Keith J. Loud
Albert C. Hergenroeder
In 2005, more than half (56%) of students nationwide had played on sports teams sponsored by their school or community groups during the preceding 12 months (Youth Risk Behavior Surveillance [YRBS], Centers for Disease Control and Prevention, 2005). This is a marked increase from 1991 (43.5%) but has remained relatively stable since 1999 at between 55% and 57%.
Beyond organized sports participation, physical inactivity is a priority health risk behavior identified by the Centers for Disease Control and Prevention. The following are two of the objectives from Healthy People 2010 (Department of Health and Human Services, 2000), which highlight the need for improved physical activity in youth:
All health care professionals caring for adolescents should therefore be prepared to:
Is Athletic Participation Safe for Adolescents in General? Promoting Physical Activity and Fitness
Maturational Issues
Although it has been suggested that teens before midpuberty should not play contact sports or that teens playing contact sports should be segregated based on early, middle, or late puberty to reduce the risk of injury, there are no data to support the idea that these interventions decrease injury rates. It has been demonstrated that injury rates increase with pubertal maturation. In contact sports (Table 18.1) this finding is consistent with the understanding that injury is related to the force of impact, which increases with the speed and body mass of the athletes involved. For noncontact sports, this finding may reflect greater force generation related to greater body mass and greater fat-free mass, as well as the increase in training intensity that tends to occur as the level of competition increases with age.
Another issue is whether adult stature could be compromised by excessive sports activities and exercise in the prepubertal and pubertal years. Evidence for reduction in growth potential was reported for a group of adolescent gymnasts with a mean bone age of 12.3 ± 0.2 years who exercised for an average of 22 hour/week, compared with swimmers who exercised for a mean of 8 hour/week (Theintz et al., 1993).
A second study suggested a negative impact of gymnastics training (10–20 hour/week) on statural growth (Lindholm et al., 1994). However, the preponderance of evidence in the literature suggests that short stature in gymnastics is related to selection bias rather than intense training (Daly et al., 2000; Damsgaard et al., 2000).
Intense training by prepubertal and pubertal athletes has raised the concern that repetitive microtrauma to epiphyseal plates could affect ultimate adult height. Runners, figure skaters, and ballet dancers may train as hard as gymnasts. As for gymnasts, the consensus is that participation in sports and exercise does not have adverse effects on adult stature, timing of peak height, or rate of growth (Malina, 1994, 1995).
Physical Fitness and Conditioning
The proportion of high school students attaining the Healthy People activity objectives has been described. In addition, 54.2% of students nationwide were enrolled in a physical education class and 33% of students attended such a class daily in the 2005 YRBS (Centers for Diseases Control and Prevention, 2006).
Fitness has four principal components:
P.265
Body Composition
Although a common notion is that the fitness of today's youth is poor, the only component of fitness that has been documented to have declined in the past three decades is body composition: obesity has increased in both teens and young adults (Gortmaker et al., 1987; National Heart, Lung, and Blood Institute, 1994) (see Chapter 32).
|
TABLE 18.1 |
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
More than one fourth (31.5%) of high school students nationwide thought they were overweight in the 2005 YRBS (Centers for Disease Control and Prevention, 2006). Overall, female students were significantly more likely than male students to consider themselves overweight (38.1% versus 25.1%, respectively). Overall, 45.6% of high school students were trying to lose weight during the 30 days preceding the YRBS survey. Female students were significantly more likely than male students to be trying to lose weight (61.7% versus 29.9%, respectively).
With respect to reducing obesity, adolescents need both reduced caloric intake and increased energy expenditure (Hergenroeder and Phillips, 1994). More adolescents choose to exercise than to diet in an attempt to lose weight in the 2005 YRBS (Centers for Disease Control and Prevention, 2006).
Cardiovascular Fitness
If the goal is to improve cardiovascular fitness, a recommended training program would include aerobic exercise
P.266
(continuous large muscle contractions that involve maintenance of 50% to 85% of the maximum heart rate) for 20 to 25 minutes, three or four times a week. More than two thirds (68.7%) of high school students nationwide had participated in activities that made them sweat and breathe hard (i.e., vigorous physical activity) for at least 20 minutes for 3 or more of the preceding 7 days in the 2005 YRBS (Centers for Disease Control and Prevention, 2006).
Recently, emphasis has been placed on the health benefits of adopting a lifestyle approach to increasing activity, rather than a structured exercise program that may appeal least to sedentary adolescents. The Centers for Disease Control and Prevention and the American College of Sports Medicine guidelines recommend moderate-intensity physical activity on most days—either in a single session or in accumulated multiple bouts, each lasting 8 to 10 minutes (Pate et al., 1995). This involves common activities such as climbing stairs (rather than taking the elevator), brisk walking, doing more house and yard work, and engaging in active recreational pursuits.
The objective is to incorporate moderate physical activity into the lifestyle of those who are sedentary. For those who desire more intensive training, an exercise prescription should be tailored to the adolescent's current level of fitness, desired level of fitness, motivation, and discipline to adhere to a training regime. More detailed goals and practical suggestions for reaching them can be found at the Bright Futures in Practice: Physical Activity Online Guide (http://www.brightfutures.org/physicalactivity/).
Strength
Approximately half (51.4%) of students nationwide had done strengthening exercises (e.g., push-ups, sit-ups, weight lifting) on at least 3 of the 7 days preceding the 1997 YRBS survey (Centers for Disease Control and Prevention, 1998). Regarding strength training, it is established that pre-pubescent and pubescent subjects, like adults, can increase strength safely by resistance training. The training program should include close adult supervision, a preparticipation examination, and the use of well-maintained equipment (including sturdy shoes). Guidelines for resistance training in teens have been reviewed (Blimpke, 1993). Resistance training is associated with strength gains and neuromuscular adaptation inpreadolescents, but it is not associated with muscle hypertrophy. Short-term resistance training has no effect on somatic growth or body composition and is not associated with increased injury rate or recovery or improved sports performance. Muscle hypertrophy will occur with resistance training in pubertal subjects. The American Academy of Pediatrics (AAP) endorses strength training for children and adolescents, if done properly (see policy statement, American Academy of Pediatrics, Committee on Sports Medicine and Fitness, 2001); a suggested resistance training program could include the following:
When 15 repetitions are easily performed during the third set, the weight can be increased by no more than 10% each week. The weight should be lifted through the entire ROM of the joint to avoid loss of flexibility. Warm-up and cool-down periods, which could include stretching exercises, should accompany each session. Three sessions per week on alternate days, allowing for a day of rest in between weight training sessions, is all that is recommended.
One-repetition maximum weight lifting should be avoided because it is a mechanism of injury. Gains in strength are more resistant to detraining than are gains in aerobic fitness, with up to 50% of the strength capacity retained for 1 year or longer in a person who is no longer training.
Flexibility
Nationwide, 51.3% of students had done stretching exercises (e.g., toe touching, knee bending, leg stretching) on 3 or more of the 7 days preceding the 1997 YRBS survey. There is no study demonstrating that stretching in healthy, previously uninjured subjects prevents injuries. However, improving flexibility and strength in previously injured athletes decreases the likelihood of subsequent injuries. A flexibility program for injured joints should include pain-free stretching. If a healthy teen desires a stretching program, the following may be offered: the program should consist of daily stretching. Each stretch should be held statically for 20 seconds, for five to ten repetitions.
Is Athletic Participation Safe for this Adolescent? the Preparticipation Evaluation
While 30 to 40 years ago the preparticipation physical evaluation (PPE) consisted of simply asking the teen, “Are you okay?,” listening to the heart, and checking for a hernia, it has evolved in sophistication more recently. In 1992, five major medical organizations (the American Academy of Family Physicians, AAP, American Medical Society for Sports Medicine, American Orthopedic Society for Sports Medicine, and American Osteopathic Academy of Sports Medicine) produced a consensus monograph on the PPE. Updated in 1997 to include the American Heart Association's (AHA) recommendations specifically concerning cardiovascular screening (Maron et al., 1996), it is now in its third edition (Preparticipation Physical Evaluation, American Academy of Family Physicians, American Academy of Pediatrics, American College of Sports Medicine, 2005). The interested reader is directed to the sponsoring organizations' Web sites or the Physician and Sports medicine Web site (www.physsportsmed.com) to obtain a copy of what is referred to as The Monograph.
The American Medical Association (AMA) Guidelines for Adolescent Preventive Services (GAPS) recommends that a comprehensive health evaluation should occur at least every other year during the adolescent period. In addition, the AAP recommends that adolescents involved in strenuous activity should have a sport-specific examination on entry into both junior and senior high school and that this examination should be updated with an annual questionnaire emphasizing recent injuries and any health condition affecting sports participation. Ideally, an adolescent athlete would have an annual to biennial comprehensive health evaluation performed by his or her primary care physician (PCP), with additional sport-specific PPEs performed by a
P.267
team physician who is responsive to the sponsoring athletic body and knowledgeable about the sport in question. In reality, the PPE monograph acknowledges that the PPE, which is performed primarily to meet legal requirements in 49 of 50 states, is often the only interaction that many adolescents (particularly male adolescents) have with the health care system. Therefore, it is recommended that the PPE be incorporated into a more general health maintenance visit with an established PCP. A multiexaminer, private station-based setup is less preferred, but acceptable alternative; mass screenings in large rooms such as gymnasiums are no longer consered appropriate. Details of how to structure a PPE outside the office setting can be found in The Monograph; the remainder of this section highlights the important elements of a history and physical examination to be performed for a PPE within a health maintenance visit. Chapter 4 details the other components of a thorough health maintenance evaluation.
Objectives
The primary objectives of the PPE, as stated in THE MONOGRAPH, include the following:
Acknowledging that the PPE may “serve as an entry point to the health care system for adolescents,” the third edition also lists determining general health and providing opportunity to initiate discussion on health-related topics as objectives, further emphasizing the central role the adolescent primary care provider performs in this evaluation.
Logistical Considerations for the Preparticipation Physical Evaluation
Ideally, the PPE should occur at least 6 weeks before preseason practice begins, to allow time for evaluation, treatment, and rehabilitation of identified problems before the first weeks of practice.
History
The medical history form from The Monograph is shown in Figure 18.1. An earlier version can be downloaded from the American Academy of Family Physicians at their Web site (http://www.aafp.org/afp/20000815/765.html) to be completed by the athlete and/or parents for review by the physician before the examination. A partnership between the athlete and the parent in completing the form is strongly recommended.
The sport-specific history should be relatively brief to assess for the following factors:
In addition, the AHA recommends the following questions for cardiovascular screening (Maron et al., 1996):
Physical Examination
GAPS does not currently require comprehensive physical examinations at each health maintenance visit. The PPE, however, does necessitate a directed examination to identify medical problems or deficits that could worsen the athlete's performance or conditions that might be worsened by athletic participation.
