Updated: Jun 15, 2009
Exercise-induced asthma (EIA) is a condition of respiratory difficulty that is triggered by aerobic exercise and lasts several minutes. Symptoms of EIA may resemble those of allergic asthma, or they may be much more vague and go unrecognized, resulting in probable underreporting of the disease.
Exercise-induced urticaria, or anaphylaxis, is often presumed to be related to EIA, even though this condition is extremely rare and unrelated. EIA is related to histamine release.1,2,3 Only 500-1000 cases of exercise-induced urticaria have been reported in the literature. In this condition, there is an early stage of exercise-related fatigue and itchiness, followed by early onset of urticaria and angioedema, which is initially mild.4 If progression occurs, there is choking, stridor, nausea, vomiting, and even hypotension. A late stage that is marked by headache may also occur. As implied by the alternative name of anaphylaxis, EIA can be life threatening; however, this can be prevented by exercise modification or avoidance of certain conditions (see Sport-Specific Biomechanics, below).
Related eMedicine articles:
Angioedema [in the Emergency Medicine section]
Asthma [in the Pulmonology section]
Exercise-Induced Anaphylaxis [in the Pediatrics section]
Urticaria [in the Allergy and Immunology section]
EIA affects 12-15% of the population. Ninety percent of asthmatic individuals and 35-45% of people with allergic rhinitis experience EIA, but even when those with rhinitis and allergic asthma are excluded, a 3-10% incidence of EIA is seen in the general population.3
EIA seems to be more prevalent in some winter or cold-weather sports.5 Some studies have demonstrated rates as high as 35% or even 50% in competitive-caliber figure skaters, ice hockey players, and cross-country skiers.6,7
The problem in EIA occurs distal to the glottis, in the lower airway. Bronchoconstriction is involved that is distinguishable from laryngospasm, which can occur in other exercise-related conditions. One such example is the condition known as vocal cord dysfunction in which there is paradoxical narrowing of the vocal cords during inspiration, resulting in stridor that is often misconstrued as audible wheezing.8,9 Normally, the vocal cords open with inspiration. (See also the eMedicine article Vocal Cord Dysfunction.)
EIA usually affects individuals who participate in sports that include an aerobic component. The condition can be seen in any sport, but EIA is much less common in predominantly anaerobic activities. This is likely due to the role of consistent and repetitive air movement through the airways (seen in aerobic sports), which affect airway humidity and temperature. EIA triggers an unknown biochemical and neurochemical pathway, resulting in the bronchospasm, which manifests as the symptoms of the disease.
Although the exact mechanism of EIA is unknown, there are 2 predominant theories as to how the symptom complex is triggered. One is the airway humidity theory, which suggests that air movement through the airway results in relative drying of the airway. This, in turn, is believed to trigger a cascade of events that results in airway edema secondary to hyperemia and increased perfusion in an attempt to combat the drying. The result is bronchospasm.
The other theory is based on airway cooling and assumes that the air movement in the bronchial tree results in a decreased temperature of the bronchi, which may also trigger a hyperemic response in an effort to heat the airway. Again, the result is a spasm in the bronchi.
Many authors think that there may be a combination of the above 2 theories that takes place, but the biochemical or physical pathways that mediate these responses are unclear. Evidence may even exist to support the idea that the resulting cascades are not the inflammatory pathways to which we attribute allergic asthma.
Likewise, certain sports and their environments predispose individuals with asthma to experience EIA. Sports played in cold and dry environments usually result in more symptom manifestation for athletes with this condition. On the other hand, when the environment is warm and humid, the incidence and severity of EIA decrease.
Patients usually present complaining of exercise-related respiratory symptoms. This complaint is much more common among children and younger athletes but can be seen at any age.
The patient's physical examination is often unremarkable in the clinical setting; a higher yield is obtained on the field or after an exercise challenge.10 Exercise challenge, for the purpose of the physical examination, may be informal. For example, the clinician may have the athlete come to the office wearing athletic clothing and run on a treadmill or around the parking lot for 10 minutes, which is then followed by another pulmonary examination.
The causes of EIA can be divided into the categories of medical, environmental, and drug related. Eliminating some causes can diminish—but may not eliminate—the athlete's symptoms. EIA may also exist without the presence of any of these causes.
