sports medicine Volume 39 Issue 7 July 2009

Sports Med 2009; 39 (7): 513-522 0112-1642/09/0007-0513/$49.95/0

LEADING ARTICLE

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Youth Sports in the Heat Recovery and Scheduling Considerations for Tournament Play Michael F. Bergeron National Institute for Athletic Health and Performance and Center for Youth Sports and Health, Sanford USD Medical Center, Sioux Falls, South Dakota, USA

Abstract

One of the biggest challenges facing numerous young athletes is attempting to perform safely and effectively in the heat. An even greater performance challenge and risk for incurring exertional heat injury is encountered when a young athlete has to compete multiple times on the same day, with only a short rest period between rounds of play, during a hot-weather tournament. Within the scope of the rules, tournament directors frequently provide athletes with only the minimum allowable time between same-day matches or games. Notably, prior same-day exercise has been shown to increase cardiovascular and thermal strain and perception of effort in subsequent activity bouts, and the extent of earlier exercise-heat exposure can affect performance and competition outcome. Incurred water and other nutrient deficits are often too great to offset during short recovery periods between competition bouts, and the athletes are sometimes ‘forced’ to compete again not sufficiently replenished. Providing longer rest periods between matches and games can significantly improve athlete safety and performance, by enhancing recovery and minimizing the ‘carryover’ effects from previous competitionrelated physical activity and heat exposure that can negatively affect performance and safety. Governing bodies of youth sports need to address this issue and provide more specific, appropriate and evidence-based guidelines for minimum rest periods between same-day contests for all levels of tournament play in the heat. Youth athletes are capable of tolerating the heat and performing reasonably well and safely in a range of hot environments if they prepare well, manage hydration sufficiently, and are provided the opportunity to recover adequately between contests.

Youth sports provide myriad physical and social health-enhancing benefits, improvements in fitness, and enjoyment for participating young athletes.[1-3] Measurable gains in cardiorespiratory health and capacity, motor skills, and general and functional muscular strength, endurance and power, as well as better body composition and bone mineral content and density, have been shown in boys and girls as a result of regular

participation in organized youth sports.[4-16] With increased participation, training and competition, however, there is also a greater risk of injury,[1,17-23] and for those sporting events held in hot, humid environments, a particular concern to athletes, parents, coaches and medical support staff is the potential for adverse effects on cardiovascular and thermal strain, performance, and exertional heat injury risk.[24-40] The physical

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challenges are even greater when children and adolescents attempt to perform safely and effectively through multiple strenuous competition bouts on the same day during a hot-weather tournament. This is a common scenario for numerous young athletes involved in organized youth sports – soccer and tennis tournaments are notable examples. Unfortunately, reasonable safety and optimal performance are often compromised by short rest periods between same-day contests during tournament play in the heat. This article addresses the physiological challenges in youth sports during tournament format competitions in the heat, where multiple contests (games or matches) played on the same day can put young athletes at greater risk for poor performance and exertional heat injury, seemingly due, in large part, to insufficient rest and recovery time between competition bouts. 1. Same-Day Repeated Bouts During tournament play in organized youth sports, young athletes often must compete two or more times on the same day. Within the scope of the rules, tournament directors frequently provide athletes with only the minimum allowable time between same-day matches or games. Empirical observations from parents and coaches indicate that, with only a short recovery period between contests, a young athlete generally has considerably less tolerance to the subsequent activity and often succumbs to the strain of the cumulative physiological demands by way of poor performance or withdrawal from play. This is particularly obvious in hot environments. 1.1 Rest and Recovery Period Guidelines

Depending on the sport, level and age-group of event, number of team or individual entries, and other logistical and administrative considerations, the amount of time between competitions in organized youth sports tournaments can vary considerably. With certain sports such as softball and baseball, tournament rules have a particular focus on pitching limitations (number of pitches and innings per day and subsequent ª 2009 Adis Data Information BV. All rights reserved.

rest days), although most governing associations also provide recommendations, based on age, for limiting the number of games that can be played per day or throughout a tournament. Minimum time between same-day contests for these and many other organized youth sports, however, is not typically defined in the tournament playing rules. Table I shows examples of youth tournament (or meet) single-day scheduling from actual events at the divisional or regional level. It is particularly worth noting the minimum rest periods between tournament games and matches in youth sports such as soccer and tennis, given the extensive physical demand on these young athletes throughout each round of play.[41,42] In the US, the duration of youth soccer games (e.g. 25to 45-minute halves) and overtime periods are based on age, and the prescribed minimum rest period between tournament games can typically range from 1 to 2 hours depending on the sanctioning association, although local tournament events often provide much less time. In junior tennis, minimum rest periods between tournament matches are defined by the national governing body. Again, in the US, where a young player can have up to five matches scheduled in one day (singles and doubles combined), the minimum rest period between matches in the junior divisions is 1 hour (30 minutes for shorter pro set formats),[43] with no consideration for the duration of each previous same-day match or Table I. Examples of youth tournament (or meet) single-day scheduling from actual events at the divisional or regional level. Recommendation: longer recovery periods (minimum two times longer than shown here), especially in hot environmental conditions and/or following a long match or game Sport

Competition load

Basketball (indoor) 3–6 games/day

Between-contests rest 1 game duration (or less)

Soccer

2–3 games/day

1–2 h or 1–2 time slots

Softball

2–3 games/day

15 min (minimum)

Baseball

2–5 games/day

15 min–1 h

Track and field

3–5 running events/day

1 h (or less)

Tennisa

3 singles, 2 doubles 1 h (singles), 30 min matches/day (doubles)

a

No time limit for each match; a singles match can last, for example, less than 1 h or up to 4 h or more.

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level of environmental heat stress. In any junior division in tennis, a match can take less than 1 hour to complete or go on for up to 4 hours or more. Notably, public school systems generally have very specific (albeit quite variable between systems) guidelines for scheduling and suspending practice and competition in extreme heat. In contrast, such restrictions are typically not as specifically outlined for or consistently utilized in organized youth sports tournaments, and it is often left up to the discretion of the on-site tournament administrator or referee to adjust or alter the competition format based on the environment. National-level and scholastic tournament events also typically provide more conservative guidelines to minimize the number of same-day contests, compared with regional, state and local non-scholastic events where tournament directors and referees often do not follow the same recommendations and practices. Unfortunately, the potential negative impact of previous competition-related physical activity and heat exposure on subsequent same-day performance and exertional heat injury risk in children and adolescents participating in organized youth sports is not well described or sufficiently appreciated. However, related field and laboratory studies on repeated-bout exercise in adults and those very few similar new studies on young athletes can provide some valuable insight into these potential after- or ‘carryover’ effects during tournament play in youth sports. 1.2 Adult Studies

Examining the effects of environmental heat stress during successive days of Marine Corps basic training, Wallace et al.[44] found that exertional heat illness risk increased with hourly wetbulb-globe temperature (WBGT; 11% increase in risk per F [~0.5C]). Although limiting physical activity during hot weather measurably reduced exertional heat illness risk, there was still an elevated relative risk and 17% of exertional heat illness cases occurring across the cautionary flag conditions for training activities. Moreover, exertional heat illness risk was associated with the ª 2009 Adis Data Information BV. All rights reserved.

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current WBGT as well as with the previous day’s average WBGT – that is, they observed a strong cumulative effect on exertional heat illness risk resulting from current environmental conditions and certain exercise-heat strain effects carried over from the day before. According to Wallace et al., those who schedule training or sports activities should consider the carryover effects of previous-day exercise and heat stress exposure to better anticipate heat-related problems and minimize exertional heat injury risk. These data further suggest that exertional heat illness risk should still be considered on a day that appears ‘safe’, if the previous day’s heat stress was high. In contrast, McLellan et al.[45] reported no carryover effects from previous-day moderate exercise-heat exposure on core body temperature or perceived exertion in sedentary non-heatacclimated (but well hydrated) adults during similar exercise on the next morning. Notably, the previous day’s afternoon exercise bout lasted only 1 hour and was followed by a single morning bout in less hot conditions. Despite these factors, a number of subjects failed to complete the exercise trial in the heat on day 2. Ronsen et al.[46] examined the residual effects of prior same-day exercise (cycling for 75 minutes) and varying recovery times on metabolic responses during a subsequent bout of the same exercise in elite endurance-trained athletes. They found augmented metabolic stress and greater cardiovascular and thermal strain (higher heart rate and core body temperature, respectively) in the second exercise bout with 3 hours between bouts, which were significantly attenuated by providing a longer rest and recovery period (6 hours) between the exercise sessions. These data underscore how the residual effects of prior exercise can affect one’s response to a subsequent same-day exercise session (even without a hot environment) and how the extent of these carryover effects can be modulated by increasing the length of the rest and recovery time between exercise bouts. Several other relevant studies provide some additional insight into same-day repeated-bout exercise. Sawka et al.[47] observed a higher core body temperature response and greater cardiovascular Sports Med 2009; 39 (7)

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strain (elevated heart rate and lower stroke volume and cardiac output) in trained runners during a second of two 80-minute bouts of highintensity treadmill running at room temperature, separated by a 90-minute rest period. Kruk et al.[48] examined consecutive moderate exercise bouts (cycling for 30 minutes) with 30-minute rest periods in between and found progressively higher core body temperature and heart rate responses with each successive exercise period, despite replacement of sweat fluid loss and no environmental heat stress. Similarly, in examining the cumulative effect of prior cycling exercise for 30 minutes in a hot environment on another identical exercise bout following a 45-minute post-exercise recovery period of seated rest in the same heat, Brenner et al.[49] reported greater rectal temperature and cardiovascular responses during the second session, as well as greater perceived exertion. Lastly, Yamada and Golding[50] also observed greater rectal temperature and heart rate during a second exercise bout (walking for 23 minutes) in the heat, following rehydration and rest during a short (12-minute) recovery period after the first identical bout of exercise. Notably, the subjects in these studies were either insufficiently or inappropriately hydrated during the test sessions and/or core body temperature had not returned to baseline between exercise bouts. These findings are particularly relevant to certain youth sports (e.g. soccer and tennis) in also highlighting how a 10-minute break between halves or sets (or a little longer between games or matches) is insufficient time to sufficiently lower rectal temperature and avert incurring greater physiological strain when activity in the heat is resumed, even with rehydration, especially if the players stay in the heat during the break. 1.3 Youth Studies

To test the hypothesis that young athletes would experience an increase in physiological strain and related ratings of perceived discomfort during a subsequent identical exercise bout (compared with the first), even when maintaining adequate hydration, Bergeron et al.[51] examined 24 healthy, young athletes (12–13 and 16–17 years ª 2009 Adis Data Information BV. All rights reserved.

old) during two 80-minute intermittent exercise (treadmill and cycle ergometer) sessions in the heat (33C), with a 1-hour rest and recovery period (21C) between bouts. Core body temperature, physiological strain index[52] and perceived thermal stress were similar during the second exercise bout. However, a 1-hour recovery period was not sufficient to avert greater perception of effort and, for some, greater physiological strain during the second bout of identical exercise, even when the young athletes consumed ample fluid during exercise, drank enough between the exercise bouts to offset any remaining fluid deficit, and core body temperature returned to baseline prior to starting exercise again. It is important to recognize that there were still apparent carryover effects to the second bout of exercise, even in ‘ideal’ recovery conditions – i.e. immediate rest and no heat exposure, full rehydration, and complete cool-down. Such circumstances are in contrast to more typical ‘real life’ tournament scenarios, where incomplete thermoregulatory recovery and subsequent increased thermal strain[48,49] are more likely to occur, because the players cannot immediately begin and maintain complete rest and cool-down procedures during the recovery period, and the next round of play may be contested in more stressful environmental conditions a little later in the day. Coyle[53] examined data from a national boys 14s (14-year-olds) junior tennis championships event over a 7-year period to show how cumulative heat stress can affect a second (same-day) match outcome during tournament play. With the effect of seeding removed, the winner of an afternoon singles match could be effectively predicted from the same-day degree minutes (product of WBGT in C and length of match [including warm-up] in minutes) acquired during the morning matches by the two respective players. Coyle found no statistical differences in hometown heat stress zone between match winners and losers, although all of these young athletes had been training and competing in the heat for some time prior to this event and thus were likely heat-acclimatized and able to tolerate the heat better than if they began play without sufficient recent exercise-heat exposure.[38,54-56] Sports Med 2009; 39 (7)

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From the same national boys 14s event, Bergeron et al.[28] also showed how junior tennis players tend to not fully rehydrate from earlier sameday play and how even just doubles competition in the afternoon following singles play can elicit an appreciable thermal challenge in a hot environment. 2. Nutrient Recovery Needs and Challenges Fluid and electrolyte deficits and carbohydrate needs can be substantial following a long and intense contest in the heat. It might be argued that those young athletes who incur a substantial fluid deficit and perform poorly or develop heatrelated problems in subsequent tournament rounds simply are not rehydrating sufficiently. Accordingly, from this perspective, the focus should be on education and compliance versus adjusting the schedule. Indeed, as with adults, a child’s or adolescent’s hydration status has a direct impact on cardiovascular and thermal strain and heat tolerance during exercise and sports.[28,38,39,57-59] With sweat rates potentially ranging from 300 to 700 mL/h in 9- to 12-year-olds[38,39,51,60] and 1–2 L or more per hour in older adolescents,[28,29,51] it is not surprising that young athletes can incur significant water and electrolyte losses from sweating during competition.[61] Much of this can be compensated by appropriate fluid intake during play, if opportunities to rehydrate are sufficiently frequent. However, in certain sports (e.g. soccer), a very active and continuously engaged participant may have few to no opportunities to consume fluid during the game (except at breaks between periods). The process of offsetting a post-play body water deficit can usually begin right away; however, there is a practical limit (often short of sufficiently eliminating the deficit) to the amount of fluid a young athlete can comfortably and safely consume with only a short recovery period.[62] For example, a moderate sweating rate of only 1.5 L/h could lead to a ‡5 L total sweat fluid loss for an adolescent player over the course of a long tennis match. Even with drinking regularly throughout the match, this young player could readily be facing a ª 2009 Adis Data Information BV. All rights reserved.

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>2 L fluid deficit by the end of play. Full rehydration (»2–3 L)[63] before the next match begins may not be possible if the time between matches is only an hour or so. If the cycle continues over the course of several matches on the same day, the player could potentially reach a point where the fluid deficit is too great to perform well or safely. Although fluid intake and hydration status are not always statistically associated with core body temperature when young players have the opportunity and desire to reduce exercise intensity and effort,[29] during a meaningful and intense tournament competition in the heat, the negative effects of insufficient hydration on thermal strain can be more readily apparent.[28] Notably, during and after play, effective rehydration requires more than just ample fluid intake. Sodium losses need to be replaced as well, so that the ingested fluid is more optimally retained and distributed to all fluid compartments, resulting in more complete rehydration.[63-66] Given the extensive sweat losses and deficits of fluid and electrolytes and energy (carbohydrate) depletion potentially incurred during play, the nutrient intake, absorption and distribution required to replace these deficits may sometimes be too great to achieve or tolerate in the allotted recovery time.[67-72] Thus, the young athlete is ‘forced’ to begin play again not optimally or sufficiently replenished. Incomplete rehydration and a sodium deficit can prompt lower heat tolerance, greater cardiovascular and thermal strain, and reduced performance,[73-77] as well as an increased risk for developing muscle cramps[61,78] during the next game or match. Moreover, low glycogen stores following a previous exercise bout and short recovery period[79] can prompt a greater pro-inflammatory cytokine response,[80] further increase the inherent challenge to maintain euglycaemia,[81] and prompt earlier fatigue[82-87] during the next round of play.

3. Who Should Assume Responsibility? The responsibility for preparing to compete in the heat should be assumed by the athlete, parent(s) or primary care provider(s), and coach.[88] Sports Med 2009; 39 (7)

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Young athletes also have the responsibility to rehydrate adequately when there is sufficient time to offset a post-play fluid deficit. This is not always the case, and players often begin competition not well hydrated when there was ample opportunity to do so;[28,89] albeit, being well hydrated prior to beginning play does not guarantee minimum thermal strain or exertional heat illness risk. However, tournament directors and other event administrators, referees, medical support personnel, and ultimately the various sport governing bodies, have the responsibility to provide safe and appropriate venues and scheduling in youth sports.[88] Some might argue that the body of published scientific and clinical evidence is not yet conclusive and therefore any changes to the current scheduling rules and practices are premature. However, an alternative perspective is emphasized by Emery et al.,[88] who point to a broadened interpretation of the precautionary principle as a guide for injury prevention in youth sports: ‘‘When there is suspected harm and the scientific evidence is inconclusive, the prescribed course is precautionary action’’ – i.e. to side with safety and reduce the risk.[90] This seems particularly appropriate when considering potential harm to children and adolescents. As indicated earlier, there is growing evidence in the literature strongly supporting the perspective that insufficient rest and recovery time, especially when competing in an already unsafe climate, can further reduce performance and put certain young athletes at increased clinical risk, even if they are fit, willing to play and motivated to win. Although desirable, these attributes are no match for a schedule that is inappropriate and does not emphasize athlete safety over completing multiple rounds of competition quickly.