Many conditions that preclude participation in sports are identified in the preadolescent age-group and are not subtle. For example, congenital heart disease and hemophilia are typically detected before adolescence. However, subtle presentations of congenital defects or acquired diseases may go undetected. The most commonly detected abnormalities on PPEs are previously undetected or unrehabilitated musculoskeletal injuries. The annual PPE, especially for teenagers, should serve as “quality control” for the diagnosis and rehabilitation of injuries. With this in mind, the physical examination should include assessment of the following:
P.268
|
FIGURE 18.1 Preparticipation sports evaluation form. (From the Ohio High School Athletic Association (OHSAA), http://www.ohsaa.org, with permission.) |
P.269
P.270
P.271
P.272
|
TABLE 18.2 |
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
P.273
|
FIGURE 18.2 Body symmetry. (From Ross Laboratories. For the practitioner: orthopedic screening examination for participation in sports. Columbus, OH: Ross Products Division, Abbott Laboratories, 1981, with permission, copyright 1981 Ross Products Division, Abbott Laboratories.) |
Laboratory Tests
Blood for hemoglobin and a dipstick of the urine for protein, glucose, and blood have been recommended as screening tests for athletic participation. Although the hemoglobin test may be indicated for general health maintenance evaluation, it is not recommended for teens who are asymptomatic. There is a particular problem diagnosing anemia in highly trained aerobic athletes, who have a reduced hematocrit due to intravascular volume expansion but a normal oxygen-carrying capacity. The urine dipstick test is not indicated in the absence of symptoms suggesting genitourinary tract dysfunction (Vehaskari and Rapola, 1982). Screening for iron deficiency in menstruating female athletes, especially those who participate in long-distance events, by measurement of serum ferritin is advocated by some experts. However, empirical iron therapy in the form of a daily multivitamin with iron may be the most cost-effective approach to preventing iron deficiency in healthy female athletes (Elliot et al., 1991).
Some centers use isokinetic or isotonic equipment to screen for muscle weakness, especially quadriceps and hamstring weakness or imbalance. This testing may be reasonable if the equipment is available free of cost to the athletes and to evaluate those with previous injuries where there is question about their recovery. However, its utility in screening all athletes has not been established. Muscle weakness can be determined through the history and physical examination.
Estimating body composition with the use of anthropometric measurements (i.e., skin folds) is indicated in wrestling because prediction equations for minimum wrestling weights have been established. Use of skin-fold measurements as screening tests is not indicated for most
P.274
athletes. Body weight measurement and BMI calculation is sufficient for tracking patients who choose to gain or lose weight.
|
FIGURE 18.3 Neck symmetry. (From Ross Laboratories. For the practitioner: orthopedic screening examination for participation in sports. Columbus, OH: Ross Products Division, Abbott Laboratories, 1981, with permission, copyright 1981 Ross Products Division, Abbott Laboratories.) |
Clearance for Sport Participation
Table 18.2 lists disqualifying medical conditions for sports participation as recommended by the AAP. These are only guidelines; they may not apply in specific cases. However, it is notable that all except three (carditis, diarrhea, and fever) allow for individualized or modified athletic participation after further evaluation. The goal of the PPE, once again, is promotion of safe physical activity for all adolescents.
After the PPE, the patient should be given one of the following recommendations:
If there are restrictions on participation, these should be discussed with the athlete and a parent or guardian, with clearly documented recommendations transmitted to a certified athletic trainer or coach. Otherwise, the message to the athlete may be misinterpreted. If a physician is not going to clear an athlete for participation, the physician should be prepared to discuss the risks associated with continued participation. This requires an understanding of the medical problem and the demands placed on the athlete in that sport. For instance, a football lineman with
P.275
an ankle sprain would be able to return to participation earlier than a ballet dancer.
The physician must also consider the importance of this sport compared with another activity; some young athletes may be willing to switch to an activity with a lower risk of reinjury.
|
FIGURE 18.4 Shoulder symmetry. (From Ross Laboratories. For the practitioner: orthopedic screening examination for participation in sports. Columbus, OH: Ross Products Division, Abbott Laboratories, 1981, with permission, copyright 1981 Ross Products Division, Abbott Laboratories.) |
|
FIGURE 18.5 Elbow and hand symmetry. (From Ross Laboratories. For the practitioner: orthopedic screening examination for participation in sports. Columbus, OH: Ross Products Division, Abbott Laboratories, 1981, with permission, copyright 1981 Ross Products Division, Abbott Laboratories.) |
Medical–Legal Issues and Exclusion from Sports Participation
Athletes and their parents may seek to participate in a sport against medical advice, citing section 504(a) of the Rehabilitation Act of 1973, which prohibits discrimination against an athlete who is disabled if that person has the capabilities and skills required to play a competitive sport, or the Americans with Disabilities Act of 1990. Athletes with physical disabilities have successfully argued to retain their right to participate in professional athletics using these legal statues. However, an amateur athlete does not have an absolute right to decide whether to participate in competitive sports. Competition in sports is generally considered a privilege, not a right. The case of Knapp versus Northwestern Universityestablished that “difficult medical decisions involving complex medical problems can be made by responsible physicians exercising prudent judgment (which will be necessarily conservative when definitive scientific evidence is lacking or conflicting) and relying on the recommendations of specialist consultants or guidelines established by a panel of experts” (Maron et al., 1998). Physicians should clear athletes for participation according to generally agreed-on guidelines for participation with known medical conditions. As Table 18.2indicates, each decision must be made on an individual basis, and there may not be expert panel guidelines for all conditions. However, such guidelines do exist in many instances, an example being the 36th Bethesda Conference guidelines (see later discussion).
Adolescents with Special Health Care Needs
In addition to identifying in which sports adolescents with special health care needs can participate, the physician should assess current physical fitness activities for these youth. If the fitness activities are inadequate, and the youth and family are interested in more sports or fitness
P.276
opportunities, the physician should either write an exercise prescription for more fitness activities or refer the teen to a physical therapist, physiatrist, exercise physiologist, or sports medicine clinic to design appropriate fitness activities. This should be done in conjunction with the adolescent's subspecialty physicians. Youth with special health care needs have limited access to exercise facilities, and physicians should advocate increasing the availability of facilities for these adolescents.
|
FIGURE 18.6 Elbow and hand symmetry, continued. (From Ross Laboratories. For the practitioner: orthopedic screening examination for participation in sports. Columbus, OH: Ross Products Division, Abbott Laboratories, 1981, with permission, copyright 1981 Ross Products Division, Abbott Laboratories.) |
|
FIGURE 18.7 Elbow and hand symmetry, continued. (From Ross Laboratories. For the practitioner: orthopedic screening examination for participation in sports. Columbus, OH: Ross Products Division, Abbott Laboratories, 1981, with permission, copyright 1981 Ross Products Division, Abbott Laboratories.) |
Clearance for Specific Cardiac Conditions
Mortality during athletic participation is extraordinarily rare (7.8 deaths per million athletes per year—Bundy and Feudtner, 2004), but devastating to the athlete's family, team, and community. Most young athletes who die during sports participation die from sudden cardiac events; most of these athletes are asymptomatic before the event. Therefore, a major focus of the PPE screening is cardiovascular risk conditions.
Any athlete complaining of true angina, syncope, presyncope, or palpitations while exercising, independent of the physical examination, should be excluded from participation until further evaluation. Full evaluation could include, in consultation with a cardiovascular specialist, a 12-lead electrocardiogram, a continuous ambulatory (Holter) or event capture monitor, a maximal stress test, and a two-dimensional echocardiogram.
The best reference for giving guidance to individual athletes with known cardiac conditions is the 36th Bethesda Conference, 2005 Report: Eligibility Recommendations for Competitive Athletes With Cardiovascular Abnormalities, accessed at http://www.acc.org/clinical/bethesda/beth36/index.pdf. Specific conditions are discussed in the subsequent text.
P.277
prolapse who die while exercising is rare. A midsystolic click, with or without a late systolic murmur, is the auscultatory hallmark of this condition. However, patient reports of having mitral valve prolapse based on previous physician diagnosis were confirmed definitively on echocardiogram in only 0.45% of cases (Flack et al., 1999). Mitral valve prolapse is a clinical diagnosis generally not requiring echocardiography unless a murmur is present, in which case an echocardiogram is indicated to assess for mitral insufficiency.
|
FIGURE 18.8 Back and leg symmetry. (From Ross Laboratories. For the practitioner: orthopedic screening examination for participation in sports. Columbus, OH: Ross Products Division, Abbott Laboratories, 1981, with permission, copyright 1981 Ross Products Division, Abbott Laboratories.) |
|
FIGURE 18.9 Back symmetry. (From Ross Laboratories. For the practitioner: orthopedic screening examination for participation in sports. Columbus, OH: Ross Products Division, Abbott Laboratories, 1981, with permission, copyright 1981 Ross Products Division, Abbott Laboratories.) |
P.278
|
FIGURE 18.10 Leg symmetry. (From Ross Laboratories. For the practitioner: orthopedic screening examination for participation in sports. Columbus, OH: Ross Products Division, Abbott Laboratories, 1981, with permission, copyright 1981 Ross Products Division, Abbott Laboratories.) |
|
FIGURE 18.11 Leg symmetry, continued. (From Ross Laboratories. For the practitioner: orthopedic screening examination for participation in sports. Columbus, OH: Ross Products Division, Abbott Laboratories, 1981, with permission, copyright 1981 Ross Products Division, Abbott Laboratories, with permission.) |
P.279
sports for 6 months and then have their ventricular function evaluated at rest and with exercise before being allowed to return to sports.
|
FIGURE 18.12 Classification of Sports. This classification is based on peak static and dynamic components achieved during competition. It should be noted, however, that higher values may be reached during training. The increasing dynamic component is defined in terms of the estimated percent of maximal oxygen uptake (MaxO2) achieved and results in an increasing cardiac output. The increasing static component is related to the estimated percent of maximal voluntary contraction (MVC) reached and results in an increasing blood pressure load. *Danger of bodily collision. †Increased risk if syncope occurs. (From Mitchell JH, Haskel W, Snell P, et al. Task Force 8: Classification of sports. J Am Coll Cardiol 2005;45:1364, with permission.) |
Clearance for Adolescents with Solitary Kidney
Current recommendations of the American Academy of Pediatrics Committee on Sports Medicine and Fitness discuss individual assessments for adolescents with a solitary kidney and their possible disqualification from participating in contact sports. Johnson et al. (2005) evaluated the incidence and outcome of blunt renal injury in
P.280
children and adolescents by mechanism of injury. Of 49,651 pediatric trauma cases there were 813 involving renal injury. In those individuals with sports-related injuries, there were four nephrectomies and these were associated with sledding (two), skiing (one), and in-line skating (one). There were no kidneys lost in any contact sports, therefore the likelihood of kidney loss related to contact sports is very small.
|
TABLE 18.3 |
||||||||||||||||||||||||||||||||||||||||||
|
||||||||||||||||||||||||||||||||||||||||||
Effectiveness of the Preparticipation Sports Examination
Pfister et al. (2000) examined 1,110 National Collegiate Athletic Association (NCAA) colleges and universities and found that only 25% had forms that contained at least 9 of the recommended 12 AHA screening guidelines, and 24% contained 4 or fewer of these parameters. Maron (1998) also reviewed this issue and found that 40% of states have no formal screening requirement or approved history and physical examination questionnaires or forms. Authors of the 3rd Edition of the PPE monograph acknowledge that there is a significant need for national standardization of preparticipation screening to better assess its effectiveness and have called for utilization of new technologies such as the Internet for information gathering and sharing. Even with perfect implementation Bundy and Feudtner (2004) cogently argue that the prevalence of sports-related death is too low for the PPE to ever qualify as an effective screening program unless the focus is shifted to and systems created for appropriate rehabilitation of identified musculoskeletal deficits.
