Adolescent Health Care: A Practical Guide

Chapter 18

Guidelines for Physical Activity and Sports Participation

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:

  1. Increase the proportion of adolescents in grades 9 through 12 who engaged in moderate physical activity for at least 30 minutes on 5 or more of the previous 7 days from 20% in 1997 to 30%.
  2. Increase the proportion of adolescents in grades 9 through 12 who engaged in vigorous physical activity that promotes cardiorespiratory fitness for 20 or more minutes per occasion on 3 or more days per week from 64% in 1997 to 85%.

All health care professionals caring for adolescents should therefore be prepared to:

  1. Promote physical activity for all adolescents
  2. Assess the risks associated with athletic participation for individual adolescents
  3. Advise on prevention strategies for athletic injury and illness
  4. Diagnose and manage common activity-related morbidities and conditions

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:

  1. Body composition
  2. Cardiovascular fitness—maximum oxygen consumption (VO2max) being the gold standard
  3. Strength
  4. Flexibility


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
Classification of Sports by Contact

Contact or Collision

Limited Contact


a Participation not recommended by the American Academy of Pediatrics.
b The American Academy of Pediatrics recommends limiting the amount of body checking allowed for hockey players 15 years and younger to reduce injuries.
c Snowboarding has been added since previous statement was published.
d Dancing has been further classified into ballet, modern, and jazz since previous statement was published.
e A race (contest) in which competitors use a map and compass to find their way through unfamiliar territory.
From Committee on Sports Medicine and Fitness. Medical conditions affecting sports participation. Pediatrics 2001;107:1205, with permission.









Body building

Field hockey

Canoeing or kayaking (white water)




Canoeing or kayaking (flat water)



Crew or rowing

Ice hockeyb

 High jump



 Pole vault


Martial arts

Floor hockey








Ski jumping






Team handball

Horseback riding


Water polo


 Shot put









Power lifting



Race walking






Rope jumping









Scuba diving






Table tennis





Ultimate frisbee




Weight lifting


Windsurfing or surfing


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


(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 (


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:

  1. Establish a 10-repetition maximum (i.e., the maximum weight that can be lifted 10 times), called the 10-rep max.
  2. To start resistance training, perform one set of 10 repetitions at 50% to 75% of the 10-rep max.
  3. Then perform a second set of 10 repetitions at 75% of the 10-rep max.
  4. Perform a third set at 100% of the 10-rep max, doing as many repetitions as possible.

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.


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 ( 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


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.


The primary objectives of the PPE, as stated in THE MONOGRAPH, include the following:

  1. Screening for conditions that may be life-threatening or disabling
  2. Screening for conditions that may predispose to injury or illness
  3. Meeting administrative requirements

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.


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 ( 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:

  1. Past injuries that caused the athlete to miss a game or practice. The clinician may need to ask, for example: Have you ever had a muscle pull? A pinched nerve? A back injury? The clinician may have to ask the same question in different ways: Have you ever fractured a bone? Have you ever broken a bone? Other athletes may not volunteer information if they think it will result in exclusion from sports participation.
  2. Any loss of consciousness or memory occurring after a head injury.
  3. Previous exclusion from sports for any reason.
  4. Allergies, asthma, or exercise-induced bronchospasm.
  5. Medications and supplements, used currently or in the last 6 months.
  6. The menstrual history in females.
  7. A history of relatively rapid increase or decrease in body weight and the athlete's perception of current body weight.

In addition, the AHA recommends the following questions for cardiovascular screening (Maron et al., 1996):

  1. Family history of premature death (sudden or otherwise).
  2. Family history of heart disease in surviving relatives; significant disability from cardiovascular disease in close relatives younger than 50 years; or specific knowledge of the occurrence of certain conditions (hypertrophic cardiomyopathy [HCM], long QT syndrome, Marfan syndrome, or clinically important arrhythmias).
  3. Personal history of heart murmur.
  4. Personal history of systemic hypertension.
  5. Personal history of excessive fatigability.
  6. Personal history of syncope, excessive or progressive shortness of breath, or chest pain or discomfort, particularly with exertion.

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:

  1. Height, weight, and body mass index (BMI): Obesity, by itself, is not a reason for exclusion. However, the increased risk of heat illness and how that risk might be reduced must be mentioned to the athlete, parent, and coach.
  2. Blood pressure and pulse: Blood pressure and pulse: Blood pressure should be taken in the right arm with the athlete sitting. Athletes with hypertension should be evaluated further but not excluded from participation unless the hypertension is severe, as discussed later. Pulse rate can be as low as 25 bpm in highly trained aerobic athletes. A pulse in the 40- to 50-bpm range is routine and does not need evaluation if the athlete is asymptomatic.
  3. Visual acuity and pupil equality: Visual acuity and pupil equality: Teens with corrected visual acuity worse than 20/40 in one or both eyes should be referred for further evaluation but are not excluded from participation if protective eyewear is worn. It is important that anisocoria be noted before any closed head injury occurs.




FIGURE 18.1 Preparticipation sports evaluation form. (From the Ohio High School Athletic Association (OHSAA),, with permission.)