4. Specific Research Needs Previous studies claim that children have a disadvantage compared with adults during exercise in the heat because boys and girls are less effective in regulating body temperature, and thus are less tolerant to and capable of performing well in a hot environment.[57,59,91-94] However, ª 2009 Adis Data Information BV. All rights reserved.

recent research and more appropriate comparisons do not indicate that children (9–12 years old) have less effective thermoregulation, insufficient cardiovascular capacity or lower tolerance during exercise in the heat when environmental and exercise conditions, aerobic fitness and heat acclimatization status are relatively the same for the children and adults and, importantly, hydration is maintained.[38,39,60] Considerably more research specific to exercise-heat tolerance in children needs to be done, however, before any definitive conclusions can be made to defend or dismiss the notion of inherently greater cardiovascular or thermal strain or other clinical risk in children or adolescents compared with adults during sports competition in the heat, especially with multiple same-day contests in a tournament format. Prospectively examining the effects of different recovery approaches (including utilizing various rehydration strategies and cooling methods[95] and durations between bouts of competition, based on environmental conditions) on subsequent physiological strain and other outcome measures related to athlete performance and safety is essential. This would provide important insight to minimizing the potential negative carryover effects of previous competition-related physical activity and heat stress exposure on clinical risk and performance during subsequent same-day competition bouts. Comprehensive epidemiological studies[96,97] on exertional heat injury and performance during outdoor tournament play is also a priority. Such research is critical in being able to provide the most appropriate evidencebased guidelines to youth sports tournament directors, administrators and sport governing bodies for safely and effectively scheduling multiple competition bouts in the heat. This will help to optimize performance, while reducing the risk of exertional heat injury, for numerous young athletes who regularly participate in a number of different organized youth sports. It is important to also consider other influential factors from a previous bout of demanding competition-related physical activity that affect athlete functional capacity and safety. Especially if recovery time between matches or games Sports Med 2009; 39 (7)

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Table II. Key scheduling challenges and related effects on young athletes, and recommended responses for event administration, that can improve athlete safety and performance in the heat Challenges

Effects

Recommended responses

Hot and humid environment Multiple same-day contests Long matches or games (i.e. extensive exercise-heat exposure)

Increased physiological strain Reduced activity tolerance and performance Incomplete recovery between competition bouts Greater risk for exertional heat injury

Increase recovery time between same-day contests Minimize number of contests per day for each athlete Monitor athletes more closely Provide verbal reminders regarding hydration and cooling strategies Schedule contests during cooler times of day Consider cancelling the event altogether, if environmental conditions are extreme

is short, muscle and central fatigue and acute muscle injury/soreness can independently or in combination measurably affect sensorimotor acuity, neuromuscular control, joint stability, and even temperature regulation[95,98-106] and thus potentially decrease performance and increase injury risk during the next same-day contest. These aspects should be comprehensively addressed as well in organized youth sports to fully appreciate the clinical and performance impact of too much same-day competition and insufficient rest and recovery between rounds of play. 5. Key Points and Recommendations1 The key points and recommendations below should be considered by youth sports event administrators and others when developing policies and event schedules, so as to enhance the health and safety of the participating athletes. Key challenges and effects, and recommended responses for event administration, that can improve athlete safety and performance in the heat are also highlighted in table II.  Multiple matches or games on the same day can pose particular performance and safety challenges to young athletes and increase exertional heat injury risk, due to insufficient recovery time and rehydration, as well as physiological ‘carryover’ effects from previous- and sameday competition-related physical activity and heat exposure.

 Youth sports tournament directors, administrators and governing bodies should recognize and appreciate that providing longer rest and recovery periods between matches and games (much more than many current governing bodies’ rules indicate) as environmental heat stress increases can improve athlete safety and performance without necessarily having to adjust the playing format (e.g. scoring or duration of the individual contests).  Following a long and intense match or game in the heat, a young athlete may have substantial water, electrolyte, carbohydrate and other macronutrient recovery needs. This requires a proportionately longer rest and recovery period, so that s/he has the opportunity to begin the next contest without one or more significant nutrient deficits or a full stomach and consequent performance and safety disadvantages.  Recovery time between contests is not the only significant scheduling-related concern when running a tournament in hot weather. Competing at all in an unsafe environment can put young athletes at great risk, even if they are well rested and sufficiently hydrated before play. In conditions of uncompensable heat stress (where evaporative cooling is insufficient to maintain thermal balance), player safety should be the priority, and contests should be cancelled or rescheduled to cooler times, even if it means playing very early or later in the evening under the lights.

1 Repeated same-day training sessions in the heat also present similar safety and performance risks; accordingly, the recovery and scheduling considerations for tournament competition and the recommendations presented here should be considered and applied to youth sports training and practice in the heat as well.

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Acknowledgements No sources of funding were used to assist in the preparation of this article. The author has no conflicts of interest that are directly relevant to the content of this article.

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53. Coyle J. Cumulative heat stress appears to affect match outcome in a junior tennis championship [abstract]. Med Sci Sports Exerc 2006; 38: S110 54. Rowland T, Hagenbuch S, Pober D, et al. Exercise tolerance and thermoregulatory responses during cycling in boys and men. Med Sci Sports Exerc 2008; 40: 282-7 55. Shapiro Y, Moran D, Epstein Y. Acclimatization strategies: preparing for exercise in the heat. Int J Sports Med 1998; 19 Suppl. 2: S161-3 56. Sunderland C, Morris JG, Nevill ME. A heat acclimation protocol for team sports. Br J Sports Med 2008; 42: 327-33 57. Bar-Or O, Dotan R, Inbar O, et al. Voluntary hypohydration in 10- to 12-year-old boys. J Appl Physiol 1980; 48: 104-8 58. Dougherty KA, Baker LB, Chow M, et al. Two percent dehydration impairs and six percent carbohydrate drink improves boys basketball skills. Med Sci Sports Exerc 2006; 38: 1650-8 59. Falk B, Bar-Or O, MacDougall JD. Thermoregulatory responses of pre-, mid-, and late-pubertal boys to exercise in dry heat. Med Sci Sports Exerc 1992; 24: 688-94 60. Inbar O, Morris N, Epstein Y, et al. Comparison of thermoregulatory responses to exercise in dry heat among prepubertal boys, young adults and older males. Exp Physiol 2004; 89: 691-700 61. Bergeron MF. Heat cramps: fluid and electrolyte challenges during tennis in the heat. J Sci Med Sport 2003; 6: 19-27 62. Gisolfi CV. Is the GI system built for exercise? News Physiol Sci 2000; 15: 114-9 63. Shirreffs SM, Maughan RJ. Volume repletion after exercise-induced volume depletion in humans: replacement of water and sodium losses. Am J Physiol 1998; 274: F868-75 64. Mitchell JB, Phillips MD, Mercer SP, et al. Postexercise rehydration: effect of Na+ and volume on restoration of fluid spaces and cardiovascular function. J Appl Physiol 2000; 89: 1302-9 65. Sanders B, Noakes TD, Dennis SC. Sodium replacement and fluid shifts during prolonged exercise in humans. Eur J Appl Physiol 2001; 84: 419-25 66. Sanders B, Noakes TD, Dennis SC. Water and electrolyte shifts with partial fluid replacement during exercise. Eur J Appl Physiol Occup Physiol 1999; 80: 318-23 67. Burke LM. Nutrition for post-exercise recovery. Aust J Sci Med Sport 1997; 29: 3-10 68. Burke LM, Kiens B, Ivy JL. Carbohydrates and fat for training and recovery. J Sports Sci 2004; 22: 15-30 69. Goetze O, Steingoetter A, Menne D, et al. The effect of macronutrients on gastric volume responses and gastric emptying in humans: a magnetic resonance imaging study. Am J Physiol Gastrointest Liver Physiol 2007; 292: G11-7 70. Ivy JL. Muscle glycogen synthesis before and after exercise. Sports Med 1991; 11: 6-19 71. Jentjens RLPG, Wagenmakers AJM, Jeukendrup AE. Heat stress increases muscle glycogen use but reduces the oxidation of ingested carbohydrates during exercise. J Appl Physiol 2002; 92: 1562-72

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72. Shirreffs SM, Taylor AJ, Leiper JB, et al. Post-exercise rehydration in man: effects of volume consumed and drink sodium content. Med Sci Sports Exerc 1996; 28: 1260-71 73. Cheung SS, McLellan TM. Heat acclimation, aerobic fitness, and hydration effects on tolerance during uncompensable heat stress. J Appl Physiol 1998; 84: 1731-9 74. Montain SJ, Coyle EF. Influence of graded dehydration on hyperthermia and cardiovascular drift during exercise. J Appl Physiol 1992; 73: 1340-50 75. Moran DS, Montain SJ, Pandolf KB. Evaluation of different levels of hydration using a new physiological strain index. Am J Physiol 1998; 275: R854-60 76. Sawka MN. Physiological consequences of hypohydration: exercise performance and thermoregulation. Med Sci Sports Exerc 1992; 24: 657-70 77. Sawka MN, Montain SJ, Latzka WA. Hydration effects on thermoregulation and performance in the heat. Comp Biochem Phys 2001; 128: 679-90 78. Bergeron MF. Heat cramps during tennis: a case report. Int J Sport Nutr 1996; 6: 62-8 79. Blom PC, Hostmark AT, Vaage O, et al. Effect of different post-exercise sugar diets on the rate of muscle glycogen synthesis. Med Sci Sports Exerc 1987; 19: 491-6 80. Ronsen O, Lea T, Bahr R, et al. Enhanced plasma IL-6 and IL-1ra responses to repeated versus single bouts of prolonged cycling in elite athletes. J Appl Physiol 2002; 92: 2547-53 81. Galassetti P, Mann S, Tate D, et al. Effect of morning exercise on counterregulatory responses to subsequent, afternoon exercise. J Appl Physiol 2001; 91: 91-9 82. Costill DL. Sweating: its composition and effects on body fluids. Ann NY Acad Sci 1977; 301: 160-74 83. Burke LM, Hawley JA. Fluid balance in team sports: guidelines for optimal practices. Sports Med 1997; 24: 38-54 84. Maughan R, Shirreffs S. Recovery from prolonged exercise: restoration of water and electrolyte balance. J Sport Sci 1997; 15: 297-303 85. Mohr M, Krustrup P, Bangsbo J. Fatigue in soccer: a brief review. J Sports Sci 2005; 23: 593-9 86. Rockwell MS, Rankin JW, Dixon H. Effects of muscle glycogen on performance of repeated sprints and mechanisms of fatigue. Int J Sport Nutr Exerc Metab 2003; 13: 1-4 87. Williams MB, Raven PB, Fogt DL, et al. Effects of recovery beverages on glycogen restoration and endurance exercise performance. J Strength Cond Res 2003; 17: 12-9 88. Emery CA, Hagel B, Morrongiello BA. Injury prevention in child and adolescent sport: whose responsibility is it? Clin J Sport Med 2006; 16: 514-21 89. Petrie HJ, Stover EA, Horswill CA. Nutritional concerns for the child and adolescent competitor. Nutrition 2004; 20: 620-31 90. Pless IB. Expanding the precautionary principle. Inj Prev 2003; 9: 1-2

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Bergeron

91. Drinkwater B, Kupprat I, Denton J, et al. Response of prepubertal girls and college women to work in the heat. J Appl Physiol 1977; 43: 1046-53 92. Falk B. Effects of thermal stress during rest and exercise in the paediatric population. Sports Med 1998; 25: 221-40 93. Haymes EM, Buskirk ER, Hodgson JL, et al. Heat tolerance of exercising lean and heavy prepubertal girls. J Appl Physiol 1974; 36: 566-71 94. Wagner J, Robinson S, Tzankoff S, et al. Heat tolerance and acclimatization to work in the heat in relation to age. J Appl Physiol 1972; 33: 616-22 95. Barnett A. Using recovery modalities between training sessions in elite athletes: does it help? Sports Med 2006; 36: 781-96 96. Caine D, Caine C, Maffulli N. Incidence and distribution of pediatric sport-related injuries. Clin J Sport Med 2006; 16: 500-13 97. Goldberg AS, Moroz L, Smith A, et al. Injury surveillance in young athletes: a clinician’s guide to sports injury literature. Sports Med 2007; 37: 265-78 98. Benjaminse A, Habu A, Sell TC, et al. Fatigue alters lower extremity kinematics during a single-leg stop-jump task. Knee Surg Sports Traumatol Arthrosc 2008 Apr; 16 (4): 400-7 99. Cheung SS, Sleivert GG. Multiple triggers for hyperthermic fatigue and exhaustion. Exerc Sport Sci Rev 2004; 32: 100-6 100. Davey PR, Thorpe RD, Williams C. Fatigue decreases skilled tennis performance. J Sports Sci 2002; 20: 311-8 101. Girard O, Lattier G, Maffiuletti NA, et al. Neuromuscular fatigue during a prolonged intermittent exercise: application to tennis. J Electromyogr Kinesiol 2008 Dec; 18 (6): 1038-46 102. Girard O, Lattier G, Micallef JP, et al. Changes in exercise characteristics, maximal voluntary contraction, and explosive strength during prolonged tennis playing. Br J Sports Med 2006; 40: 521-6 103. Montain SJ, Latzka WA, Sawka MN. Impact of muscle injury and accompanying inflammatory response on thermoregulation during exercise in the heat. J Appl Physiol 2000; 89: 1123-30 104. Ronglan LT, Raastad T, Borgesen A. Neuromuscular fatigue and recovery in elite female handball players. Scand J Med Sci Sports 2006; 16: 267-73 105. Rozzi SL, Lephart SM, Fu FH. Effects of muscular fatigue on knee joint laxity and neuromuscular characteristics of male and female athletes. J Athl Train 1999; 34: 106-14 106. Tripp BL, Yochem EM. Uhl TL. Functional fatigue and upper extremity sensorimotor system acuity in baseball athletes. J Athl Train 2007; 42: 90-8

Correspondence: Prof. Michael F. Bergeron, National Institute for Athletic Health and Performance, Sanford USD Medical Center, 1210 W 18th Street, Suite 204, Sioux Falls, SD 57104, USA. E-mail: [email protected]

Sports Med 2009; 39 (7)

Sports Med 2009; 39 (7): 523-546 0112-1642/09/0007-0523/$49.95/0

REVIEW ARTICLE

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Medial Tibial Stress Syndrome A Critical Review Maarten H. Moen,1 Johannes L. Tol,2 Adam Weir,2 Miriam Steunebrink2 and Theodorus C. De Winter2 1 Department of Sports Medicine of the University Medical Centre Utrecht and Rijnland Hospital, Leiderdorp, the Netherlands 2 Department of Sports Medicine of the Medical Centre Haaglanden, the Hague, the Netherlands

Contents Abstract. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1. Methods. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1.1 Literature Search . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2. Aetiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.1 Functional Anatomy. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.2 Biomechanics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3. Histology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4. Patient Examination . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.1 History . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.2 Physical Examination . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.3 Imaging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.3.1 Radiograph . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.3.2 Bone Scan . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.3.3 Magnetic Resonance Imaging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.3.4 High-Resolution Computed Tomography Scan . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.3.5 Imaging Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5. Risk Factors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5.1 Risk Factor Studies. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5.2 Risk Factor Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6. Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6.1 Conservative . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6.2 Surgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7. Prevention . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7.1 Prevention Studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7.2 Prevention Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8. Discussion. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9. Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Abstract

523 525 525 525 525 532 532 533 533 533 534 534 534 535 536 537 537 537 538 538 538 539 540 540 541 541 543

Medial tibial stress syndrome (MTSS) is one of the most common leg injuries in athletes and soldiers. The incidence of MTSS is reported as being between 4% and 35% in military personnel and athletes. The name given to this condition refers to pain on the posteromedial tibial border during exercise, with pain on palpation of the tibia over a length of at least 5 cm. Histological studies fail to provide evidence that MTSS is caused by periostitis as a result of traction. It is caused by bony resorption that outpaces bone

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formation of the tibial cortex. Evidence for this overloaded adaptation of the cortex is found in several studies describing MTSS findings on bone scan, magnetic resonance imaging (MRI), high-resolution computed tomography (CT) scan and dual energy x-ray absorptiometry. The diagnosis is made based on physical examination, although only one study has been conducted on this subject. Additional imaging such as bone, CT and MRI scans has been well studied but is of limited value. The prevalence of abnormal findings in asymptomatic subjects means that results should be interpreted with caution. Excessive pronation of the foot while standing and female sex were found to be intrinsic risk factors in multiple prospective studies. Other intrinsic risk factors found in single prospective studies are higher body mass index, greater internal and external ranges of hip motion, and calf girth. Previous history of MTSS was shown to be an extrinsic risk factor. The treatment of MTSS has been examined in three randomized controlled studies. In these studies rest is equal to any intervention. The use of neoprene or semi-rigid orthotics may help prevent MTSS, as evidenced by two large prospective studies.