Can we Prevent Athletic Injury and Illness?
Morbidity and Mortality
Although football has been associated with a high incidence of injuries, the number of injury events resulting in permanent disability or death has been on the decline since the 1970s. However, catastrophic injuries and fatalities still occur in high school and college football and in other sports. A full report is available at the Web site for the National Center for Catastrophic Sports Injury Research, (www.unc.edu/depts/nccsi). At this site, the reader can find a breakdown of injuries and fatalities stratified by high school and college and by type of sport and by year. The sports with the highest incidence of fatalities from direct injuries per 100,000 participants from the 1982–1983 season through 2003–2004 were the following:
|
P.281
|
Nonfatal injuries also were similar in regard to the common sports involved. However, for female student-athletes, the leading cause of fatalities and catastrophic injuries between 1982 and 2003 was cheerleading.
There have been dramatic reductions in the number of football fatalities and nonfatal catastrophic injuries since 1976. While football is still associated with the greatest number of catastrophic injuries among all sports, the incidence of injury per 100,000 participants is higher for both gymnastics and ice hockey.
Catastrophic injuries to female athletes have increased over the years from one in 1982 to 1983 to an average of 6.7 in the last 22 years. A major factor in this increase has been the change in cheerleading which increasingly involves gymnastic stunts. Cheerleading now accounts for 50% of all high school catastrophic injuries to female athletes and 64.5% of catastrophic injuries at the college level.
Injury Prediction
Well-defined risk factors for athletic injury are scarce due to the paucity of good epidemiological research in the field. Factors that may predispose the athlete to injury include the following:
Injury Prevention Strategies
There are several ways of preventing injuries.
Returning to Participation
In general, athletes should not be allowed to return to participation in sports until the following criteria have been satisfied:
The following are examples of injuries or conditions that preclude returning to sports until the criteria just listed have been fulfilled:
The physician caring for the athlete should be familiar with common injuries and their therapy. A few are discussed in the following section. For further information on specific injuries, also see Chapter 16 and the References section at the end of this chapter.
P.282
Diagnosis and Management of Sports-Related Conditions and Morbidities
Neurological Concussion
The field of concussion, or sports-related mild traumatic brain injury (MTBI) is evolving rapidly and health care providers should look at recent guidelines to remain upto-date. A panel of international experts in the field met in Prague in November 2004 to revise and update the consensus recommendations they had made in Vienna in November 2001 (McCrory et al., 2005).
Definition
Sports concussion is now defined as “a complex pathophysiological process affecting the brain, induced by traumatic biomechanical forces” (McCrory et al., 2005). There are approximately 300,000 sports-related traumatic brain injuries in the United States, annually (Sosin et al., 1996).
Grading
The Vienna and Prague groups, which included authors of some of the most widely used concussion grading scales, recommend abandoning such crude systems in favor of individual assessment and guidance based on combined measures of recovery. The grading scales have not reliably correlated with any physiological or psychometric measures so far studied to be useful for predicting risk, sequelae, resolution of symptoms, or return to play.
Classification
The consensus panel recommends that clinicians appreciate that concussion in sport may either be simple or complex, but that this classification is made retrospectively.
Diagnosis and Management
Essentially any athlete who complains of any neurological symptoms or demonstrates any neurological signs (Fig. 18.13) or memory loss after any bodily contact (not just the head) with another athlete, the ground or other playing surface, or a projectile such as a ball or puck should be managed as an acute concussion.
The Sport Concussion Assessment Tool (SCAT) Card (Fig. 18.13) is a handheld standardized method to evaluate the concussed athlete. It also provides a suggested approach to management, which can be summarized as “When in doubt, sit them out!” In more detail this is as follows:
Return to Play
Return to play follows a stepwise process, with advance of no more than one step per day:
If any postconcussion symptoms occur at a level, the athlete must wait until asymptomatic for at least 24 hours before resuming the progression at the previous level.
The minimum time in which such a progression can be completed is a week, but may take much longer depending on the individual case. Lack of progression should prompt referral to a neurologist, neurosurgeon, or sports medicine physician comfortable with the management of sports concussion. Formal neuropsychological testing may be indicated at this time, although its interpretation may be hampered by a lack of baseline assessment. Although they, too, are hindered by issues of validation, particularly in younger age-groups, commercially available computerized neuropsychological batteries performed before participation may be helpful in this regard.
Second Impact Syndrome
One of the goals of the above guidelines is to prevent diffuse cerebral swelling with delayed catastrophic deterioration, a known complication of brain trauma. This has been postulated to occur after repeated concussive brain injury in sports and is known as the second impact syndrome (SIS). All cases of SIS to date have been diagnosed in adolescent boys. Some authors have suggested a different mechanism of cerebral autoregulation in children and adolescents as compared with adults (Snoek et al., 1984).
However, McCrory (1998) reviewed the 17 cases of SIS reported in the literature as of the year 2000, using strict diagnostic criteria, and established that only 5 were probably SIS. He suggested that, because all of the SIS cases have been reported in North America, because player and teammate recall of traumatic brain injury during sports is poor, and because diffuse cerebral edema after initial traumatic brain injury has been described for <100 years, SIS may in fact be the cerebral response to the
P.283
P.284
P.285
first traumatic brain injury. Nonetheless, it appears most prudent to limit contact sports in adolescent athletes until all postconcussive symptoms have disappeared, regardless of which concussion management protocol is followed.
|
FIGURE 18.13 Sport Concussion Assessment Tool (SCAT) Card. (From Clinical Journal of Sports Medicine 2005, with permission.) |
Sequelae of Chronic Head Trauma
There is evidence that traumatic brain injury occurring over an extended period (i.e., months or years) can result in cumulative neurological and cognitive deficits (Gronwall and Wrightson, 1975; Leininger et al., 1990). “Dementia pugilistica” was the description given to the punchy boxer's condition in 1928, and the syndrome also occurs in other sports characterized by repeated head trauma. This syndrome includes the following:
Neuropsychiatric abnormalities can persist for up to 6 months after a concussion (not only in sports). This has led to the definition of the postconcussional disorder described in theDiagnostic and Statistical Manual of Mental Disorders, 4th ed. (American Psychiatric Association 1994), as follows:.
Dementia (decreased cognition, memory, or any of the above symptoms) resulting from a single head injury is usually not progressive. If the dementia or behavior grows progressively worse, consider another diagnosis, such as hydrocephalus or major depressive disorder.
Collins et al. (1999) evaluated the relationship between concussion and neuropsychological performance in college football players. They found that both a history of multiple concussions and learning disabilities were associated with reduced cognitive performance, and that the effects were most pronounced in concussed athletes with a history of learning disabilities.
Heading in Soccer
The results of cross-sectional, retrospective studies of head injuries in soccer players have been used to suggest that “heading” of the soccer ball by young athletes should be banned. However, it is not the heading of the ball that appears to be the culprit so much as concussions incurred during the course of play. Matser et al. (1999) found that concussion in soccer players was associated with impaired performance in memory and planned functions. Concussions in soccer players should be managed using guidelines as discussed previously. Other suggestions include the following:
Cervical Spinal Injuries
Most catastrophic sports injuries involve the head and neck. The reader is again referred to the Web site for the National Center for Catastrophic Sports Injury Research listed at the end of the chapter.
General Management
P.286
Cervical Muscle Strain
Cervical muscle strains are common and can be painful. The mechanisms of injury include rapid acceleration of a muscle or muscles as a result of a collision; a quick movement causing the muscle to tear; or repetitive contractions causing muscle fatigue and eventually muscle tearing. There should be no motor or sensory deficits on examination. The athlete will complain of pain typically in the trapezius area. There will be tenderness over the muscle body, limitation of ROM, and pain with resistance. Midline pain and tenderness are consistent with a cervical fracture and should be treated as such in the acute setting. Any player without full ROM and strength is excluded from further contact sports. Ice, analgesic medication, and physical therapy should be initiated immediately. A cervical collar may be used rarely; for example, when the patient is in intractable pain after physical therapy and medication has been started. The physician should reassess the diagnosis if pain is intractable. Once physical therapy has yielded some relief, the player should receive continued physical therapy as needed in the therapist's office, complemented by home exercises. Clearance for return to contact sport requires a normal range of cervical motion and strength.
“Stingers” or “Burners”
A “stinger” is a common injury in American football and is the result of trauma to the brachial plexus that occurs when a player hits another opponent with the head or shoulder. The player describes a burning pain or weakness, or both, in the distribution of a branch of the brachial plexus. The physician who initially evaluates a stinger should first think about the possibility that the paresthesia is secondary to a spinal cord injury, as discussed previously, although unilateral signs and symptoms make this less likely. Once the cervical spine has been cleared (i.e., no midline cervical tenderness and full cervical ROM), then the diagnosis of brachial plexopathy can be made. Typically, these injuries are mild and the player recovers in minutes or less. The athlete may return to full participation if motor and sensory examination of the extremity is normal. However, some patients have dysesthesia and/or weakness that can last days to weeks. We suggest that patients with symptoms persisting longer than 12 hours or weakness documented to be 3/5 or less should be referred to a sports medicine specialist or a neurosurgeon. A nerve conduction or electromyographic study can be considered to assess for the extent of nerve injury after 21 days of symptoms, especially if the patient is not making clinical improvement.
Other Musculoskeletal Injuries and Conditions
The common injuries sustained by athletes and other active (and inactive!) adolescents are detailed in Chapters 16 and 17.
