing a unique combination of high-velocity, high collision and repetitive stress, blended with ritualistic tradition and individualism that is unparalleled in modern sports.[1] Quantification of this sport, from a scientific standpoint, may minimize the potential for future trauma, enhance performance potential and ensure career longevity.[1,19,20] ª 2010 Adis Data Information BV. All rights reserved.

This review focuses on the sport science for rodeo, the history behind the sport and what is currently known about the physical and physiological status, coronary risk profile, strength and power levels, event-specific kinesiological and biomechanical aspects, nutritional habits and psychological indices associated with the rodeo athlete. In addition, future directions for optimal performance and prevention of unnecessary injury in this non-traditional sport are discussed. A subsequent instalment to this review[21] will discuss the incidence and mechanisms of trauma in rodeo, and recommendations to minimize injury potential. To ensure comprehensiveness, the literature search/data retrieval methodology that we employed included all sport science and medicine databases encompassing an unlimited time period and all sub-disciplines, as well as all references cited by prior authors in their respective areas of research. 1. The History of Rodeo The popularity of rodeo in the US and throughout the world is well documented.[22-25] Based on the tradition, history and lore of the American West and the individualistic nature and Sports Med 2010; 40 (5)

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lifestyle of the sport of rodeo, the rodeo athlete has achieved iconic status in sport, literature, art and entertainment.[22,26-29] Rodeo has become a staple of organized sport programmes in high schools, universities and international competitions for over half a century. The origins of rodeo grew from ranch work dating back to the Spanish vaqueros in the 1700s.[6,27,30] Although there is some discrepancy as to the first documented rodeo held in the US, informal ranch competitions developed into a spectator sport in many frontier towns as early as the 1880s. The sport was officially organized in 1929 through the Rodeo Association of America, was later developed into the Cowboy Turtle Association in 1936 and eventually became the Professional Rodeo Cowboy Association (PRCA) in 1975. By the 1930s, championships were determined, and the sport of rodeo surpassed baseball and auto racing in spectator attendance. The popularity grew from traditional US towns such as Cheyenne, WY; Pendleton, OR; and Salinas, CA and Canadian towns such as Calgary, AB to indoor shows at Madison Square Gardens in New York, the Boston Gardens in MA, USA, and even to unique venues such as the Yankee Stadium in New York. The National Intercollegiate Rodeo Association (NIRA) brought the sport into the academic setting in 1949, followed by the National High School Rodeo Association and the National Little Britches Rodeo Association, both formed in 1961 for the junior/adolescent ranks. Since then, sponsorship for the sport has grown and it gained extensive worldwide popularity after its exposure as an exhibition sport at the Winter Olympics in 1988 and through coverage from major media outlets (e.g. ESPN [Entertainment and Sports Programming Network], ABC [American Broadcasting Company], NBC [National Broadcasting Company]). In the early 1980s, sports medicine care soon followed, with the Justin Boot Company (Fort Worth, TX, USA) sponsoring the Justin Heeler programme at the PRCA level.[31] In 1992, Professional Bull Riders, Inc. was formed to take the bull riding event to urban areas through a season-long tour ª 2010 Adis Data Information BV. All rights reserved.

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and, even more recently, the team roping event has seen tremendous growth with over 127 000 members enrolled in the US Team Roping Championships.[30] Today, the sport draws over 33 million spectators annually, with an estimated 30 000 individuals competing in over 2800 sanctioned rodeos each year. Many of these contestants are young and/or have had limited, part-time experience.[3,31,32] The sport has experienced similar popularity in Canada, Brazil, New Zealand and Australia, and continues to spread worldwide, with bull riding now being considered as an ‘extreme’ sport.[22,23] Athletes either compete during a rodeo performance before spectators or in the ‘slack’ period before or following the performance, with many athletes often competing in more than one event. Traditional rodeo events typically include roughstock riding, steer wrestling and roping for male competitors and barrel racing for female competitors. Goat tying and breakaway calf roping are additional events sanctioned at the collegiate level. Roughstock riding, comprised of bull riding, bareback and saddlebronc riding is a subjectively scored event consisting of a competitor riding either an uncooperative bull or horse for 8 seconds. Steer wrestling is a timed event involving a competitor dismounting from a horse and attempting to turn and flip a moving steer off its feet. Both roughstock and steer wrestling events are considered high-contact activities resulting in extensive injuries to rodeo athletes. Calf roping, also referred to as tie-down roping, is a noncontact, timed event consisting of a competitor attempting to catch a young calf with the use of a rope while on horseback, then dismounting and flipping the calf and tying three of its legs. Team roping involves two equine-mounted contestants, comprised of a ‘header’ who ropes the steer’s horns, dallying/wrapping the rope around the saddle horn and turning the animal for the ‘heeler’ to rope the steer’s hind legs. Time is stopped when the ropes are pulled taut with the horses facing the steer. Barrel racing is a noncontact, timed event involving a competitor racing around a clover-leaf pattern of barrels while on horseback and seeking the fastest time. Sports Med 2010; 40 (5)

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2. Physiology Sports medicine specialists and coaches have continually searched for ways to identify and enhance athletic performance and minimize the risk of injury. Early characterization of athletes was not sport specific and was primarily based on subjective analyses derived from limited measurements of strength and speed. Subsequent conditioning or training programmes were also modified from this general concept. Within the last decade, a better understanding of the physiological responses to exercise and concomitant advances in technology have generated sportspecific training and rehabilitation programmes for traditional athletes that are based on a wide array of quantitative measurements.[33,34] Rodeo competition is an activity that is basically intermittent in nature, with short periods of highly intense activity. However, as in many other sports requiring anaerobic metabolism, several authors have suggested that an aerobic base significantly influences the onset of fatigue, performance potential and the adequate recovery of athletes from repetitive, high-intensity activity.[13,14,35-37] Physiological testing of athletes has demonstrated that those athletes who exhibit low-aerobic capacity and a high percentage of body fat have a higher incidence of fatigue, show decreases in performance levels and are predisposed to injury.[38-40] Although not conclusive, numerous authors have indicated the potential for significant improvements in athletic performance and a significant reduction in musculoskeletal injuries resulting from the identification and subsequent enhancement of muscular strength, flexibility and endurance in various athletes.[13,41-43] Sport science research on the sport of rodeo is limited. Currently, only two studies exist that have examined the exercise performance of rodeo athletes.[13,14] During the 1988–9 collegiate rodeo season, physiological assessments were performed on 20 male and 10 female athletes from the NIRA in the Central Rocky Mountain Region. The majority of athletes were present or former high school or college champions in their respective events. Data were collected on all athª 2010 Adis Data Information BV. All rights reserved.

letes to determine anthropometric status and body composition, cardiovascular endurance, resting blood chemistry, coronary risk, muscular strength and power, and visual reaction/movement time.[13] 2.1 Anthropometry and Body Composition

In this initial benchmark study (table I), steer wrestlers were found to be heavier and possessed more lean body mass than competitors in the roughstock and roping events. Roughstock athletes were shorter and revealed a lower percentage of body fat than males in the roping and steer wrestling events.[13] Past studies have indicated that lower percentages of body fat are typically observed in athletes involved in extreme anaerobic competition.[44] Whether this is a physical requirement for success in various sports or simply because of stereotypic selection by coaches is not conclusive. However, in rodeo athletes, the mean body fat of 12% was lower than that reported in football, baseball, ice hockey and field event athletes, and higher than that reported among athletes competing in cycling, basketball, soccer and wrestling.[45] Since performance is inversely related to excess body fat,[38,40] the higher percentage of body fat observed among steer wrestlers and female rodeo athletes, in relation to established athletic norms, poses some concern for improvement in the physical conditioning of athletes in this sport. However, the higher body-fat percentages reported among the steer wrestlers might be useful when noting the nature of the event, in which a larger and heavier body size may be advantageous when wrestling animals of considerable size. A similar argument could be considered for a higher body-fat percentage for athletes in other sports such as football; particularly, for the linemen and linebackers. Steer wrestlers possessed greater body size than was found among athletes in other male events which, in this study, led to a greater lean body mass. When compared with other intermittent activity sports, lean body mass among college rodeo competitors was lower than the lean body mass found in athletes competing in football, basketball, baseball and hockey.[45] Sports Med 2010; 40 (5)

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Table I. Mean anthropometric, body composition, exercise and reaction/movement response of collegiate rodeo athletes by eventa (reproduced from Meyers et al.,[13] with permission. The final, definitive version of Meyers et al.,[13] has been published by SAGE Publications Ltd./SAGE Publications, Inc., All rights reserved.ª) Variable

Event roughstock

roping

steer wrestling

barrel racing

21.8 – 0.7

20.1 – 0.8

20.7 – 1.2

20.2 – 0.7

Height (cm)

175.2 – 1.9

182.7 – 2.3

186.3 – 3.5

167.7 – 1.9

Weight (kg)

70.7 – 2.0

75.3 – 2.4

89.7 – 3.7

61.5 – 2.0

Body fat (%)

9.4 – 1.4

13.1 – 1.7

17.7 – 2.6

24.2 – 1.4

Age (y)