Medial tibial stress syndrome (MTSS) is one of the most common causes of exercise-induced leg pain.[1] Incidences varying from 4% to 35% are reported, with both extremes being derived from military studies.[2-4] This condition is most frequent among military personnel, runners and athletes involved in jumping, such as basketball players and rhythmic gymnasts.[5,6] There is much controversy about the definition and terminology of this condition. Different authors have used different names, such as ‘shin soreness’,[7] ‘tibial stress syndrome’,[8] ‘medial tibial syndrome’,[9] ‘medial tibial stress syndrome’,[10] ‘shin splints syndrome’[11] and ‘shin splints’.[12] In this review we chose to use ‘medial tibial stress syndrome’ because, in our opinion, this best reflects the aetiology of the syndrome. MTSS is characterized by exercise-related pain on the posteromedial side of the mid- to distal tibia. In 1966 the American Medical Association defined the condition (then termed shin splints) as: ‘‘pain or discomfort in the leg from repetitive running on hard surfaces or forcible excessive use of the foot flexors; diagnosis should be limited to musculotendinous inflammations, excluding fracture or ischaemic disorder.’’[13] This definition is the only available official definition given in the literature, but in our opinion is outdated and was never well accepted among clinicians. It does not ª 2009 Adis Data Information BV. All rights reserved.

describe signs on physical examination. Frequently when in the (older) literature the term ‘shin splints’ is used, ‘medial tibial stress syndrome’ is meant. More recently, an updated and better definition was proposed by Yates and White.[4] They described MTSS as ‘‘pain along the posteromedial border of the tibia that occurs during exercise, excluding pain from ischaemic origin or signs of stress fracture.’’ Additionally, they stated that on palpation with physical examination, a diffuse painful area over a length of at least 5 cm should be present. However, since no official definition exists, many authors use their own definition of MTSS. This makes comparison between studies difficult. Before diagnosing MTSS, the diagnosis of tibial stress fracture and exertional compartment syndrome should be excluded (see section 4). Detmer[14] in 1986 developed a classification system to subdivide MTSS into three types: (i) type I – tibial microfracture, bone stress reaction or cortical fracture; (ii) type II – periostalgia from chronic avulsion of the periosteum at the periosteal-fascial junction; and (iii) type III – chronic compartment syndrome. In the recent literature, stress fracture and compartment syndrome are qualified as separate entities. The objective of this review is to provide a critical analysis of the existing literature on MTSS. Aetiology, biomechanics, histology, patient Sports Med 2009; 39 (7)

Medial Tibial Stress Syndrome

evaluation, diagnostic imaging, risk factors, therapy and prevention are discussed.

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Table I. Assessment of methodological quality and level of evidence (reproduced from Institute for Quality and Healthcare, the Netherlands,[15] with permission)

1. Methods

Assessment of methodological quality of studies concerning intervention (treatment/prevention)

1.1 Literature Search

A1: Systematic review of at least two independently conducted studies of A2 level

The electronic databases MEDLINE (1966–2009), EMBASE (1980–2009), CINAHL (1982–2009), SPORTDiscus (1975–2009) and Cochrane Library were searched for articles. The search terms ‘shin splints’, ‘medial tibial syndrome’, ‘medial tibial stress syndrome’ and ‘tibial stress syndrome’ were used with no restrictions for language. The references from the articles were screened and in this way additional articles were obtained. Using the search terms, 382 possible titles were screened. Of these, 334 were not relevant as they discussed sports injuries in general, stress fractures, compartment syndromes or other topics. The 48 relevant titles were screened for related titles in the references. In total, 110 references were found, of which 104 articles could be obtained. Articles were judged using the Institute for Quality of Healthcare (CBO [Centraal Begeleidings Orgaan]) classification system[15] (table I) and methodological quality and level of evidence were assessed. Methodological quality status (A1, A2, B, C, D) and level of evidence status (1, 2, 3, 4) were assessed (see tables II and III). The assessment was done independently by two researchers (MM and MS). If methodological quality and level of evidence were scored differently, a third author (AW) made the final decision (on two occasions). Randomized controlled studies on the prevention and treatment of MTSS were also assessed using the Delphi scoring list[39] (table IV and V). This is a list of criteria for quality assessment of randomized clinical trials when conducting systematic reviews. This list contains nine points and each was scored as being present or not. The maximal score for the Delphi list is nine points. 2. Aetiology 2.1 Functional Anatomy

There is much controversy about the anatomical basis for MTSS. Post-mortem studies have been performed to examine the relationship ª 2009 Adis Data Information BV. All rights reserved.

A2: Randomized double-blind clinical comparing study of good quality and size B: Randomized clinical study, with moderate quality and size, or other comparing research (case-control study, cohort study) C: Case series D: Expert opinion Assessment of methodological quality of studies concerning imaging and aetiology A1: Systematic review of at least two independently conducted studies of A2 level

Imaging A2: Research comparing against a gold standard/reference test, with an adequate number of participants B: Research comparing against a gold standard/reference test, with an inadequate number of participants

Aetiology A2: Prospective research with adequate and non-selective follow-up, with control for confounding B: Prospective research with not all criteria mentioned under A2, or retrospective research

Imaging and aetiology C: Case series D: Expert opinion Level of evidence 1: One systematic review (A1) or at least two independently conducted studies of A2 level (strong evidence) 2: One study of A2 level, or at least two independently conducted studies of B level (moderate evidence) 3: One study of B or C level (limited evidence) 4: Expert opinion (no evidence)

between the location of the pain and the anatomical structures. In these studies the distal attachments of different leg muscles were compared with the site of symptoms in MTSS. Michael and Holder[49] dissected 14 specimens and found fibres of the soleus muscle but not the posterior tibialis muscle on the posteromedial tibial border. Saxena et al.[50] dissected ten cadavers and found that the distal attachment of the tibialis posterior muscle was 7.5 cm proximal to the medial malleolus. He concluded from this that the tibialis posterior muscle caused MTSS. Sports Med 2009; 39 (7)

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Table II. Study characteristics and quality scores of studies involving imaging Study design

Inclusion criteria

Imaging type

No. of subjects

Population/type of activity

Outcome

Methodological quality

Level of evidence

Holder and Michael[16] (1984)

Prospective cohort

Pain on palpation of middle and distal posteromedial tibial border

Bone scan

10

Athletes, 50% M, 50% F; 6 running, 2 hockey, 1 ballet, 1 basketball, 16–31 y

9 scans abnormal uptake, 1 normal

B

2

Chisin et al.[17] (1987)

Prospective cohort

Not clearly stated

Bone scan

171 scanned with suspicion of stress fracture

Male soldiers, 18–21 y

171 bone scans: 53% sharply defined abnormality, stress fracture, 35% irregular poorly defined uptake, 12% normal

B

2

Batt et al.[18] (1998)

Prospective cohort

Exercise-induced lower leg pain, pain on palpation >5 cm on posteromedial tibial border

MRI/bone scan/x-ray

23: 41 symptomatic tibias, 4 asymptomatic athletes

Athletes and students, 14–58 y; 48% F, 52% M

x-Ray: 9% periosteal elevation; bone scan: 88% tibias abnormal; MRI: 83% abnormal

B

2

Gaeta et al.[19] (2005)

Case control

Lower leg pain 5 cm along tibial shaft

MRI

12: 14 tibias

Male soldiers, 17–25 y

93% periosteal oedema; 29% intraosseous bright signal and periosteal oedema

C

3

Aoki et al.[27] (2004)

Case series

Pain in the middle or distal portion of the medial side of the leg; normal xray

MRI

14 MTSS, 8 stress tibial fracture

Athletes (runners, basketball, volleyball, kendo, soccer players), 13–33 y; 59% M, 41% F

14/14: linear abnormally high signal along posteromedial border, 50% abnormally high signal of bone marrow, 36% both abnormal signals seen. After 4 wk, with continued exercise, MRI signals diminished in 5 patients

C

3

CT = computed tomography; F = female; M = male; MRI = magnetic resonance imaging; MTSS = medial tibial stress syndrome; T1 = T1 weighted; T2 = T2 weighted.

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Study (year)

Medial Tibial Stress Syndrome

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Table II. Contd

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Table III. Study characteristics and quality of studies concerning intrinsic risk factors Study (year)

Inclusion criteria

No. of subjects

Population

Risk factors (specification of determinant)

Outcome

Methodological Level of quality evidence

DeLacerda[28] Prospective (1980) cohort

Pain along the posteromedial aspect of the tibia

81

Female, physical education students, 18–21 y

Navicular displacement weight bearing/ non-weight bearing

Incidence MTSS 37%. Navicular drop 8.90 – 2.89 mm in MTSS group, control 5.56 – 2.32 mm

A2

2

Bennett Prospective et al.[3] (2001) cohort

Pain with palpation 125 over the distal 2/3 of the posterior medial tibia

Cross-country runners, 14–17 y; 46% M, 54% F

Navicular drop test

Navicular drop test (p = 0.01), female sex (p = 0.003)

A2

2

Burne et al.[29] Prospective (2004) cohort

At least 1 wk medial 158 tibial pain on exertion and >10 cm pain on palpation at distal 2/3 of posteromedial tibia

Military cadets, 17–21 y; 77% M, 23% F

Men only: greater internal and external hip ROM, leaner calf girth

Incidence MTSS 15%. A2 Incidence 15% F, 10% M. Greater internal and external ROM (p < 0.05), leaner calf girth (p = 0.04)

2

Prospective cohort

Pain, due to 125 exercise along the posteromedial tibial border, on palpation diffuse >5 cm

Naval recruits, 17–35 y; 75% M, 25% F

Female sex (RR 2.03), Incidence MTSS 36%. A2 more pronated foot Incidence 53% F, 28% M type (RR 1.70)

2

Plisky et al.[30] Prospective (2007) cohort

Pain along the distal 105 2/3 of the tibia exacerbated with repetitive weightbearing activity

Cross-country runners, 14–19 y; 56% M, 44% F

Higher BMI (RR 5.0)

Incidence MTSS 15%. 4.3/1000 athletic exposures (F), 1.7/1000 athletic exposures (M)

A2

2

Yates and White[4] (2004)

Study design

Prospective cohort

Exercise-related pain along the posteromedial side of the tibia for at least 5 cm with diffuse pain on palpation

146

Collegiate athletes from NCAA division I and II, 20 – 1.7 y; 45% M, 55% F

Athletic activity 46 months in a study investigating athletes, mainly runners) MRI scans were normal in seven patients.[25] Despite abnormalities found on MRI in symptomatic patients, Bergman et al.,[93] in a study with 21 distance runners, showed that 43% had a tibial stress reaction while asymptomatic ª 2009 Adis Data Information BV. All rights reserved.

(figure 3a and 3b). These runners ran 80–100 km a week for 8 weeks and continued doing this. None of these runners developed complaints. 4.3.4 High-Resolution Computed Tomography Scan

With high-resolution CT scan, Gaeta et al.[19,20] showed osteopenic changes in the tibial cortex and few resorption cavities (figure 4). A case-control study reported a sensitivity and specificity of 42% and 100%, respectively (LR 0.58).[19] In ten asymptomatic non-athlete controls, one tibia showed mild abnormalities (slightly reduced cortical attenuation). In 20 asymptomatic runners, 18 of the 40 tibias showed abnormalities (ranging from slightly reduced cortical attenuation to cortical osteopenia). All

Fig. 4. Axial CT scan showing cortical osteopenia (black arrows) and small resorption cavitations (white arrows) [reproduced from Gaeta et al.,[20] with permission].

Sports Med 2009; 39 (7)

Medial Tibial Stress Syndrome

symptomatic tibias in patients with MTSS showed cortical osteopenia.[20] 4.3.5 Imaging Summary

The diagnosis of MTSS should be made clinically. In cases where the diagnosis is unclear the physician may perform a bone scan or an MRI, which have approximately the same sensitivity and specificity. Compared with these values the sensitivity of CT scanning is lower, with a higher specificity. 5. Risk Factors 5.1 Risk Factor Studies

A number of prospective case-control and retrospective studies have examined intrinsic risk factors. Extrinsic risk factors have been poorly studied. The methodological quality and results of the risk studies are described in table III. One of these intrinsic risk factors is overpronation.[4,32,33] However, the definition of pronation in different articles varies. Pronatory foot type was shown to be a risk factor in a prospective military study by Yates and White (relative risk [RR] 1.70),[4] using the Foot Posture Index.[94,95] Gehlsen and Seger[32] and Viitasalo and Kvist[33] found increased pronation upon heelstrike to be a risk factor in two athlete casecontrol studies. In the study by Gehlsen and Seger,[32] the angular displacement between the calcaneus and the midline of the leg while running was significantly greater (p < 0.01) in the MTSS group compared with the non-MTSS group. Viitasalo and Kvist described the same finding as Gehlsen and Seger.[32] The angle between the lower leg and calcaneus at heel strike was higher for the symptomatic group (p < 0.01). Equivalents of pronation, measured with the navicular drop test and the standing foot angle, have also been studied. Four prospective studies were published examining the navicular drop test (the difference in distance between the lower border of the navicular and the ground – loaded and unloaded).[3,28,30,31] The navicular drop test is an indicator of midfoot pronation. Attention to the navicular prominence is also paid in the Foot Posture Index.[94,95] The navicular drop test was ª 2009 Adis Data Information BV. All rights reserved.

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measured in the study by Bennett et al.[3] of 125 runners. The mean drop distance in runners with complaints was 6.8 mm (– 3.7 mm), compared with 3.7 mm (– 3.3 mm) in the asymptomatic group (p = 0.003). In the second study, a significant correlation was found between navicular tuberosity displacement and the incidence of MTSS (8.9 – 2.9 compared with 5.6 – 2.3 mm) [p < 0.01].[28] A recent case-control study conducted among athletes showed a significant difference (p = 0.046) in navicular drop between loaded and unloaded groups (MTSS group 7.7 – 3.1 mm, control group 5.0 – 2.2 mm).[37] A third and fourth prospective study failed to find a significant relationship between navicular drop and MTSS.[30,31] The standing foot angle measures the angle between medial malleolus, navicular prominence and first metatarsal head. Sommer and Vallentyne[34] found that a standing foot angle 0.05). Another prospective study showed that increased plantar flexion range of motion was associated with MTSS (p = 0.004). This study was conducted among collegiate athletes.[31] A case-control study published in 1980 reported significantly increased plantar flexion strength values (p < 0.05), using cable tension procedures, in ten athletes with MTSS compared with ten healthy athletes.[32] In an Australian military prospective study by Burne et al.,[29] greater internal and external ranges of hip motion was a risk factor (p = 0.01–0.04 for left and right hip). This was measured with the hip and knee flexed to 90, with the hip rotated until a firm end feel. The extra amount of internal and external hip ranges of motion among patients was 8–12. In the same study[29] the lean calf girth (the maximal calf perimeter corrected for skin thickness) was 10–15 mm less among symptomatic cadets compared with asymptomatic cadets. This finding was only significant among males (p < 0.04). Leaner calf girth may also be biomechanically (see section 2.2) associated with MTSS due to reduced shock-absorbing capacity.[66-69] However, lean calf girth is not strictly correlated with calf muscle strength.[96] In a case-control study, Madeley et al.[35] found a significant difference in the number of heel raises that could be performed. MTSS patients succeeded with 23 repetitions per minute compared with 33 in the controls (p < 0.001). The study demonstrated muscular endurance deficits in athletes with MTSS. A higher body mass index (BMI > 20.2) was shown to be an intrinsic risk factor in the prospective study by Plisky et al. (OR 5.3).[30] The study investigated risk factors in a group of crosscountry runners. Female sex is also an intrinsic risk factor.[3,4,29] In a prospective study of naval recruits in Australia the incidence was 52.9% in females compared with 28.2% in males (RR 2.03).[4] The ª 2009 Adis Data Information BV. All rights reserved.

incidence of MTSS in a group of high school cross-country runners in another prospective study was 19.1% in females and 3.5% in males (p < 0.003).[3] A prospective study among the Australian Defence Force Academy also showed female sex to be a risk factor (MTSS incidence: females 30.6%, males 9.8%; OR 3.1).[29] A retrospective Canadian study found that a below-average activity history (8.5 or 90% of HRmax and 30.4% of the time with heart rates >95% of HRmax. This suggests that the intensity of female collegiate basketball is high enough to require large contributions from anaerobic metabolic pathways. 3.2 Male Players 3.2.1 Time-Motion Analysis