  1. Skin: Infections that are highly contagious (e.g., varicella, impetigo) should be identified. Players with these infections need to be noninfectious before returning to sports in which skin-to-skin contact is possible (Table 18.2).
  2. Teeth and mouth: These are examined only if the history suggests an acute problem.
  3. Cardiac examination: AHA recommendations for PPE cardiac examination include the following (Maron et al., 1996):
  4. Perform precordial auscultation in supine and standing positions to identify heart murmurs consistent with dynamic left ventricular outflow obstruction.
  5. Assess femoral artery or lower extremity pulses to exclude coarctation of the aorta.
  6. Recognize the physical stigmata of Marfan syndrome; refer the teenager for further evaluation if a male taller than 6 ft or a female taller than 5 ft 10 in. has a family history of two of the following:
  • Kyphosis
  • High-arched palate
  • Pectus excavatum
  • Arachnodactyly
  • Arm span > height
  • Murmur (mitral valve prolapse or aortic)
  • Myopia
  • Lens dislocation
  • Thumb or wrist signs
  1. Assess brachial artery blood pressure in the sitting position.
  2. Document the presence of murmurs, clicks, or rubs (see Chapter 14). Normal or physiological murmurs are characteristically <4/6 systolic murmurs that decrease from supine to standing with no diastolic component, and with a normal physiological split second heart sound (S2). The murmur of HCM, if one is present, may sound like a normal murmur except that it increases in intensity when the patient moves from the supine to the standing position.
  3. Abdomen: Organomegaly is a disqualifying condition for collision/contact or limited-contact sports until definitive evaluation and individual assessment for clearance has been completed.
  4. Genitalia: An undescended testicle is not a contraindication to participation in contact sports; however, the player should wear a protective cup to protect the other, descended testis. An evaluation for the unidentified testis is necessary.
  5. Sexual maturation stage: Tanner stage assessment for sexual maturity is appropriate for adolescents, but it has no role in deciding whether the teen should play a given sport.
  6. Musculoskeletal screening: General musculoskeletal screening should include muscle strength, range-of-motion and joint-stability testing, and evaluation for structural abnormalities of major joints (e.g., ankle, knee, shoulder, elbow, back). An efficient musculoskeletal screening examination is demonstrated in Figures 18.2, 18.3, 18.4, 18.5,18.6, 18.7, 18.8, 18.9, 18.10, 18.11. A more in-depth examination of the specific body parts should be pursued if there are concerns from the history or general screening examination (listed in parentheses are diagnoses to consider if the examination finding is abnormal):
  7. Body symmetry (Figs. 18.2, 18.3, 18.4, 18.5, 18.6, 18.7, 18.8, 18.9, 18.10, 18.11): Observe the adolescent standing with arms at the sides, dressed in shorts and a shirt that allows inspection of the distal quadriceps muscles and acromioclavicular joints, respectively. Look for the following:
  • Head tilted or turned to side (consider primary cervical spine injury, primary or secondary trapezius, or cervical muscle spasm)
  • Asymmetry of shoulder heights (trapezius spasm, shoulder injury, scoliosis)
  • Enlarged acromioclavicular joint (previous acromioclavicular joint sprain, shoulder separation)
  • Asymmetrical iliac crest heights (scoliosis or leg length difference, back spasm)
  • Swollen knee; prominent tibial tuberosity (any knee injury, Osgood-Schlatter disease). Ask the athlete to contract (“tighten”) the quadriceps muscles, and look for atrophy of the vastus medialis obliquus, a characteristic of any knee or lower extremity injury in which the athlete avoids normal use of that leg.
  • Swollen ankle (unrehabilitated ankle sprain)
  1. Neck examination (Fig. 18.3): This is especially important in players with a previous history of neck injury and brachial plexopathy (referred to as stingersor burners).
  • Have the athlete do the following maneuvers:
  • –Look at the floor (cervical flexion).
  • –Look at the ceiling (cervical extension).
  • –Look over the left shoulder, then over the right shoulder (left and right rotation, respectively).
  • –Put right ear on right shoulder, then left ear on left shoulder (right and left lateral flexion).
  • Look for limited or asymmetrical motion with the maneuvers listed (neck injury, congenital cervical abnormalities). Any athlete with limitation of range of motion(ROM),weakness or pain on neck examination is excluded from contact or collision sports until further evaluation.
  1. Shoulder examination (Fig. 18.4)
  • Have the athlete raise the arms from the side and touch the hands above the head, keeping elbows extended (full abduction). Look for the following:
  • –Asymmetric elevation of shoulder before arms reach 90 degrees (shoulder weakness due to a brachial plexopathy, shoulder instability, impingement syndrome).
  • –Inability to raise arms to full abduction position (shoulder weakness due to brachial plexopathy, impingement syndrome, or apprehension from subluxation or dislocation).
  • Have athlete hold the arms in front of the body (forward flexion) and then to the side (90 degrees abduction); examiner should push the hands down. Look for asymmetrical atrophy or fasciculations of anterior and middle deltoid muscles and pain and/or weakness (may be indicative of a variety of shoulder problems).
  • Have athlete put hands behind head (maximal external rotation/abduction). Look for the following:
  • –Inability to get hand behind head (i.e., lack of external rotation of shoulder).
  • –Apprehension or inability to pull the elbows, symmetrically, posterior to the shoulder (anterior subluxation or dislocation).
  • – An athlete with limitation of motion should be evaluated further before clearance is granted for further participation.