Anxiety
Hyperventilation Syndrome
Vocal Cord Dysfunction
Deconditioning syndrome
Seasonal asthma
Upper airway obstruction
Although rare, as with any asthma attack, progression of EIA can result in status asthmaticus and even death. Treatment for this condition should be provided immediately and the situation taken seriously.
On the playing field, consultation is rarely available and is not needed in the acute EIA attack; however, access to the emergency medical system should be readily available.
Treatment of the athlete who is experiencing an acute attack of EIA is the same as in any asthma attack situation and includes the following:
If the initial response to treatment was adequate, patient observation and monitoring need to continue for several hours in case of a relapse.
If patient relapse is immediate, transportation to an emergency facility should be initiated.
If mild, residual symptoms persist in the patient after relief of the acute symptoms, a repeat administration of albuterol is advisable; the recommended dosing interval is 4 hours.
Long-term treatment of EIA is prevention of the condition (see Medication).1
Nonpharmacologic measures can also be taken in the treatment of EIA.
The optimal treatment for EIA is to prevent the onset of symptoms. After controlling the patient's underlying and contributing factors (eg, respiratory infection, allergy, allergic asthma), a combination of drugs can be used to prevent EIA.1 The basis of treatment is with preexercise short-acting β2 -agonist administration.1 A role also exists for long-acting β2 -agonists and mast cell stabilizers. Antileukotriene drugs have been shown to be effective as well.12,13 Traditional asthma medications (eg, corticosteroids, theophylline) have less of a role in the treatment of pure EIA. There is ongoing investigation regarding other agents (eg, heparin, calcium-channel blockers, diuretics).
These agents are used for prophylactic bronchodilation to prevent the onset of symptoms with exercise and have been shown to have a 90% efficacy.
DOC and first-line agent. β 2 -agonist for bronchospasm that is refractory to epinephrine. Relaxes bronchial smooth muscle by action on β 2 -receptors with little effect on cardiac muscle contractility.
2 puffs via metered dose inhaler 15-30 min preexercise
1-2 puffs via metered dose inhaler 15-30 min preexercise
Caution with other sympathomimetics, MAOIs, tricyclic antidepressants, other agents that decrease potassium
Documented hypersensitivity; tachyarrhythmias; hypokalemia
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
May cause jitteriness and tachycardia; caution with hypokalemia from repetitive and frequent use
By relaxing the smooth muscles of the bronchioles in conditions that are associated with bronchitis, emphysema, asthma, or bronchiectasis, salmeterol can relieve bronchospasms. Effect may also facilitate expectoration.
Adverse effects are more likely to occur when this agent is administered at high or more frequent doses than recommended; the incidence of side effects is then higher.
2 puffs via metered dose inhaler 30-45 min preexercise or bid
1-2 puffs via metered dose inhaler 30-45 min preexercise or bid
Caution with other sympathomimetics, MAOIs, tricyclic antidepressants
Documented hypersensitivity; tachyarrhythmias; hypokalemia
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Educate patient that this agent is not to be used as a rescue treatment for acute bronchospasm; long-acting β 2 -agonists may cause more tachyphylaxis than short-acting agents.
These agents are 70-80% effective in preventing bronchospasm during exercise. An additive effect is noted when used in combination with albuterol.
First- or second-line agent in the prevention of EIA.
2 puffs via metered dose inhaler 30-45 min preexercise
1-2 puffs via metered dose inhaler 30-45 min preexercise
None reported
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Educate patient that this agent is not to be used as a rescue treatment for acute bronchospasm; avoid use with isoproterenol during pregnancy.
These agents provide no bronchodilatory effect but are useful in controlling the underlying inflammation of allergic asthma.
Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability. Does not depress the hypothalamus. Considered a third-line agent.
2-4 inhalations qd/qid; varies with preparation
<6 years: Some preparations are contraindicated
>6 years: 1-4 inhalations qd/qid; varies with preparations
None reported
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Educate patient that this agent is not to be used as a rescue treatment for acute bronchospasm.
Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability. Considered a third-line agent.