LBM (kg) VEmax (L/min) . VO2max (mL/kg/min) RERmax

64.0 – 1.6

65.3 – 1.9

73.5 – 2.9

46.6 – 1.6

153.8 – 4.7

160.9 – 5.6

165.3 – 8.6

103.8 – 4.7

50.1 – 1.6

47.9 – 1.9

47.2 – 2.9

36.9 – 1.6

1.4 – 0.02

1.4 – 0.02

1.3 – 0.04

1.4 – 0.02

HRmax (beats/min)

193.0 – 3.5

198.0 – 4.2

194.0 – 6.4

186.0 – 3.5

Tmax (min:sec)

12:35 – :27

12:22 – :33

12:15 – :50

10:25 – :27 118 – 3.0

BP (mmHg) rest systolic

128 – 3.0

120 – 3.5

130 – 5.4

rest diastolic

85 – 3.1

80 – 3.7

81 – 5.7

84 – 3.1

max systolic

187 – 5.9

180 – 7.1

192 – 9.8

166 – 5.9

81 – 2.4

80 – 2.8

88 – 4.3

83 – 2.4

max diastolic Lactate (mM/L) pre-exercise

2.3 – 0.5

3.5 – 0.7

2.9 – 0.9

2.3 – 0.5

post-exercise

14.8 – 1.3

15.5 – 1.8

13.7 – 2.6

11.3 – 1.4

Reaction (ms)

252.7 – 7.2

269.1 – 8.2

275.3 – 12.5

267.0 – 6.8

Movement (ms)

151.9 – 9.4

139.3 – 10.6

123.3 – 16.2

156.7 – 8.9

Total (ms)

404.6 – 8.0

408.4 – 9.0

398.6 – 13.6

423.7 – 7.6

a

Values are means – SEM.

BP = blood pressure; HRmax = maximal heart rate; LBM = lean body mass; max = maximal; ms = milliseconds; RERmax = maximal respiratory . exchange ratio; SEM = standard error of the mean; Tmax = maximal time on treadmill; VEmax = maximal expiratory volume; VO2max = maximal oxygen uptake.

2.2 Oxygen Uptake and Energy Expenditure

As most rodeo events are of a fast timeframe duration, athletes may employ mainly anaerobic requirements; other mechanisms (i.e. respiratory and cardiac muscle) also dictate critical power, especially post-exercise to return the body to homeostasis.[35,36]. Interestingly, when maximal oxygen uptake (VO2max) and energy expenditure data were compared with established norms, male and female rodeo athletes were considered to possess average aerobic capacity.[46,47] This suggests that training and competing in the male rodeo events (i.e. roughstock, roping, steer wrestling) may elicit an aerobic component that has not been previously considered or investigated. No differences in maximal expiratory volume ª 2010 Adis Data Information BV. All rights reserved.

. (VEmax), VO2max, maximal respiratory exchange ratio, energy expenditure, maximal heart rate, blood pressure or maximal time on the treadmill were found between males in the roughstock, roping and steer wrestling events.[13] When comparing maximal aerobic capacity with athletes involved in intermittent-activity . sports, male rodeo athletes exhibited VO2max values similar to those of elite Olympic basketball, football, water polo, tennis and gymnastic athletes, as well as values higher than those reported in weight lifters.[47] As expected, when compared with high-aerobic events, both male and female rodeo athletes possessed lower . VO2max and VEmax than observed in middle- and long-distance runners, cyclists, swimmers, soccer players, triathletes and speed skaters.[47,48] Sports Med 2010; 40 (5)

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When considering that experience and, thus, improvement in rodeo is achieved solely through constant and punishing practices involving actual, repetitive human versus livestock competition, practices closely imitate a sport-specific form of interval training. This offers a plausible . explanation for the higher than expected VO2 values observed in this population. Although performance decrements and the potential for injury can be related to low levels of fitness,[39,40,42] this may not be applicable to this group, since they possess comparable levels of aerobic capacity to other athletes successfully competing in intermittent sports. Regardless of the anecdotal arguments, the impact of aerobic training on the performance of rodeo athletes remains to be determined and is an area for future study. 2.3 Blood Chemistry

In a single study, selected mean resting blood chemistry parameters of collegiate rodeo athletes were within the normal range across all events and were comparable to athletes in other sports.[13] However, testing revealed three male athletes with iron concentrations ranging from 15 to 47 mg/dL, which is well below the accepted norms[46,49] and is in contrast to research that has traditionally indicated iron deficiency to be prevalent in female athletes following chronic physical training.[50,51] Although transferrin, apoferritin and ferritin levels were not established in the study to substantiate possible iron-deficient anaemia, no evidence of negative iron balance or subnormal haemoglobin concentration was observed in the female group. Possible causes may include an inadequately balanced diet with concomitant repetitive stress encountered by male rodeo athletes in their daily practices and competition.[45,52,53] With the typical US diet containing 5–6 mg per 1000 kilocalories, many athletes demonstrate difficulty in re-establishing optimal iron levels on their own.[52,54] The identification of the nutritional status of an individual as a contributor to iron (as well as other essential nutrients) continues to be a challenge that plagues the athletic population. ª 2010 Adis Data Information BV. All rights reserved.

2.4 Coronary Risk

Research has indicated hypertension as a major predictor of impending coronary dysfunction.[46] No evidence of hypertension, either pre- or postexercise, was identified within this group of athletes, with results falling within accepted ranges for normal populations.[55] When analysing the normotensive and body composition data with total cholesterol and high-density lipoprotein cholesterol ratios ranging from 3.0 to 4.0 across groups, results indicate an average-to-low risk for coronary heart disease in this population.[13,46] An additional coronary-risk concern is the use of tobacco products among athletes. Studies have consistently associated tobacco use with increased risk of oral cancer and adverse effects on the cardiovascular system.[56,57] There was no reported use of cigarette smoking found in this group of athletes; however, 30% of male athletes reported current use of smokeless tobacco or snuff. These results are similar to those found by Connolly et al.,[58] who reported smokeless tobacco use in 34% of professional baseball players. However, the interrelations and ramifications of oral tobacco use in this group of athletes are not well known and warrant further research. 2.5 Muscular Strength and Power

An isolated study on preseason isokinetic knee extension/flexion strength and power, in addition to handgrip strength, was reported in 20 male and 10 female athletes from the NIRA.[14] Peak quadriceps torques at 30 sec-1 ranged from 67 kg to 96 kg and 31 kg to 48 kg at 180 sec-1, with peak hamstring torques of 45–76 kg at 30 sec-1 and 24–36 kg at 180 sec-1 being documented across events. Peak quadriceps and hamstring power at 30 sec-1 of 77–165 W and 49–99 W were observed, with power outputs of 208–407 W and 157–343 W being reported at 180 sec-1, respectively. Although sex differences existed, there was a trend for steer wrestlers to exhibit higher torque and power, which is likely to be a function of greater body size and lean body mass than athletes in the other events. Findings were somewhat lower than those



















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reported for college football and baseball players and alpine skiers, but were still considered to be within normal limits.[59-61] When quadriceps-to-hamstring ratios were calculated, they ranged from 72.4% to 79.5% for the men, which is very high compared with normal ratios of 50–65%.[62,63] The enhanced hamstring strength of rodeo athletes in this study was similar to that reported for college football players,[43] and this finding probably reflects the involvement of the hamstring muscle group while spurring/riding the animals during all male events. The female rodeo athletes reflected normal ratios of 65–67%. Peak handgrip strengths ranged from 55 kg to 67 kg and from 39 kg to 41 kg among male and female rodeo competitors, respectively. Findings were similar to those of collegiate baseball players,[64] although lower than that reported for elite ice hockey players.[65] The overall inconsistency of leg and handgrip strength and power outputs across events may reflect event-specific training and/or the lack of structured uniform strength and conditioning programmes not often considered relevant among these athletes.[1] 2.6 Flexibility, Agility and Balance

It is commonly observed that flexibility, agility and balance are essential for optimizing performance and minimizing the risk of injury during sport, and has been addressed from a sport- and position-specific standpoint for most sports.[39,42,66-69] Although flexibility for improving range of motion has been recommended in rodeo,[2] no studies on rodeo athletes in these areas have been published. However, the lack of specificity of traditional conditioning techniques brings into question the validity of such attempts in this unique sport. Therefore, standard investigation may not be an essential determinant of rodeo success and may only be of value in regards to predisposition to injury.[39,42,68] 3. Kinesiology and Biomechanics Extensive technical skill is required to successfully compete in rodeo and, interestingly, ª 2010 Adis Data Information BV. All rights reserved.