TABLE 18.2
Medical Conditions and Sports Participation


May Participate?

aThis table is designed for use by medical and nonmedical personnel.
“Needs evaluation” means a physician with appropriate knowledge and experience should assess the safety of a given sport for an athlete with the listed medical condition. Unless otherwise noted, this is because of the variability of the severity of the disease, the risk of injury for the specific sports listed in the preceding text, or both.
From Committee on Sports Medicine and Fitness. Medical conditions affecting sports participation. Pediatrics 2001;107:1205, with permission.

Atlantoaxial instability (instability of the joint between cervical vertebrae 1 and 2)

Qualified yes

 Explanation: Athlete needs evaluation to assess risk of spinal cord injury during sports participation.


Bleeding disorder

Qualified yes

 Explanation: Athlete needs evaluation.


Cardiovascular diseases


 Carditis (inflammation of the heart)


  Explanation: Carditis may result in sudden death with exertion.


 Hypertension (high blood pressure)

Qualified yes

  Explanation: Those with significant essential (unexplained) hypertension should avoid weight and power lifting, body building, and strength training; those with secondary hypertension (hypertension caused by a previously identified disease) or severe essential hypertension need evaluation. The National High Blood Pressure Education Working group defined significant and severe hypertension.


 Congenital heart disease (structural heart defects present at birth)

Qualified yes

  Explanation: Those with mild forms may participate fully; those with moderate or severe forms and those who have undergone surgery need evaluation. The 36th Bethesda Conference defined mild, moderate, and severe disease for common cardiac lesions.


 Dysrhythmia (irregular heart rhythm)

Qualified yes

  Explanation: Those with symptoms (chest pain, syncope, dizziness, shortness of breath, or other symptoms of possible dysrhythmia) or evidence of mitral regurgitation (leaking) on physical examination need evaluation. All others may participate fully.


 Heart murmur

Qualified yes

  Explanation: If the murmur is innocent (does not indicate heart disease), full participation is permitted; otherwise the athlete needs evaluation (see Congenital heart disease and Mitral valve prolapse discussed earlier).


Cerebral palsy

Qualified yes

 Explanation: Athlete needs evaluation.


Diabetes mellitus


 Explanation: All sports can be played with proper attention to diet, blood glucose concentration, hydration, and insulin therapy. Blood glucose concentration should be monitored every 30 min during continuous exercise and 15 min after completion of exercise.



Qualified no

 Explanation: Unless disease in mild, no participation is permitted, because diarrhea may increase the risk of dehydration and heat illness (see “Fever” in this table).


Eating disorders

Qualified yes

 Anorexia nervosa


 Bulimia nervosa


  Explanation: These patients need both medical and psychiatric assessment before participation.




 Functionally one-eyed athlete

Qualified yes

 Loss of an eye


 Detached retina


 Previous eye surgery or serious eye injury


  Explanation: A functionally one-eyed athlete has a best corrected visual acuity of <20/40 in the eye with worse activity. These athletes would suffer significant disability if the better eye were seriously injured, as would those with loss of an eye. Some athletes who have previously undergone eye surgery or had a serious eye injury may have an increased risk of injury because of weakened eye tissue. Availability of eye guards approved by the American Society for Testing Materials (ASTM) and other protective equipment may allow participation in most sports, but this must be judged on an individual basis.




 Explanation: Fever can increase cardiopulmonary effort, reduce maximum exercise capacity, make heat illness more likely, and increase orthostatic hypotension during exercise; fever may rarely accompany myocarditis or other infections that may make exercise dangerous.


Heat illness, history of

Qualified yes

 Explanation: Because of the increased likelihood of recurrence, the athlete needs individual assessment to determine the presence of predisposing conditions and to arrange a prevention strategy.




 Explanation: Because of the apparent minimal risk to others, all sports may be played that the athlete's state of health allows. In all athletes, skin lesions should be covered properly and athletic personnel should use universal precautions when handling blood or body fluids with visible blood.


Human immunodeficiency virus infection


 Explanation: Because of the apparent minimal risk to others, all sports may be played as allowed by the athlete's state of health; in all athletes, skin lesions should be covered properly, and athletic personnel should use universal precautions when handling blood or body fluids with visible blood.


Kidney, absence of one

Qualified yes

 Explanation: Athlete needs individual assessment for contact/collision and limited-contact sports.


Liver, enlarged

Qualified yes

 Explanation: If the liver is acutely enlarged, participation should be avoided because of risk of rupture; if the liver is chronically enlarged, individual assessment is needed before collision/contact or limited-contact sports are played.


Malignant neoplasm

Qualified yes

 Explanation: Athlete needs individual assessment.


Musculoskeletal disorders

Qualified yes

 Explanation: Athlete needs individual assessment.