Only four time-motion analysis studies on male basketball players[19,20,46,47] were found. This is a low number for this kind of study, compared, for example, with another popular ball game – soccer.[48-55] A time-motion analysis was conducted by Ben Abdelkrim et al.[19] of elite under-19-year-old male basketball players. In this study, the authors defined nine specific movements, and the average total number of movements performed by the players during the game was 1050 – 51. McInnes et al.[46] defined eight specific movements (e.g. stand/walk, jog, run and stride/sprint), and examined their frequency and duration during a basketball game. The mean frequency of all movements was 997 – 183 and the mean duration of all movements was 85% of HRmax in 75% of their playing time. Such high heart rates are usually associated with high intensity. However, it was indicated in the same study that high-intensity movements were performed during only 15% of the players’ playing time. The authors explained this discrepancy by suggesting that a variety of high-intensity movements – such as maintaining a position against physical resistance, passing, rebounding and shooting – were not measured in this study. A similar observation was made by Ben Abdelkrim et al.,[19] who compared heart rates among male players playing different positions. They found that guards had heart rates that were higher by 2–3 beats/min than forwards and centres. This difference suggested a slightly higher play intensity in guards, which is in line with the finding that guards were engaged in more moderate- and high-intensity movements. However, heart rate is also influenced by other variables, such as nutritional status,[11] environmental conditions,[11] psychological arousal,[19] anxiety[19] Sports Med 2009; 39 (7)

Attributes of Female and Male Basketball Players

and stoppage in game play.[19] Therefore, these data should be carefully interpreted. 3.2.3 Blood Lactate

Obtaining information on the metabolic pathways that are utilized during a basketball game – both aerobic and anaerobic – should also be of interest to the basketball coach and the strength and conditioning coach. Ben Abdelkrim et al.[19] reported that guards had higher blood lactate levels than centres (6.0 – 1.2 vs 4.9 – 1.1 mmol/L, respectively). Narazaki et al.[20] reported a mean value of 4.2 – 1.3 mmol/L in 20-minute practice games, while Castagna et al.[56] reported a mean of 3.72 – 1.39 in 20-min games of young basketball players (mean age 16.8 – 2 years). McInnes et al.[46] reported elevated lactate levels throughout a basketball game, with high variability among male players (mean maximum 8.5 – 3.1 mmol/L). The elevated lactate values suggested that glycolytic pathways made an important contribution to energy production during an actual game.[46] However, caution is warranted when interpreting blood lactate values. Blood lactate concentration is a snapshot of lactate turnover. Lactate is being produced by muscles working at high intensity, and at the same time it is being removed from those muscles to be used by other skeletal muscles, the cardiac muscle, or for gluconeogenesis in the liver. Therefore, the simple fact that blood lactate is elevated above resting levels does not tell us directly what percentage of energy comes from aerobic or anaerobic pathways. 4. Nutritional Strategies and Oxidative Stress It is widely accepted that maintaining proper nutrition is beneficial to athletic performance.[57] A number of studies examining the contribution of nutritional strategies to facilitating improved performance in basketball are reviewed. It is beyond the objectives and scope of our article to provide a more extensive review on nutritional strategies and oxidative stress in elite basketball players than that given here. Basketball players (female and male), as with other athletes, should maintain a positive energy ª 2009 Adis Data Information BV. All rights reserved.

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balance and avoid low-energy intakes. Energy intake should be balanced between carbohydrates (55–58% of energy), proteins (12–15%) and fats (25–30%).[57] Special care should be taken in the vegetarian athlete, who might be at risk for low protein intake, as well as low micronutrients intake (specifically vitamin B12, zinc, iron and calcium). While most macronutrients and micronutrients can be supplied from foods in a balanced diet, additional supplements may be useful during an intense basketball season. Maintaining a positive and balanced energy intake can prove difficult between the practice sessions and games, and during long travels in a competitive basketball season. Schroder et al.[58] found that 32 (58%) of a sample of 55 basketball players in the First Spanish Basketball League reported using dietary supplements. Of those players, 81% used supplements on a daily basis, with multivitamins and vitamins being taken most frequently (50%). The authors suggested that the consumption of multivitamins might help in preventing temporary vitamin imbalances that may be caused by the frequency and timing of training sessions, travel and poor food selection. 4.1 Hydration

One nutrient that is often overlooked is water. Maintaining euhydration is important to aerobic performance, and it is suggested that a water deficit of 2% of bodyweight can lead to decreased performance.[59,60] A number of studies on hydration in basketball players suggest that dehydration is detrimental to performance.[61-63] In one study of eleven 17- to 28-year-old male basketball players, dehydration led to impaired vigilance-related attentional performance.[61] In another study of 17 male basketball players aged 17–28 years old, a progressive decline in basketball skills was associated with dehydration levels of 1–4% of bodyweight.[62] The threshold of water deficit at which overall performance deterioration became statistically significant was 2% of bodyweight.[62] Consumption of carbohydrate solutions (sports drinks) during intermittent exercise appears to improve sports performance.[64] In a study of 15 male adolescent players aged Sports Med 2009; 39 (7)

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12–15 years,[63] it was found that 2% dehydration was associated with deterioration in basketball skill performance, and that euhydration with a 6% carbohydrate solution improved both shooting skills and on-court sprinting compared with euhydration with a placebo. Clearly, teaching basketball players to maintain hydration is important. This can be effectively accomplished by weighing each player before and after practices. In this manner, players can learn their individual sweat loss ratios and know how much fluid intake is required of them to maintain euhydration. 4.2 Oxidative Stress

Free radicals occur naturally in the body and can have negative effects on lipids, proteins and DNA oxidation. The antioxidant system alleviates these negative effects. When there is an imbalance between the production of free radicals and the antioxidant defence, oxidative stress occurs. Oxidative stress may be involved in the aging process, cell damage, some pathology, muscular fatigue and overtraining.[65] Exercise training increases the production of free radicals and the utilization of antioxidants. Therefore, proper nutrition is important in maintaining the antioxidants.[65] Since basketball players perform intense physical activity, their free radical production is likely to increase. Hence, it is important to supply the needed micronutrients that serve as antioxidants to alleviate the possible negative effects of the free radicals. When a balanced diet is not maintained, antioxidant supplements may be warranted. In one study,[66] researchers examined the effects of antioxidant supplements – a-tocopherol (vitamin E), b-carotene and ascorbic acid (vitamin C) – on exercise stress markers in 13 professional male basketball players (seven players in a supplement group, six players in a placebo group). After 32 days of treatment, elevated plasma levels of a-tocopherol and b-carotene were found in the supplement group but not in the placebo group. However, plasma levels of ascorbic acid were not elevated in the supplement ª 2009 Adis Data Information BV. All rights reserved.

group, while there was a significant decrease in the placebo group. The authors cautiously suggested the ascorbic acid levels remaining similar despite the supplementation might be explained by its use to scavenge free radicals and regenerate vitamin E. Importantly, lipid peroxide (lipid peroxidation is the degradation of lipids and can cause cell membrane damage) plasma concentration decreased in the supplement group by 27%, although the difference was not statistically significant (p < 0.09). The authors suggested that this may be related to a reduction in muscle cell damage during training.[66] Similar results were observed in another study,[67] which found an improvement in oxidative stress in elite male basketball players during a competitive season when antioxidant supplements were taken. A third study[68] found that a-tocopherol supplementation may reduce the DNA oxidation induced by training. In this study, total antioxidant status was higher after 1 month of supplementation. These studies suggest that basketball players may benefit from supplementing their diet with antioxidants. Interestingly, vegetarian athletes have higher antioxidant status for vitamin C, vitamin E and b-carotene compared with omnivores.[69] While the negative effects of free radicals do not usually affect performance, it is possible that they can lead to overtraining. This may be because muscular cell damage, which can be caused by free radicals, can reduce the metabolic capacities of muscle cells.[65] This speculation should be considered cautiously as there is no direct evidence to support it.[65] 5. Conditioning for Basketball A number of articles looked at conditioning for basketball.[43,70-74] Although an extensive review of the basketball conditioning literature is beyond the scope of our article, a few concepts are noteworthy. (For a detailed review of conditioning practices in basketball see Hoffman and Maresh.[43]) Conditioning practices for basketball players can be complex, as the players require good aerobic capacity, anaerobic power, speed, agility and strength. The limited time for conditioning Sports Med 2009; 39 (7)

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during the season means that the coaching staff working with the players need to decide what aspect of conditioning the strength and conditioning coach needs to concentrate on. Tavino et al.[28] suggested that during the offseason, players should use a combination of aerobic and anaerobic training to maintain fitness levels. During pre-season, athletes should concentrate more on developing anaerobic capacity, and during the season, high-intensity training should be done twice a week to maintain anaerobic capacity. In addition, weight training should be employed throughout the year, while during the season weight training should be carried out moderately twice a week to maintain strength.[28] Relevant information on conditioning programmes was obtained from NBA strength and conditioning coaches (NBA-SC) in a large survey of 20 NBA-SC where it was found that all worked with their players on flexibility, speed development, plyometrics and strength/power development. Much variation was seen in the types of drills, frequency, duration and intensity of training.[73] It was also found that most coaches (90%) divided their programmes into periods by taking into account the specific needs of their players in different phases of the season. NBA-SC also assessed the fitness level of their players. More coaches reported testing for aerobic capacity (n = 12) than anaerobic capacity (n = 10). It is unclear why less than half the coaches tested for anaerobic capacity, as it is clearly of great importance to the game. A time-motion analysis can be used by strength and conditioning coaches when planning conditioning programmes for their elite players. Taylor,[74] for example, suggested that four videotapes of game performance should be chosen for analysis for each player: (a) the best game of year; (b) the worst game of year; (c) the game with fewest fouls; and (d) a post-season game. After the analysis performed by the coach, he or she can plan workouts that simulate intensity and rest periods in order to mimic what players do in actual games. Including such workouts in the year-round conditioning programme can improve the physical preparation of the players for practices and games. ª 2009 Adis Data Information BV. All rights reserved.

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Time-motion analysis can also be used in order to establish specific testing protocols for basketball players. This was the objective of Castagna et al.,[42] who decided on a repeatedsprint test protocol based on a time-motion analysis. They found that 93% of sprint stride sequences included no more than ten consecutive bouts and that sprint lengths were 5–32 m. Based on these data, they decided on a basketballspecific repeated-sprint test of ten shuttle run sprints of 15 m. As Hoffman et al.[75] indicated, once an aerobic base has been established, further increases in aerobic capacity may not increase performance in basketball players. Therefore, a maintenance programme consisting of running three times per week for a duration of 30–40 minutes may be sufficient. However, there is reason to believe that an aerobic training programme targeted at increasing the anaerobic threshold is beneficial as well. According to a recent study, the mean oxygen . is 66.7% of . consumption during game play VO2max in female and 64.7% of VO2max in male basketball players.[20] These values are probably in the vicinity of the anaerobic threshold of these players and perhaps a bit higher, although this was not measured in the study. That is to say that the players worked at an intensity that was at or slightly above their anaerobic threshold. Increasing .the anaerobic threshold to a realistic 70% of VO2max will allow players to use more aerobic metabolic pathways, which can lead to decreased fatigue during games. However, this recommendation should be considered with caution as it is inferred from only one study of six female and six male players. 5.1 Hormonal Status and the Overtraining Syndrome

One aspect of conditioning that should not be overlooked is overtraining. Peak performance can be achieved by the right combination of volume and intensity of training, as well as by providing the player with adequate resting periods in between.[76] If volume and intensity are too high, and if not enough recovery time is given to the player, overtraining can occur. The Sports Med 2009; 39 (7)

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overtraining syndrome is characterized by diminished performance, increased fatigue and stress.[77] It has been suggested that disturbances of several hormones (e.g. growth hormone, cortisol,[77] hypothalamopituitary dysregulation[78]) can be reliable markers of overtraining. In addition, biochemical markers such as creatine kinase and urea can be indicative of muscle damage.[66] However, one study suggested that their validity in indicating overtraining may be overestimated.[78] It should be noted that there are no definite diagnostic criteria for the overtraining syndrome.[79] It should also be noted that the ratio between testosterone and cortisol represents the balance between anabolic and catabolic processes, and is also likely to represent the physiological strain of training.[77] One study was found that examined hormonal and biochemical changes in ten male basketball players participating in a 4-week training camp.[76] No difference in testosterone and luteinizing hormone levels in over 4 weeks of training was indicated. The training camp was scheduled 1 month after the end of the 9-month regular season. Plasma cortisol increased significantly in week 4 of the training programme, but remained within the normal range. The ratio between testosterone and cortisol was decreased by 22% in week 4, although this finding was not statistically significant. Between week 1 and week 2 of the training programme, creatine kinase levels increased by 60%; however, this was not statistically significant. This finding probably represented local muscle trauma only. It was concluded that a 4-week training camp for elite basketball players did not appear to cause any disturbance to the hormonal or biochemical profile of the players. Since it can be difficult to notice decrements in performance in basketball players, unlike sports like swimming or track and field in which measures of performance are quite clear,[76] more studies of hormonal and biochemical markers of overtraining that are evaluated over an entire basketball season are warranted. Such objective markers of overtraining can help coaches to start tapering early enough to prevent overtraining from developing. ª 2009 Adis Data Information BV. All rights reserved.

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6. Five Limitations Observed from the Physical and Physiological Measurements The studies reviewed in this article provide useful information to both researchers and practitioners on various physical and physiological characteristics of female and male basketball players. Among these characteristics are height, mass, aerobic and anaerobic capacities, strength and agility. However, five limitations associated with the testing protocols used in the reviewed studies are presented here. (a) Lack of a longitudinal approach. In the majority of the reviewed studies the physical and physiological tests were given to the players only once. No replicated measurements across different periods of time were performed. In order to systematically examine characteristics of elite performers (e.g. basketball players), a longitudinal approach should be used as well. In this approach, one group of performers is observed over a long period of time,[80] enabling the researchers to collect data on a variety of dependent variables, as well as to study developmental perspectives of the observed group. From an expert theory perspective, it has been established[81] that a period of at least 10 years is required to achieve expertise in sport, as well as in other domains such as art, music and science. Therefore, it would be useful for researchers and practitioners alike to obtain information on the physical and physiological characteristics of elite players during different periods of time across the season/s, and among different groups of skill level and age. This information would result in improving the ability of coaches to compare achievements among players as well as to plan more effectively training programmes for elite basketball players. (b) Lack of tests performed under physical exertion conditions. The physical and physiological tests used in the reviewed studies were performed in a rested state, i.e. the players performed when they felt ready, according to the protocols of the tests. Fatigue primarily affects the central processes that take place between information receipt and the initiation of a movement.[82] In this Sports Med 2009; 39 (7)

Attributes of Female and Male Basketball Players

respect, it was shown that fatigue can influence certain mechanisms as they operate from the input of information to the output. Moderately high fatigue will impair performances requiring strength, endurance and rapid movements. Therefore, it is of particular interest to the coach to assess his or her players’ ability not only under rested conditions, but also under physical exertion conditions that reflect what is required of them in actual games. (c) Lack of studies using a time-motion analysis. The majority of the studies described in our review were conducted under laboratory conditions and sterile settings, where the players were instructed to perform the tests individually. In only a few studies were data collected on physical and physiological performances of players during actual games. In order to plan effective strength and conditioning programmes for basketball players, more information should be gathered on what actions players actually perform during the game. A systematic analysis of the main actions demonstrated by the players during the game should be carefully made, and then, based on this analysis, field observations using a timemotion analysis should be conducted on players of different skill levels as well as on players playing different positions. In addition, studying the work/rest ratio during competitive games by recording live physiological measurements (via a portable metabolic system) can allow coaches to gather additional relevant information on the players, and plan better conditioning programmes accordingly. (d) Reported HR values can be difficult to interpret. These values should be interpreted as a percentage of HRmax; however, these interpretations will be accurate only if the actual HRmax is known for the players, since the estimation of HRmax from age is inaccurate. In addition, HR values should be reported for the total game time, including stoppages. Recording HR only in live time ignores important recovery information during rest periods such as time-outs and half-time. (e) The results of blood lactate concentration can also be difficult to interpret. As mentioned earlier (section 3.2.3), blood lactate concentration is a result of lactate rate of appearance and rate of ª 2009 Adis Data Information BV. All rights reserved.