2-4 inhalations qd/qid; varies with preparation
<6 years: Some preparations are contraindicated
>6 years: 1-4 inhalations qd/bid/tid/qid; varies with preparations
None reported
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Educate patient that this agent is not to be used as a rescue treatment for acute bronchospasm; do not exceed recommended doses.
Inhibits bronchoconstriction mechanisms; produces direct smooth muscle relaxation; may decrease number and activity of inflammatory cells, in turn decreasing airway hyperresponsiveness. Considered a third-line agent.
2-4 inhalations qd/qid; varies with preparation
<6 years: Some preparations are contraindicated
>6 years: 1-4 inhalations qd/qid; varies with preparations
Coadministration with ketoconazole may increase plasma levels but do not appear to be clinically significant
Documented hypersensitivity, bronchospasm, status asthmaticus, other types of acute episodes of asthma
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Educate patient that this agent is not to be used as a rescue treatment for acute bronchospasm.
Xanthine derivatives have been used in allergic asthma for their bronchodilatory and anti-inflammatory properties; however, these agents have multiple side effects. Therefore, monitoring for nontoxic levels is necessary.
Potentiates exogenous catecholamines, stimulates endogenous catecholamine release and diaphragmatic muscular relaxation, which in turn stimulates bronchodilation.
For bronchodilation, near-toxic (>20 mg/dL) levels are usually required.
5.6 mg/kg loading dose (based on aminophylline) IV over 20 min, followed by maintenance infusion of 0.1-1.1 mg/kg/h
6 weeks to 6 months: 0.5 mg/kg/h loading dose IV in first 12 h (based on aminophylline), followed thereafter by maintenance infusion of 12 mg/kg/d; may administer continuous infusion by dividing total daily dose by 24 h
6 months to 1 year of age: 0.6-0.7 mg/kg/h, loading dose IV in first 12 h, followed by maintenance infusion of 15 mg/kg/d; may administer as continuous infusion, as above
>1 year: Administer as in adults
Aminoglutethimide, barbiturates, carbamazepine, ketoconazole, loop diuretics, charcoal, hydantoins, phenobarbital, phenytoin, rifampin, isoniazid, and sympathomimetics may decrease effects of theophylline; theophylline effects may increase with allopurinol, β -blockers, ciprofloxacin, corticosteroids, disulfiram, quinolones, thyroid hormones, ephedrine, carbamazepine, cimetidine, erythromycin, macrolides, propranolol, and interferon.
Documented hypersensitivity; patients with uncontrolled arrhythmias, peptic ulcers, hyperthyroidism, and uncontrolled seizure disorders
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in patients with peptic ulcer disease, hypertension, tachyarrhythmias, hyperthyroidism, and compromised cardiac function; do not inject IV solution >25 mg/min; patients with pulmonary edema or liver dysfunction are at greater risk of toxicity because of reduced drug clearance.
Leukotriene receptor antagonists can be used as adjuncts in cases of incompletely controlled EIA with the use of other agents; however, leukotriene receptor antagonists should be reserved for more frequent and persistent cases of EIA rather than for intermittent cases. Leukotriene receptor antagonists should not to be used alone for the treatment of EIA.
Inhibits effects by the leukotriene receptor, which has been associated with asthma, including airway edema, smooth muscle contraction, and cellular activity associated with the symptoms. Third-line agent and used as adjunct only.
20 mg PO bid
10 mg PO bid
Erythromycin and theophylline decrease serum levels; aspirin increases levels of zafirlukast; zafirlukast increases toxicity of warfarin.
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Educate patient that this agent is not to be used as a rescue treatment for acute bronchospasm; may cause liver inflammation; not for use as monotherapy in the management of EIB
Neuropsychiatric events have been reported, and following further FDA evaluation, the prescribing information has been updated to include case reports during postmarketing surveillance that include agitation, aggression, anxiousness, dream abnormalities, hallucinations, depression, insomnia, irritability, restlessness, suicidal thinking and behavior (including suicide), and tremor
Inhibits the leukotriene receptor effects associated with asthma, including airway edema, smooth muscle contraction, and cellular activity associated with the symptoms. Third-line agent and used as an adjunct only. European studies have suggested an improvement in gas exchange versus β 2 -agonist medication.