Neurological disorders


 History of serious head or spine trauma, severe or repeated concussions, or craniotomy

Qualified yes

  Explanation: Athlete needs individual assessment for collision, contact or limited-contacted sports, and also for noncontact sports if deficits in judgment or cognition are present; research supports a conservative approach to management of concussion.


  Seizure disorder, well controlled


   Explanation: Risk of seizure during participation is minimal.


  Seizure disorder, poorly controlled

Qualified yes

   Explanation: Athlete needs individual assessment for collision/contact or limited-contact sports. The following noncontact sports should be avoided: archery, riflery, swimming, weight or power lifting, strength training, and sports involving heights. In these sports, occurrence of a seizure may be a risk to self or others.



Qualified yes

 Explanation: Because of the risk of heat illness, obese persons need careful acclimatization and hydration.


Organ transplant recipient

Qualified yes

 Explanation: Athlete needs individual assessment.


Ovary, absence of one


 Explanation: Risk of severe injury to the remaining ovary is minimal.


Respiratory conditions


 Pulmonary compromise including cystic fibrosis

Qualified yes

  Explanation: Athlete needs individual assessment, but generally all sports may be played if oxygenation remains satisfactory during a graded exercise test. Patients with cystic fibrosis need acclimatization and good hydration to reduce the risk of heat illness.




  Explanation: With proper medication and education, only athletes with the most severe asthma will have to modify their participation.


 Acute upper respiratory infection

Qualified yes

  Explanation: Upper respiratory obstruction may affect pulmonary function; athlete needs individual assessment for all but mild disease (see “Fever” in this table).


Sickle cell disease

Qualified yes

 Explanation: Athlete needs individual assessment. In general, if status of the illness permits, all but high-exertion, collision, or contact sports may be played. Overheating, dehydration, and chilling must be avoided.


Sickle cell trait


 Explanation: It is unlikely that individuals with sickle cell trait have an increased risk of sudden death or other medical problems during athletic participation except under the most extreme conditions of heat, humidity, and possibly increased altitude. These individuals, like all athletes, should be carefully conditioned, acclimatized, and hydrated to reduce any possible risk.


Skin disorders: boils, herpes simplex, impetigo, scabies, molluscum contagiosum

Qualified yes

 Explanation: While the patient is contagious, participation in gymnastics with mats, martial arts, wrestling, or other collision, contact, or limited-contact sports is not allowed.


Spleen, enlarged

Qualified yes

 Explanation: Patients with acutely enlarged spleens should avoid all sports because of risk of rupture; those with chronically enlarged spleens need individual assessment before playing collision, contact, or limited-contact sports.


Testicle, absent or undescended


 Explanation: Certain sports may require a protective cup.

  1. Elbow and hand
  • Have athlete extend and flex elbows with arms to the side (90 degrees abduction) (Fig. 18.5). Look for asymmetrical elbow extension or flexion (prior dislocation or fracture, osteochondritis dissecans).
  • With arms at sides and elbows flexed 90 degrees, have the athlete pronate and supinate forearms (Fig. 18.6). Look for asymmetrical loss of motion (residual of forearm fractures, Little League elbow, osteochondritis dissecans of elbow). The cause of a limitation in ROM of the elbow should be established before a young athlete is cleared for participation, especially in throwing sports.
  • In the same position, have the athlete spread fingers, then make a fist (Fig. 18.7). Look for lack of finger flexion, swollen joints, finger deformities (residuals of sprains, fractures). Hand injuries should be evaluated and recommendations for sports participation based on the severity of the injury and the specific sport the athlete desires to play should be made. Typically, the athlete is not excluded from participation unless there is a complication of a previous fracture or tendon rupture that needs further assessment.
  1. Back and leg observation
  • Have the patient stand facing away from the examiner (Fig. 18.8). Look for the following:
  • –Asymmetry of waist (scoliosis, leg-length difference)
  • –Elevated shoulder (scoliosis or trapezius spasm from shoulder or neck injury)
  • –Depressed shoulder (scoliosis, muscle weakness)
  • –Prominent rib cage (scoliosis)
  • –Increased lordosis (spondylolysis, tight hip flexors, weak hamstrings)
  • –Idiopathic scoliosis is not a contraindication for sports participation in almost all cases, unless the angle is severe (i.e., a Cobb angle >45 degrees). If pain is present or there is a left major thoracic or lumbar scoliosis, then the diagnosis may not be idiopathic scoliosis and a definitive diagnosis should be established. This should include a neurological examination and magnetic resonance imaging (MRI) of the spine.