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disappearance. Blood lactate and muscle lactate can be different during intermittent exercise, and blood lactate is not necessarily a good predictor of muscle lactate.[83] Moreover, while some of the working muscles produce lactate, other muscles that work at lower intensities may actually be consumers of lactate as a substrate. It is suggested that measuring or estimating the anaerobic threshold of each player, followed by the measurements of muscle and blood lactate over several games, as Ben Abdelkrim et al.[19] suggested, can enhance our understanding of the workload and metabolic pathways being used during a game. Several test protocols are available for the measurement of the anaerobic threshold. Performing those tests and interpreting their results require a knowledgeable and experienced staff. (For a review of the concept of the anaerobic threshold and the methods of measurement, see Svedahl and MacIntosh.[84])

7. Practical Advice for Basketball and Strength and Conditioning Coaches We have three recommendations for the basketball coach and the strength and conditioning coach. (a) Training programmes should be planned for the athlete according to his or her playing position. Guards, forwards and centres have different physical and physiological characteristics. Although relevant information on training programmes for basketball players can be found in the literature,[43] it is suggested that more emphasis be placed on developing specific programmes for forwards, centres and, particularly, for guards. Ultimately, basketball and strength and conditioning coaches should plan their training programmes according to the unique characteristics of each player. (b) A careful selection of the physical and physiological tests should be made. As reported in our review, there are a large number of different tests assessing physical and physiological abilities in basketball players. Therefore, it is recommended to carefully select the test most Sports Med 2009; 39 (7)

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appropriate for assessing abilities in female and male basketball players. It is also recommended that the same test be used for comparing achievements in a specific ability among the basketball players. Different tests yield different values, and thus the resulting comparison would not be effective. (c) Coaches should be aware of changes in the rules of the game. They should take any changes made in the rules of the game into account while planning their training programmes. Practically speaking, the physical preparation as part of the annual training programme should also help the player adjust to any new changes made in the rules of the game.

8. Conclusions This paper reviewed several issues related to basketball players and their performance. Despite the five limitations observed in the reviewed studies, three practical recommendations for basketball coaches were noted. We suggest that future research should concentrate on timemotion analyses, physiological demands during game-play, and the effects of fatigue on performance. Acknowledgements The authors would like to thank Dinah Olswang for her editorial assistance during the preparation of this manuscript. No sources of funding were used to assist in the preparation of this review, and the authors have no conflicts of interest that are directly relevant to the content of this review.

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logical attributes. J Sci Med Sport 2000 Dec; 3 (4): 91-405 Hoffman JR, Epstein S, Einbinder M, et al. A comparison between the Wingate Anaerobic Power Test to both vertical jump and line drill tests in basketball players. J Strength Cond Res 2000; 14 (3): 261-4 Kalinski MI, Norkowski H, Kerner MS, et al. Anaerobic power characteristics of elite athletes in national level teamsport games. Eur J Sport Sci 2002; 2 (3): 1-14 Markovic G. Does plyometric training improve vertical jump height? A meta-analytical review. Br J Sports Med 2007 Jun; 41 (6): 349-55 Castagna C, Abt G, Manzi V, et al. Effect of recovery mode on repeated sprint ability in young basketball players. J Strength Cond Res 2008 May; 22 (3): 923-9 Hoffman JR, Maresh CM. Physiology of basketball. In: Garrett Jr WE, Kirkendall DT, editors. Exercise and sport science. Philadelphia (PA): Lippincott Williams & Wilkins, 2000: 733-44 Beam WC, Merrill TL. Analysis of heart rates recorded during female collegiate basketball [abstract]. Med Sci Sports Exerc 1994; 26 (5 Suppl.): S66 Ainsworth BE, Haskell WL, Whitt MC, et al. Compendium of physical activities: an update of activity codes and MET intensities. Med Sci Sports Exerc 2000 Sep; 32 (9 Suppl.): S498-504 McInnes SE, Carlson JS, Jones CJ, et al. The physiological load imposed on basketball players during competition. J Sports Sci 1995 Oct; 13 (5): 387-97 Miller SA, Bartlett RM. Notational analysis of the physical demands of basketball [abstract]. J Sports Sci 1994; 12 (2): 181 Mohr M, Krustrup P, Bangsbo J. Match performance of high-standard soccer players with special reference to development of fatigue. J Sports Sci 2003 Jul; 21 (7): 519-28 Krustrup P, Mohr M, Ellingsgaard H, et al. Physical demands during an elite female soccer game: importance of training status. Med Sci Sports Exerc 2005 Jul; 37 (7): 1242-8 Burgess DJ, Naughton G, Norton KI. Profile of movement demands of national football players in Australia. J Sci Med Sport 2006 Aug; 9 (4): 334-41 Di Salvo V, Baron R, Tschan H, et al. Performance characteristics according to playing position in elite soccer. Int J Sports Med 2007 Mar; 28 (3): 222-7 Stroyer J, Hansen L, Klausen K. Physiological profile and activity pattern of young soccer players during match play. Med Sci Sports Exerc 2004 Jan; 36 (1): 168-74 Anastasiadis S, Anogeianaki A, Anogianakis G, et al. Real time estimation of physical activity and physiological performance reserves of players during a game of soccer. Stud Health Technol Inform 2004; 98: 13-5 Drust B, Atkinson G, Reilly T. Future perspectives in the evaluation of the physiological demands of soccer. Sports Med 2007; 37 (9): 783-805 Hill-Haas S, Coutts A, Rowsell G, et al. Variability of acute physiological responses and performance profiles of youth soccer players in small-sided games. J Sci Med Sport 2008; 11 (5): 487-90 Castagna C, Manzi V, Marini M, et al. Effect of playing basketball in young basketball players [abstract]. In:

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Hoppeler H, Reilly T, Tsolakidis E, et al., editors. Book of abstracts of the 11th Annual Congress of the European College of Sport Science 2006. Lausanne: 2006: 325 Joint Position Statement: nutrition and athletic performance. American College of Sports Medicine, American Dietetic Association, and Dietitians of Canada. Med Sci Sports Exerc 2000 Dec; 32 (12): 2130-45 Schroder H, Navarro E, Mora J, et al. The type, amount, frequency and timing of dietary supplement use by elite players in the First Spanish Basketball League. J Sports Sci 2002 Apr; 20 (4): 353-8 Casa DJ, Clarkson PM, Roberts WO. American College of Sports Medicine roundtable on hydration and physical activity: consensus statements. Curr Sports Med Rep 2005 Jun; 4 (3): 115-27 Cheuvront SN, Carter 3rd R, Sawka MN. Fluid balance and endurance exercise performance. Curr Sports Med Rep 2003 Aug; 2 (4): 202-8 Baker LB, Conroy DE, Kenney WL. Dehydration impairs vigilance-related attention in male basketball players. Med Sci Sports Exerc 2007 Jun; 39 (6): 976-83 Baker LB, Dougherty KA, Chow M, et al. Progressive dehydration causes a progressive decline in basketball skill performance. Med Sci Sports Exerc 2007 Jul; 39 (7): 1114-23 Dougherty KA, Baker LB, Chow M, et al. Two percent dehydration impairs and six percent carbohydrate drink improves boys basketball skills. Med Sci Sports Exerc 2006 Sep; 38 (9): 1650-8 Coombes JS, Hamilton KL. The effectiveness of commercially available sports drinks. Sports Med 2000 Mar; 29 (3): 181-209 Finaud J, Lac G, Filaire E. Oxidative stress: relationship with exercise and training. Sports Med 2006; 36 (4): 327-58 Schroder H, Navarro E, Mora J, et al. Effects of alphatocopherol, beta-carotene and ascorbic acid on oxidative, hormonal and enzymatic exercise stress markers in habitual training activity of professional basketball players. Eur J Nutr 2001 Aug; 40 (4): 178-84 Schroder H, Navarro E, Tramullas A, et al. Nutrition antioxidant status and oxidative stress in professional basketball players: effects of a three compound antioxidative supplement. Int J Sports Med 2000 Feb; 21 (2): 146-50 Tsakiris S, Parthimos T, Tsakiris T, et al. Alpha-tocopherol supplementation reduces the elevated 8-hydroxy-2-deoxyguanosine blood levels induced by training in basketball players. Clin Chem Lab Med 2006; 44 (8): 1004-8 Venderley AM, Campbell WW. Vegetarian diets: nutritional considerations for athletes. Sports Med 2006; 36 (4): 293-305

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70. Chandler J. Basketball: goals and activities for athletic conditioning in basketball. Strength Cond 1986; 8 (5): 52-5 71. Hilyer J, Hunter GR. Bridging the gap-practical application: a year-round strength development and conditioning program for men’s basketball. Strength Cond 1989; 11 (6): 16-9 72. Kroll WA. Conditioning for basketball. Strength Cond 1983; 5 (2): 24-6 73. Simenz CJ, Dugan CA, Ebben WP. Strength and conditioning practices of National Basketball Association strength and conditioning coaches. J Strength Cond Res 2005 Aug; 19 (3): 495-504 74. Taylor J. Basketball: applying time motion data to conditioning. Strength Cond 2003; 25 (2): 57-64 75. Hoffman JR, Epstein S, Einbinder M, et al. The influence of aerobic capacity on anaerobic performance and recovery indices in basketball players. J Strength Cond Res 1999; 13 (4): 407-11 76. Hoffman JR, Epstein S, Yarom Y, et al. Hormonal and biochemical changes in elite basketball players during a 4-week training camp. J Strength Cond Res 1999; 13 (3): 280-5 77. Urhausen A, Gabriel H, Kindermann W. Blood hormones as markers of training stress and overtraining. Sports Med 1995 Oct; 20 (4): 251-76 78. Urhausen A, Gabriel HH, Kindermann W. Impaired pituitary hormonal response to exhaustive exercise in overtrained endurance athletes. Med Sci Sports Exerc 1998 Mar; 30 (3): 407-14 79. Meeusen R, Duclos M, Gleeson M, et al. Prevention, diagnosis and treatment of the overtraining syndrome. Eur J Sport Sci 2006; 6 (1): 1-14 80. Thomas JR, Nelson JK. Research methods in physical activity. 5th ed. Champaign (IL): Human Kinetics, 2005 81. Ericsson KA. How the expert performance approach differs from traditional approaches to expertise in sports. In: Starkes JL, Ericsson KA, editors. Expert performance in sports-advances in research on sport expertise. Champaign (IL): Human Kinetics, 2003: 371-402 82. Pack M. Effects of four fatigue levels on performance and learning of novel dynamic balance skill. J Mot Behav 1974; 6: 191-7 83. Krustrup P, Mohr M, Steensberg A, et al. Muscle and blood metabolites during a soccer game: implications for sprint performance. Med Sci Sports Exerc 2006 Jun; 38 (6): 1165-74 84. Svedahl K, MacIntosh BR. Anaerobic threshold: the concept and methods of measurement. Can J Appl Physiol 2003 Apr; 28 (2): 299-323

Correspondence: Dr Ronnie Lidor, Associate Professor, The Zinman College of Physical Education and Sport Sciences, Wingate Institute, Netanya 42902, Israel. E-mail: [email protected]

Sports Med 2009; 39 (7)

Sports Med 2009; 39 (7): 569-590 0112-1642/09/0007-0569/$49.95/0

REVIEW ARTICLE

ª 2009 Adis Data Information BV. All rights reserved.

Shoulder Muscle Recruitment Patterns and Related Biomechanics during Upper Extremity Sports Rafael F. Escamilla1, 2 and James R. Andrews1 1 Andrews-Paulos Research and Education Institute, Gulf Breeze, Florida, USA 2 Department of Physical Therapy, California State University, Sacramento, California, USA

Contents Abstract. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1. Shoulder Electromyography (EMG) during the Overhead Baseball Pitch . . . . . . . . . . . . . . . . . . . . . . . 1.1 Wind-Up Phase . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1.2 Stride Phase . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1.3 Arm Cocking Phase . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1.4 Arm Acceleration Phase . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1.5 Arm Deceleration Phase . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2. Shoulder EMG during the Overhead American Football Throw. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3. Shoulder EMG during Windmill Softball Pitching. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4. Shoulder EMG during the Volleyball Serve and Spike . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5. Shoulder EMG during the Tennis Serve and Volley . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6. Shoulder EMG during Baseball Batting . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7. Shoulder EMG during the Golf Swing. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8. Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Abstract

569 571 572 572 573 574 576 577 578 580 583 585 586 588

Understanding when and how much shoulder muscles are active during upper extremity sports is helpful to physicians, therapists, trainers and coaches in providing appropriate treatment, training and rehabilitation protocols to these athletes. This review focuses on shoulder muscle activity (rotator cuff, deltoids, pectoralis major, latissimus dorsi, triceps and biceps brachii, and scapular muscles) during the baseball pitch, the American football throw, the windmill softball pitch, the volleyball serve and spike, the tennis serve and volley, baseball hitting, and the golf swing. Because shoulder electromyography (EMG) data are far more extensive for overhead throwing activities compared with non-throwing upper extremity sports, much of this review focuses on shoulder EMG during the overhead throwing motion. Throughout this review shoulder kinematic and kinetic data (when available) are integrated with shoulder EMG data to help better understand why certain muscles are active during different phases of an activity, what type of muscle action (eccentric or concentric) occurs, and to provide insight into the shoulder injury mechanism. Kinematic, kinetic and EMG data have been reported extensively during overhead throwing, such as baseball pitching and football passing. Because

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shoulder forces, torques and muscle activity are generally greatest during the arm cocking and arm deceleration phases of overhead throwing, it is believed that most shoulder injuries occur during these phases. During overhead throwing, high rotator cuff muscle activity is generated to help resist the high shoulder distractive forces »80–120% bodyweight during the arm cocking and deceleration phases. During arm cocking, peak rotator cuff activity is 49–99% of a maximum voluntary isometric contraction (MVIC) in baseball pitching and 41–67% MVIC in football throwing. During arm deceleration, peak rotator cuff activity is 37–84% MVIC in baseball pitching and 86–95% MVIC in football throwing. Peak rotator cuff activity is also high is the windmill softball pitch (75–93% MVIC), the volleyball serve and spike (54–71% MVIC), the tennis serve and volley (40–113% MVIC), baseball hitting (28–39% MVIC), and the golf swing (28–68% MVIC). Peak scapular muscle activity is also high during the arm cocking and arm deceleration phases of baseball pitching, with peak serratus anterior activity 69–106% MVIC, peak upper, middle and lower trapezius activity 51–78% MVIC, peak rhomboids activity 41–45% MVIC, and peak levator scapulae activity 33–72% MVIC. Moreover, peak serratus anterior activity was »60% MVIC during the windmill softball pitch, »75% MVIC during the tennis serve and forehand and backhand volley, »30–40% MVIC during baseball hitting, and »70% MVIC during the golf swing. In addition, during the golf swing, peak upper, middle and lower trapezius activity was 42–52% MVIC, peak rhomboids activity was »60% MVIC, and peak levator scapulae activity was »60% MVIC.