Special Considerations: the Female Athlete
In general, female athletes have injuries and injury rates similar to those of male athletes in the same sport. The exception to this rule is female athletes in jumping sports, who have a higher rate of anterior cruciate ligament sprains than their male counterparts. The reason for this difference is not established. A reduction in the incidence of acute knee injuries in female athletes after a 6-week neuromuscular training course, compared with a group that did not have this training, has been reported (Hewett et al., 1999). The results of this study and others imply a role for improved neuromuscular control in stabilizing the knee and, potentially, preventing anterior cruciate ligament injuries. It does not establish that neuromuscular control is inadequate in young female athletes as compared with young male athletes, because the latter were not studied with a similar intervention program. The issue of overtraining and adult height in female gymnasts was addressed earlier in this chapter.
Female Athlete Triad
The effects of excessive exercise on the reproductive system in young females deserve special mention. The so-called female athlete triad—disordered eating, amenorrhea, and osteoporosis—highlights the effects of excessive exercise (Yeager et al., 1993). Female athletes with amenorrhea or oligomenorrhea have lower bone mineral density (BMD) and higher rates of stress fracture than eumenorrheic athletes (Barrow and Saha, 1988; Myburgh et al., 1990; Bennell et al., 1999). A long-term consequence of amenorrhea and osteopenia during the second decade may be an increased risk of postmenopausal osteoporosis. Nichols et al., 2006 examined the prevalence rate for the female athlete triad among high schools athletes. They found that among female athletes studied (N = 170), 18.2%, 23.5%, and 21.8% met the criteria for disordered eating, menstrual irregularity, and low bone mass, respectively. Ten girls (5.9%) met the criteria for two components of the triad, and two girls (1.2%) met criteria for all three components.
Evaluation and Treatment
The first step in addressing hypothalamic amenorrhea/oligomenorrhea in female athletes is to make a correct diagnosis. Hypothalamic amenorrhea associated with exercise and/or inadequate caloric intake is a diagnosis of exclusion. The diagnosis is made on the basis of a careful history (menstrual, diet, and exercise history) and appropriate physical examination.
The menstrual history includes the following:
The diet history includes the following:
P.287
The exercise history includes the following:
The conditions that need to be ruled out in the evaluation of amenorrhea are reviewed in Chapter 52.
If a diagnosis of hypothalamic amenorrhea or oligomenorrhea associated with exercise and/or inadequate caloric intake is made, reductions in training intensity and/or enhanced caloric intake need to be made. Amenorrheic athletes who gain weight through reduced training and improved diet may resume menses spontaneously and increase their BMD (Drinkwater et al., 1986; Lindberg et al., 1987).
If the athlete has a diagnosable eating disorder, then treatment needs to include coordinated medical, nutritional, and psychological therapy. In our experience, this condition is best approached as a chronic condition, with long-term treatment and follow-up (months–years) being typical. Weight gain is the mainstay of treatment in trying to restore BMD in a patient with an eating disorder. However, weight gain is not always associated with improved BMD, and, when BMD is improved, it still tends to be below normal (Hotta et al., 1998;Jonnavithula et al., 1993). Therefore, estrogen replacement should be considered (see “Other Forms of Estrogen and/or Progestin Replacement” section).
The lifestyle changes (i.e., improved caloric intake and reduced exercise training) should be made in consultation with a dietitian. An example of changing the training intensity and dietary intake for a competitive athlete who is at less than 100% of her estimated ideal body weight (IBW) would be to reduce training time by one third and to add a snack containing at least 250 kilocalories (kcal) to the daily diet (Dueck et al., 1996), or at least enough to ensure that available daily energy is >35 kcal/kg fat-free mass (approximately 45–50 kcal/kg of body weight per day). If the athlete weighs 85% to 90% of estimated IBW and is exercising daily, we would recommend more aggressive changes: reduce exercise by one half and add 500 kcal/day (e.g., two dietary supplemental drinks or snacks). We do not recommend exercise if the body weight is <85% of estimated IBW, unless the athlete is >80% of estimated IBW, is eumenorrheic, and her weight is increasing weekly. There appears to be a subgroup of these athletes who have a more robust hypothalamic–pituitary–ovarian axis and maintain their menses better than women with anorexia nervosa, who resume menses only when their weight is >90% of estimated IBW. Exercise may attenuate bone loss in patients with bulimia nervosa compared to those with anorexia nervosa (Sundgot-Borger, 1998). We support exercise in patients with bulimia nervosa if their weight is >90% of the estimated IBW and they are menstruating. Strain on bone (through exercise) and estrogen appear to have additive effects on improving bone strength. The effectiveness of bone modeling through exercise could be limited when estrogen levels are reduced (Damien et al., 1998).
Appropriate Follow-up
The athlete should be monitored weekly until weight increases consistently. The visits can then be reduced to once every 2 weeks assuming the teen's weight progresses toward 90% of estimated IBW. This assumes the coach is supportive of the plan. We usually give a written plan to the athlete and encourage her to show it to her coach and ask the coach to call the physician or dietitian with any questions.
Low Bone Density
Measurement of Bone Mineral Density
Measurement of the BMD of the lumbar spine and hip by dual-energy x-ray absorptiometry (DXA) should be considered if the patient has been amenorrheic for longer than 6 months or oligomenorrheic, with fewer than 4 menses in the previous year. If the subject has been amenorrheic for longer than 1 year and is malnourished, the DXA scan is more strongly recommended. If DXA scanning is done, it should not be repeated at an interval of <12 months.
World Health Organization Criteria for Osteopenia and Osteoporosis
The World Health Organization (1994) has established criteria for the diagnosis of osteopenia and osteoporosis using a T-score. The T-score is the number of standard deviations (SDs) above or below the average peak BMD value for young, healthy women (age 20–29). Osteoporosis is defined as a T-score of -2.5 SD or lower; osteopenia is defined as a T-score between -1 and -2.5 SD. How this designation applies to the risk for subsequent stress fracture, or ultimately to clinical osteoporosis manifested as a fracture, in young athletes with amenorrhea is not known. Therefore, the International Society for Clinical Densitometry (ISCD, www.iscd.org) recommends utilizing only Z-scores (age, gender, and ethnicity matched as best possible) for patients younger than 20 years. Furthermore, because the fracture threshold in children and adolescents has not been established, terminology such as “below the expected range for age” is preferred for Z-scores < - 2.0. Osteoporosis is a clinical, not densitometric, diagnosis in pediatrics. Finally, the physician should exercise caution in interpreting either T-scores or Z-scores in patients with short stature because DXA tends to underestimate BMD in short subjects and overestimate BMD in tall subjects (Leonard et al., 1999).
Hormonal Therapy
Does hormonal therapy reduce stress fractures and/or improve BMD?
It has not been established that estrogen/progestin, in the form of oral contraceptive pills (OCPs), increases BMD more than no treatment. One longitudinal, randomized study (Hergenroeder et al., 1997) demonstrated improvement in total body and lumbar BMD in young amenorrheic females treated for 12 months with OCPs, compared with those treated with medroxyprogesterone or placebo. A second longitudinal, randomized clinical trial (Gibson et al., 1999) reported no improvement in amenorrheic subjects treated over 18 months with an estrogen/progestin preparation (Trisequens) containing 1 to 2 mg estradiol plus
P.288
0.5 to 1 mg estriol (equivalent to 35 µg of ethinyl estradiol) every day plus norethisterone (1 mg) for 10 days in a 28-day cycle. Two milligrams of estradiol is estimated to be similar to 25 µg of ethinyl estradiol (Fagan, 1998). The ethinyl estradiol dose that would be equivalent to 1 mg of estriol is not known to us at this time, but the combination of estradiol (2 mg) and estriol (1 mg) appears to be similar.
It has also not been established that OCPs prevent stress fractures (Bennell et al., 1999). Two retrospective cohort studies reported lower rates of stress fractures in women who used OCPs (Barrow and Saha, 1988; Myburgh et al., 1990). One prospective study found no relationship between current or past use of OCPs and the rate of stress fractures of the lower extremity, compared with athletes who had never used OCPs (Bennell et al., 1999).
One study demonstrated that conjugated estrogen (Premarin, 0.625 mg taken daily on days 1 through 25 of each month) and medroxyprogesterone (Provera, 5 mg taken daily on days 16 through 25 of each month) taken for a mean of 1.5 years improved lumbar BMD in females with anorexia nervosa compared with a placebo group if the patient's weight at the initiation of therapy was <70% of the estimated IBW (Klibanski et al., 1995). However, the authors did not state that this study was conclusive that weight <70% of estimated IBW was the criterion for starting this estrogen/progestin therapy. One report demonstrated an improvement of BMD in adult women taking medroxyprogesterone, 10 mg/day, for 10 days a month, but that study has not been replicated and this is not an accepted treatment protocol for adolescents (Prior et al., 1990).
Other Pharmacological Treatments to Prevent Osteoporosis
Selective estrogen receptor modulators (SERMs) have been developed to maximize the effect of estrogen on bone while minimizing the effect of estrogen on the breast and endometrium. Raloxifene is a SERM that has been approved by the U.S. Food and Drug Administration (FDA) for the prevention and treatment of osteoporosis in postmenopausal women. Its effect on the skeletons of adolescent and young adult females is not known.
Bisphosphonates such as alendronate are utilized to improve BMD in postmenopausal women by intercalating into the bone matrix, inhibiting osteoclastic resorption of bone. Because bisphosphonates may remain in the skeleton for a decade or more and may cross the placenta, they are not recommended for women of child-bearing age or younger. Studies are underway to investigate the safety and efficacy of these agents in young women with eating disorders. Recombinant parathyroid hormone and its active polypeptide components have been shown to improve bone density and strength in postmenopausal women and in elderly men as well.
Recombinant insulin like growth factor has been demonstrated to increase markers of bone turnover in women with anorexia nervosa (Grinspoon et al., 1996). Further research is needed to determine the role of these agents in improving BMD status in young women with amenorrhea.
The effects of all of the above agents on the skeletons of adolescent and young adult females are not known. Therefore, they must all be considered investigational, to be used only in research settings or by specialized skeletal centers.
Osteoporosis Prevention with Oral Contraceptive Pills
It has been suggested that use of OCPs in premenopausal women will reduce the risk of postmenopausal osteoporosis (Michaelsson et al., 1999). This effect has not been demonstrated for those who took OCPs at an age younger than 30 years.
With insufficient evidence for clinical benefit, the decision to treat with estrogen/progestin should be individualized. One concern is the psychological effects of taking OCPs. Patients may be falsely reassured by the resumption of menses so as to interfere with recovery. Other patients may be stressed by fears of hormonally mediated weight gain. Some users perceive weight gain even if they do not gain weight (Reubinoff et al., 1995). A prospective, longitudinal, randomized trial is urgently needed to resolve the effect of OCPs on BMD in amenorrheic athletes. However, the dropout rate in studies of amenorrheic subjects treated with hormonal therapy is 25% to 50%, making longitudinal studies difficult to perform (Gulekli et al., 1994; Hergenroeder et al., 1997; Gibson et al., 1999).