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there is a paucity of research on the kinesiological and biomechanical aspects for the sport. With the exception of the kinematic analysis of rope velocity,[70] the biomechanics of bull riding, steer wrestling and roping have been discussed in lieu of computerized motion analysis.[37,71,72] Early computerized kinematic investigation of roping during simulated competition recorded mean, initial, mid-trajectory and final rope velocities of 16.2, 8.7 and 4.5 m/sec, respectively, resulting in an overall mean velocity of 10.1 m/sec, over a total throwing distance of 2.4 m.[70] In comparison, mean initial/release velocities of a thrown rope were 30–60% lower than traditional sport projectiles.[9] Subsequent kinesiological analyses divided the roping motion into five distinct phases: windup, primary arm acceleration, arm cocking, secondary arm acceleration and arm deceleration/ follow-through, with the motion being continually modified to accommodate split-second changes in environmental and competitive conditions.[72] These conditions, which are unique to this sport, include maintaining optimal plane of motion in relation to a non-stationary bovine target, overcoming inertia during completion of the throw while travelling on horseback at a speed of up to 55 km/hour, maintaining trajectory, direction and acceleration of a non-aerodynamic projectile in the absence of gyroscopic action, and adjusting to the influence and instability of equine footing. In summary, compared with traditional sport, the throwing task is considered extremely dynamic, requiring an extensive array of subconscious articular adjustments to maximize velocity and reach the elusive target. With the extensive impact forces and subsequent trauma observed in bull riding following dismount, recent attempts have been directed toward quantifying ground reaction forces (GRFs) of rodeo bucking bulls.[73] Utilizing computer simulation following filming during actual competition, authors reported mean GRFs of 2.9–4.0 times the bodyweight of the bull at the fore hooves, and 9.4–13.0 times the bodyweight in the hind hooves. Maximal forces achieved at the fore and hind hooves were 112 kN (10.0–14.2 times bodyweight) and 198.5 kN Sports Med 2010; 40 (5)

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(17.6–25.2 times bodyweight), respectively. Although GRFs varied based on the weight of the bull (500–885 kg), findings indicate that the flakjacket style of vests presently worn by roughstock athletes, offer limited protection from compression forces if stepped on by the animal at the end of the ride. It is well established that the analysis and subsequent training of skill-related components (i.e. speed, agility, coordination) enhances sport performance and minimizes predisposition to injury.[67,74,75] Limited investigation of the reaction/movement response of athletes in this sport (table I) indicated visual reaction time by event ranged from 253 to 275 milliseconds and movement time from 123 to 157 milliseconds, which are within the normal ranges commonly observed in athletes at the collegiate level, with no significant differences between gender and event.[13,76,77] Improvements in movement response and, ultimately, performance in this sport, are primarily achieved by ‘playing yourself into shape’, as substantiated in both early and recent studies.[1,78] There is a lack of adherence to traditionally organized conditioning/training programmes similar to other sports. In lieu of training protocols that closely duplicate the biomechanical and mental aspects of this unique sport, as well as various bucking-/roping-simulation machines, actual competition is primarily relied on for hand/eye-response refinement. This sole method of training is typically not observed in other sports, which usually encompass both competitive and non-competitive tasks and drills to optimize performance and minimize predisposition to injury. 4. Nutrition As previously mentioned, only one study has indirectly discussed nutritional concerns among rodeo athletes as a result of the indications of negative iron balance.[13] Possible potential causes cited include an inadequately balanced diet with concomitant overtraining commonly observed by rodeo athletes in their daily practices and competition. Typically not considered a training table sport, primary sources of information for most rodeo ª 2010 Adis Data Information BV. All rights reserved.

athletes stem from exposure to media-related nutritional advertisements and interaction with other competitors; therefore, in general, rodeo athletes are lacking optimal dietetic support. Coupled with the constant travel, self-coaching and inconsistent nutritional oversight, nonadherence to proper nutrition may be more prevalent than initially suggested,[13] although present data are insufficient to determine the extent of a disordered eating behaviour among these athletes.[53] The identification of nutritional status as a logical contributor to iron balance, as well as injury, has recently been readdressed.[52,79] 5. Psychology An extensive body of literature exists on the psychological characteristics of elite and collegiate athletes involved in traditional sporting events. Unfortunately for the rodeo athlete, the sophisticated sport psychology knowledge that exist, remains out of reach or is nonspecific in a sport receiving increased attention and financial support. Interestingly, there has been some debate as to whether or not participants in rodeo events perceive themselves as actual athletes or just performers.[15,24] With the advent and popularity of sports medicine care during the 1980s, rodeo competitors have evolved socially from their traditional role in Western lore to achieving athletic status.[24,31] In other words, society has elevated this population from simply cowboy status to a recognized athlete in sport.To date, there are a limited but growing number of published studies that provide quantitative information concerning the psychological make-up of the rodeo athlete. 5.1 Personality Traits

Investigation addressing psychological constructs conducive to performance in the nontraditional sport of rodeo has been varied and limited, with efforts primarily descriptive in nature in an attempt to quantify personality characteristics, sensation seeking and competitive anxiety at the professional level.[15,16] Initial Sports Med 2010; 40 (5)

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findings indicated a high level of independence, goal orientation and stress. In addition, these athletes experienced similar competitive trait anxiety, and did not espouse a sensation-seeking mentality, contrary to initial assertions posited by researchers and common belief among the general public. Psychological responsiveness was later assessed in collegiate athletes of the NIRA Southern Region to determine enduring and temporary psychological traits consisting of tension, depression, anger, vigour, fatigue, confusion, extraversion, neuroticism and conformity in barrel racers, ropers, roughstock riders and steer wrestlers.[17] Findings revealed that collegiate rodeo performers scored significantly higher in vigour and extraversion and significantly lower in depression, fatigue, confusion, total mood disturbance and conformity than collegiate norms. These rodeo cowboys/cowgirls exhibit the ‘iceberg profile’ as described by Morgan.[80] When compared with previous studies on mood states, rodeo participants were comparable to football players, body builders, cyclists and triathletes.[81-84] Interestingly, female rodeo performers scored significantly higher on neuroticism than their male counterparts in the roping, roughstock riding and steer wrestling events. Contestants involved in roping events scored higher in conformity than those individuals competing in barrel racing or roughstock riding events, but did not score any differently to steer wrestlers. No other significant differences were found between events, although there was a trend for roughstock performers to exhibit greater depression, anger, total mood disturbance and extraversion than indicated in other events. Some researchers have asserted that quality of sport performance can be delineated from personality constructs.[80,85,86] Previous research with highly successful athletes indicate high scores on extraversion and low scores on neuroticism when compared with the norms appropriate for their population.[80] This agrees with the current findings with rodeo performers in extraversion across all events and neuroticism in the male faction. When compared with higher levels of sport performance, the reflected similaª 2010 Adis Data Information BV. All rights reserved.

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rities between the collegiate rodeo athlete and earlier studies with elite athletes suggest that rodeo contestants are an athletic population. 5.2 Precompetitive Mindset

The effect of precompetitive mindset on athletic performance in sport is well documented. Investigation of collegiate gymnasts, wrestlers and elite Olympic athletes by Morgan and Johnson[87] and Silva and colleagues[88] indicated an inverse relationship between diminished tension, depression, anger, fatigue and confusion scores and enhanced performance outcome. Recent work has indicated that precompetitive anxiety levels dictated the type of coping strategies observed during competition.[89] Further research has revealed variations in precompetitive mindsets among athletes associated with the type of sport involved.[90-93] Murphy[94] proposed that the level of competitive stress was a function of the following: (i) the athlete’s self-perception at a given moment; (ii) the goal determination of the athlete; and (iii) the inherent atmosphere unique to the sport involved. Certainly, rodeo elicits a unique atmosphere that lends itself to the potential for shifts in precompetitive mood states as a function of the particular event. In an attempt to determine the magnitude and diversity of stress imposed upon rodeo athletes immediately prior to competition, mood states were quantified in 115 college rodeo athletes within 20 minutes preceding specific rodeo competition, while athletes were on horseback or in the immediate chute area while the participants were awaiting individual competition.[12] Findings indicated that collegiate rodeo athletes exhibited higher tension and vigour levels with concomitant decreases in depression, anger and fatigue prior to competition, in contrast to baseline profiles (i.e. initial psychological status away from the competitive environment) independent of competitive influence. Interestingly, no significant precompetitive effects between rodeo events and sex were found. Although one might expect distinctive differences in contact (roughstock, steer wrestling) versus non-contact (roping, barrel racing) events, non-perceptualization of inherent injury among younger Sports Med 2010; 40 (5)

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competitors in many sports has been reported and rodeo may be no exception.[5,95-97] 5.3 Injury Incidence and Mood States

Although numerous multifactorial models have indicated the role of psychology in injury incidence,[67,79,98,99] conflicting results and inconsistent replication have complicated attempts to substantiate a relationship between the occurrence of injury and psychological status in sport. Although early studies have found no relationship between psychological variables and injury prediction among football, basketball and volleyball athletes,[100-103] other studies have documented significant association between psychosocial response (i.e. self-concept, attentional style, life stress, mood states) and increased levels of trauma across various sports and levels of competition.[85,104-107] Differences may be attributed to the diversity of scales used, the difference between sports and subsequent levels of stress or the administration of inventories with limited correlation to sport injury.[108-110] Furthermore, only a single study has addressed the psychology-injury relationship in rodeo. Based on the premise that increased arousal state (i.e. tension, anxiety, vigour) typically occurs during competition,[111] which may subsequently enhance the potential for injury or effect treatment,[85,106] pre- and non-competition mood states and injury data were compiled during a single collegiate season.[112] Findings revealed no significant association between precompetitive mood states and the incidence of upper body, lower body or total injuries; however, a significant inverse relationship was found between a higher incidence of injury and non-competitive vigour. 5.4 Athletic and Pain Coping Skills

Over the last decade, the area of coping skills has evolved with an increased emphasis directed toward identifying skills that are relevant to adjusting to the sport environment. Based on the premise that the ability to effectively cope during competition dictates performance outcome,[69,113] the plethora of potential constructs ª 2010 Adis Data Information BV. All rights reserved.