Electromyography (EMG) is the science of quantifying muscle activity. Several studies have reported shoulder muscle activity during a variety of upper extremity sports.[1-7] Understanding when and how much specific shoulder muscles are active during upper extremity sports is helpful to physicians, therapists, trainers and coaches in providing appropriate treatment, training and rehabilitation protocols to these athletes, as well as helping health professionals better understand the shoulder injury mechanism. When interpreting EMG data it should be emphasized that while the EMG amplitude does correlate reasonably well with muscle force for isometric contractions, it does not correlate well with muscle force as muscle contraction velocities increase, or during muscular fatigue (both of which occur in sport).[8] Nevertheless, EMG analyses are helpful in determining the timing and quantity of muscle activation throughout a given movement. This review focuses on shoulder muscle activity in upper extremity sports, specifically: baseball pitching, American football throwing, windmill ª 2009 Adis Data Information BV. All rights reserved.

softball pitching, the volleyball serve and spike, the tennis serve and volley, baseball hitting, and the golf swing. Most of the movements that occur in the aforementioned sports involve overhead throwing type movements. Shoulder EMG data in the literature are far more extensive for overhead throwing activities, such as baseball pitching, compared with other upper extremity sports that do not involve the overhead throwing motion, such as baseball hitting. Therefore, much of this review focuses on shoulder EMG during activities that involve the overhead throwing motion. To help better interpret the applicability and meaningfulness of shoulder EMG data, EMG data will be integrated with shoulder joint kinematics (linear and angular shoulder displacements, velocities and accelerations) and kinetics (shoulder forces and torques) when these data are available. In the literature, kinematic, kinetic and EMG measurements have been reported extensively in overhead throwing activities,[2,9-12] such as baseball pitching and football throwing, but these data are sparse in other upper extremity activities, such as Sports Med 2009; 39 (7)

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the volleyball serve and spike, the tennis serve and volley, baseball hitting, and the golf swing. Overhead throwing activities in particular are commonly associated with shoulder injuries.[13,14] When EMG is interpreted with shoulder kinematics and kinetics, it not only provides a better understanding of why certain muscles are active during different phases of an activity, but also provides information as to what type of muscle action (eccentric or concentric) is occurring, and insight into the shoulder injury mechanism. Although shoulder muscle activity is the primary focus of this review, shoulder injuries will be dis-

cussed briefly relative to joint loads, joint motions and muscle activity when these data are available. 1. Shoulder Electromyography (EMG) during the Overhead Baseball Pitch Shoulder muscle activity during baseball pitching has been examined extensively by Jobe and colleagues,[2,15-18] with their initial report published in 1983.[18] Using 56 healthy male college and professional pitchers, DiGiovine and colleagues[2] quantified shoulder muscle activity

Table I. Shoulder activity by muscle and phase during baseball pitchinga (adapted from DiGiovine et al.,[2] with permission) Muscles

No. of subjects

Phase wind-upb (% MVIC)

Upper trapezius

11

18 – 16

64 – 53

37 – 29

Middle trapezius

11

7–5

43 – 22

51 – 24

Lower trapezius

13

13 – 12

39 – 30

Serratus anterior (6th rib)

11

14 – 13

Serratus anterior (4th rib)

10

Rhomboids Levator scapulae

stridec (% MVIC)

arm cockingd (% MVIC)

arm acceleratione (% MVIC)

arm decelerationf (% MVIC)

follow-throughg (% MVIC)

69 – 31

53 – 22

14 – 12

71 – 32

35 – 17

15 – 14

38 – 29

76 – 55

78 – 33

25 – 15

44 – 35

69 – 32

60 – 53

51 – 30

32 – 18

20 – 20

40 – 22

106 – 56

50 – 46

34 – 7

41 – 24

11

7–8

35 – 24

41 – 26

71 – 35

45 – 28

14 – 20

11

6–5

35 – 14

72 – 54

76 – 28

33 – 16

14 – 13

Anterior deltoid

16

15 – 12

40 – 20

28 – 30

27 – 19

47 – 34

21 – 16

Middle deltoid

14

9–8

44 – 19

12 – 17

36 – 22

59 – 19

16 – 13

Posterior deltoid

18

6–5

42 – 26

28 – 27

68 – 66

60 – 28

13 – 11

Supraspinatus

16

13 – 12

60 – 31

49 – 29

51 – 46

39 – 43

10 – 9

Infraspinatus

16

11 – 9

30 – 18

74 – 34

31 – 28

37 – 20

20 – 16

Teres minor

12

5–6

23 – 15

71 – 42

54 – 50

84 – 52

25 – 21

Subscapularis (lower 3rd)

11

7–9

26 – 22

62 – 19

56 – 31

41 – 23

25 – 18

Subscapularis (upper 3rd)

11

7–8

37 – 26

99 – 55

115 – 82

60 – 36

16 – 15

Pectoralis major

14

6–6

11 – 13

56 – 27

54 – 24

29 – 18

31 – 21

Latissimus dorsi

13

12 – 10

33 – 33

50 – 37

88 – 53

59 – 35

24 – 18

Triceps brachii

13

4–6

17 – 17

37 – 32

89 – 40

54 – 23

22 – 18

Biceps brachii

18

8–9

22 – 14

26 – 20

20 – 16

44 – 32

16 – 14

Scapular

Glenohumeral

a

Data are given as means and standard deviations, and expressed for each muscle as a percentage of an MVIC.

b

From initial movement to maximum knee lift of stride leg.

c

From maximum knee lift of stride leg to when lead foot of stride leg initially contacts the ground.

d

From when lead foot of stride leg initially contacts the ground to maximum shoulder external rotation.

e

From maximum shoulder external rotation to ball release.

f

From ball release to maximum shoulder internal rotation.

g

From maximum shoulder internal rotation to maximum shoulder horizontal adduction.

MVIC = maximum voluntary isometric contraction.

ª 2009 Adis Data Information BV. All rights reserved.

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Knee up

Phases

Wind-up

Foot contact

Stride

Max ER

Arm cocking

Release

Arm acceleration

Arm deceleration

Max IR

Follow-through

Fig. 1. Pitching phases and key events (adapted from Fleisig et al.,[12] with permission). ER = external rotation; IR = internal rotation; max = maximum.

during baseball pitching (data summarized in table I). To help generalize phase comparisons in muscle activity from table I, 0–20% of a maximum voluntary isometric contraction (MVIC) is considered low muscle activity, 21–40% MVIC is considered moderate muscle activity, 41–60% MVIC is considered high muscle activity and >60% MVIC is considered very high muscle activity.[2] From these initial reports, the baseball pitch was divided into several phases, which later were slightly modified by Escamilla et al.[9] and Fleisig et al.[11] as the wind-up, stride, arm cocking, arm acceleration, arm deceleration and follow-through phases (figure 1). 1.1 Wind-Up Phase

Shoulder activity during the wind-up phase, which is from initial movement to maximum knee lift of stride leg (figure 1), is generally very low due to the slow movements that occur. From table I, it can be seen that the greatest activity is from the upper trapezius, serratus anterior and anterior deltoids. These muscles all contract concentrically to upwardly rotate and elevate the scapula and abduct the shoulder as the arm is initially brought overhead, and then contract eccentrically to control downward scapular rotation and shoulder adduction as the hands are lowered to approximately chest level. The rotator ª 2009 Adis Data Information BV. All rights reserved.

cuff muscles, which have a duel function as glenohumeral joint compressors and rotators, have their lowest activity during this phase. Because shoulder activity is low, it is not surprising that the shoulder forces and torques generated are also low;[9,11] consequently, very few, if any, shoulder injuries occur during this phase. 1.2 Stride Phase

There is a dramatic increase in shoulder activity during the stride phase (table I), which is from the end of the balance phase to when the lead foot of the stride leg initially contacts the ground (figure 1). During the stride the hands separate, the scapula upwardly rotates, elevates and retracts, and the shoulders abduct, externally rotate and horizontally abduct due to concentric activity from several muscles, including the deltoids, supraspinatus, infraspinatus, serratus anterior and upper trapezius. It is not surprising that there are many more muscles activated and to a higher degree during the stride compared with the windup phase. Interestingly, the supraspinatus has its highest activity during the stride phase as it works to not only abduct the shoulder but also help compress and stabilize the glenohumeral joint.[2] The deltoids exhibit high activity during this phase in order to initiate and maintain the shoulder in an abducted position.[2] Moreover, the trapezius Sports Med 2009; 39 (7)

Shoulder Muscle Activity in Upper Extremity Sports

and serratus anterior have moderate to high activity, as they assist in stabilizing and properly positioning the scapula to minimize the risk of impingement as the arm abducts.[2] 1.3 Arm Cocking Phase

The arm cocking phase begins at lead foot contact and ends at maximum shoulder external rotation. During this phase the kinetic energy that is generated from the larger lower extremity and trunk segments is transferred up the body to the smaller upper extremity segments.[10,19,20] The pitching arm lags behind as the trunk rapidly rotates forward to face the hitter, generating a peak pelvis angular velocity around 600/sec occurring 0.03–0.05 sec after lead foot contact, followed by a peak upper torso angular velocity of nearly 1200/sec occurring 0.05–0.07 sec after lead foot contact.[10] Consequently, high to very high shoulder muscle activity is needed during this phase in order to keep the arm moving with the rapidly rotating trunk (table I), as well as control the resulting shoulder external rotation (table I), which peaks near 180.[10] Moderate activity is needed by the deltoids (table I) to maintain the shoulder at approximately 90 abduction throughout this phase.[10] Activity from the pectoralis major and anterior deltoid is needed during this phase to horizontally adduct the shoulder with a peak angular velocity of approximately 600/sec, from a position of approximately 20 of horizontal abduction at lead foot contact to a position of approximately 20 of horizontal adduction at maximum shoulder external rotation.[10] Moreover, a large compressive force of »80% bodyweight is generated by the trunk onto the arm at the shoulder to resist the large ‘centrifugal’ force that is generated as the arm rotates forward with the trunk.[11] The supraspinatus, infraspinatus, teres minor and subscapularis achieve high to very high activity (table I) to resist glenohumeral distraction and enhance glenohumeral stability. While it is widely accepted that strength and endurance in posterior shoulder musculature is very important during the arm deceleration phase to slow down the arm, posterior shoulder musª 2009 Adis Data Information BV. All rights reserved.

573

culature is also important during arm cocking. The posterior cuff muscles (infraspinatus and teres minor) and latissimus dorsi generate a posterior force to the humeral head that helps resist anterior humeral head translation, which may help unload the anterior capsule and anterior band of the inferior glenohumeral ligament.[11,15,21] The posterior cuff muscles (infraspinatus and teres minor) also contribute to the extreme range of shoulder external rotation that occurs during this phase. A peak shoulder internal rotation torque of 65–70 N m is generated near the time of maximum shoulder external rotation,[11,22] which implies that shoulder external rotation is progressively slowing down as maximum shoulder external rotation is approached. High to very high activity is generated by the shoulder internal rotators (pectoralis major, latissimus dorsi and subscapularis) [table I], which contract eccentrically during this phase to control the rate of shoulder external rotation.[2] The multiple functions of muscles are clearly illustrated during arm cocking. For example, the pectoralis major and subscapularis contract concentrically to horizontally adduct the shoulder and eccentrically to control shoulder external rotation. This duel function of these muscles helps maintain an appropriate length-tension relationship by simultaneously shortening and lengthening, which implies that these muscles may be maintaining a near constant length throughout this phase. Therefore, some muscles that have duel functions and simultaneous shortening and lengthening as the shoulder performs duel actions at the same time may in effect be contracting isometrically. The importance of scapular muscles during arm cocking is demonstrated in table I. High activity from these muscles is needed in order to stabilize the scapula and properly position the scapula in relation to the horizontally adducting and rotating shoulder. The scapular protractors are especially important during this phase in order to resist scapular retraction by contracting eccentrically and isometrically during the early part of this phase and cause scapular protraction by contracting concentrically during the latter




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part of this phase. The serratus anterior generates maximum activity during this phase. Scapular muscle imbalances may lead to abnormal scapular movement and position relative to the humerus, increasing injury risk. Because both the triceps brachii (long head) and biceps brachii (both heads) cross the shoulder, they both generate moderate activity during this phase in order to provide additional stabilization to the shoulder. In contrast to the moderate triceps activity reported by DiGiovine et al.[2] during arm cocking, Werner et al.[23] reported the highest triceps activity during arm cocking. Because elbow extensor torque peaks during this phase,[23,24] high eccentric contractions by the triceps brachii are needed to help control the rate of elbow flexion that occurs throughout the initial 80% of this phase.[10] High triceps activity is also needed to initiate and accelerate elbow extension, which occurs during the final 20% of this phase as the shoulder continues externally rotating.[10] Therefore, during arm cocking the triceps initially contract eccentrically to control elbow flexion early in the phase and concentrically to initiate elbow extension later in the phase. Gowan and colleagues[16] demonstrated that subscapularis activity is nearly twice as great in professional pitchers compared with amateur pitchers during this phase. In contrast, muscle activity from the pectoralis major, supraspinatus, serratus anterior and biceps brachii was »50% greater in amateur pitchers compared with professional pitchers. From these data, professional pitchers may exhibit better throwing efficiency thus requiring less muscular activity compared with amateurs. Glousman and colleagues[15] compared shoulder muscle activity between healthy pitchers with no shoulder pathologies to pitchers with chronic anterior shoulder instability due to anterior glenoid labral tears. Pitchers diagnosed with chronic anterior instability exhibited greater muscle activity from the biceps brachii and supraspinatus and less muscle activity from the pectoralis major, subscapularis and serratus anterior. Chronic anterior instability results in excessive stretch of the anterior capsular, which may stimulate mechanoª 2009 Adis Data Information BV. All rights reserved.

receptors within the capsule resulting in excitation in the biceps brachii and supraspinatus and inhibition in the pectoralis major, subscapularis and serratus anterior.[15] Increased activity from the biceps brachii and supraspinatus helps compensate for anterior shoulder instability, as these muscles enhance glenohumeral stability. Rodosky et al.[25] reported that as the humerus abducts and maximally externally rotates, the biceps long head enhances anterior stability of the glenohumeral joint and also decreases the stress placed on the inferior glenohumeral ligament. Decreased activity from the pectoralis major and subscapularis, which contract eccentrically to decelerate the externally rotating shoulder, may accentuate shoulder external rotation and increase the stress on the anterior capsule.[15] Decreased activity from the serratus anterior may cause the scapula to be abnormally positioned relative to the externally rotating and horizontally adducting humerus, and a deficiency in scapular upward rotation may decrease the subacromial space and increase the risk of impingement and rotator cuff pathology.[26] Interestingly, infraspinatus activity was lower in pitchers with chronic anterior shoulder instability compared with healthy pitchers.[16] During arm cocking, the infraspinatus not only helps externally rotate and compress the glenohumeral joint, but also may generate a small posterior force on the humeral head due to a slight posterior orientation of its fibres as they run from the inferior facet of the greater tubercle back to the infraspinous fossa. As previously mentioned, this posterior force on the humeral head helps resist anterior humeral head translation and unloads strain on the anterior capsule during arm cocking.[16] It is unclear whether chronic rotator cuff insufficiency results in shoulder instability, or whether chronic shoulder instability results in rotator cuff insufficiency due to excessive activity. 1.4 Arm Acceleration Phase

The arm acceleration phase begins at maximum shoulder external rotation and ends at ball release[10,11,22] (figure 1). Like the arm cocking phase, high to very high activity is generated from the glenohumeral and scapular muscles during Sports Med 2009; 39 (7)

Shoulder Muscle Activity in Upper Extremity Sports

this phase in order to accelerate the arm forward (table I). Moderate activity is generated by the deltoids[2] to help produce a fairly constant shoulder abduction of approximately 90–100,[10] which is maintained regardless of throwing style (i.e. overhand, sidearm, etc.). The glenohumeral internal rotators (subscapularis, pectoralis major and latissimus dorsi) have their highest activity during this phase[2] (table I) as they contract concentrically to help generate a peak internal rotation angular velocity of approximately 6500/sec near ball release.[9] This rapid internal rotation, with a range of motion of approximately 80 from maximum external rotation to ball release, occurs in only 30–50 msec.[10,27] The very high activity from the subscapularis (115% MVIC) occurs in part to help generate this rapid motion, but it also functions as a steering muscle to maintain the humeral head in the glenoid. The teres minor, infraspinatus and supraspinatus also demonstrate moderate to high activity during this phase to help properly position the humeral head within the glenoid. With these rapid arm movements that are generated to accelerate the arm forward, it is not surprising that the scapular muscles also generate high activity,[2] which is needed to help maintain proper position of the glenoid relative to the rapidly moving humeral head. Strengthening scapular musculature is very important because poor position and movement of the scapula can increase the risk of impingement and other related injuries,[28] as well as reduce the optimal length-tension relationship of both scapular and glenohumeral musculature. Although DiGiovine et al.[2] reported that the triceps had their highest activity during this phase,[2] Werner et al.[23] reported relatively little triceps EMG during the arm acceleration phase. In addition, elbow extensor torque is very low during this phase compared with the arm cocking phase.[23,24] It should be re-emphasized that elbow extension initially begins during the arm cocking phase as the shoulder approaches maximum external rotation.[9] Kinetic energy that is transferred from the lower extremities and trunk to the arm is used to help generate a peak elbow extension angular velocity of approximately 2300/sec during this phase.[9] In fact, a conª 2009 Adis Data Information BV. All rights reserved.