10 mg PO at least 2 h before exercise; do not repeat dose within 24 h
<15 years: Not established; some pediatric subspecialists recommend 5 mg PO qd
> 15 years: Administer as in adults
Phenobarbital and rifampin reduce effects.
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Not indicated to reverse acute asthma attacks; not for use as monotherapy in the management of EIB; use appropriate short-acting, inhaled β 2 -agonist for exacerbations; if already taking montelukast daily (eg, chronic asthma, allergic rhinitis), do not take an additional dose to prevent EIB; administration for chronic asthma has not been established to prevent acute EIB; chewable tab contains phenylalanine: caution in patients with phenylketonuria
Neuropsychiatric events have been reported, and following further FDA evaluation, the prescribing information has been updated to include case reports during postmarketing surveillance that include agitation, aggression, anxiousness, dream abnormalities, hallucinations, depression, insomnia, irritability, restlessness, suicidal thinking and behavior (including suicide), and tremor
Inhibits leukotriene formation, which in turn decreases neutrophil and eosinophil migration, neutrophil and monocyte aggregation, leukocyte adhesion, capillary permeability, and smooth muscle contractions. Third-line therapy and used as an adjunct only.
600 mg PO qid
Not established
Monitor drugs that are metabolized by cytochrome p3A4; potentiates theophylline, warfarin, and propranolol
Documented hypersensitivity; patients with active liver disease or transaminase elevation greater than or equal to 3 times the upper limit of the normal value
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Educate patient that this agent is not to be used as a rescue treatment for acute bronchospasm; monitor liver enzymes; neuropsychiatric events have been reported, and following further FDA evaluation, the prescribing information has been updated to include case reports during postmarketing surveillance that include agitation, aggression, anxiousness, dream abnormalities, hallucinations, depression, insomnia, irritability, restlessness, suicidal thinking and behavior (including suicide), and tremor
Adrenergic agonists are used in the emergency treatment of life-threatening situations, when β-agonists are unavailable or treatment with β-agonists has failed.
Has α -agonist effects that include increased peripheral vascular resistance, reversed peripheral vasodilatation, systemic hypotension, and vascular permeability. β -agonist effects of epinephrine include bronchodilation, chronotropic cardiac activity, and positive inotropic effects. Indicated in the emergency treatment of bronchospasm.
0.2-1 mg SC q4h prn
0.01 mg/kg SC q4h prn; not to exceed 0.5 mg
May potentiate the pressor effects of tricyclic antidepressants, furazolidone, antihistamines, levothyroxine, β- blockers, and guanethidine; epinephrine may be antagonized by nitrites and α-b lockers; should avoid digitalis and other arrhythmia-producing agents
Documented hypersensitivity; cardiac arrhythmias; angle-closure glaucoma; local anesthesia in areas such as fingers or toes because vasoconstriction may produce sloughing of tissue; during labor (may delay second stage of labor)
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in elderly patients and in patients with prostatic hypertrophy, hypertension, cardiovascular disease, diabetes mellitus, hyperthyroidism, and cerebrovascular insufficiency; rapid IV infusions may cause death from cerebrovascular hemorrhage or cardiac arrhythmias
The severity of an EIA attack varies greatly. Although cases of respiratory arrest and even death have been reported, the usual scenario is of a mild respiratory difficulty during play, which either spontaneously resolves or immediately responds to inhaled albuterol. Oftentimes, the athlete self-medicates and never leaves play or alerts the trainer or doctor. Although no clear-cut guidelines exist, a player who is removed from play for an asthma attack should be kept out of play until his or her respiration has normalized. This should occur within 5-10 minutes of medication administration. The athlete should be monitored closely for signs of relapse over the next several hours. If the symptoms do not completely resolve with sideline medication, the athlete should not return to play and should be referred for further treatment. Depending on the severity of the patient's symptoms, this may require transportation via ambulance.
Complications of an untreated asthma attack include status asthmaticus, respiratory failure, and even death. More commonly, an anxiety attack can be precipitated secondary to dyspnea.
The optimal treatment of EIA is to prevent the onset of symptoms. See the Medication section for a discussion of drugs used to prevent EIA.