The following points should also be considered:
In the absence of compelling evidence and an established standard, the use of combination OCPs should be considered for those female athletes who have been amenorrheic for longer than 6 months, especially if they are malnourished, as manifested by weight <85% of their estimated IBW. In addition, because 60% to 80% of the variance in BMD is likely attributable to heritable factors, a family history of osteoporosis should lower the threshold for hormonal treatment. If the athlete has been amenorrheic for longer than 12 months, stronger consideration should be given to starting OCP treatment, in addition to effecting lifestyle changes discussed earlier (Castro et al., 2000).
Estrogen Therapy in Younger Teens
Some groups have recommended that estrogen replacement must not be prescribed for patients younger than 16 years (American Academy of Pediatrics, 1989). The dilemma is that delaying estrogen therapy may compromise BMD but premature use of estrogen could compromise adult height. Bone age determination may be helpful in the decision to prescribe estrogen/progestin to female adolescents with amenorrhea related to excessive exercise and calorie restriction.
A 15-year old with a bone age of 13 years has achieved 96.4% of her full adult height; with a bone age of 14 years this same teen has achieved 98.3%, and with a bone age of 15 years 99%, of her adult height (Gruelich and Pyle, 1959). The mean height of females in North America is 163 cm at 19 years of age (Tanner and Davies, 1985). If estrogen
P.289
therapy completely arrested height gain from the onset of therapy, then the adolescent with a bone age of 15 years and a potential adult height of 163 cm could potentially lose only 1.6 cm of height. If statural growth were only partially or minimally arrested, then some additional height growth would occur and any lost height potential would be trivial.
On the other hand, bone loss resulting from an eating disorder occurring before menarche could lead to significant arrest of BMD development, compared with bone loss after menarche. The onset of bone loss in relation to bone development is important in that onset of anorexia nervosa before 15 years of age affects bone size and volumetric BMD more than onset after age 15 does (Seeman et al., 2000). Bone fragility is a function of both bone size and volumetric BMD, and these are partly established during pubertal growth. There is a risk of delaying the start of estrogen/progestin therapy until epiphyseal growth is complete.
It is therefore reasonable to prescribe estrogen/progestin replacement for females with amenorrhea at 15 years of age and a bone age of 15 years, and to consider such therapy for those with a bone age of 14 years, depending on the degree of osteopenia and malnutrition. This is an area that requires further investigation.
Calcium Intake
Amenorrheic athletes, like all adolescent females, have a daily elemental calcium recommended daily intake (RDI) of 1,300 to 1,800 mg. It must be noted, however, that in a group of healthy adolescents followed up longitudinally, changes in BMD were independent of calcium intake, which ranged from 500 to 1,500 mg/day (Lloyd et al., 2000).
Ergogenic Aids and Drug Use in Athletes
Background
Evidence suggests that substance use among high school and college athletes may be greater in some cases than in nonathletes, with important differences depending on gender and the individual drug being studied (Anderson and McKeag, 1989; Wadler and Hainline, 1989). Specifically, there is recent evidence that marijuana and alcohol use are higher in male students who compete in competitive sports than in those not competing in sports; the reverse is true for female athletes (Ewing, 1998; Aaron et al., 1995). Neither marijuana nor alcohol has ergogenic effects on athletic performance. Cigarettes tend to be used less by athletes (Aaron et al., 1995). Anabolic steroids are used more by athletes. Drugs are often readily available starting in junior high school.
The major categories of drugs used to improve performance by athletes include stimulants, pain relievers, and anabolic steroids (Wadler and Hainline, 1989). In addition, over the last decade there has been increased recognition of the use of dietary supplements as ergogenic aids. These supplements include creatine, androstenedione, and dehydroepiandrosterone (DHEA), γ-hydroxybutyrate, and protein powders.
For more information about drugs of abuse, contact the National Clearinghouse for Alcohol and Drug Information on-line at http://ncadi.samhsa.gov.
Therapeutic Drugs
Over-the-counter analgesics, decongestants, antihistamines, laxatives, antidiarrheal agents, and weight-loss medications are commonly used by athletes. Athletes should be asked specifically about use of these medications during office or training room visits, because they may not perceive them to be as important as prescription drugs and may not report their use. In addition, these medications have important side effects that can affect performance, and some are banned by sports governing bodies (NCAA and United States Olympic Committee). Physicians are encouraged to consult the United States (www.usantidoping.org) and World Anti-Doping Agencies (www.wada-ama.org) when advising athletes, especially college and elite athletes, about medication and prescription drug use.
Performance-Enhancing Drugs
Stimulants
Stimulants have been used extensively to combat psychological and muscular fatigue. These substances are banned by the International Olympic Committee (IOC) and can be detected by urine tests.
Amphetamines
Fine motor coordination and performance on tasks requiring prolonged attention have been shown to improve with amphetamine use. Side effects include anxiety, restlessness, tremors, tachycardia, irritability, confusion, and poor judgment, and these effects occur at higher doses.
Cocaine
No evidence supports ergogenic effects of cocaine. Effects include increased heart rate, reflexes, and blood pressure, with accompanying euphoria. In the inexperienced user, reflexes are often more rapid but dyssynchronous, leading to a decrement in athletic performance. Lethal toxicity can occur unexpectedly, particularly with intravenous use, because the doses of cocaine available on the street vary widely. Symptoms of acute overdose are difficult to treat and include arrhythmias, seizures, hyperthermia, and death. Metabolites can be found in the urine within 24 to 36 hours of ingestion and up to 4 days after acute ingestion.
Caffeine
Caffeine is probably the most commonly used stimulant. Several studies have documented increased muscle work output for endurance activities. Significant side effects mimic those of other stimulants. Caffeine has a direct diuretic effect, potentially complicating fluid and electrolyte status in prolonged exercise activities. Caffeine is banned by the IOC in quantities >12 µg/mL (approximately equivalent to 4–8 cups of coffee or 8–16 cups of cola).
Anabolic Steroids
Anabolic steroid use is associated with increased muscle size and strength, especially in athletes who are weight training when the steroid use is initiated and in those who are consuming a high-calorie diet. Animal models demonstrate that anabolic steroids result in muscle hypertrophy in nonexercising muscle. There is no evidence that steroid use enhances aerobic power. There is evidence that anabolic steroids may aid in the healing of muscle contusion injury, in contrast to corticosteroids, raising potential
P.290
ethical issues in the future regarding the use of steroids in muscle healing in response to contusion. FDA-approved uses of anabolic steroids include weight gain in patients with acquired immunodeficiency syndrome (AIDS), severe anemia, hereditary angioedema, metastatic breast cancer, or male adrenal insufficiency.
Anabolic steroids may be injected or taken orally, and they are often freely available from peers and coaches. Buckley et al. (1988) reported that 6.6% of 12th grade male adolescents had used anabolic steroids. Approximately 21% indicated that their primary source was a health professional. The lifetime prevalence of illegal steroid use among high school students in the United States as reported by the YRBS rose from 2.2% in 1993 to 6.1% in 2003 but has since fallen to 4.0%, in the 2005 YRBS (Centers for Disease Control and Prevention, 2006). In the Monitoring the Future study of 12th graders, the lifetime prevalence rates were 2.3% in 1995, 2.9% in 1999, 3.5% in 2003, and 2.6% in 2005(www.monitoringthefuture.org,Johnston et al., 2006). For 8th graders, the lifetime prevalence rates rose from 2.0% in 1995 to 3.5% in 2003, but fell dramatically to 1.7% in 2005.
Side effects of anabolic steroids include the following:
Injected steroids are detectable in the urine for 6 months or longer. Orally administered anabolic steroids disappear from the urine after days to weeks. More information on anabolic steroids can be obtained at the NIDA Web site on steroid use: www.steroidabuse.org.
Narcotic Analgesics
Narcotic analgesics may allow an athlete to perform despite pain and/or injury, but they do not enhance athletic performance. In standard doses, there also does not appear to be a detriment. However, they may be abused in an attempt to return to play prematurely. The effects include psychomotor retardation, sedation, dysphoria, and nausea and vomiting.
Dietary Supplements as Ergogenic Aids
The potency, purity, and long-term effects of most dietary supplements (also see Chapter 83) are not known because they are not regulated by the FDA. Unfortunately, the 1994 Dietary Supplement Health and Education Act (DSHEA), which removed the FDA regulation, has lead to an explosion in the availability and use of these products among teens. Reputable information about dietary supplements can be found at http://dietary-supplements.info.nih.gov, but our awareness of the “latest” agents likely lags far behind their actual use by our patients. None of these supplements are recommended for use in adolescents.
Androstenedione
Androstenedione is an androgen produced by the gonads and adrenal glands. It is a precursor to estradiol and testosterone, yet it is marketed as a prohormone or nutritional supplement and is not regulated by the FDA. Individuals taking androstenedione experience no beneficial effect on strength as compared with controls. It has been associated with increased serum estradiol levels, no change in serum testosterone levels, and an increased LDL:HDL ratio at 12 weeks in healthy adult men (King et al., 1999; Broeder et al., 2000).
There is no medically approved use for androstenedione, and its use is banned by the IOC, the NCAA, the National Football League, and other athletic organizations. However, because of its perceived benefit and because testing for androstenedione is not possible, its use is likely to continue.
Dehydroepiandrosterone
DHEA is an adrenal androgen marketed as a food supplement. It is a precursor of androgens and estradiol. Ergogenic effects have not been demonstrated in athletes. DHEA has been reported to increase IGF. The side effects are androgenic, including hair loss and irreversible deepening of the voice in females. Androgens can hasten the growth of prostatic cancer, and estrogens can similarly affect the growth of breast and endometrial cancer. The effects of DHEA on the growth of these tumors are unknown.
Creatine
Creatine is synthesized in the liver, kidney, and pancreas. Creatine is supplied in the diet in the form of meat and fish. The usual U.S. diet supplies approximately 1 to 2 g of creatine daily to replenish that which is lost in the urine. Theoretically, creatine works as an ergogenic aid by increasing the cellular concentration of high-energy phosphocreatine, the immediate transport entity in the synthesis of adenosine triphosphate (ATP) from adenosine diphosphate (ADP). It has been suggested that those with lower intracellular creatine concentration may benefit most from creatine supplementation, yet there is no method to assay for low intracellular concentration at this time. There may be some benefit for short-duration (i.e., <30 seconds), high-intensity exercise, but this effect has been demonstrated in laboratory settings and has not translated into improved performance on the athletic field. In addition, there have been case reports of renal injury with the use of creatine and long-term safety has not been established.