assessing anxiety management, concentration, self-confidence, mental preparation, dissociation, problem solving and motivation continue to be investigated.[89,114] Subsequent work was directed toward the areas of coping skills and athletic injury, as well as pain coping styles across various sport populations.[18,109,115] Investigation into the athletic coping skills of athletes has also resulted in equivocal findings. Although some studies have indicated motivation differences among elite and non-elite Olympic weightlifters, and greater anxiety management skills and self-confidence in elite versus subelite equestrian athletes,[116,117] others have found no differences in athletic coping styles and increased performance in judo and tennis athletes.[118,119] A more positive coping response was significantly associated with a lower incidence of injury and a higher level of athletic success.[109,115] In a single study addressing athletic coping skills among college rodeo athletes, highly skilled competitors revealed a significantly higher response in anxiety management, concentration, confidence and motivation than lower skilled athletes, but with no significant differences observed across rodeo events.[120] In a subsequent focus on pain coping styles at the collegiate level, significant differences existed between topand bottom-ranked athletes, sex and athletes competing in high versus low injury-potential events.[18] In conclusion, rodeo athletes exhibit personality constructs, mood state patterns and coping skills similar to athletes in more traditional sports, with a mindset reflecting a substantial relationship with performance outcome and prevalence of injury.[17,86,120] The high variability of these traits within and between events and sexes coincide with highly individualized responsiveness found in other cognitive, somatic and behavioural research on sports.[18,121] Additional multivariate research, which defines and delineates precompetitive effects in rodeo with subsequent performance outcome and physiological parameters, as well as establishing a possible association between precompetitive psychological response and injury potential (as confirmed in Sports Med 2010; 40 (5)

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other sports), is a possibility.[80,122] Continued research may be useful in the identification of personality structure as it relates to current performance and injury status, future performance level and the establishment of sport-specific psychological techniques that may accentuate performance response and lead to career longevity of the rodeo athlete. 6. Training With the voluminous amounts of literature and recommendations written on training regimens,[9,42,66,69,123-125] limited efforts have been directed toward rodeo. Tuza[126] made an initial attempt to define training components deemed essential for optimal rodeo performance based on traditional parameters. Later work attempted to improve bull riding and steer wrestling performance through periodization training.[37,71] However, no quantification of the efficacy of the proposed conditioning regimens were conducted, although physiological testing of the rodeo athlete was emphasized before any training programme could be considered adequate.[126] However, with limited scientific support, traditional training regimens may provide a firm foundation of strength and endurance, although they should be interpreted with caution from a sport-specific standpoint as they relate to the physical requirements of this sport. It is recognized that past performance levels, livestock draw and task difficulty influence present physiological and psychological outcome.[12,127] As found/shown in other sports, physiological and psychological variables beyond standard-training benchmarks may be at play.[67,124] 7. Conclusions Although the efforts to quantify this nontraditional sport are still in the initial stages, information concerning what the optimal fitness level of rodeo athletes should be for maximal performance levels, in a basically anaerobic sport, remains to be determined and is an area for future study.[13,128] Additional development of event-specific strength and conditioning protoª 2010 Adis Data Information BV. All rights reserved.

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cols should then be derived from objective criteria and incorporated in weekly practice regimens. Regardless of the anecdotal arguments, based on a substantial body of sport research,[42,69,123] the effect of a comprehensive, criterion-based conditioning programme should significantly improve the resilience and performance of these athletes. Continued research should be directed toward optimizing performance outcome as well as preventive aspects of sports medicine and postinjury care. As extensively conducted in other sports,[20,129,130] there is an increased need for research that addresses the kinematic and kinetic techniques that are specifically involved in each event, and the respective relationship these have to optimal sport performance and injury potential.[131,132] For instance, studies have not quantified the specific phases and muscle-firing activity of the riding and steer wrestling motion, as documented in other sports. These efforts could provide information to enhance the conditioning and/or rehabilitation of event-specific muscles. The additional health risk concerning the use of smokeless tobacco products among a small percentage of this athletic population also needs to be further investigated. Since the majority of the studies were descriptive, no direct effects of the measured variables on performance of the incidence of injuries is known, although speculation is possible. With regard to nutrition, potential non-adherence to correct caloric intake needs to be further identified, and this will consequently lead to realistic nutritional expectations, sportspecific dietary planning and sound educational support. Psychological profiles may be useful in the identification of personality structure, current performance and injury status, future performance level and the establishment of sport-specific psychological techniques that may accentuate performance response and lead to career longevity of the rodeo athlete.[17,86] How psychological preparation truly relates to success in the rodeo athlete is a question that warrants further investigation. Proposed theories of self-concept affecting injury potential, the dissociation of Sports Med 2010; 40 (5)

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pain as a function of individual perception, cognitive approaches to performance demands, and emotional/somatic response on rehabilitative processes also need further understanding.[94,106] Investigation of psychological influence upon performance, injury potential, pain and, ultimately, rehabilitation in rodeo may also provide additional insight into these unique athletes.[1,86] Finally, as with all sports, rodeo performance is based on a multifactorial array of variables and, therefore, interdisciplinary efforts encompassing expertise across medicine, science and coaching are encouraged.[69,133,134] Taking a comprehensive approach in the assessment of athletes, as well as the development and quantification of event-specific training protocols, may ultimately enhance athletic potential, minimize the potential for injury and possibly provide information to coaches and allied health professionals for optimal medical care and the appropriate development of these athletes. Acknowledgements No sources of funding were used to assist in the preparation of this review. The authors have no conflicts of interest that are directly relevant to the content of this review.

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124. Giles LV, Rhodes EC, Taunton JE. The physiology of rock climbing. Sports Med 2006; 36 (6): 529-45 125. Mermier CM, Janot JM, Parker DL, et al. Physiological and anthropometric determinants of sport climbing performance. Br J Sports Med 2000; 34: 359-66 126. Tuza G. Training considerations for rodeo. Nat Strength Cond Assoc J 1985; 6: 38-41 127. Heyman S. Comparisons of successful and unsuccessful competitors: a reconsideration of methodological questions and data. J Sport Psych 1982; 4: 295-300 128. Meyers MC, Sterling JC, Souryal TO. Radiographic findings of the upper extremity in collegiate rodeo athletes. Med Sci Sports Exerc 2003; 35 (4): 543-7 129. Elliott B, Khangure M. Disk degeneration and fast bowling in cricket: an intervention study. Med Sci Sports Exerc 2002; 34 (11): 1714-8 130. Hintermeister RA, O’Connor DD, Dillman CJ, et al. Muscle activity in slalom and giant slalom skiing. Med Sci Sports Exerc 1995; 27: 315-22 131. Whiting W, Zernicke R. Biomechanics of musculoskeletal injury. Champaign (IL): Human Kinetics, 1998: 113-35 132. Winston F, Schwarz D, Baker S. Biomechanical epidemiology: a new approach to injury control. J Trauma 1996; 40: 820-4 133. St Clair Gibson A, Noakes TD. Evidence from complex system integration and dynamic neural regulation of skeletal muscle recruitment during exercise in humans. Br J Sports Med 2004; 38: 797-806 134. Sawka MN, Noakes TD. Does dehydration impair exercise performance? Med Sci Sports Exerc 2007; 39 (8): 1209-17

Correspondence: Adjunct Professor Michael C. Meyers, Department of Health and Human Development, Montana State University, 139 Reid Hall, Bozeman, MT 59717-2940, USA. E-mail: [email protected]

Sports Med 2010; 40 (5)

REVIEW ARTICLE

Sports Med 2010; 40 (5): 433-447 0112-1642/10/0005-0433/$49.95/0

ª 2010 Adis Data Information BV. All rights reserved.

The Effect of Exercise on Haemodynamics in Intermittent Claudication A Systematic Review of Randomized Controlled Trials Belinda J. Parmenter,1 Jacqueline Raymond1 and Maria A. Fiatarone Singh1,2,3 1 Exercise, Health and Performance Faculty Research Group, Faculty of Health Sciences, University of Sydney, Sydney, New South Wales, Australia 2 Sydney Medical School, University of Sydney, Sydney, New South Wales, Australia 3 Hebrew SeniorLife and Jean Mayer USDA Human Nutrition Research Center on Aging, Tufts University, Boston, Massachusetts, USA

Contents Abstract. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1. Methods. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1.1 Search Strategy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1.2 Inclusion and Exclusion Criteria. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1.3 Study Selection and Data Extraction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1.4 Data Analysis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2. Results . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.1 Quality Assessment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.2 Study Characteristics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.3 Lower Limb Haemodynamic Outcome Measures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.3.1 Resting Ankle Brachial Index (ABI) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.3.2 Post-Exercise ABI . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.3.3 Resting Arterial Calf Blood Flow . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.3.4 Reactive Hyperaemic Blood Flow Post-Ischaemia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.3.5 Resting Toe Systolic Pressure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.4 Relationship of Prescriptive Elements to Haemodynamic Measures . . . . . . . . . . . . . . . . . . . . . . . . 2.5 Relationship of Medication Use to Haemodynamic Measures . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.6 Relationship of the Improvement in Function to Changes in Haemodynamic Measures . . . . . . 3. Discussion. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.1 Future Research and Quality of Trials . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4. Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Abstract