  • Have athlete bend forward at waist/hips (lumbar flexion) to touch toes (Fig. 18.9). Look for the following:
  • –Twisting or deviating of side (paraspinous muscle spasm)
  • –Asymmetrical prominence of rib cage (scoliosis)
  • –Inability to reverse the lumbar lordosis (spondylolysis, paraspinous muscle spasm caused by a chronic inflammatory condition such as ankylosing spondylitis)
  • Have athlete stand straight and rise onto toes (Fig. 18.10). Look for the following:
  • –Asymmetry of heel elevation (calf weakness, restricted ankle motion from sprain or fracture)
  • –Asymmetry of gastrocnemius (atrophy from incompletely rehabilitated ankle or leg injury)
  • Have athlete rise onto heels. Look for the following:
  • –Asymmetry of elevation of forefoot or toes (weakness of ankle dorsiflexors, limitation of ankle motion from ankle fracture or sprain)
  • –If asymmetry on toe or heel raising is detected, further evaluation and treatment is indicated before the athlete is cleared for full sports participation.
  1. Hip, knee, and ankle screening: Have athlete slowly assume a painless squatting position (buttocks on heels) (Fig. 18.11). If the athlete cannot do this, then further evaluation is indicated. Ask athlete to take four steps forward in this squatting position (“duck walk”), then turn 180 degrees in this squatting position and take four more steps. Look for the following:
  • Asymmetry of heel height off ground (limited ankle motion or Achilles tendon tightness from tendonitis or injury).
  • Asymmetrical knee flexion, that is, difference in heel-to-buttock height from the rear view or inability to get down as far on one side as on the other (knee effusion, residual limitation of motion from sprain, torn meniscus, quadriceps tightness or weakness, patellofemoral pain, Osgood-Schlatter disease).
  • Pain at any point in the range of knee flexion. The cause of the pain should be established and the patient rehabilitated before allowing return to participation without restrictions.
  1. Ankle screening: Have the athlete hop five times as high as possible on each foot. Inability to do so suggests an undiagnosed or unrehabilitated lower leg, ankle, or foot injury. The ankle should be evaluated and fully rehabilitated before full participation is allowed.

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


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:

  1. Cleared without restriction
  2. Cleared, with recommendations for further evaluation or treatment
  3. Clearance withheld pending further evaluation, treatment, or rehabilitation
  4. Not cleared for certain types of sports or for all sports

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


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


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 Specific conditions are discussed in the subsequent text.

  1. Mitral valve prolapse (see Chapter 14)
  2. Studies of mitral valve prolapse in healthy young adults with no known cardiac disease report a prevalence of 0.6% to 2.7% (Flack et al., 1999; Gilon et al., 1999).
  3. Mitral valve prolapse is generally a benign, asymptomatic condition. Patients can have palpitations, dizziness, supraventricular and ventricular arrhythmias, and chest pain, in which case they should be excluded from sports until they are fully evaluated. Sudden cardiac death in patients with mitral valve


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.)

  1. Patients with mitral valve prolapse can participate in all competitive sports unless the following exist:
  • A history of syncope documented to be arrhythmogenic in origin.
  • A family history of sudden death associated with mitral valve prolapse.
  • Repetitive forms of supraventricular and ventricular arrhythmias, particularly if exaggerated by exercise.
  • Moderate to marked mitral regurgitation.
  • Prior embolic event.
  • LV systolic ejection fraction <50%.
  1. Athletes with mitral valve prolapse andany of the symptoms just listed may participate only in low-intensity sports (i.e., low static, low dynamic—see Figure 18.12, Class IA).
  2. Asymmetrical septal hypertrophy or HCM
  3. This is a primary abnormality of the myocardium manifested as an asymmetrically hypertrophied, nondilated left ventricle in the absence of a cardiac or systemic disease that could cause left ventricular hypertrophy (LVH).
  4. The mechanism of sudden death is not established, but a factor may be arrhythmia or myocardial ischemia related to myocardial bridging across coronary arteries. This suggests a role for angiography in patients with HCM (Yetman et al., 1998).
  5. In many cases there are no symptoms before the sudden death. When present, the symptoms include exertional dyspnea, angina pectoris, fatigue, and/or syncope.
  6. There is increased intensity of murmur from supine to standing.



  1. There may be a family history of early sudden death, particularly related to exercise.
  2. The diagnosis is made by demonstrating left ventricular wall thickness >15 mm, although some highly trained athletes can have a left ventricular thickness of up to 16 mm, and some patients with HCM, especially young, growing adolescents, can have a thickness <15 mm.
  3. Athletes with HCM must be evaluated by a cardiologist before participation.
  4. Recommendations for participation in sports are as follows:
  • Athletes with the unequivocal diagnosis of HCM should not participate in most competitive sports, with the possible exception of low-intensity sports (Fig. 18.12, Class IA). This applies to athletes with and without evidence of left ventricular outflow obstruction.
  • There is currently no compelling evidence to preclude athletes with genotype positive for HCM who do not have phenotypic manifestations (i.e., normal echocardiogram), family history of sudden death, or any cardiac symptoms on history.

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.)

  1. Coronary artery anomalies
  2. These are rare overall; they should be suspected if the evaluation of syncope or anginal chest pain during exercise is normal.
  3. They may lead to sudden death. Identification before death is difficult because many patients are asymptomatic before the sudden death event.
  4. The cardiac examination is normal.
  5. Cardiac consultation before participation is mandatory if this condition is suspected.
  6. If coronary artery anomalies are identified, there is complete exclusion from sports participation.
  7. Myocarditis
  8. The incidence in young athletes is controversial because of the imprecise criteria for diagnosis.
  9. It is a process characterized by an inflammatory infiltrate of the myocardium with necrosis and/or degeneration of myocytes. The disease progresses through active, healing, and healed phases, and arrhythmias may occur at any time.
  10. Recommendations regarding sports participation are as follows:
  • Athletes in whom a presumptive diagnosis has been made should be excluded from all competitive


sports for 6 months and then have their ventricular function evaluated at rest and with exercise before being allowed to return to sports.