575

centric contraction from the triceps brachii alone could not come close to generating this 2300/sec elbow extension angular velocity. This is supported by findings reported by Roberts,[29] who had found that subjects who threw with paralyzed triceps could obtained ball velocities >80% of the ball velocities obtained prior to the triceps being paralyzed. This is further supported by Toyoshima et al.,[20] who demonstrated normal throwing using the entire body generated almost twice the elbow extension angular velocity compared with extending the elbow by throwing without any lower extremity, trunk and shoulder movements. These authors concluded that during normal throwing the elbow is swung open like a ‘whip’, primarily due to linear and rotary contributions from the lower extremity, trunk and shoulder, and to a lesser extent from a concentric contraction of the triceps. Nevertheless, the triceps do help extend the elbow during this phase, as well as contribute to shoulder stabilization by the triceps long head. These findings illustrate the importance of lower extremity conditioning, because weak or fatigued lower extremity musculature during throwing may result in increased loading of the shoulder structures, such as the rotator cuff, glenoid labrum, and shoulder capsule and ligaments. Further research is needed to substantiate these hypotheses. Gowan and colleagues[16] demonstrated that rotator cuff and biceps brachii activity was 2–3 times higher in amateur pitchers compared with professional pitchers during this phase. In contrast, subscapularis, serratus anterior and latissimus dorsi activity was much greater in professional pitchers. These results imply that professional pitchers may better coordinate body segment movements to increase throwing efficiency. Enhanced throwing mechanics and efficiency may minimize glenohumeral instability during this phase, which may help explain why professional pitchers generate less rotator cuff and biceps activity, which are muscles that help resist glenohumeral joint distraction and enhance stability. Compared with healthy pitchers, pitchers with chronic anterior shoulder instability due to anterior labral injuries exhibit greater muscle activity from the biceps brachii, supraspinatus and Sports Med 2009; 39 (7)

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infraspinatus, and less muscle activity from the latissimus dorsi, subscapularis and serratus anterior.[15] The increased activity from rotator cuff and biceps musculature in pitchers with chronic anterior instability is needed in order to provide additional glenohumeral instability that is lacking in these pitchers due to a compromised anterior labrum. With shoulder internal rotation, the long biceps tendon is repositioned anteriorly at the shoulder, providing compressive and posterior forces to the humeral head, both of which enhance anterior stability. Therefore, throwers with chronic anterior instability activate their biceps to a greater extent (32% vs 12% MVIC), as well as their supraspinatus and infraspinatus (37% vs 13% MVIC), compared with asymptomatic throwers.[15] However, increased and excessive biceps activity due to anterior instability results in increased stress to the long biceps anchor at the superior labrum, which over time may result in superior labral pathology that is anterior to posterior in direction (SLAP lesions). In addition, chronic anterior shoulder instability inhibits normal contributions from the internal rotators and serratus anterior,[15] which may adversely affect throwing mechanics and efficiency, as well as increase shoulder injury risk. 1.5 Arm Deceleration Phase

The arm deceleration phase begins at ball release and ends at maximum shoulder internal rotation (figure 1).[10,11,22] Large loads are generated at the shoulders to slow down the forward acceleration of the arm. The purpose of this phase is to provide safety to the shoulder by dissipating the excess kinetic energy not transferred to the ball, thereby minimizing the risk of shoulder injury. Posterior shoulder musculature, such as the infraspinatus, teres minor and major, posterior deltoid and latissimus dorsi, contract eccentrically not only to decelerate horizontal adduction and internal rotation of the arm, but also help resist shoulder distraction and anterior subluxation forces. A shoulder compressive force slightly greater than bodyweight is generated to resist shoulder distraction, while a posterior shear force of 40–50% bodyweight is generated to resist ª 2009 Adis Data Information BV. All rights reserved.

shoulder anterior subluxation.[9,11] Consequently, high activity is generated by posterior shoulder musculature,[2] in particular the rotator cuff muscles. For example, the teres minor, which is a frequent source of isolated tenderness in pitchers, exhibits its maximum activity (84% MVIC) during this phase (table I). In addition, scapular muscles also exhibit high activity to control scapular elevation, protraction and rotation during this phase. For example, the lower trapezius – which generate a force on the scapula in the direction of depression, retraction and upward rotation – generated their highest activity during this phase (table I). High EMG activity from glenohumeral and scapular musculature illustrate the importance of strength and endurance training of the posterior musculature in the overhead throwing athlete. Weak or fatigued posterior musculature can lead to multiple injuries, such as tensile overload undersurface cuff tears, labral/biceps pathology, capsule injuries and internal impingement of the infraspinatus/ supraspinatus tendons on the posterosuperior glenoid labrum.[14] Compared with healthy pitchers, pitchers with chronic anterior shoulder instability exhibited less muscle activity from the pectoralis major, latissimus dorsi, subscapularis and serratus anterior, which is similar to what occurred in the arm cocking and acceleration phases.[15] However, muscle activities from the rotator cuff and biceps brachii are similar between healthy pitchers and pitchers with chronic anterior shoulder instability during this phase, which is in contrast to the greater rotator cuff and biceps brachii activity demonstrated in pitchers with chronic anterior shoulder instability during the arm cocking and acceleration phases.[15] This difference in muscle activity may partially be explained by the very high compressive forces that are needed during arm deceleration to resist shoulder distraction, which is a primary function of both the rotator cuff and biceps brachii. The biceps brachii generate their highest activity (44% MVIC) during arm deceleration (table I). The function of this muscle during this phase to 2-fold. Firstly, it must contract eccentrically along with other elbow flexors to help Sports Med 2009; 39 (7)

Shoulder Muscle Activity in Upper Extremity Sports

decelerate the rapid elbow extension that peaks near 2300/sec during arm acceleration.[9] This is an important function because weakness or fatigue in the elbow flexors may result in elbow extension being decelerated by impingement of the olecranon in the olecranon fossa, which may lead to bone spurs and subsequent loose bodies within the elbow. Secondly, the biceps brachii works synergistically with the rotator cuff muscles to resist distraction and anterior subluxation at the glenohumeral joint. Interestingly, during arm deceleration biceps brachii activity is greater in amateur pitchers compared with professional pitchers,[16] which may imply that amateur pitchers employ a less efficient throwing pattern compared with professional pitchers. As previously mentioned, excessive activity from the long head of the biceps brachii may lead to superior labral pathology. 2. Shoulder EMG during the Overhead American Football Throw There is only one known study that has quantified muscle activity during the football throw.[3] Using 14 male recreational and college athletes,

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Kelly et al.[3] quantified activity from nine glenohumeral muscles throughout throwing phases specific for football; their results are summarized in table II. The defined phases for football throwing (table II) are similar but slightly different to the defined phases for baseball pitching (table I). Early arm cocking in the football throw was similar to the stride phase in baseball, while late cocking in the football throw was the same as arm cocking in baseball. The acceleration phase was the same for both the football throw and the baseball pitch. The arm deceleration and follow-through phases in the baseball pitch were combined into a single arm deceleration/follow-through phase in the football throw. From table II, rotator cuff activity progressively increased in each phase of the football throwing, being least in the early cocking phase and peaking in the arm deceleration/followthrough phase. This is a slightly different pattern than the baseball pitch, where rotator cuff activity was generally greatest during either the arm cocking phase or the arm deceleration phase (table I). For both baseball pitching and football throwing, deltoid and biceps brachii activity were generally greatest during the arm deceleration

Table II. Shoulder activity by muscle and phase during the overhead football throwa (adapted from Kelly et al.,[3] with permission) Muscles

No. of subjects

Phase early cockingb (% MVIC)

late cockingc (% MVIC)

arm accelerationd (% MVIC)

arm deceleration and follow-throughe (% MVIC)

total throwf (% MVIC)

Supraspinatus

14

45 – 19

62 – 20

65 – 30

87 – 43

65 – 22

Infraspinatus

14

46 – 17

67 – 19

69 – 29

86 – 33

67 – 21

Subscapularis

14

24 – 15

41 – 21

81 – 34

95 – 65

60 – 28

Anterior deltoid

14

13 – 9

40 – 14

49 – 14

43 – 26

36 – 9

Middle deltoid

14

21 – 12

14 – 14

24 – 14

48 – 19

27 – 9

Posterior deltoid

14

11 – 6

11 – 15

32 – 22

53 – 25

27 – 11

Pectoralis major

14

12 – 14

51 – 38

86 – 33

79 – 54

57 – 27

Latissimus dorsi

14

7–3

18 – 9

65 – 30

72 – 42

40 – 12

Biceps brachii

14

12 – 7

12 – 10

11 – 9

20 – 18

14 – 9

a

Data are given as means and standard deviations, and expressed for each muscle as a percentage of a MVIC.

b

From rear foot plant to maximum shoulder abduction and internal rotation.

c

From maximum shoulder abduction and internal rotation to maximum shoulder external rotation.

d

From maximum shoulder external rotation to ball release.

e

From ball release to maximum shoulder horizontal adduction.

f

Mean activity throughout the four defined phases.

MVIC = maximum voluntary isometric contraction.

ª 2009 Adis Data Information BV. All rights reserved.

Sports Med 2009; 39 (7)

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phase (tables I and II). The greatest activity of the pectoralis major, latissimus dorsi and subscapularis was during arm cocking and arm acceleration in baseball pitching (table I), while peak activity occurred in these muscles during arm acceleration and arm deceleration in football throwing (table II). The pectoralis major, latissimus dorsi and subscapularis are powerful internal rotators. These muscles contract eccentrically and help generate a shoulder internal rotation torque of »50 N m during arm cocking to slow down the externally rotating shoulder, and they contract concentrically during arm acceleration to help generate a peak shoulder internal rotation angular velocity of approximately 5000/sec.[19] The pectoralis major and subscapularis also help horizontally adduct the shoulder during arm cocking and arm acceleration, but in a different kinematic pattern compared with the baseball pitch. In football passing, the quarterback tends to ‘lead with the elbow’ as the elbow moves anterior to the trunk in achieving approximately 30 of horizontal adduction during arm cocking and arm acceleration, generating a peak horizontal adduction torque of »75 N m.[19] In contrast, in the baseball pitch the elbow remains slightly in the back of the trunk during arm cocking (»15) and slightly in front of the trunk (»5) during arm acceleration.[19] The greatest activity in the rotator cuff muscles and latissimus dorsi occurred during the arm deceleration/follow-through phase of the football throw. These muscles work to generate a peak shoulder compressive force »80% bodyweight during arm deceleration/follow-through to resist shoulder distraction, which is 20–25% less than the shoulder compressive force that is generated during baseball pitching during this phase.[19] The latissimus dorsi, posterior deltoid and infraspinatus also contract eccentrically to slow down the rapid horizontal adducting arm. Fleisig and co-authors[19] reported a shoulder horizontal abduction torque »80 N m, which is needed to help control the rate of horizontal adduction that occurs during arm deceleration/follow-through. Moreover, the peak activity that occurred in the latissimus dorsi, posterior deltoid and infraspinatus during arm deceleration/follow-through










ª 2009 Adis Data Information BV. All rights reserved.

helps resist anterior translation of the humeral head within the glenoid by, in part, generating a peak shoulder posterior force »240 N.[19] The aforementioned kinematic and kinetic differences between football passing and baseball pitching help explain the differences in muscle activity between these two activities, and they occur in part because a football weighs three times more than a baseball. Therefore, a football cannot be thrown with the same shoulder range of motion and movement speeds compared with throwing a baseball. This results in smaller loads (i.e. less shoulder forces and torques) overall applied to the shoulder in football passing compared with baseball pitching,[19] which may in part account for the greater number of shoulder injuries in baseball pitching compared with football passing. 3. Shoulder EMG during Windmill Softball Pitching Maffet et al.[4] conducted the only known study that quantified shoulder muscle firing patterns during the softball pitch. These authors used ten female collegiate softball pitchers who all threw the ‘fast pitch’ and quantified activity in the anterior and posterior deltoid, supraspinatus, infraspinatus, teres minor, subscapularis, pectoralis major and serratus anterior. The ‘fastpitch’ motion starts with the throwing shoulder extended and then as the pitcher strides forward the arm fully flexes, abducts and externally rotates and then continues in a circular (windmill) motion all the way around until the ball is released near 0 shoulder flexion and adduction. The six phases that define the pitch[4] are as follows: (i) wind-up, from first ball motion to 6 o’clock position (shoulder flexed and abducted approximately 0); (ii) from 6 o’clock to 3 o’clock position (shoulder flexed approximately 90); (iii) from 3 o’clock to 12 o’clock position (shoulder flexed and abducted approximately 180); (iv) from 12 o’clock to 9 o’clock position (shoulder abducted approximately 90); (v) from 9 o’clock position to ball release; and (vi) from ball release to completion of the pitch. The total circumduction of the arm about the shoulder from the wind-up to the follow-through Sports Med 2009; 39 (7)

Shoulder Muscle Activity in Upper Extremity Sports

is approximately 450–500.[30] Moreover, this circumduction occurs while holding a 6.25–7 oz (177–198 g) ball with the elbow near full extension, which accentuates the ‘centrifugal’ distractive force acting at the shoulder. EMG results by muscle and phase during the softball pitch are shown in table III. Muscle activity was generally lowest during the wind-up and increased during the 6–3 o’clock phase as the arm began accelerating upwards. Both the supraspinatus and infraspinatus generated their highest activity during this phase. During the 6–3 o’clock phase the arm accelerates in a circular motion and achieves a peak shoulder flexion angular velocity of approximately 5000/sec.[30] The anterior deltoid was moderately active to help generate this rapid shoulder flexion angular velocity, and the serratus anterior was moderately active in helping to upwardly rotate and protract the scapula. The arm rapidly rotating upwards in a circular pattern results in a distractive force of »20–40% bodyweight, which is resisted in part by the shoulder compressive action of the supraspinatus and infraspinatus. As the arm continues its upward acceleration during the 3–12 o’clock phase, the posterior deltoids, teres minor and infraspinatus all reach their peak activity. These muscles not only help externally rotate the shoulder during this phase but also help resist the progressively increasing shoulder distractive forces, which are »50% bodyweight during this phase.[30] These muscles

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are also in good position to resist shoulder lateral forces, which peak during this phase.[30] The arm begins accelerating downward during the 12–9 o’clock phase. It is during this phase that the shoulder begins to rapidly internally rotate 2000–3000/sec.[30] It is not surprising that the internal rotators (subscapularis and pectoralis major) exhibit high activity during this phase. High activity from the pectoralis major also helps adduct the shoulder. The subscapularis helps stabilize the humeral head and may help unload anterior capsule stress caused by the overhead and backward position of the arm as it begins accelerating forward. The serratus anterior exhibited a marked increase in activity to help stabilize the scapula and properly position the glenoid with the rapidly moving humerus. The subscapularis, pectoralis major and serratus anterior collectively generated their highest activity during the 9 o’clock to ball release phase. The serratus anterior continues to work to stabilize the scapula and properly position it in relation to the rapidly moving humerus. High subscapularis and pectoralis major activity is needed during this phase to resist distraction at the shoulder, which peaks during this phase with a magnitude of approximately bodyweight.[30,31] These muscles also help generate a peak shoulder internal rotation of approximately 4600/sec[30] and help adduct and flex the arm until the arm contacts the lateral thigh. However, not all softball pitchers exhibit the same pattern of motion

Table III. Shoulder activity by muscle and phase during the windmill softball pitcha (adapted from Maffet et al.,[4] with permission) Muscles

No. of subjects

Phase wind-up (% MVIC)

6–3 o’clock position (% MVIC)

3–12 o’clock position (% MVIC)

12–9 o’clock position (% MVIC)

10 o’clock to ball release (% MVIC)

follow-through (% MVIC)

Anterior deltoid

10

25 – 11

38 – 29

17 – 23

22 – 24

43 – 38

28 – 21

Supraspinatus

10

34 – 17

78 – 36

43 – 32

22 – 19

37 – 27

19 – 12

Infraspinatus

10

24 – 13

93 – 52

92 – 38

35 – 22

29 – 17

30 – 15

Posterior deltoid

10

10 – 5

37 – 27

102 – 42

52 – 25

62 – 29

34 – 29

Teres minor

10

8–7

24 – 25

87 – 21

57 – 21

41 – 23

44 – 11

Pectoralis major

10

18 – 11

17 – 12

24 – 18

63 – 23

76 – 24

33 – 20

Subscapularis

10

17 – 4

34 – 23

41 – 33

81 – 52

75 – 36

26 – 22

Serratus anterior

10

23 – 9

38 – 19

19 – 9

45 – 39

61 – 19

40 – 14

a

Data are given as means and standard deviations, and expressed for each muscle as a percentage of an MVIC.

MVIC = maximum voluntary isometric contraction.

ª 2009 Adis Data Information BV. All rights reserved.