433 435 435 435 436 436 437 437 438 439 439 439 440 440 441 442 442 442 442 444 445

Changes in lower limb haemodynamics such as arterial pressure and/or flow have often been, and continue to be, cited as possible mechanisms for the improvement in walking performance that occurs with exercise training in individuals with peripheral arterial disease (PAD), but data are conflicting in this regard. There are a small number of literature reviews examining the effects of exercise on PAD, however, there has been insufficient analysis synthesizing possible mechanisms of effect, overall benefits and limitations of these trials. Our objective was therefore to systematically review the evidence

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for the effect of exercise on lower limb haemodynamic measures of resting and post-exercise ankle brachial index (ABI), resting toe pressure, and resting and reactive hyperaemic calf blood flow in PAD. A systematic search of studies published between 1934 and March 2010 was conducted using MEDLINE, EMBASE, AMED, SportDiscus, CINAHL, PEDro, Premedline, Google Scholar and Web of Knowledge databases. Eligible studies included randomized controlled trials using an exercise intervention for the treatment of intermittent claudication with haemodynamic measures of disease severity as outcomes. Relative effect sizes (ESs) and 95% confidence intervals were calculated for outcomes. Correlation and regression analyses were performed to establish relationships between symptoms and haemodynamic outcomes. Thirty-three trials including 1237 subjects with mild to moderate claudication met the eligibility criteria. Exercise did not significantly change lower extremity haemodynamics in most trials; nor were clinical improvements related to changes in resting ABI (mean ES 0.09 – 0.26; r = 0.02; p = 0.94), post-exercise ABI (mean ES 0.18 – 0.3; r = -0.33; p = 0.52) or reactive hyperaemic calf blood flow (mean ES 0.38 – 0.67; r = 0.35; p = 0.26). A relationship may exist between a change in symptoms and changes in resting toe pressure (mean ES 0.22 – 0.22; r = 0.75; p = 0.25) and resting calf blood flow (mean ES 0.09 – 0.16; r = 0.59; p = 0.22). Changes in resting and post-exercise ABI and reactive hyperaemic calf blood flow do not appear to explain the clinical benefits of exercise in PAD. More study is required in the areas of resting toe pressure and resting calf blood flow.

Lower extremity peripheral arterial disease (PAD) is a chronic occlusive disease of the aorta, its branches and the lower extremity arteries. Total disease prevalence has been estimated at 3–10%, increasing to 15–20% in persons >70 years of age.[1] Between 3% and 7% of individuals with PAD suffer with intermittent claudication (IC),[2] which can progressively impair functional mobility, consequently reducing quality of life. Ten to 20% of those patients with IC will develop worsening claudication and a further 1–2% will develop critical limb ischaemia.[3] Exercise is one form of management for PAD that has been shown to significantly improve function, with two independent meta-analyses reporting mean improvements in walking ability of 150%[4] and 179%.[5] In contrast to its clear effect on function, the mechanism by which exercise training improves IC is controversial. Numerous randomized controlled trials (RCTs) investigating possible mechanisms of effects of exercise on function have been conducted.[4-7] One suggested mechanism involves lower limb haemodynamic measures such as arterial presª 2010 Adis Data Information BV. All rights reserved.

sure and blood flow.[8-11] However, there has been insufficient analysis synthesizing the overall benefits and limitations of these trials, as well as the relative effects of the various exercise prescriptions utilized. Assessments of the key reviews that are currently referred to in the literature are presented in table I. The review currently most referred to was first completed in 2000 by Leng et al.[4] for the Cochrane Database of Systematic Reviews. This analysis identified ten RCTs and was updated in 2005 and 2007 with no further inclusions. In 2008, Watson et al.[7] updated this review, with 12 further inclusions. However, this review also included trials in which there was an active control treatment that the exercise group did not receive, minimizing any benefits attributable to the experimental exercise condition. These trials should have been designed as ‘non-inferiority’ trials, and appropriately powered for such comparisons of two active treatments, but close inspection suggests that this was not the case. Thus, the magnitude of the exercise effect relative to ‘control’ concluded by this review would Sports Med 2010; 40 (5)

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Table I. Assessment of previous reviews available on current literature

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exercise training programmes, or clinical improvements, were related to these outcomes.

Study (y)

Assessments

Gardner and Poehlman[5] (1995)

Not limited to RCTs (3 RCTs + 18 UCTs and NRTs)

1. Methods

Excluded results from RCTs in final conclusion

1.1 Search Strategy

Did not analyse effect of supervision Outcome measures did not include haemodynamics Leng et al.[4] (2000) Watson et al.[7] (2008)

Included trials in which the control group received an alternative treatment to the intervention group, therefore did not isolate the benefits of exercise Did not analyse effect of supervision Analysed some prescriptive elements, but comparisons between different modes and intensities were not made Outcome measures did not include all measures of haemodynamics examined in the literature

Bendermacher et al.[6] (2006)

Not limited to RCTs Did not analyse prescriptive elements Outcome measures did not include haemodynamics

NRTs = non-randomized trials; RCTs = randomized controlled trials; UCTs = uncontrolled trials.

have been attenuated because of this analytic approach. This Cochrane publication[7] identified four RCTs with peak exercise calf blood flow and seven RCTs with ankle brachial index (ABI) as outcome measures, and deemed the effect on peak exercise blood flow as inconclusive because of limited data. As they included five trials in which the control group received an alternative treatment to the intervention group, conclusions about the isolated effect of exercise on outcomes compared with usual care are precluded. Therefore, our objective was to systematically review the literature to identify the relative efficacy of various modes of structured exercise in individuals with PAD on all measures of lower extremity arterial pressure and flow, including resting and post-exercise ABI, resting toe pressure, and resting and reactive hyperaemic calf blood flow. A secondary objective was to identify whether various prescriptive elements such as duration, intensity, supervision and/or length of ª 2010 Adis Data Information BV. All rights reserved.

The literature search was performed, with no language restrictions, using the electronic databases MEDLINE, EMBASE, AMED, SportDiscus, CINAHL, PEDro, Premedline, Google Scholar and Web of Knowledge. Databases were searched initially from the earliest records up until 15 January 2009, with the search repeated on the 22 March 2010. Bibliographies of all eligible papers and reviews identified from the electronic search were manually searched. Search terms included ‘peripheral vascular’, ‘claudica* (where * was used for truncation)’, ‘peripheral arter*’, ‘arterial occlusive Outcome measures did not include disease’, ‘thrombosis’, ‘ischaemia’, ‘exercise’, ‘physical activity’, ‘aerobic’, ‘resist*’, ‘weight lifting’, ‘strength’, ‘muscular exercise’, ‘squat’, ‘lunge’, ‘knee bend’, ‘calf raise’, ‘heel raise’, ‘circuit training’, ‘endurance’, ‘stretch’, ‘physical training’, ‘fitness’, ‘cardiovascular training’, ‘walk’, ‘cycling’, ‘step’, ‘exertion’, ‘exercise therapy’, ‘muscle stretching exercise’, ‘random*’ and ‘clinical trial’. 1.2 Inclusion and Exclusion Criteria

Studies were included if they met the following criteria: (i) an RCT that employed any mode of prescribed structured exercise (defined as any modality of physical activity where clear prescriptive instructions were provided, whether supervised or unsupervised, and conducted in any setting) for the treatment of IC; (ii) inclusion of haemodynamic measures of disease severity, including resting and post-exercise ABI, resting toe pressure, resting and reactive hyperaemic calf blood flow; and (iii) inclusion of functional assessments such as initial and absolute claudication time/distance, or subjective measures of symptom progression as outcomes. We included studies that compared two different types of exercise prescription, where they differed in one variable (e.g. supervision, intensity, mode, duration). A non-exercising control group was deemed not Sports Med 2010; 40 (5)

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essential for these analyses. Trials were excluded if: (i) they included subjects with asymptomatic lower limb atherosclerosis; (ii) the control group was prescribed medications or surgical interventions for treatment of symptoms of PAD and the exercise/treatment group was not; or (iii) only acute bouts or <4 weeks of exercise were used. 1.3 Study Selection and Data Extraction

One author (BP) conducted the search and extracted all data. After eliminating duplications, all papers identified by the search strategy were screened by the author, first by title and then by abstract using the above eligibility criteria. Papers retrieved for evaluation were screened by two authors (BP and JR). Quality assessment of all eligible papers was undertaken separately and in duplicate by these two authors using a modified version of the Physiotherapy Evidence Database (PEDro) scale.[12] As per PEDro guidelines, points are only awarded when a criterion is clearly satisfied. Supervision of exercise was added to the quality assessment as a variable considered important in assessing the quality of the trials,[6] but not included in the final score. Any disputes were resolved by consensus, or by a third author (MFS) when necessary. Subjects were graded according to the Rutherford clinical categories of chronic limb ischaemia.[13] Tests for reactive hyperaemic blood flow post-ischaemia were grouped together regardless of ischaemic procedure. Authors were contacted for missing data whenever possible. 1.4 Data Analysis

Due to the heterogeneity of exercise prescriptions, outcomes assessed and measurement tools used, a systematic review was conducted rather than a meta-analytic approach. Trials were split into two groups: (1) exercise versus control; and (2) exercise versus exercise. Mean differences and between-group and/or intra-group effect sizes (ESs) were calculated for both groups. For group 1, between-group ES adjusted via Hedges’ bias-corrected for small sample sizes and 95% confidence intervals (CIs) were calculated for each outcome measure where applicable using formula 1: between-group ES = (Dtreatment ª 2010 Adis Data Information BV. All rights reserved.