  • Athletes can return to sports when their ventricular function and dimensions are normal and clinically relevant arrhythmias are absent on ambulatory monitoring.
  • There is no strong evidence for endomyocardial biopsy as a precondition for returning to sports participation.
  1. Regarding the athlete with an acute febrile illness characterized by fever and myalgia, it seems prudent to withhold that athlete from competition. However, there is no evidence that this precaution protects against sudden death. In athletes diagnosed with sudden death related to myocarditis, there is no clear temporal pattern between the febrile illness and the sudden death.
  2. Systemic hypertension (also see Chapter 13)
  3. Although hypertension is associated with an increased risk for sudden death and complex ventricular arrhythmias, to date it has not been incriminated as a cause of sudden cardiac death in young, competitive athletes.
  4. To be consistent with JNC 7 guidelines for adults, classification of hypertension in adolescents has been revised as shown in Table 18.3. Proper measurement of blood pressure and diagnosis of hypertension is discussed in Chapter 13. Athletes with stage 1 or 2 hypertension should be screened for LVH with an echocardiogram.
  5. Athletes with stage 1 hypertension in the absence of end-organ damage, including LVH and heart disease have no restrictions, but should have BP measured every 2 to 4 months to assess the impact of exercise.
  6. Those with stage 2 hypertension should be restricted, especially from high-static sports (Fig. 18.12, Classes IIIA–C), until their blood pressure is controlled.
  7. If athletes have true LVH (in distinction from “athlete's heart”) on screening, they should be restricted from participation in high-static sports (Fig. 18.12, Classes IIIA–C) until the hypertension is controlled.

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


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
Classification of Hypertension in Adolescents


Adolescents and Childrenb (mm Hg)

Adults (mm Hg)

aBlood pressure values are based on the average of three or more readings taken at each of three or more visits after the initial screening. These definitions apply to individuals who are not taking antihypertensive drugs and are not acutely ill.
b Or adult parameters if greater.
Adapted from the 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.




<90th percentile for age, gender, and heightb








90th–95th percentile for age, gender, and heightb





Stage 1 hypertension



95th–99th percentile for age, gender, and height plus 5 mm Hgb





Stage 2 hypertension



>99th percentile for age, gender, and height plus 5 mm Hgb





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, ( 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:

High School

Incidence per 100,000 Participants





 Ice hockey















Incidence per 100,000 Participants



















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:

  1. Weakness and/or inflexibility related to a previous injury.
  2. Accelerated growth.
  3. Training errors, including too-rapid increases in pace, distance, repetitions, or weight/resistance. Training errors are the most common factor associated with overuse injuries.
  4. Inappropriate equipment (improper shoes, equipment not sized appropriately).
  5. Change in the environment, such as running up hills or on a banked track instead of a flat surface.

Injury Prevention Strategies

There are several ways of preventing injuries.

  1. Individual level interventions
  2. Recognize and fully rehabilitate old injuries. As mentioned, the most important function of the PPE may be as a quality control point for injuries and rehabilitation during the past year (Keller et al., 1987).
  3. Stretching is not likely to prevent injuries unless there is an identified deficit. Pope et al. (2000) confirmed this in a group of military recruits. The stretching methods described in that report are typical of a stretching routine for middle school and high school teams, but they are not ideal stretching exercises because they were done only once for 20 seconds. We recommend stretching of the lower extremities after weight-bearing exercise. This should include gastrocnemius, soleus, hamstring, and quadriceps stretches, held for 20 seconds each, twice per muscle-group.
  4. See “The Female Athlete” section, later in this chapter, regarding prevention of acute knee injuries in female athletes.
  5. System or environment-level interventions are far more effective in reducing injury rates.
  6. Breakaway bases (bases in baseball and softball that are not anchored to the ground) have been associated with fewer and less significant ankle and lower-leg injuries from sliding. The incidence of serious neck injuries decreased after the trampoline was removed from gymnastics competition (National Institutes of Health, 1992).
  7. Enforce rules to eliminate behavior that places athletes at high risk for injury. Serious neck injuries in football dropped precipitously after spear tackling was made illegal in football (Mueller and Cantu, 2001). As mechanisms of injury are elucidated, preventive measures can be planned. This underscores the need for continued research into the causes of sports injuries. An excellent review of the approach to the epidemiology of youth sports was published by the Conference on Sports Injuries in Youth (National Institutes of Health, 1992), but its calls have been largely unheeded in the intervening years.
  8. Future injury is best prevented by minimizing the consequences of an index injury as it occurs.

Returning to Participation

In general, athletes should not be allowed to return to participation in sports until the following criteria have been satisfied:

  1. The injury has been accurately diagnosed.
  2. The examiner is reasonably certain that the injury will not significantly worsen with continued play.
  3. The examiner is reasonably certain that continued participation (with the injury) will not result in a secondary injury.
  4. The athlete has achieved full ROM and strength in the injured joint.
  5. The athlete wants to return to play.