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during this phase, as none of the 53 youth softball pitchers studies by Werner et al.[31] adopted the release strategy of contacting the lateral thigh at ball release. This may partially explain why the collegiate pitchers in the Maffet et al.[4] study generated relatively low posterior cuff activity and relatively low activity in general during the follow-through. With contact of the arm with the lateral thigh near ball release, the deceleration forces and torques generated by muscles to slow down the arm are much less compared with no contact of the arm with the lateral thigh. With no arm contact with the lateral thigh, shoulder compressive and related forces and torques may be higher during follow-through, as relatively high shoulder forces and torques have been reported.[30,31] However, these forces and torques are less during follow-through compared with the 9 o’clock to ball release acceleration phase. This is one major difference between overhand throwing and the ‘windmill’ type motion. In overhead throwing the deceleration phase after ball release generates greater shoulder forces and torques compared with the acceleration phase up to ball release. In softball pitching the greatest forces and torques occur during the acceleration phase of the delivery. The rapid shoulder movements and high shoulder forces that are generated during the ‘windmill fast pitch’ makes the shoulder susceptible to injury. There is also a higher risk of subacromial impingement due to the extreme shoulder flexion and abduction that occurs during the pitch. A significant number of shoulder injuries have been reported in softball pitchers, including bicipital and rotator cuff tendonitis, strain and impingement.[32] 4. Shoulder EMG during the Volleyball Serve and Spike Both the volleyball serve and spike involve an overhead throwing motion that is similar to baseball pitching and football throwing. Unlike baseball pitching and football passing, there are no known studies that have quantified the shoulder forces and torques that are generated during the volleyball serve and spike. Nevertheless, because the motion is overhead and exª 2009 Adis Data Information BV. All rights reserved.

tremely rapid, similar to baseball pitching, it is hypothesized that high shoulder forces and torques are generated, especially during the volleyball spike. To support this hypothesis, numerous injuries occur each year in volleyball, primarily involving muscle, tendon and ligament injuries during blocking and spiking.[33] It has been reported that approximately one-quarter of all volleyball injuries involve the shoulder.[33-36] Moreover, in athletes who engage in vigorous upper arm activities, shoulder pain ranks highest in volleyball players, which is largely due to the repetitive nature of the hitting motion.[33-36] Therefore, understanding muscle firing patterns of the shoulder complex is helpful in developing muscle-specific treatment and training protocols, which may both minimize injury and enhance performance. There are no known studies that have quantified muscle activity from the scapular muscles during the volley serve or spike. This is surprising given the importance of the scapular muscles in maintaining proper position of the scapula relative to the humerus. Volleyball players with shoulder pain often have muscle imbalances of the scapula muscles.[37] Therefore, the firing pattern of the scapular muscles during the volleyball serve and spike should be the focus of future research studies. Rokito et al.[6] conducted the only known study that quantified muscle firing patterns of glenohumeral muscles during the volleyball serve and spike. These authors studied 15 female college and professional volleyball players who performed both the volleyball serve and spike. The shoulder muscles quantified included the anterior deltoid, supraspinatus, infraspinatus, teres minor, subscapularis, teres major, latissimus dorsi and pectoralis major. The serve and spike motions were divided into five phases, which collectively are 1.95 sec in duration for the serve[6] and 1.11 sec for the spike:[6] (i) wind-up (comprises 39% of total serve time and 33% of total spike time) begins with shoulder abducted and extended and ends with the initiation of shoulder external rotation; (ii) cocking (comprises 20% of total serve time and 23% of total spike time) – initiation of shoulder external rotation to maximum Sports Med 2009; 39 (7)

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shoulder external rotation; (iii) acceleration (comprises 6% of total serve time and 8% of total spike time) – maximum shoulder external rotation to ball impact; (iv) deceleration (comprises 8% of total serve time and 9% of total spike time) – ball impact to when upper arm is perpendicular to trunk; and (v) follow-through (comprises 28% of total serve time and 27% of total spike time) – upper arm perpendicular to trunk to end of arm motion. Shoulder EMG results by muscle and phase during the volleyball serve and spike are shown in table IV. Similar to other overhead throwing activities, muscle activity during the serve was relatively low during the wind-up and followthrough phases. However, during the wind-up

phase of the spike, peak activity was recorded in the anterior deltoid, infraspinatus and supraspinatus. These muscles are important to help rapidly elevate the arm overhead (anterior deltoid and supraspinatus) and initiate external rotation (infraspinatus). The rotator cuff muscles are also active to help stabilize the humeral head in the glenoid fossa. During the cocking phase the shoulder rapidly externally rotates, which helps explain the high activity in the infraspinatus and teres minor during both the serve and spike. As mentioned during the section on baseball pitching, these muscles also produce a posterior force on the humerus that may help unload the anterior capsule due to the humeral head attempting to translate

Table IV. Shoulder activity by muscle and phase during the volleyball serve and spikea (adapted from Rokito et al.,[6] with permission) Muscles

Anterior deltoid

No. of subjects

Phase wind-up (% MVIC)

cocking (% MVIC)

acceleration (% MVIC)

deceleration (% MVIC)

follow-through (% MVIC)

15

Serve

21 – 11

31 – 13

27 – 22

42 – 17

16 – 16

Spike

58 – 26

49 – 19

23 – 17

27 – 10

15 – 7

Supraspinatus

15

Serve

25 – 10

32 – 18

37 – 25

45 – 13

24 – 16

Spike

71 – 31

40 – 17

21 – 27

37 – 23

27 – 15

Infraspinatus

15

Serve

17 – 10

36 – 16

32 – 22

39 – 21

13 – 11

Spike

60 – 17

49 – 16

27 – 18

38 – 19

22 – 11

Serve

7–8

44 – 20

54 – 26

30 – 23

8–9

Spike

39 – 20

51 – 17

51 – 24

34 – 13

17 – 7

Teres minor

Subscapularis

15

15

Serve

8–8

27 – 25

56 – 18

27 – 15

13 – 11

Spike

46 – 16

38 – 21

65 – 25

23 – 11

16 – 15

Teres major

15

Serve

1–1

11 – 7

47 – 24

7–8

3–3

Spike

28 – 14

20 – 11

65 – 31

21 – 18

15 – 16

Latissimus dorsi

15

Serve

1–2

9 – 18

37 – 39

6–9

3–3

Spike

20 – 13

16 – 17

59 – 28

20 – 21

15 – 10

Serve

3–6

31 – 14

36 – 14

7 – 11

7–6

Spike

35 – 17

46 – 17

59 – 24

20 – 16

21 – 12

Pectoralis major

a

15

Data are given as means and standard deviations, and expressed for each muscle as a percentage of an MVIC.

MVIC = maximum voluntary isometric contraction.

ª 2009 Adis Data Information BV. All rights reserved.

Sports Med 2009; 39 (7)

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anteriorly as the shoulder externally rotates. Also, the rotator cuff muscles have high activity to generate glenohumeral compression and resist distraction. The relatively high activity from the subscapularis and pectoralis major (both internal rotators) help provide support to the anterior shoulder (without such support anterior instability may ensue), as these muscles also contract eccentrically to slow down and control the rate of the rapid shoulder external rotation. An important distinction between the serve and spike occurs during the acceleration phase. During the serve the objective is not to impart maximum velocity to the ball but rather hit the ball so it ‘floats’ over the net with a parabolic trajectory in an area that would be most difficult for the opponent to return. In contrast, during the spike the primary objective is to hit the ball as hard as possible so as to convey maximum velocity to the ball. Consequently, muscle activity was higher in the powerful acceleratory muscles during the spike compared with during the serve. Because overhead throwing motions such as baseball pitching, football passing and the tennis serve achieve shoulder internal rotation angular velocities between 4000 and 7000/sec,[9,19,38] it is reasonable to assume that similar internal rotation angular velocities occur during the volleyball spike. The shoulder internal rotators (teres major, subscapularis, pectoralis major and latissimus dorsi) all generated their highest activity for both the serve and the spike in order to both internally rotate the shoulder and accelerate the arm forward. During the acceleration phase, teres minor activity peaked to provide a stabilizing posterior restraint to anterior translation. In contrast, infraspinatus activity was relatively low. The differing amounts of EMG activity between the teres minor and infraspinatus throughout the different phases of the serve and spike is interesting, especially since both the teres minor and infraspinatus provide similar glenohumeral functions and they are both located adjacent to each other anatomically. However, the spatial orientations of these two muscles are different, with the teres minor in a better mechanical position to extend the shoulder in a sagittal plane and ª 2009 Adis Data Information BV. All rights reserved.

Escamilla & Andrews

the infraspinatus in a better mechanical position to extend the shoulder in a transverse plane. There are also clinical differences between these two muscles, as they are typically not injured together but rather an isolated injury occurs to either the teres minor or infraspinatus.[2,6] These different clinical observations between the teres minor and infraspinatus are consistent with the different muscle firing patterns that occur within any given phase of overhead throwing, such as baseball pitching (table I).[2] During the deceleration phase, infraspinatus and supraspinatus activity was greatest during the serve, but not during the spike. In fact, rotator cuff activity was generally lower in the spike compared with the serve, which may be counterintuitive. For example, because a primary function of the rotator cuff is to generate shoulder compressive force to resist shoulder distraction, and since shoulder compressive forces from similar overhead throwing motions (such as baseball pitching and football passing) generate large shoulder compressive forces during this phase,[9,19] it is plausible to assume large compressive forces are also needed during the spike. The relatively low activity from the rotator cuff muscles during the spike is a different pattern compared with the moderate to high rotator cuff activity generated during the baseball pitch and football pass (tables I and II). The higher rotator cuff activity during baseball pitching and football passing is needed during this phase to resist the large distractive forces that occur at the shoulder, which are near or in excess of bodyweight. These EMG differences between varying overhead throwing motions may be due to mechanical differences between these different activities. For example, in both baseball pitching and football passing a weighted ball (5 oz [142 g] baseball and 15 oz [425 g] football) is carried in the hands throughout throwing phases but is released just prior to the beginning of the deceleration phase. With these weighted balls no longer in hand, the arm may travel faster just after ball release (beginning of deceleration phase) and thus more posterior shoulder forces and torques may be generated by the posterior musculature to slow down the rapidly moving arm. In the Sports Med 2009; 39 (7)

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volleyball spike there is no weighted implement in the hand throughout the entire motion. Moreover, when the hand contacts the ball, the ball generates an equal and opposite force on the hand, which acts to slow down the forward moving hand. Therefore, a slower moving arm may result in smaller forces and torques at the shoulder to decelerate the arm and less muscle activity. This explanation may partially explain the lower rotator cuff activity in the volleyball spike compared with baseball pitching and football passing, especially from the posterior musculature (table IV). However, a biomechanical analysis of the volleyball spike is needed to quantify shoulder forces and torques to help confirm this hypothesis. 5. Shoulder EMG during the Tennis Serve and Volley There is a scarcity of shoulder EMG data during the tennis serve and volley. Ryu and colleagues[39] conducted the only known study that extensively quantified shoulder EMG during the tennis serve. EMG data were collected during the serve from eight shoulder muscles using six male collegiate tennis players. One of the limitations of this study is there were no standard deviations reported and only a few subjects were used. The serve was divided into four phases: (i) wind-up start of service motion to ball release; (ii) cockingball release to maximum shoulder external

rotation; (iii) acceleration-maximum shoulder external rotation to racquet-ball contact; and (iv) deceleration and follow-through-racquetball contact to completion of serve. Shoulder EMG results during the serve are shown in table V. Mean EMG peaked for the infraspinatus and supraspinatus during the cocking phase. During this phase the shoulder externally rotates approximately 170 with a peak shoulder internal rotator torque of »65 N m.[38] These kinematic and kinetic data help explain the high activity from the infraspinatus, which is active to initiate shoulder external rotation during the first half of the cocking phase. The infraspinatus and supraspinatus also contract to resist shoulder distractive forces during the cocking phase. Although not quantified during the tennis serve, the shoulder compressive force needed to resist distraction is »80% bodyweight during the cocking phase in baseball pitching, which is a similar motion to the tennis serve.[11] The biceps brachii may also help generate shoulder compressive force during the cocking phase,[15] which may help explain the relatively high activity from this muscle. Pectoralis major, latissimus dorsi and subscapularis activity was greatest during the acceleration phase, as they contract to help generate a peak shoulder internal rotation angular velocity »2500/sec,[38] as well as accelerate the arm forward. Serratus anterior activity also peaked during the acceleration phase to properly




Table V. Shoulder activity by muscle and phase during the tennis servea (adapted from Ryu et al.,[39] with permission) Muscles

No. of subjects

Phase wind-up (% MVIC)

cocking (% MVIC)

acceleration (% MVIC)

deceleration and follow-through (% MVIC)

Biceps brachii

6

6

39

10

Middle deltoid

6

18

23

14

34 36

Supraspinatus

6

15

53

26

35

Infraspinatus

6

7

41

31

30

Subscapularis

6

5

25

113

63

Pectoralis major

6

5

21

115

39

Serratus anterior

6

24

70

74

53

Latissimus dorsi

6

16

32

57

48

a

Data are given as means (standard deviations not reported), and expressed for each muscle as a percentage of an MVIC.

MVIC = maximum voluntary isometric contraction.

ª 2009 Adis Data Information BV. All rights reserved.

Sports Med 2009; 39 (7)

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position the scapula relative to the rapidly moving humerus. These EMG findings during the tennis serve are similar to EMG findings during baseball pitching, which is not surprising considering there are numerous kinematic and kinetic similarities between the tennis serve and baseball pitch.[9-11,38] EMG activity during arm deceleration and follow-through demonstrated moderate to high activity, but less than the EMG observed during baseball pitching and football passing. One reason for this, as previously explained for the volleyball spike, is that the force the ball exerts against the racquet acts to slow down the arm, which may result in less posterior force and torque needed from muscle contractions. The rela-

tively high activity from the biceps brachii helps stabilize the shoulder, resist distraction and decelerate the rapid elbow extension angular velocity, which peaks at »1500/sec.[38] The moderate to high activity from the rotator cuff muscles generate compressive force to help resist shoulder distractive forces, with peak forces »75% bodyweight during the serve.[38] A few studies have examined shoulder activity during the tennis backhand and forehand.[1,39,40] Ryu and colleagues[39] collected EMG data from eight shoulder muscles using six male collegiate tennis players. This study is weakened by the low number of subjects, no standard deviations are reported and there are no statistical analyses between the forehand and backhand volleys. The

Table VI. Shoulder activity by muscle and phase during the tennis forehand and backhand volleya (adapted from Ryu et al.,[39] with permission) Muscles

Biceps brachii

No. of subjects

Phase racquet preparation (% MVIC)

acceleration (% MVIC)

deceleration and follow-through (% MVIC)

6

Forehand

17

86

53

Backhand

11

45

41

Middle deltoid

6

Forehand

27

17

20

Backhand

22

118

48

Supraspinatus

6

Forehand

22

25

14

Backhand

10

73

41

Infraspinatus

6

Forehand

29

23

40

Backhand

7

78

48

Forehand

28

102

49

Backhand

8

29

25

Subscapularis

Pectoralis major

6

6

Forehand

10

85

30

Backhand

15

29

14

Serratus anterior

6

Forehand

14

76

60

Backhand

12

45

31

Forehand

6

24

23

Backhand

4

45

10

Latissimus dorsi

a

6

Data are given as means (standard deviations not reported), and expressed for each muscle as a percentage of an MVIC.

MVIC = maximum voluntary isometric contraction.

ª 2009 Adis Data Information BV. All rights reserved.

Sports Med 2009; 39 (7)

Shoulder Muscle Activity in Upper Extremity Sports

forehand and backhand volleys have been divided into three phases:[39] (i) racquet preparation – shoulder turn to initiation of weight transfer to front foot; (ii) acceleration-initiation of weight transfer to front foot to racquet-ball contact; and (iii) deceleration and follow-through-racquet-ball contact to completion of stroke. Shoulder EMG results from this study are shown in table VI. Muscle activity was relatively low during the racquet preparation phase, which is consistent with forehand and backhand shoulder EMG data from Chow et al.[1] Relatively large differences in muscle activity have been reported between the forehand and backhand during the acceleration phase.[1,39] High activity has been reported in the biceps brachii, anterior deltoid, pectoralis major and subscapularis during the forehand volley, but these same muscles exhibited low activity during the backhand volley.[1,39,40] The high activity during the forehand volley from the pectoralis major, anterior deltoid and subscapularis is not surprising given their role as horizontal flexors and internal rotators. However, the high activity from the biceps brachii is somewhat surprising. Morris et al.[41] also reported high biceps activity during the forehand in the acceleration phase. The biceps are in a mechanically advantageous position to horizontally flex the shoulder during the forehand motion, and they also may work to stabilize both the shoulder and elbow. Moreover, they may also help cause the slight amount of elbow flexion that occurs, or at least stabilize the elbow and keep it from extending (due to inertial forces and torques the arm applies to the forearm at the elbow as the arm rapidly horizontally flexes). The serratus anterior is also more active during the forehand compared with the backhand to help protract the scapula during the acceleration phase and help properly position the scapula relative to the rapidly moving humerus. Posterior deltoids, middle deltoids, supraspinatus, infraspinatus, latissimus dorsi and triceps brachii exhibit high activity during the backhand volley, but relatively low activity during the forehand volley.[1,39] These muscles all work synergistically during the backhand to horizontally extend and externally rotate the ª 2009 Adis Data Information BV. All rights reserved.

585

shoulder. The triceps are also active to extend the elbow and help stabilize both the shoulder and elbow. The high activity from the supraspinatus and infraspinatus help provide shoulder compressive forces to resist shoulder distraction. The supraspinatus and deltoids also help maintain the shoulder in abduction. 6. Shoulder EMG during Baseball Batting There is only one known study that has quantified muscle activity of the shoulder during baseball hitting.[7] Using the swings of 18 professional male baseball players during batting practice, these investigators quantified posterior deltoid, triceps brachii, supraspinatus and serratus anterior activity during the following swing phases: (i) wind-up – lead heel off to lead forefoot contract; (ii) pre-swing – lead forefoot contact to beginning of swing; (iii) early swing – beginning of swing to when bat was perpendicular to ground; (iv) middle swing – when bat was perpendicular to ground to when bat was parallel with ground; (v) late swing – when bat was parallel with ground to bat-ball contact; and (vi) follow-throughbat-ball contact to maximum abduction and external rotation of lead shoulder. Muscle activity was relatively low during the wind-up and follow-through phases, with EMG magnitudes generally