Dcontrol)/pooled baseline standard deviation (SD), where D indicates change.[14] For group 2, an intra-group ES was calculated for each treatment arm using formula 2: intra-group ES = (post-score - pre-score)/baseline SD.[14] For group 2, a between-group ES was also calculated using formula 1 outlined above. Final sample sizes excluding dropouts were used to calculate ESs, unless there had been imputation of missing data from dropouts. Prior to calculating ESs, data were manipulated if necessary to derive means and SDs as follows: 1. When sample size exceeded 25 and the mean was not reported, the median was substituted for the mean. In sample sizes <25, means were calculated using the following formula: x » (a + 2m + b)/4, where m = median, a = the smallest/ minimum value, and b = the largest/maximum value.[15] 2. If data were presented as mean and range or interquartile range then SDs were calculated using the following formulae: SD = one quarter of the range or SD = four fifths of the interquartile range[15] 3. Values reported as standard error (SE) were converted to SD using the following formula: SD = SE · On, where n = number of subjects. ESs were interpreted according to Cohen’s interpretation of ‘trivial’ (<0.20), ‘small’ (‡0.20 to <0.50), ‘moderate’ (‡0.50 to <0.80) and ‘large’ (‡0.80).[16] ESs and 95% CIs were graphed as forest plots, with the triangle representing the between-group ES for group 1, and the square representing the intra-group ES for group 2. The horizontal line represents the 95% CI. For group 1 and group 2, the between-group and intragroup ESs, respectively, were deemed to have no statistical significance when the CI crossed the vertical midline (i.e. included 0).[17] In addition, for group 2, if the between-group ES and its 95% CI were inclusive of 0 then one form of exercise was deemed non-inferior to the other. In calculating between-group ESs for group 2, walking and lower intensity prescriptions were classified as usual prescription and therefore allocated as ‘control’ group. The subsequent between-group ES analysis indicated whether the novel exercise was ‘inferior’ (negative ES) or superior (positive ES) to the standard exercise Sports Med 2010; 40 (5)

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prescription (e.g. walking). In the leg cycling versus arm crank trials, leg cycling was allocated as the ‘control’ group. Finally, correlation and regression analyses were performed to establish relationships between symptoms and haemodynamic outcomes. Measurements are presented as mean – standard deviations and significance was set at p < 0.05 unless otherwise indicated. 2. Results Results of the search strategy are presented in figure 1. Thirty-three intervention trials met all inclusion criteria.[8-11,18-48] Among the 134 papers fully assessed for inclusion in this review, 92 were excluded for the following reasons: 58 were not RCTs; 12 were duplicate data sets and had no further outcome measures relevant to the review;

four papers were not, at least, 4-week training interventions; seven papers did not supply the control group with the same active treatment that the intervention group received; two papers investigated the effect of medication rather than exercise; two papers included subjects with asymptomatic disease; one paper did not provide structured exercise advice to its intervention group; one paper did not provide enough information on exercise prescription to determine whether it fit the eligibility criteria for structured exercise; and five papers were unable to be located. 2.1 Quality Assessment

An assessment of the study quality according to a modified PEDro scale is presented in table I in the Supplemental Digital Content 1, at http://

Search results n = 14 833 Duplicates n = 1783 After removal of duplicates n = 13 050

Excluded on basis of title or abstract n = 12 974

Retrieved for evaluation n = 76

Added from hand searching n = 58 References fully assessed n = 134

Excluded on basis of eligibility criteria n = 92

Included papers n = 42 Included trials n = 401

Haemodynamic outcomes n = 33 trials Claudication symptom outcomes n = 37 trials Fitness outcomes n = 20 trials Quality of life and psychosocial function outcomes n = 15 trials

Aerobic exercise trials n = 36

PRT trials n=4

n = 31

n=2

Haemodynamic outcomes n = 33 Fig. 1. Flow of papers identified from search strategy. 1 Seven trials subsequently excluded as a result of non-reporting on lower limb haemodynamic outcomes. PRT = progressive resistance training.

ª 2010 Adis Data Information BV. All rights reserved.

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links.adisonline.com/SMZ/A4. Overall quality of the included trials was only moderate, with, on average, five of the ten quality criteria being met (mean 4.9 – 0.9, range 2–6/10). The most common limitations were in the areas of concealment of randomization, blinding of subjects, therapists and assessors and intent-to-treat analyses. In assessing robustness of the evidence provided by these trials, all studies included in this review were RCTs. Thirty trials[8-11,19-28,30,32-48] (91%) reported that groups were similar at baseline for all the factors that determine the clinical outcomes. One trial[18] reported a significant difference at baseline in the potentially relevant clinical outcome of ABI. The two remaining trials[29,31] did not report similarities or differences between groups at baseline with respect to at least one measure of the severity of the condition. Twentytwo trials (67%)[11,19-22,24,25,27,28,30-34,37-39,42,44-48] reported measurement of at least one key outcome from more than 85% of the subjects initially allocated to groups. Therefore, a >15% dropout rate may have disguised the true treatment effect of the intervention in 11 of the trials. Only 11 of the trials[8,10,21-25,28,31,37,41,44] performed an intent-to-treat analysis, where analysis was performed based on participants receiving treatment or control conditions as originally allocated. No trials blinded participants or the therapists who administered the therapy, and only three trials[11,19,36] blinded assessors who measured at least one key outcome. Thus, the assessor’s belief in the effectiveness of the intervention in 30 of the 33 trials may have subconsciously distorted the measurement of treatment outcomes.[49] However, it is recognized that blinding of participants and therapists in an exercise intervention trial is extremely difficult unless ‘sham’ exercise was used. Overall, between-group statistics (85%)[8-11,18-21,23,24,26,27,29,30,32-45,47,48] and point measures, and measures of variability (91%)[8,9,11,18,20-28,30-48] were well reported. Seventy-six percent of trials provided complete supervision for subjects during training interventions. Seven trials[18,19,26,30,31,34,43] (21%) provided the intervention group with a level of supervision ranging between zero and three suª 2010 Adis Data Information BV. All rights reserved.

pervised sessions per week. One trial did not report whether the training of the intervention group was supervised.[33] In summary, the overall quality of the literature reviewed was moderate. Taking all of the above design and analysis features into account, only two[11,19] of the 30 trials fulfilled most of the recommended PEDro criteria for trial validity and would therefore be considered relatively robust.[49] 2.2 Study Characteristics

The 33 trials included 1237 subjects (698 of whom underwent exercise training), ranging in sample size from 12 to 149. Nearly 80% of subjects were male, and aged 56–72 years. Overall, duration of illness, if reported, was relatively short. Most trials selected subjects with mild to moderate IC or Rutherford grade 1, categories 1 or 2 classification.[50] Four trials[11,32,40,47] incorporated subjects with severe claudication in their inclusion criteria; however, inclusion was not confirmed nor analysed separately in the results. No trials included subjects with severe PAD defined as Rutherford grade II, category 4 (ischaemic rest pain) or grade III, category 5 and 6 (minor or major tissue loss).[3] Almost all subjects were overweight or obese, with hypertension, coronary artery disease and diabetes mellitus as co-morbidities. See table II in the Supplemental Digital Content for more information. Most control groups were commenced on usual medical care and instructed either to maintain the usual level of activity or not to exercise on a regular basis. Two trials[32,33] compared surgical revascularization versus surgical revascularization plus exercise training, and two compared pharmacotherapy, namely dipyridamole plus aspirin,[34] and cilostazol[28] with pharmacotherapy plus exercise training. Ten trials[9,10,18,19,37,39-41,44,48] compared two exercise training modalities. Aerobic exercise training was the most common form of training (94% of trials), with walking and lower extremity aerobic (LEA) exercise the most common modes. LEA was defined by one trial[43] as a series of active and passive leg exercises, in another[24,51] as a Sports Med 2010; 40 (5)

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combination of walking, running, dancing and playing ball, and in one further[34] as raising, lowering, flexing and extending the lower extremities, and making lateral foot movements. Four trials[19,28,42,46] based aerobic training on circuittype exercises involving the calf and quadriceps muscle groups, two of which[28,46] also included a small amount of arm swinging exercise. Four of the eleven LEA trials[22,29,32,33] reported the training mode as dynamic leg exercise, but they did not expand on exactly what this entailed. The remaining seven aerobic exercise trials[18,20,21,30,39,44,48] prescribed training such as lower limb cycling, arm cranking, pole-striding and stepping, with one trial[48] comparing arm cranking to combined arm crank/walking training. One trial[27,38] compared aerobic exercise versus progressive resistance training (PRT), and one trial[35] examined the effect of PRT alone. Frequency ranged from 2 to 7 days per week, but most commonly 3 days per week (61% of trials). Most trials (87%) used the subject’s claudication pain – either to onset, mild to moderate or maximum levels tolerable – as a measure of intensity, and chose workload based on a percentage achieved at baseline testing. Most trials (76%) were fully supervised. Follow-up of subjects and repeated outcome measure assessment varied from every 4 weeks throughout the duration of the programme, to pre- and postprogramme only with the majority of trials (70%), repeating outcome measures at regular intervals during the exercise programme. Eleven trials[9,10,20,21,25,26,28,30,34,36,40,43] excluded subjects who were taking medications specifically for symptoms of PAD (i.e. vitamin E, pentoxifylline, cilostazol), and/or medications that may have a direct impact on haemorheology or haemodynamic outcomes (e.g. warfarin, b-blockers or vasodilators). See table III in the Supplemental Digital Content for more information. 2.3 Lower Limb Haemodynamic Outcome Measures

A complete summary of outcomes measured, mean differences and ESs are presented in tables IV–XII of the Supplemental Digital Content. ª 2010 Adis Data Information BV. All rights reserved.

