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Exercise induced asthma
ICD-9 493.81
DiseasesDB 31728
eMedicine sports/155 
MeSH D001250

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Overview

Exercise-induced asthma, or E.I.A., is a medical condition characterized by shortness of breath induced by sustained aerobic exercise. It shares many features with other types of asthma, and responds to some typical asthma medications, but does not appear to be caused by the same inflammatory reaction as the other types.

Etiology

While the potential triggering events for E.I.A. are well delineated, the underlying pathogenesis is poorly understood. It usually occurs after at least several minutes of vigorous, "aerobic" activity, which demands that normal nasal breathing be supplemented by mouth-breathing. The resultant inhalation of air that has not been warmed and humidified by the nasal passages seems to generate increased blood flow to the linings of the bronchial tree, resulting in edema. Constriction of these vessels then follows, worsening the degree of obstruction to airflow. This sequence generates symptoms similar to those seen in other forms of asthma, but occurs without the inflammatory changes that underlie them.

Signs and symptoms

During an attack, the E.I.A. victim will likely be short of breath and/or coughing, with an elevated respiratory rate and wheezing, which may be audible even without a stethoscope. Examination will usually reveal the wheezing and a prolonged expiratory phase. In the occasional severe attack, altered level of consciousness and cyanosis due to depressed oxygenation of the blood may occur. Severe attacks are often the result of someone with both allergic and exercise-induced asthma exercising in a high-allergen environment (e.g. walking uphill alongside slowly moving traffic at dusk), and can be fatal.

In most cases, a relative "refractory period" follows resolution of an attack. During this approximately one hour period, resumption of exercise will likely produce either none or mild symptoms. Curiously as well, some 6-10 hours after the initial attack, a rebound attack with milder symptoms often develops without precipitating exertion.

Treatment

As with any asthma, the best treatment is avoidance, when possible, of conditions predisposing to attacks. In athletes who wish to continue their sport, and/or do so at times in adverse conditions, preventive measures, including altered training techniques and medications, can be taken.

Some athletes take advantage of the refractory period by precipitating an attack by "warming up," and then timing their competition such that it occurs during the refractory period. Step-wise training works in a similar fashion. An athlete warms up in stages of increasing intensity, using the refractory period generated by each stage to get up to a full workload.

The most common medication approach is to use a beta agonist about twenty minutes before exercise. Some physicians prescribe inhaled anti-inflammatory mists such as corticosteroids or leukotriene antagonists, and mast cell stabilizers have also proven effective. A randomized crossover study compared oral montelukast with inhaled salmeterol, both given two hours before exercise. Both drugs had similar benefit but montelukast lasted 24 hours.[1]

Prognosis

As evidenced by the many professional athletes who have overcome E.I.A. using some combination of the above treatments, the prognosis is usually very good. Olympic swimmers Tom Dolan, Amy Van Dyken, and Nancy Hogshead, baseball Hall of Famer Catfish Hunter, and American football player Jerome Bettis are among the many who have done so.

At the same time, it should be noted that according to International Olympic Committee statistics, during most of Olympic Games in last 20 years from 1/3 to 2/3 of athletes claimed to have asthma. Some medical experts tie such inordinate rates of reported asthma with athletes' desire to use complex medication to help them achieve better results.

References

  1. Philip G, Pearlman DS, Villarán C; et al. (2007). "Single-dose montelukast or salmeterol as protection against exercise-induced bronchoconstriction". Chest. 132 (3): 875–83. doi:10.1378/chest.07-0550. PMID 17573489.

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