The following are examples of injuries or conditions that preclude returning to sports until the criteria just listed have been fulfilled:

  1. Unconsciousness, however brief (see “Neurological Concussion” section)
  2. Any neurological abnormalities
  3. Obvious swelling
  4. Limited ROM
  5. Pain within the normal ROM
  6. Bleeding
  7. An injury the examiner does not know how to manage
  8. Obvious loss of normal function
  9. Athlete's lack of desire to return to play

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.



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).


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).


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.


The consensus panel recommends that clinicians appreciate that concussion in sport may either be simple or complex, but that this classification is made retrospectively.

  1. Simple concussion: An athlete suffers an injury that progressively resolves without complication over 7 to 10 days.
  2. Complex concussion: Cases in which athletes suffer persistent symptoms, any other sequelae (such as seizure), prolonged loss of consciousness (>1 minute), or prolonged cognitive impairment after the injury. Recurrent concussions, especially those triggered by progressively less impact force, fall into this category as well.

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:

  1. The athlete should not be allowed to return to play in the current game or practice session.
  2. The athlete should not be left alone, and regular monitoring for deterioration is essential over the initial few hours after injury.
  3. The player should be medically evaluated after the injury.
  4. Any abnormalities on sideline neurological screening necessitate immediate formal neurological evaluation by a physician on-site or at a medical facility.
  5. Neuroimaging may play a part in the assessment of complex sports concussion, but are not essential for simple concussive injury if not indicated by physical examination findings.
  6. Return to play must follow a medically supervised stepwise process (i.e., no predetermined time frames for exclusion).

Return to Play

Return to play follows a stepwise process, with advance of no more than one step per day:

  1. No physical activity. When completely asymptomatic for 24 hours, proceed to step 2.
  2. Light aerobic exercise such as walking or stationary cycling, but no resistance (strength) training.
  3. Sport-specific exercise may resume—for example skating in ice hockey, running with no pads in football—or beginning of resistance training.
  4. Noncontact training drills—for example with helmet and pads in football, shooting and passing in ice hockey—or increased resistance training.
  5. After medical clearance (reevaluation by physician), may participate in controlled full-contact training such as practice sessions.
  6. Game play.

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






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:

  1. Injury in and around the third ventricle, leading to memory deficits, emotion lability, and euphoria.
  2. Injury to the inferior cerebellar tonsils, manifested as slurred speech and abnormal balance.
  3. Degeneration of the basal ganglia, leading to Parkinson disease.
  4. Diffuse neuronal loss, leading to a picture that is similar to Alzheimer disease.

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:.

  1. History of head trauma including loss of consciousness and posttraumatic amnesia
  2. Evidence of difficulty in attention (concentrating, shifting focus of attention, performing simultaneous cognitive tasks) or memory
  3. Three or more of the following occurring shortly after the injury and lasting 3 months or longer:
  4. Easily fatigued
  5. Disordered sleep
  6. Headache
  7. Dizziness
  8. Irritability or aggression with little provocation
  9. Anxiety or depression
  10. Change in personality (social or sexual inappropriateness)
  11. Apathy or lack of spontaneity

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:

  1. Adequate on-site medical care for acute brain injuries
  2. Full medical evaluation of concussed players
  3. Strict rule enforcement
  4. Padding of the goal posts
  5. Requiring use of mouth guards
  6. Teaching proper heading technique (Green and Jordan, 1998)

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

  1. Initially, when a player's head or neck is injured, a spinal cord injury must be assumed to be present. The patient should not be moved until a diagnosis is established that would allow cervical movement. If a cervical spine injury is suspected, the first priority is to determine that the patient's cardiopulmonary status is normal. If not, basic life support measures must be instituted. The second priority is to do no harm. For a potential unstable cervical spine fracture or dislocation, this means allowing no one to move the athlete, including not taking off the helmet or rolling the patient over, until the appropriate emergency personnel are present. After personnel are present who can prepare the patient for transport, the cervical spine should be stabilized and the patient transported. Physicians who cover football games should be comfortable stabilizing and preparing for the transport of an athlete with a potential cervical spine fracture. This can be learned only through hands-on training. Of special note is the instruction to not remove any helmets. In sports where an athlete wears a helmet, they often also wear shoulder pads. Proper alignment of the cervical spine is maintained by the combination of helmet and shoulder padding. Because it is unsafe, typically, to remove the shoulder pads, it is unsafe to remove the helmet. Axial traction can be maintained through a properly fit helmet.
  2. If the patient is unconscious and has neck pain and/or radiating pain to an extremity, or has paresis or paresthesia, it should be assumed that a cervical spine injury is present. The athlete should be immobilized on a board and transported to an emergency room.
  3. If there is no motor or sensory abnormality of the extremities, no neck pain, and the patient is conscious, he/she can be allowed to walk off the field for further evaluation. If at any time the patient complains of radiating pain, paresthesia, or neck pain, the physician should consider that a cervical spine fracture is present and initiate appropriate procedures. If the physician is not comfortable with the above scenarios, then he or she should know what the protocol is for activating emergency medical services.