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2.3.1 Resting Ankle Brachial Index (ABI)

Twenty-nine trials measured resting ABI, and analysis suggests that resting ABI did not increase to a statistically significant degree following exercise training. Exercise prescription elements (supervision, dose and modality) were notably not related to this outcome. In the exercise versus control group comparisons (table IV, in the Supplemental Digital Content), 22 between-group ESs were calculated from 25 trials, but only one trial[11] reported a significant effect of exercise training. In this trial, the between-group ES was negligible and nonsignificant. For the remaining 21 ESs calculated, although the range was broad (-0.35 to 0.63), the mean ES (0.09 – 0.26) was trivial, and all 21 were non-significant (figure 2). In addition, the magnitude of non-significant absolute change in ABI was trivial (mean 0.03 – 0.06). Only one trial in the exercise versus exercise group (table V, in the Supplemental Digital Content) reported a significant time effect[10] with exercise training, and no trials reported a significant group · time effect. Twelve intra-group ESs were calculated and all but one were negligible and non-significant (figure 2). In addition, six between-group ESs were calculated and although the range was broad (-0.22 to 0.52), the mean -0.03 was trivial and all six were non-significant. Thus, there were no differences among the exercise prescriptions used in these trials with respect to improving resting ABI. 2.3.2 Post-Exercise ABI

Exercise did not increase post-exercise ABI in the eight trials reporting it. In the exercise versus control group (table VI, figure 1, in the Supplemental Digital Content) five between-group ESs were calculated and, though the range was broad (-0.29 to 0.54), the mean 0.18 was trivial and all were non-significant. In addition, the magnitude of non-significant change (mean 0.03 – 0.05) reported in these trials was negligible. The intra-group ESs we calculated for the exercise versus exercise group (table VII, figure 1, in the Supplemental Digital Content) were trivialmoderate and non-significant. The between-group ES was trivial and non-significant, indicating no Sports Med 2010; 40 (5)

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Zwierska et al. (2005) Zwierska et al. (2005) Gardner et al. (2005) Gardner et al. (2005) Kakkos et al. (2005) Kakkos et al. (2005) Savage et al. (2001) Savage et al. (2001) Regensteiner et al. (1997) Regensteiner et al. (1997) Hiatt et al. (1994), Regensteiner et al (1996) Hiatt et al. (1994), Regensteiner et al (1996) McGuigan et al. (2001) Hiatt et al. (1994), Regensteiner et al (1996) Zwierska et al. (2005) Zwierska et al. (2005) Collins et al. (2005) Collins et al. (2003) Stewart et al. (2008) Stewart et al. (2008) Hobbs et al. (2006) Tisi et al. (1997) Mannarino et al. (1991) Lundgren et al. (Clin Sci 1989) Lundgren et al. (Ann Surg 1989) Crowther et al. (2008) Crowther et al. (2008) Wood et al. (2006) Sandri et al. (2005) Mika et al. (2005) Gardner et al. (2001) Gibellini et al. (2000) Hiatt et al. (1994), Regensteiner et al (1996) Hiatt et al. (1990)

Exercise vs exercise

Control vs exercise

−3

−2

−1

0

1

2

3

ES (95% CI) Favours control Standard exercise

Favours exercise Experimental exercise

Fig. 2. Forest plot of control vs exercise between-group effect size (ES; triangles) and exercise vs exercise intra-group ES (squares) and 95% confidence intervals (CIs) for resting ankle brachial index. Included studies: Zwierska et al.,[44] Gardner et al.,[8,9] Kakkos et al.,[10] Savage et al.,[40] Regensteiner et al.,[37,38] Hiatt et al.,[26,27] McGuigan et al.,[35] Collins et al.,[20,21] Stewart et al.,[42] Hobbs et al.,[46]; Tisi et al.,[43] Mannarino et al.,[34] Lundgren et al.,[32,33] Crowther et al.,[45] Wood et al.,[47]; Sandri et al.,[11] Mika et al.,[36] Gibellini et al.[25]

difference between walking and PRT with respect to improving post-exercise ABI in this trial. 2.3.3 Resting Arterial Calf Blood Flow

Few trials measured resting arterial calf blood flow, and it is unclear what amount of change in this outcome would translate to a clinically meaningful increase in walking distance. In the exercise versus control group (table VIII, in the Supplemental Digital Content), the between-group ESs calculated were mostly trivial (mean 0.09; range -0.12 to 0.24), and all were non-significant (figure 3). The magnitude of non-significant changes with exercise training was small, ranging from -0.13 (-3%) to 0.25 mL/100 mL/min (7%). In the exercise versus exercise group (table IX, in the Supplemental Digital Content), Gardner et al.[9] reported a significant time effect with both low and high intensity walking. The intra-group ESs we calculated were both small and inclusive ª 2010 Adis Data Information BV. All rights reserved.

of zero and the net magnitude of change reported was 0.49 for low intensity (15.5%) and 0.26 mL/100 mL/min for high intensity (8%). The between-group ES was small and also inclusive of zero. The remaining trial in this group also compared high with low intensity walking and reported no significant time or group · time effect with exercise training. All intra-group and between-group ESs were negligible and non-significant (figure 3). 2.3.4 Reactive Hyperaemic Blood Flow Post-Ischaemia

The amount of change in reactive hyperaemic blood flow post-ischaemia that would translate to a clinically meaningful increase in walking distance is unknown. However, 11 trials measured this outcome and most trials reported nonsignificant change, and ESs were trivial or small. In the exercise versus control group (table X, figure 2, in the Supplemental Digital Content) Sports Med 2010; 40 (5)

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only two[8,23,33] of nine trials reported a significant group · time effect. Both trials trained subjects to ischaemic pain, three times per week for 24 weeks and reported on average, a 46% or 6.5 mL/100 mL/min increase in reactive hyperaemic blood flow with exercise training. The corresponding between-group ESs calculated in both trials were large and statistically significant. One of these trials[23] subsequently decreased the frequency of training sessions to twice weekly for a further 52 weeks. At 76 weeks, initial claudication distance improved by 12%, but flow decreased by 6.3%, relative to 24 weeks, suggesting that changes in reactive hyperaemic blood flow may not explain improved walking performance. Six of the seven remaining trials in the exercise versus control group reported a mean 9.6 – 10.3% (range -6.3 to 24.5%) increase in this outcome, representing an absolute change of -0.8 to 3.04 mL/100 mL/min. The between-group ESs calculated were on average trivial (mean 0.14 – 0.47) and five of the six were non-significant. In one trial[9] the between-group ES calculated was a significant moderate negative ES, -0.78 (-1.09 to -0.47), indicating the control group had a significant improvement over the exercise group.

The final trial[29] in this group reported a nonsignificant effect of exercise training. In the exercise versus exercise group (table XI, figure 2, in the Supplemental Digital Content) two trials measured this outcome, and one trial[9] that compared low and high intensity walking reported significant time effects for both exercise groups. Gardner et al.[9] reported a net increase ranging from 2.02 to 3.11 mL/100 mL/min or 24–26%, in both the low and high intensity group and the intra-group ESs were moderate and statistically significant. Between-group ESs for this trial were trivial and non-significant. The second trial[10] reported a non-significant time effect, reporting a net decrease of 0.05 and 0.32 mL/sec (-6.7 and -29.6%) for unsupervised and supervised walking, respectively. This trial did not report on a group · time effect; however, the between-group ES we calculated was nonsignificant, suggesting the prescriptive element of supervision also does not significantly affect this outcome. 2.3.5 Resting Toe Systolic Pressure

Few trials to date have measured resting toe pressure, and it is unclear what amount of change

Slordahl et al. (2005) Slordahl et al. (2005) Exercise vs exercise Gardner et al. (2005) Gardner et al. (2005) Mannarino et al. (1991) Dahllof et al. (1974) Control vs exercise Gardner et al. (2002) Gardner et al. (2001)

−3

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0

1

2

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ES (95% CI) Favours control Standard exercise

Favours exercise Experimental exercise

Fig. 3. Forest plot of exercise vs control between-group effect size (ES; triangles) and exercise vs exercise intra-group ES (squares) and 95% confidence intervals (CIs) for resting calf blood flow. Included studies: Slordahl et al.,[41] Gardner et al.,[8,9,23] Mannarino et al.,[34] Dahllof et al.[22]

ª 2010 Adis Data Information BV. All rights reserved.