The prognosis is excellent for athletes with asthma. With proper interventions, most symptoms can be prevented, and performance should not be limited by EIA if this condition is treated properly. Newly diagnosed young athletes need to be educated that this condition should not be perceived as an insurmountable disability. Using examples of the numerous elite athletes (eg, Jackie Joyner-Kersee [perhaps the world's greatest athlete]; Amy Van Dyken [Olympic swimmer]; Jerome Bettis [former running back for the Pittsburgh Steelers]) with this condition can help young impressionable athletes continue in their endeavors without fear of failure or medical distress.
Patient education is a critical part of the treatment of EIA. Once the diagnosis is made, athletes should be encouraged to continue in their activities with the reassurance that proper treatment can allow for an unhampered performance for most individuals. In addition to reassurance, it is also important to teach individuals to recognize the signs of an impending attack. Once recognized, individuals should be taught to remove themselves from the aggravating activity and initiate treatment as necessary. This includes education about the proper choice of agents to abort an acute attack (ie, albuterol), but not cromolyn, salmeterol, or an inhaled steroid. Teaching the proper mechanics of inhalant medication administration is also important, along with, if needed, teaching and demonstrating the proper use of a spacer device to the patient; without the proper mechanics in using such devices, the medication does not reach the area of pathology and does not benefit the athlete.
For excellent patient education resources, visit eMedicine's Asthma Center. Also, see eMedicine's patient education articles Asthma, Asthma FAQs, and Exercise-Induced Asthma.
National Heart, Lung,and Blood Institute, National Asthma Education and Prevention Program. Expert Panel Report 3:Guidelines for the Diagnosis and Management of Asthma: Full Report 2007. Bethesda, Md: NHLBI; August 2007. Publication no. 07-4051. [Full Text].
Anderson SD. How does exercise cause asthma attacks?. Curr Opin Allergy Clin Immunol. Feb 2006;6(1):37-42. [Medline].
Hough DO, Dec KL. Exercise-induced asthma and anaphylaxis. Sports Med. Sep 1994;18(3):162-72. [Medline].
Beaudouin E, Renaudin JM, Morisset M, et al. Food-dependent exercise-induced anaphylaxis--update and current data. Allerg Immunol (Paris). Feb 2006;38(2):45-51. [Medline].
Stensrud T, Berntsen S, Carlsen KH. Exercise capacity and exercise-induced bronchoconstriction (EIB) in a cold environment. Respir Med. Jul 2007;101(7):1529-36. [Medline].
Butcher JD. Exercise-induced asthma in the competitive cold weather athlete. Curr Sports Med Rep. Dec 2006;5(6):284-8. [Medline].
Dickinson JW, Whyte GP, McConnell AK, Harries MG. Screening elite winter athletes for exercise induced asthma: a comparison of three challenge methods. Br J Sports Med. Feb 2006;40(2):179-82; discussion 179-82. [Medline].
Wilson JJ, Wilson EM. Practical management: vocal cord dysfunction in athletes. Clin J Sport Med. Jul 2006;16(4):357-60. [Medline].
Kenn K. [Vocal Cord Dysfunction--what do we really know? A review] [German]. Pneumologie. Jul 2007;61(7):431-9. [Medline].
Kaplan TA. Exercise challenge for exercise-induced bronchospasm: confirming presence, evaluating control. Phys Sports Med. 1995;23(8):47-57.
Rundell KW, Anderson SD, Spiering BA, Judelson DA. Field exercise vs laboratory eucapnic voluntary hyperventilation to identify airway hyperresponsiveness in elite cold weather athletes. Chest. Mar 2004;125(3):909-15. [Medline]. [Full Text].
Storms W. Update on montelukast and its role in the treatment of asthma, allergic rhinitis and exercise-induced bronchoconstriction. Expert Opin Pharmacother. Sep 2007;8(13):2173-87. [Medline].
Steinshamn S, Sandsund M, Sue-Chu M, Bjermer L. Effects of montelukast and salmeterol on physical performance and exercise economy in adult asthmatics with exercise-induced bronchoconstriction. Chest. Oct 2004;126(4):1154-60. [Medline]. [Full Text].