γ-Hydroxybutyrate, γ-Hydroxybutyrolactone, and 1,4-Butanediol
1,4-Butanediol (BD) is an industrial solvent that is rapidly converted to γ-hydroxybutyrate (GHB), which is the active metabolite for all three of these compounds. GHB is an endogenous metabolite of γ-aminobutyric acid (GABA), the predominant inhibitory
P.291
neurotransmitter in the brain. The clinical use of GHB is limited to trials in patients with narcolepsy. GHB was marketed to bodybuilders in the 1980s as a method to increase muscle and promote fat loss. Although it is a Schedule I drug, it is a common “rave” drug and is readily accessible.
The sale of GHB was banned in 1991 after it was linked to fatal and to serious nonfatal side effects, but DSHEA made it possible to legally sell the precursors of GHB as dietary supplements. Both γ-hydroxybutyrolactone (GBL) and BD were marketed as nontoxic and natural dietary supplements. The FDA subsequently issued warnings about both compounds, the health risks of which included acute intoxication (which can be fatal), addiction, and withdrawal (Zvosec et al., 2001). The FDA has recommended disposing of all supplies of GBL, and there was a voluntary recall of GBL in 1999. Subsequently, BD began being marketed as a “replacement product” despite FDA warnings.
Use of Recreational Drugs by Athletes
Smokeless Tobacco
The incidence of smokeless tobacco use among preprofessional and professional baseball players is estimated to be 30% to 40% (Ernster et al., 1990), compared to 4% to 11% for the same age-group in the general population. Cigarette smoking is less common among baseball players. Complications of smokeless tobacco include oral cancer, periodontal disease, oral leukoplakia, and mouth and gum irritation. Smokeless tobacco may have a performance-enhancing effect on cognitive tasks. There does not appear to be a demonstrable effect on reaction time, and there is no demonstrable ergogenic effect. The perception of benefit and cultural support for smokeless tobacco use in sports such as baseball, football, and rodeo sustain its use.
Alcohol
Alcohol is the leading drug of abuse among high school and college students, regardless of whether they are involved in sports. Alcohol use in college students is better correlated with participation in fraternities and sororities than with participation in athletics. Still, alcohol has become entwined in the fabric of sport in America through sponsorship use of athletic events. Beer producers spend large proportions of their advertising budgets on sports. This financial relationship between alcohol and sports appears unlikely to change, and, to the extent that advertising of alcohol influences drinking behaviors, alcohol abuse will remain a problem for adolescents and young adults.
Alcohol use acutely and chronically impairs athletic performance by impairing cognition and visual-motor coordination. However, athletes who significantly abuse alcohol may not have impaired performance until the problem is chronic. Physicians and trainers should attempt to diagnose and refer patients for treatment at the early and middle stages of alcohol abuse and not wait until performance deteriorates.
Testing for Performance-Enhancing Drugs
Readers are encouraged to contact the NCAA (telephone 1-913-339-1906) or the U.S. Olympic Committee (1-800-233-0393, Drug Control Hotline). The following five components should be included in any drug testing program:
The American College Health Association (1994) (http://acha.org/info_resources/guidelines.cfm) has also provided guidelines regarding drug education and testing of student athletes, including the following:
Given than many jurisdictions that sponsor sports may be limited financially, it may be more cost effective to advocate for balanced educational programs that increase student-athletes' knowledge than to mount an expensive testing program, particularly at the high school and youth sports levels.
Web Sites
For Teenagers and Parents
http://www.sportsmedicine.com/. Site connecting individuals interested in sports medicine.
P.292
http://www.alliedhealthrehab.com/Information/Informational_sheets.htm. Patient information from the Sports Medicine Center, Akron Children's Hospital.
http://orthoinfo.aaos.org. Your Orthopaedic Connection from the American Academy of Orthopaedic Surgeons.
For Health Professionals
http://www.aap.org/sections/sportsmedicine/. American Academy of Pediatrics Council on Sports Medicine and Fitness.
http://www.acsm.org/. American College of Sports Medicine.
http://www.sportsmed.org/. American Orthopaedic Society for Sports Medicine.
http://www.unc.edu/depts/nccsi/. National Center for Catastrophic Sports Injury Research, data on sports injuries and fatalities.
http://www.nata.org/downloads/documents/secondary_school_medcarecommunication.pdf. National Athletic Trainers' Association communication on Appropriate Medical Care for the Secondary School-Age Athlete.
http://www.asmi.org/. American Sport Medicine Institute.
http://www.ipsm.org. Institute for Preventative Sports Medicine.
http://www.newamssm.org. American Medical Society for Sports Medicine.
http://www.cdc.gov/doc.do/id/0900f3ec80017619. U.S. Centers for Disease Control and Prevention Heads Up! Tool Kit on Concussion.
References and Additional Readings
Aaron DJ, Dearwater SR, Anderson R, et al. Physical activity and the initiation on high-risk health behaviors in adolescents. Med Sci Sports Exerc 1995;27:1639.
American Academy of Family Physicians, the American Academy of Pediatrics, the American Medical Society for Sports Medicine, the American Orthopedic Society for Sports Medicine and the American Osteopathic Academy of Sports Medicine. Preparticipation physical evaluation. The Physician and Sports Medicine, 2nd ed. Minneapolis, MN: A joint publication of the American Academy of Family Physicians, the American Academy of Pediatrics, the American Medical Society for Sports Medicine, the American Orthopedic Society for Sports Medicine and the American Osteopathic Academy of Sports Medicine, 1996.
American Academy of Family Physicians, American Academy of Pediatrics, American College of Sports Medicine. Preparticipation physical evaluation, 3rd ed. Minneapolis, MN: McGraw-Hill Healthcare Information, 2005.
American Academy of Pediatrics, Committee on Sports Medicine and Fitness. Mitral valve prolapse and athletic participation in children and adolescents. Pediatrics 1995;95;789.
American Academy of Pediatrics, Committee on Sports Medicine and Fitness and American Academy of Ophthalmology. Committee on eye safety and sports ophthalmology. Protective eyewear for young athletes. Pediatrics 1996;98;311.
American Academy of Pediatrics, Committee on Sports Medicine and Fitness. Strength training by children and adolescents. Pediatrics 2001;107;1470.
American Academy of Pediatrics Committee on Sports Medicine and Fitness. Promotion of healthy weight-control practices in young athletes. Pediatrics 2005;116:1557.
American Medical Society for Sports Medicine and American Academy of Sports Medicine. Human immunodeficiency virus and other blood-borne pathogens in sports. Clin J Sports Med 1995;5:199.
American Psychiatric Association. Diagnostic and statistical manual of mental disorders, 4th ed. Washington, DC: American Psychiatric Association, 1994.
Anderson J. Stretching. Bolinas, CA: Shelter Publications, 1980.
Bader RS, Goldberg L, Sahn DJ. Risk of sudden cardiac death in young athletes: which screening strategies are appropriate? Pediatr Clin North Am 2004;51:1421.
Batts M. The etiology of spondylolisthesis. J Bone Joint Surg 1939;21:879.
Bering JR, Steen SN. Sports nutrition for the '90s. Gaithersburg, MD: Aspen Publishers, 1991.
Berger S, Kugler JD, Thomas JA, et al. Sudden cardiac death in children and adolescents: introduction and overview. Pediatr Clin North Am 2004;51:1201.
Bergfield JA, Hershman EB, Wilboiurn AJ. Brachial injuries in athletes. Orthop Trans 1988;12:743.
236th Bethesda Conference. Eligibility recommendations for competitive athletes with cardiovascular abnormalities. J Am Coll Cardiol 2005;45:1313.
Bhasin S, Storer TW, Berman N, et al. The effects of supraphysiologic doses of testosterone on muscle size and strength in normal men. N Engl J Med 1996;335:1.
Blimpke CJ. Resistance training during preadolescence. Sports Med 1993;15:389.
Bouchard C, Shepard RJ, Stephens T, eds. Physical activity, fitness, and health: international proceedings and consensus statement. Champaign, IL: Human Kinetics, 1994.
Broeder CE, Quindry J, Brittingham K, et al. The andro project: physiological and hormonal influences of androstenedione supplementation in men 35 to 65 years old participating in a high-intensity resistance training program. Arch Intern Med 2000;160:3093.
Brostrum L. Treatment and prognosis in recent ligament ruptures. Acta Chir Scand 1966;132:537.
Buckley WE, Yesalis CE, Friedl KE. Estimated prevalence of anabolic steroid use among male high school seniors. JAMA 1988;260:3441.
Bundy DG, Feudtner CF. Preparticipation physical evaluations for high school athletes: time for a new game plan. Ambul Pediatr 2004;4:260.
Calfee R, Fadale P. Popular ergogenic drugs and supplements in young athletes. Pediatrics 2006;117:e577.
Calin A, Porta J, Fries JF, et al. Clinical history as a screening test for ankylosing spondylitis. JAMA 1977;237:2613.
Cantu RC. When to return to contact sports after a cerebral concussion. Sports Med Dig 1988;10:1.
Cantu RC, Mueller FO. Fatalities and catastrophic injuries in high school and college sports, 1982–1997. Phys Sportsmed 1999;27:35.
Cassas KJ, Cassettari-Wayhs A. Childhood and adolescent sports-related overuse injuries. Am Fam Physician 2006;73:1014.
Centers for Disease Control and Prevention. Youth risk behavior surveillance—United States, 1997. Morb Mortal Wkly Rep 1998;47(SS-3);1.
Centers for Disease Control and Prevention. Youth risk behavior surveillance—United States, 2005. Morb Mortal Wkly Rep CDC Surveill Summ 2006;55(SS05);1. http://www.cdc.gov/HealthyYouth/yrbs/index.htm.
P.293
Circulation. Cardiovascular preparticipation screening of competitive athletes. 1996;94:850.
Collins MW, Grindel SH, Lovel MR, et al. Relationship between concussion and neuropsychological performance in college football players. JAMA 1999;282:964.
Colorado Medical Society, Sports Medicine Committee. Guidelines for the management of concussion in sports, revised. Denver, CO: Colorado Medical Soceity, 1991.
Creatine and androstenedione: two “dietary supplements.” Med Lett Drugs Ther 1998;40:105.
Dehydroepiandrosterone (DHEA). Med Lett Drugs Ther 1996;38:91.
Department of Health and Human Services, U.S. Public Health Service. Healthy people 2010: conference edition. Washington, DC: DHHS, 2000.
DiBello V, Bianchi M, Bertini A, et al. Effects of anabolic-anabolic steroids on weight-lifters' myocardium: an ultrasonic video-densitometric study. Med Sci Sports Exerc1999;31:514.
Drezner JA. Sudden cardiac death in young athletes. Postgrad Med 2000;108:37.
Durant RH, Rickert VI, Ashworth CS, et al. Use of multiple drugs among adolescents who use anabolic steroids. N Engl J Med 1993;328:922.