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:

  1. Age at menarche
  2. Frequency and duration of menstrual cycle
  3. Last menstrual period
  4. Longest time period without menstruation
  5. Physical signs of ovulation, such as dysmenorrhea
  6. Prior hormonal therapy

The diet history includes the following:

  1. Food history in last 3 days
  2. List of any restricted foods



  1. Highest and lowest weights since menarche
  2. Satisfaction with current weight and perceived ideal weight
  3. Bingeing and purging behaviors
  4. Use of laxatives, diuretics, appetite suppressants, supplements, or other pathological weight-control behaviors.

The exercise history includes the following:

  1. Exercise patterns and training intensity levels
  2. Exercise done outside of required training
  3. Compulsive exercise
  4. History of previous fractures
  5. Overuse injuries

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, 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


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:

  1. Young women with anorexia nervosa and secondary amenorrhea have mean serum estradiol levels that approximate those of postmenopausal women.
  2. Osteoporosis is one of the more serious, long-term consequences of prolonged amenorrhea in adolescent athletes.
  3. Hypoandrogenemia, reduced serum levels of insulin like growth factor I (IGF-I), and hypercortisolemia in anorexia nervosa contribute to loss of BMD. These factors improve with weight gain. They are not likely to be affected by estrogen/progestin therapy and unless they are improved, the effect of estrogen/progestin may be limited.

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


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


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

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 ( and World Anti-Doping Agencies ( when advising athletes, especially college and elite athletes, about medication and prescription drug use.

Performance-Enhancing Drugs


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.


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.


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 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


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(,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:

  1. Alteration of myocardial textural properties (as detected by ultrasound). These changes are not seen in weight lifters who do not use anabolic steroids, yet nonetheless experience increased left ventricular mass with weight training. The clinical significance and prognostic significance of these changes is unknown.
  2. Altered myocardial function: 17α-Methyl testosterone has been associated with reduced myocardial compliance and reduced myocardial function in rats.
  3. Risk of hepatic damage (manifested as elevated liver-specific enzymes): The risk of hepatic neoplasms is unknown, because the reports to date are anecdotal.
  4. Decreased high-density lipoprotein (HDL) and increased low-density lipoprotein (LDL) cholesterol levels.
  5. Oligospermia and azoospermia with decreased testicular size occurs.
  6. Premature epiphyseal closure in pubertal athletes.
  7. Acne.
  8. Masculinization in women: Manifested as deepening of the voice, acne, and hair loss.
  9. Feminization in men: Manifested as gynecomastia and a high voice.
  10. Adverse psychological effects, including increased aggressiveness and rage in some athletes.
  11. Association with the use of other illicit drugs.

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:

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, 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 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.


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 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


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 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:

  1. Written policy: A written policy regarding the purpose of the drug prevention program, the methods of collection, and consequences. In developing this plan, representatives from coaches, parents, athletes, medical staff, and physicians should be involved.
  2. Education: An educational component must be prepared and used.
  3. Testing: Actual testing must take place, preferably at random.
  4. Discipline for those who test positive: The mechanism of feedback to the player and coaches must be established. The physician should not be in the role of administering any disciplinary action; rather, he or she should work with the athlete to identify a problem if one exists and to facilitate appropriate care.
  5. Evaluation of treatment: A process for evaluating the treatment of drug users must be implemented.

The American College Health Association (1994) ( has also provided guidelines regarding drug education and testing of student athletes, including the following:

  1. The drug education program should reflect the institution's overall commitment to eliminating drug abuse among students, faculty, and staff. The drug education and testing programs should not be restricted to only student athletes.
  2. Each institution initiating or evaluating a drug education and testing program should have an advisory committee in place consisting of student athletes and representatives of the athletics department, student health center, counseling center, and student affairs.
  3. A single individual should direct and supervise the program.
  4. The educational program should target both the athletes and the coaches and staff of the athletic department.
  5. Legal counsel should be involved when a drug testing program is instituted.
  6. Drug testing should be done only when it is accomplished fairly and accurately.
  7. Careful review should be undertaken regarding which athletes will be tested and how often, as well as what sanctions will be imposed.
  8. The institution should guarantee that the test results and records will be handled in a strictly confidential manner.
  9. It is important that adequate counseling be available for those who test positive.
  10. Because alcohol is the most abused drug on campuses, an emphasis on alcohol education should be incorporated into the program.

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 Site connecting individuals interested in sports medicine.

P.292 Patient information from the Sports Medicine Center, Akron Children's Hospital. Your Orthopaedic Connection from the American Academy of Orthopaedic Surgeons.

For Health Professionals American Academy of Pediatrics Council on Sports Medicine and Fitness. American College of Sports Medicine. American Orthopaedic Society for Sports Medicine. National Center for Catastrophic Sports Injury Research, data on sports injuries and fatalities. National Athletic Trainers' Association communication on Appropriate Medical Care for the Secondary School-Age Athlete. American Sport Medicine Institute. Institute for Preventative Sports Medicine. American Medical Society for Sports Medicine. 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.



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.



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

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.



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.



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.