Beuther DA, Martin RJ. Efficacy of a heat exchanger mask in cold exercise-induced asthma. Chest. May 2006;129(5):1188-93. [Medline]. [Full Text].
Knöpfli BH, Luke-Zeitoun M, von Duvillard SP, et al. High incidence of exercise-induced bronchoconstriction in triathletes of the Swiss national team. Br J Sports Med. Aug 2007;41(8):486-91; discussion 491. [Medline].
[Best Evidence] Koh MS, Tee A, Lasserson TJ, Irving LB. Inhaled corticosteroids compared to placebo for prevention of exercise induced bronchoconstriction. Cochrane Database Syst Rev. 2007;3:CD002739. [Medline].
Lacroix VJ. Exercise-induced asthma. Phys Sports Med. 1999;27(12):75-92.
McFadden ER Jr, Gilbert IA. Exercise-induced asthma. N Engl J Med. May 12 1994;330(19):1362-7. [Medline].
National Asthma Education and Prevention Program. Expert Panel Report: Guidelines for the Diagnosis and Management of Asthma - Update on Selected Topics 2002. Bethesda, Md: National Institutes of Health and National Heart, Lung, and Blood Institute; June 2003. NIH publication no. 02-5074. [Full Text].
Parsons JP, Kaeding C, Phillips G, ET AL. Prevalence of exercise-induced bronchospasm in a cohort of varsity college athletes. Med Sci Sports Exerc. Sep 2007;39(9):1487-92. [Medline].
Smith BW, MacKnight JM. Pulmonary. In: Safran MR, McKeag DB, Van Camp SP, eds. Manual of Sports Medicine. Vol 1. Philadelphia, Pa: Lippincott-Raven; 1998:244-9.
Storms WW. Asthma associated with exercise. Immunol Allergy Clin North Am. Feb 2005;25(1):31-43. [Medline].
EIA, exertional asthma, exercise-induced bronchospasm, EIB, asthma, exercise-induced urticaria, allergic rhinitis, bronchoconstriction, exercise-related respiratory symptoms, wheezing, chest tightness, shortness of breath, dyspnea, difficulty breathing, aerobic exercise, environmental factors, allergic asthma, asthmogenic agents
Anthony J Saglimbeni, MD, Staff Physician, Family Practice Residency, President, South Bay Sports and Preventive Medicine Associates; Private Practice; Team Internist, San Francisco Giants; Team Internist, West Valley College; Team Physician, Bellarmine College Prep; Team Physician, Presentation High School
Disclosure: Nothing to disclose.
Joseph P Garry, MD, FACSM, FAAFP,, Director of Sports Medicine and Sports Medicine Fellowship, Associate Professor of Family Medicine and Exercise and Sport Science, Department of Family Medicine, East Carolina University Brody School of Medicine
Joseph P Garry, MD, FACSM, FAAFP, is a member of the following medical societies: American Academy of Family Physicians, American College of Sports Medicine, American Heart Association, American Medical Society for Sports Medicine, and North American Primary Care Research Group
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.
Russell D White, MD, Professor of Medicine, Department of Community and Family Medicine, University of Missouri-Kansas City School of Medicine, Truman Medical Center Lakewood
Disclosure: Nothing to disclose.
Jon B Whitehurst, MD, Clinical Instructor of Surgery, University of Illinois College of Medicine; Partner and Executive Board Member, Rockford Orthopedic Associates; Orthopedic Chairman, Rockford Memorial Hospital
Jon B Whitehurst, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Society for Sports Medicine, and Arthroscopy Association of North America
Disclosure: Nothing to disclose.
Craig C Young, MD, Professor, Departments of Orthopedic Surgery and Community and Family Medicine, Medical Director of Sports Medicine, Sports Medicine Fellowship Director, Medical College of Wisconsin
Craig C Young, MD is a member of the following medical societies: American Academy of Family Physicians, American College of Sports Medicine, American Medical Society for Sports Medicine, Phi Beta Kappa, and Wilderness Medical Society
Disclosure: Nothing to disclose.
© 1994-
by Medscape.
All Rights Reserved
(http://www.medscape.com/public/copyright)