Durant RH, Seymore C, Linder CW, et al. The preparticipation examination of athletes: comparison of single and multiple examiners. Am J Dis Child 1985;139:657.
Elster A, ed. American medical association guidelines for adolescent preventive services (GAPS) recommendations and rationale. Baltimore: Williams & Wilkins, 1994.
Ewing BT. High school athletes and marijuana use. J Drug Educ 1998;28:147.
Ernster VL, Grady DG, Greene JC, et al. Smokeless tobacco use and health effects among baseball players. JAMA 1990;264:218.
Faigenbaum AD, Zaichkowsky LD, Gardner DE, et al. Anabolic steroid use by male and female middle school students. Pediatrics 1998;101:e6.
Flack JM, Kvasnicka JH, Gardin JM, et al. Anthropometric and physiologic correlates of mitral valve prolapse in a biethnic cohort of young adults: the CARDIA study. Am Heart J1999;138:486.
Garrick JG, Requa R. Injuries in high school sports. Pediatrics 1978;61:465.
Garrick JG, Webb DR. Sports injuries: diagnosis and management, 2nd ed. Philadelphia: WB Saunders, 1999.
Gilon D, Buonanno FS, Joffe MM, et al. Lack of evidence of an association between mitral-valve prolapse and stroke in young patients. N Engl J Med 1999;341:8.
Glover DW, Maron BJ, Matheson GO. The preparticipation physical examination. Phys Sportsmed 1999;27:29.
Goldberg B, Saraniti A, Whitman P, et al. Pre-participation sports assessments: an objective evaluation. Pediatrics 1979;66:736.
Green GA, Jordan SE. Are brain injuries a significant problem in soccer? Clin Sports Med 1998;17:795.
Gronwall D, Wrightson P. Cumulative effects of concussion. Lancet 1975;2:995.
Hallagan JB, Hallagan LF, Snyder MB. Anabolic-androgenic steroid use by athletes. N Engl J Med 1989;321:1042.
Haller CA, Benowitz NL. Adverse cardiovascular and central nervous system events associated with dietary supplements containing ephedra alkaloids. N Engl J Med 2000;343:1833.
Hergenroeder AC. Diagnosis and treatment of ankle injuries: a review. Am J Dis Child 1990;144:809.
Hergenroeder AC, Garrick JG, eds. Sports medicine. Pediatr Clin North Am 1990;37(5).
Hergenroeder AC, Phillips S. Advising teenagers and young adults about weight gain and loss through exercise and diet: practical advice for the physician. In: Shenker IR, ed.Monographs in clinical pediatrics: adolescent medicine. London: Harwood Academic, 1994:113.
Jonas AP, Sickles RT, Lombardo JA. Substance abuse. In: Puffer J, ed. Clinics in sports medicine, 1992;11:379.
Johnson MD. Anabolic steroid use in adolescent athletes. Pediatr Clin North Am 1990;37:1111.
Johnson TS, Rock PB. Current concepts: acute mountain sickness. N Engl J Med 1988;319:841.
Johnston LD, O'Malley PM. Bachman JG, et al. Monitoring the future national survey results on drug use, 1975–2005: volume I, secondary school students (NIH Publication No. 06–5883). Bethesda, MD: National Institute on Drug Abuse, 2006.
Keller CS, Noyes FR, Buncher R. The medical aspects of soccer injury epidemiology. Am J Sports Med 1987;15:230.
Kelly JP, Nichols JS, Filley CM, et al. Concussion in sports: guidelines for the prevention of catastrophic outcome. JAMA 1991;266:2867.
King DS, Sharp RL, Vukovich MD, et al. Effect of oral androstenedione on serum testosterone and adaptations to resistance training in young men: a randomized controlled trial.JAMA 1999;281:2020.
Kirkwood MW, Yeates KO, Wilson PE. Pediatric sport-related concussion: a review of the clinical management of an oftneglected population. Pediatrics 2006;117:1359.
Landers DM, Crews DJ, Boutcher SH, et al. The effects of smokeless tobacco on performance and psychophysiological response. Med Sci Sports Exerc 1992;24:895.
Leddy JJ, Smolinski RJ, Lawrence J, et al. Prospective evaluation of the Ottawa Ankle rules in a university sports medicine center. Am J Sports Med 1998;26:158.
Leininger BE, Gramling SE, Fannell HD, et al. Neuropsychological deficits in symptomatic minor head injury patients after concussion and mild concussion. J Neurol Neurosurg Psychiatry 1990;53:293.
Leski M. Sudden cardiac death in athletes. South Med J 2004;97:861.
Lyznicki JM, Nielsen NH, Schneider JF. Cardiovascular screening of student athletes. Am Fam Physician 2000;62:765.
Maron BJ. Cardiovascular risks to young persons on the athletic field. Ann Intern Med 1998;129:379.
Maron BJ, Mitten Matthew J, Quandt EF, et al. Competitive athletes with cardiovascular disease: the case of Nicholas Knapp. N Engl J Med 1998;339:1634.
Maron BJ, Roberts WC, McAllister HA, et al. Sudden death in young athletes. Circulation 1980;62:218.
Maron BJ, Thompson PD, Puffer JC, et al. Cardiovascular preparticipation screening of competitive athletes. A statement for health professionals from the Sudden Death Committee and Congenital Cardiac Defects Committee, American Heart Association. Circulation 1996;94:850; (Addendum appears in Circulation 1998;97:2294).
Matser EJT, Kessels AG, Lezak MD, et al. Neuropsychological impairment in amateur soccer players. JAMA 1999;282:971.
McClain LG, Reynolds S. Sports injuries in a high school. Pediatrics 1989;84:446.
McCrory PR. Second impact syndrome. Neurology 1998;50:677.
McGrory PR, Johnston K, Meeuwisse W, et al. Summary and agreement statement of the 2nd International Conference on Concussion in Sport, Prague 2004. Br J Sports Med2005;39:196.
Metzl JD. Concussion in the young athlete. Pediatrics 2006;117(5):1813.
P.294
MMWR Morb Mortal Wkly Rep. Sports-related recurrent brain injuries—U.S. 1997;46:224.
Mueller FD, Cantu RC. National center for catastrophic injury research: 17th annual report. Chapel Hill, NC: University of North Carolina, NCCSIR, 2001. Available at www.unc.edu/depts/nccsi.
National Heart, Lung, and Blood Institute. Indexes of obesity and comparisons with the previous national survey data in 9- and 10-year-old black and white girls: the NHLBI Growth and Health Study. J Pediatr 1994;124:675.
National High Blood Pressure Education Program, Working Group on Hypertension Control in Children and Adolescents. Fourth report on the diagnosis, evaluation, and treatment of high blood pressure in children and adolescents, Pediatrics 2004;114:555.
National Institutes of Health. Proceedings of the Conference on Sports Injuries in Youth: surveillance strategies. NIH Publication No. 93–3444. Washington, DC: NIH, Department of Health and Human Services, U.S. Public Health Service, November 1992.
Nickerson HJ, Holubets MC, Weiler BR, et al. Causes of iron deficiency in adolescent athletes. J Pediatr 1989;114:657.
Oberlander MA, Shalvoy RM, Hughston JC. The accuracy of the clinical knee examination documented by arthroscopy. Am J Sports Med 1993;21:773.
O'Connor FG, Kugler JP, Oriscello RG. Sudden death in young athletes: screening for the needle in a haystack. Am Fam Physician 1998;57:2763.
O'Shea KJ, Murphy KP, Heekin RD, et al. The diagnostic accuracy of history, physical examination, and radiographs in the evaluation of traumatic knee disorders. Am J Sports Med1996;24:164.
Pate RR, Long BJ, Heath G. Descriptive epidemiology of physical activity in adolescents. Pediatr Exerc Sci 1994;6:434.
Pate RR, Pratt M, Blair SN, et al. Physical activity and public health: a recommendation from the Centers for Disease Control and Prevention and the American College of Sports Medicine. JAMA 1995;273:402.
Pfister GC, Puffer JC, Maron BJ. Preparticipation cardiovascular screening for U.S. collegiate student-athletes. JAMA 2000;283:1597.
Pope PR, Herbert RD, Kirwan JD, et al. A randomized trial of pre-exercise stretching for prevention of lower-limb injury. Med Sci Sports Exerc 2000;32:271.
Powell JW, Barber-Foss KD. Traumatic brain injury in high school athletes. JAMA 1999;282:958.
Puffer JC. Drugs and doping in athletes. In: Mellion MB, ed. Office management of sports injuries and athletic problems. Philadelphia: Handley & Belfus, 1988.
Purcell JS, Hergenroeder AC. Physical conditioning in adolescents. Curr Opin Pediatr 1994;6:373.
Reid DC. Sports injury assessment and rehabilitation. New York: Churchill Livingston, 1992.
Reider B, ed. Sports medicine: the school-age athlete, 2nd ed. Philadelphia: WB Saunders, 1996.
Ross Laboratories. For the practitioner: orthopedic screening examination for participation in sports. Columbus, OH: Ross Laboratories, 1978.
Sallis JF, ed. Physical activity guidelines for adolescents. [Special issue]. Pediatr Exerc Sci 1994;6:299.
Semon RL, Spengler D. Significance of lumbar spondylolysis in college football players. Spine 1981;6:172.
Shields BJ, Smith GA. Cheerleading-related injuries to children 5 to 18 years of age: United States, 1990–2002. Pediatrics 2006;117:122.
Snoek JW, Minderhoud JM, Wilmink JT. Delayed deterioration following mild head injury in children. Brain 1984;107:15.
Soler T, Calderon C. The prevalence of spondylolysis in the Spanish elite athlete. Am J Sports Med 2000;28:57.
Sosin DM, Sniezek JE, Thurman DJ. Incidence of mild and moderate brain injury in the United States, 1991. Brain Inj 1996;10:47.
Stewart JG, Ahlquist DA, McGill DB, et al. Gastrointestinal blood loss and anemia in runners. Ann Intern Med 1984;100:843.
Steill IG, Greenberg GH, Wells GA, et al. Prospective validation of a decision rule for the use of radiography in acute knee injuries. JAMA 1996;275:611.
Steill IG, Greenberg GH, McKnight RD, et al. The “real” Ottawa Ankle rules. Ann Emerg Med 1996;27:103.
Thacker SB, Stroup DF, Branche CM, et al. The prevention of ankle sprains in sports. Am J Sports Med 1999;27:753.
U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion. Physical activity and health: a report of the Surgeon General. Publication No. S/N 017-023-00196-5. Washington, DC: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, 1996.
Valkenburg HA, Haaneen HCM. The epidemiology of low back pain. In: White AA, Gordon SL, eds. American Academy of Orthopaedic surgeons symposium on idiopathic low back pain. St. Louis: CV Mosby, 1982:9.