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McGuigan et al. (2001)

Gelin et al. (2001) Control vs exercise Lundgren et al. (Ann Surg 1989)

Lundgren et al. (Clin Sci 1989)

−2

−1

0 ES (95% CI)

Favours control Standard exercise

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Favours exercise Experimental exercise

Fig. 4. Forest plot of exercise vs control between-group effect size (ES; triangles) and 95% confidence intervals (CIs) for resting toe systolic pressure. Included studies: McGuigan et al.,[35] Gelin et al.,[24] Lundgren et al.[32,33]

in this outcome would translate to a clinically meaningful increase in walking distance. Four trials (each comparing an exercise intervention versus a control group) measured this outcome, with no trial reporting a significant training effect. Four between-group ESs were calculated (table XII, in the Supplemental Digital Content), which were small on average (mean 0.22 – 0.22) and non-significant (figure 4). The magnitude of this non-significant increase with exercise training ranged from 1.4 to 9 mmHg. 2.4 Relationship of Prescriptive Elements to Haemodynamic Measures

There was no consistent relationship between prescriptive elements such as modality, frequency, intensity or volume of exercise and any haemodynamic outcomes (data not shown). 2.5 Relationship of Medication Use to Haemodynamic Measures

There was no consistent relationship between use or exclusion of medication that affects haemorheology/haemodynamics and any haemodynamic outcomes (data not shown). ª 2010 Adis Data Information BV. All rights reserved.

2.6 Relationship of the Improvement in Function to Changes in Haemodynamic Measures

There were no significant relationships between change in symptoms and change in resting ABI (r = 0.02; r2 = 0.0004; p = 0.94) [figure 5a], post-exercise ABI (r = -0.33; r2 = 0.11; p = 0.52) [figure 3a, in the Supplemental Digital Content] or reactive hyperaemic calf blood flow (r = 0.35; r2 = 0.12; p = 0.26) [figure 3b, in the Supplemental Digital Content]. More study is required to detect whether a change in resting calf blood flow (r = 0.59; r2 = 0.35; p = 0.22) [figure 5b] and resting toe pressure (r = 0.75; r2 = 0.56; p = 0.25) [figure 5c] correlates to a change in symptoms, given that 35% (r2 = 0.35) and 56% (r2 = 0.56) of the variance, respectively, in claudication symptoms was explained by changes in these measures in these studies. Access to individual data points in these trials, rather than study means, would have provided more evidence to substantiate these trends. 3. Discussion It has been repeatedly shown that exercise improves functional capacity and in some cases Sports Med 2010; 40 (5)

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a Change in resting ABI

0.25 0.20 0.15 0.10 0.05 0 −50

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r = 0.02 r2 = 0.0004 p = 0.94

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b 0.3 0.2 0.1 0 −0.1 0 −0.2 −0.3 −0.4 −0.5

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r = 0.59 r2 = 0.35 p = 0.22

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r = 0.75 r2 = 0.56 p = 0.25

Fig. 5. Correlation between change in symptoms and (a) resting ankle brachial index (ABI), (b) resting calf blood flow and (c) resting toe pressure. r and p values calculated via linear regression analysis. ACD = absolute claudication distance.

eliminates symptoms in subjects with IC;[4,5,7] yet, the mechanisms by which exercise training generates improvements in function remain unconfirmed and speculative. To date, several mechanisms have been suggested, including altered lower limb haemodynamics[8-11] or haemorheology,[36,52] improvements in endothelial function,[1] improved skeletal muscle oxidative metabolism,[22,26,29,31-33,35,41] improved inflammatory properties of the blood,[43] greater walking economy,[8,31] and/or improvement in pain tolerance and various psychological constructs.[20,30,44,53-55] Our findings suggest that there is currently no significant or robust evidence to suggest that changes in lower limb haeª 2010 Adis Data Information BV. All rights reserved.

modynamic measures of flow and pressure explain the improvement in the clinical symptoms of PAD. Analysis of the 26 RCTs that measured resting ABI shows, on average, a negligible change in ABI, even though significantly large improvements in claudication distances occurred with exercise training.[8,9,23,25,32,33,35,36,40,43,44] In addition, analyses of results for post-exercise ABI indicate that regardless of mode or intensity of exercise, this measure is also not significantly changed by exercise training. This review identified 11 RCTs that measured reactive hyperaemic blood flow post-ischaemia. Most trials were non-significant, regardless of exercise mode. Among the trials[8,9,23,33] that did Sports Med 2010; 40 (5)

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report significant improvements in this outcome, one trial[23] reported a decrease in this outcome once the frequency of training sessions was reduced, despite claudication distances continuing to improve. Prior to this, Lundgren et al.[33] compared reconstructive arterial surgery with exercise training and reported improvements in claudication distance for all intervention groups, but found that reactive hyperaemic blood flow post-ischaemia only improved in the surgical groups. Thus, improvements in claudication distances despite decreases or no change in reactive hyperaemic blood flow suggest that changes in this outcome are not the primary mechanism for exercise-related improvements. Two haemodynamic factors appear worthy of additional robust investigation because of their relationship to symptom improvement: resting calf blood flow and resting toe pressure. Although regression analysis suggests that 35% and 56% of the variance, respectively, in claudication symptoms may be explained by changes in these two measures, more information is required on what magnitude of change in each measure would elicit a clinically meaningful increase in claudication distance. Perhaps more sophisticated measures of calf perfusion using magnetic resonance or CT imaging techniques might provide a more definitive answer to the question of whether there is a significant relationship between lower limb haemodynamic changes and symptom improvement. 3.1 Future Research and Quality of Trials

The novelty of our review is that through our comprehensive literature search we have identified the largest number of RCTs (15 more than previously reported on) that to our knowledge have ever been analysed. In addition, the extensive statistical analysis that we have performed provides us with a clear conclusion as to what areas require future research. Past research has suggested that exercise may improve PAD symptoms via improved endothelial function,[1] improved efficiency of local oxygen delivery[8-11] and/or utilization in the claudicating muscles.[22,29,31,42] Improvements in ª 2010 Adis Data Information BV. All rights reserved.

oxygen delivery suggest that changes occur via the circulatory system. The lack of significant increases in flow and pressure in reviewed studies to date tends to make this less likely. However, in order to completely exclude improved delivery as a potential mechanism of benefit, more research is required on resting toe pressure and calf blood flow, as well as microcirculation changes such as increased capillary density on muscle biopsy, for example. An improvement in endothelial function suggests that changes in reactive hyperaemic blood flow would have been demonstrated.[56] Again, the lack of significant improvements in lower limb reactive hyperaemic blood flow in the reviewed trials suggests that this is also not the primary mechanism of exercise benefit. However, as the current standard measure for endothelial function is brachial artery flow-mediated dilation,[57] this measure should be correlated to lower limb hyperaemic measures of blood flow. In contrast, past studies in both animals and humans have provided evidence for an increase in muscle mitochondria with exercise training via an increase in oxygen extraction ratio[58] or activity of mitochondrial enzymes.[59] Several trials have shown defective energy metabolism in the mitochondria of the claudicating muscle,[60-62] and one trial has shown that training increases the activity of oxidative mitochondrial enzymes in individuals with PAD.[33] Therefore, the mechanism of oxygen utilization and improvement in cellular processes at the local muscle level that occurs with exercise training warrants further research as a possible mechanism of improvement in symptoms in individuals with PAD. Regarding the quality of the 33 trials included in this review, only two trials[11,19] fulfilled most of the recommended PEDro criteria for trial validity, including blinding of all assessors. The lack of blinding of assessors in 30 of the 33 trials is a serious limitation of this literature, although admittedly the measurement outcomes described here include objective tests in many cases with minimal opportunity for assessor bias to be interjected. Unfortunately, the true treatment effect of the third trial[36] that blinded all assessors, may have been attenuated due to a >15% dropout rate and lack of intent-to-treat analysis.[49] Future Sports Med 2010; 40 (5)

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research may benefit from, at least, blinding the assessors, and perhaps allocating the control group to ‘sham’ exercise training such as stretching or no, or very low intensity resistance training. This would eliminate the potential bias in results that can occur with the assessor’s or subject’s belief in the effectiveness of the trial. 4. Conclusions Review of the current literature suggests that there is minimal evidence to support change in lower limb haemodynamic measures of resting and post-exercise ABI and reactive hyperaemic arterial calf blood flow as a primary mechanism for clinical symptom relief and functional improvements via exercise in PAD. Underlying mechanisms remain to be established; however, the mechanism of oxygen utilization and improvement in cellular processes at the local muscle level, walking economy and/or pain tolerance and self-efficacy warrants further research. More study is required to detect whether a consistent and significant relationship exists between a change in symptoms and change in resting toe pressure and resting arterial calf blood flow. Acknowledgements The authors had full access to all of the data in the study and Belinda Parmenter takes responsibility for the integrity of the results and accuracy of the data analysis. No sources of funding were used to assist in the preparation of this review. The authors have no conflicts of interest that are directly relevant to the content of this review.

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Correspondence: Belinda J. Parmenter, Exercise, Health and Performance Faculty Research Group, Faculty of Health Sciences, University of Sydney, PO Box 170, Lidcombe, NSW 1825, Australia. E-mail: [email protected]

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