Wadler GI, Hainline B. Ryan AJ, ed. Drugs and the athlete. Contemporary Exercise and Sports Medicine Series. Philadelphia: FA Davis Co, 1989.
Zvosec DL, Smith SW, McCurcheon JR, et al. Adverse events, including death, associated with the use of 1, 4-butanediol. N Engl J Med 2001;344:87.
The Female Athlete/Maturational Issues
American Academy of Pediatrics, Committee on Sports Medicine. Amenorrhea in adolescent athletes. Pediatrics 1989;84:394.
American Academy of Pediatrics, Committee on Sports Medicine and Fitness. Medical concerns of the female athlete. Pediatrics 2000;106:610.
Ayers JWT, Gidwani GP, Schmidt IMV, et al. Osteopenia in hypoestrogenic young women with anorexia nervosa. Fertil Steril 1984;41:224.
Barrow GW, Saha S. Menstrual irregularity and stress fractures in collegiate female distance runners. Am J Sports Med 1988;16:209.
Bennell KL, Malcolm SA, Thomas SA, et al. Risk factors for stress fractures in track and field athletes. Am J Sports Med 1996;24:810.
Bennell K, White S, Crossley K. The oral contraceptive pill: a revolution for sports women? Br J Sports Med 1999;33:231.
Bernstein L, Henderson BE, Hanisch R, et al. Physical exercise and reduced risk of breast cancer in young women. J Natl Cancer Inst 1994;86:1403.
Birch K. Female athlete triad. BMJ 2005;330:244.
Cann CE, Martin MC, Genant HK, et al. Decreased spinal mineral content in amenorrheic women. JAMA 1984;251:626.
Castro J, Sazaro L, Pons F, et al. Predictors of bone mineral density reductions in adolescents with anorexia nervosa. J Am Acad Child Adolesc Psychiatry 2000;39:1365.
Constantini NW, Warren MP. Physical activity, fitness, and reproductive health in women: clinical observations. In: Bouchard C, Shepard RJ, Stephens T, eds. Physical activity, fitness, and health. Champaign, IL: Human Kinetics, 1994.
P.295
Copeland PM, Sacks NR, Herzog DB. Longitudinal follow-up of amenorrhea in eating disorders. Psychosom Med 1995;57:121.
Daly RM, Rich PA, Klein R, et al. Short stature in competitive prepubertal and early pubertal male gymnasts: the result of selection bias or intense training? J Pediatr2000;137:510.
Damien E, Price JS, Lanyon LE. The estrogen receptor's involvement in osteoblasts' adaptive response to mechanical strain. J Bone Miner Res 1998;13:1275.
Damsgaard R, Bencke J, Matthiesen G, et al. Is prepubertal growth adversely affected by sport? Med Sci Sports Exerc 2000;32:1698.
Drinkwater BL, Bruemner B, Chesnut CH III. Menstrual history as a determinant of current bone density in young athletes. JAMA 1990;263:545.
Drinkwater BL, Nelson K, Chestnut CH, et al. Bone mineral content of amenorrheic and eumenorrheic athletes. N Engl J Med 1984;311:277.
Drinkwater BL, Nilson K, Ott S, et al. Bone mineral density after resumption of menses in amenorrheic athletes. JAMA 1986;256:380.
Dueck CA, Matt KS, Manore MM, et al. Treatment of athletic amenorrhea with a diet and training intervention program. Int J Sport Nutr 1996;6:24.
Elliot DL, Goldberg L, Loprinzi M. Management of suspected iron deficiency: A cost-effectiveness model. Med Sci Sports Exerc. 1991;23:1332.
Fagan KM. Pharmacologic management of athletic amenorrhea. Clin Sports Med 1998;17:327.
Frisch RE, Wyshak G, Albright NL, et al. Lower prevalence of non-reproductive system cancer among female former college athletes. Med Sci Sports Exerc 1989;21:250.
Gibson JH, Mitchell A, Reeve J, et al. Treatment of reduced bone mineral density in athletic amenorrhea: a pilot study. Osteoporos Int 1999;10:284.
Goodman LR, Warren MP. The female athlete and menstrual function. Curr Opin ObstetrGynecol 2005;17:466.
Gortmaker SL, Dietz WH, Sobol AN, et al. Increasing pediatric obesity in the US. Am J Dis Child 1987;14:535.
Grinspoon S, Baum H, Lee K, et al. Effects of short-term recombinant human insulin-like growth factor I administration on bone turnover in osteopenic women with anorexia nervosa. J Clin Ednocrinol Metab 1996;81:3864.
Gruelich WW & Pyle SI. Radiographic atlas of the skeletal development of the hand and wrist, 2nd Edition. Stanford, CA: Stanford University Press, 1959.
Gulekli B, Davies MC, Jacos HS. Effect of treatment on established osteoporosis in young women with amenorrhea. Clin Endocrinol 1994;41:275.
Haberland CA, Seddick D, Marcus R, et al. A physician survey of therapy for exercise-induced amenorrhea: a brief report. Clin J Sports Med 1995;5:246.
Hergenroeder AC, Smith EO, Shypailo R, et al. Bone mineral changes in young women with hypothalamic amenorrhea and oligomenorrhea treated with oral contraceptive pills, medroxyprogesterone, and placebo over 12 months. Am J Obstet Gynecol 1997;176:1017.
Hewett TE, Lindenfeld TN, Riccobene JV, et al. The effect of neuromuscular training on the incidence of knee injury in female athletes. Am J Sports Med 1999;27:699.
Hobart JA, Smucker DR. The female athlete triad. Am Fam Physician 2000;61:3357.
Hotta M, Shibasaki T, Sato K, et al. The importance of body weight history in the occurrence and recovery of osteoporosis in patients with anorexia nervosa: evaluation by dual X-ray absorptiometry and bone metabolic markers. Eur J Endocrinol 1998;139:276.
Jonnavithula S, Warren MP, Fox RP, et al. Bone density is compromised in amenorrheic women despite return of menses: a 2-year study. Obstet Gynecol 1993;81:669.
Klibanski A, Biller B, Schoenfeld D, et al. The effect of estrogen administration on trabecular bone loss in young women with anorexia nervosa. J Clin Endocrinol Metab1995;80:898.
Kleerekoper M, Briensa RS, Schultz LR, et al. Oral contraceptive use may protect against low bone mass. Arch Intern Med 1991;151:1971.
Leonard MB, Properi KJ, Zemel BS, et al. Discrepancies in pediatric bone mineral density reference data: potential for misdiagnosis of osteopenia. J Pediatr 1999;135:182.
Loucks AB. Physical activity, fitness, and female reproductive morbidity. In: Bouchard C, Shepard RJ, Stephens T, eds. Physical activity, fitness, and health. Champaign, IL: Human Kinetics, 1994.
Lindberg JS, Powell M, Hunt MM, et al. Increased vertebral bone mineral in response to reduced exercise in amenorrheic runners. West J Med 1987;146:39.
Lindholm C, Hagenfeldt K, Ringertz B-M. Pubertal development in elite juvenile gymnasts: effects of physical training. Acta Obstet Gynecol Scand 1994;73:269.
Lloyd T, Chinchilli VM, Hohnson-Rollings N, et al. Adult female hip bone density reflects teenage sports-exercise patterns but not teenage calcium intake. Pediatrics 2000;106:40.
Malina RM. Physical activity and training: effects on stature and the adolescent growth spurt. Med Sci Sports Exerc 1994;26:759.
Malina RM. Issues in normal growth and maturation. Curr Opin Endocrinol Diabetes 1995;2:83.
Marcus R, Cann C, Madvig P, et al. Menstrual function and bone mass in elite women distance runners: endocrine and metabolic features. Ann Intern Med 1985;102:158.
Michaelsson K, Baron JA, Farahmand BY, et al. Oral contraceptive use and risk of hip fracture: a case-control study. Lancet 1999;353:1481.
Myburgh KH, Hutchins J, Fataar AB, et al. Low bone density is an etiologic factor for stress fractures in athletes. Ann Intern Med 1990;113:754.
National Heart Lung and Blood Institute. Indexes of obesity and comparisons with the previous national survey data in 9- and 10-year old black and white girls: The NHLBI Growth and Health Study. J Pediatr. 1994;124:675.
Nichols JF, Rauh MJ, Lawson MJ, et al. Prevalence of the female athlete triad syndrome among high school athletes. Arch Pediatr Adolesc Med 2006;160:137.
Prior JC, Vigna YM, Schechter MT, et al. Spinal bone loss and ovulatory disturbances. N Engl J Med 1990;323:1221.
Recker R, Davies KM, Hinders SM, et al. Bone gain in young adult women. JAMA 1992;68:2403.
Rencken ML, Chesnut CH, Drinkwater BL. Bone density a multiple skeletal sites in amenorrheic athletes. JAMA 1996;276:238.
Reubinoff BE, Grubstein A, Meirow D, et al. Effects of low-dose estrogen oral contraceptives on weight, body composition, and fat distribution in young women. Fertil Steril1995;63:516.
Rockwell JC, Sorensen AM, Baker S, et al. Weight training decreases vertebral bone density in premenopausal women: a prospective study. J Clin Endocrinol Metab 1990;71:988.
P.296
Seeman E, Karlsson MK, Duan Y. On exposure to anorexia nervosa, the temporal variation in axial and appendicular skeletal development predisposes to site-specific deficits in bone size and density: a cross-sectional study. J Bone Miner Res 2000;15:2259.
Seeman E, Szmukler GI, Formica C, et al. Osteoporosis in anorexia nervosa: the influence of peak bone density, bone loss, oral contraceptive use, and exercise. J Bone Miner Res1992;7:1467.
Sundgot-Borger J, et al. Normal bone mass in bulimic women. J Clin Endocrinol Metab 1998;9:3144.
Theintz GE, Howald H, Weiss U, et al. Evidence for a reduction of growth potential in adolescent female gymnasts. J Pediatr 1993;122:306.
Vehaskari V, Rapola J. Isolated proteinuria: Analysis of a school-age population. J Pediatr. 1982;101:661.
Warren MP, Brooks-Gunn J, Hamilton LH, et al. Scoliosis and fractures in young ballet dancers: relation to delayed menarche and secondary amenorrhea. N Engl J Med1986;314:1348.
World Health Organization. Assessment of fracture risk and its application to screening for postmenopausal osteoporosis. WHO technical report series. Geneva: WHO, 1994.
Yeager KK, Agostini R, Nattiv A, et al. The female athlete triad: disordered eating, amenorrhea and osteoporosis. Med Sci Sports Exerc 1993;25:775.
Yetman AT, McCrindle BW, MacDonald C, et al. Myocardial bridging in children with hypertrophic cardiomyopathy: A risk factor for sudden death. N Engl J Med. 1998;339:1201.