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Exercise-Induced Asthma: Diagnosis, Treatment, and Regulatory Issues

Beck, Kenneth C.; Joyner, Michael J.; Scanlon, Paul D.

Exercise and Sport Sciences Reviews: January 2002 - Volume 30 - Issue 1 - p 1-3
News Briefs

If you have ideas for material you would like to see in this section, please contact the NEWS BRIEFS editor: M.J. Joyner, M.D., Department of Anesthesiology, Mayo Clinic, 200 First Street SW, Rochester, MN 55905 (E-mail:

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In the summer of 2001, a football player at Northwestern University died from an apparent asthma attack at practice. This unfortunate event served to highlight a number of points concerning asthma in the elite athlete. In an editorial in the New York Times, Olympic champion Jackie Joyner-Kersee addressed several important points from the perspective of an elite athlete who has been treated for asthma for many years (5). Key points included 1) the fear on the part of many athletes regarding a diagnosis of asthma because of the implication of weakness, and 2) the fact that many athletes ignore symptoms of asthma because they are trained to tolerate discomfort with exertion. Ms. Joyner-Kersee highlighted the seriousness of the disease and the importance of appropriate treatment. Several additional points should also be discussed related to asthma in the elite athlete: First, how is the diagnosis of asthma made? Second, how much does asthma affect athletic performance? Third, what effect will the use of medications to treat asthma have on athletic performance, both in the athlete with asthma and in the nonasthmatic?

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Exercise-induced asthma (EIA) can be diagnosed on the basis of clinical history, physical examination, and laboratory investigations. The clinical history is the most helpful means of diagnosis in practice. However, the positive predictive value of diagnosis on the basis of history alone is largely unknown. Even with laboratory data, the accuracy of diagnosis is far from perfect. Laboratory studies typically include spirometry and chest radiograph (to rule out other causes of symptoms). However, a methacholine challenge test, a cold air isocapnic hyperventilation test, or an exercise challenge test may be used as well. Of these tests, the least sensitive is the routine spirometric evaluation because patients with mild asthma often have normal pulmonary function in between asthma attacks. However, even challenge tests may not be 100% sensitive because they are often performed in the laboratory and do not include all the additional stresses associated with athletic competition. Recent data from Rundell et al. (9) show that field-based trials may be more sensitive than laboratory-based trials in eliciting bronchospasm in cold weather athletes. The most specific test is the exercise challenge test while breathing either dry or cold dry air. Second to that is the hyperventilation test, also breathing cold or dry air. Use of dry or cold air is important, as it has been shown that the severity of EIA is directly related to either water loss from the airway or cooling of the airway by dry or cold air.

Several recent studies have emphasized that the prevalence of asthma or EIA is higher among elite athletes compared with the general population (14,6,3), in which the prevalence is about 8–12% in the United States, but higher in Australia and Great Britain and lower in developing countries. The methods used to determine prevalence in athletic populations have ranged from questionnaires probing the frequency of symptoms of asthma, to methacholine or histamine challenge tests, and finally measurements of lung function before and after actual or simulated competition. Some studies have suggested that specific athletic groups may be predisposed to EIA or asthma, such as cold weather athletes (cross country skiers, skaters) and swimmers (14,3). These results raise the issue of whether the repeated exposure to increased ventilation with cold or dry air, or air containing contaminants such as chlorine or internal combustion engine exhaust fumes (from ice resurfacing machines), may cause damage to the airways, leading to the hyper-responsiveness.

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In the classical model of EIA, bronchospasm does not occur during exercise, but after. In the laboratory, when an athlete is subjected to the usual exercise evaluation consisting of progressive incremental increases in exercise intensity until volitional fatigue, airway function is well preserved, and may even improve slightly during the exercise, and will only deteriorate when exercise is stopped (1). Thus, under conditions of steadily increasing exercise intensity, premedication probably does not affect performance (10). However, when exercise is varied in intensity or is continuous for longer than 12–15 min, lung function may deteriorate during exercise (1). This may be perceived as wheeziness or shortness of breath as ventilatory demand approaches the declining capacity of the lungs (4). These laboratory investigations have not been reproduced in the field, so it is largely unknown how airways respond to specific events such as cross country skiing, marathon running, or stop-and-go sports like soccer, basketball, and hockey, in which intensity varies. Thus it is likely that untreated asthma will affect athletic performance in some way. Furthermore, airway responsiveness in asthma can vary from day to day, so an athlete can have good days and bad days as a result of factors like fluid balance, the antigen or pollutant content of the air, and the psychological stresses of competition.

Untreated asthma could affect performance additionally because baseline airway function declines faster than normal in untreated asthmatics compared with nonasthmatics. If baseline lung function declines, the maximal ventilatory capacity of the lungs will decline and may become a limiting factor for exercise performance.

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Drugs used to treat EIA range from drugs intended to treat the airway inflammation that is thought to be the underlying cause of asthma (steroids and mast cell-stabilizing agents) to drugs that act to relax airway smooth muscle, which essentially treat the symptoms of the disease. These drugs are likely to improve performance in the athlete with EIA or asthma. An important issue is whether they will also improve performance in nonasthmatic athletes. The β2 adrenergic agonist medications have been implicated as ergogenic and have been used by nonasthmatic athletes seeking a competitive advantage. There are compelling theoretical reasons to expect that these agents may be ergogenic, because adrenergic receptors are involved in glucose mobilization and metabolism, control of heart rate and cardiac contractility, and regulation of vascular smooth muscle. They may also be involved in skeletal muscle contractility.

Are there good data to indicate β2 agonists are ergogenic? The picture from the literature is inconsistent. Two studies showed an ergogenic effect of inhaled β2 agonist: Bedi et al. (2) studied 14 nonasthmatic athletes by subjecting them to a 1-h cycle ergometer ride followed by a maximal sprint. Subjects were studied after double-blind administration of inhaled albuterol, a β2 agonist. As expected, the forced expiratory volume in 1 sec from preexercise spirometry improved slightly after the β2 agonist but not after placebo. The sprint times improved significantly on the albuterol treatment compared with placebo treatment. These results suggest that an athlete’s “finishing kick” might be improved. Likewise, Signorile et al. (12) found a significant improvement in performance time during a maximal anaerobic power test after treatment with inhaled β2 agonist. However, several other studies with similar designs have not found a significant effect in any physiological or performance parameters (7,8,11,13). After reviewing all of these studies, the negative findings seem to come from studies determining maximal exercise capacity or endurance tests, whereas the positive results are likely related to short-term anaerobic power measurements. Further work is warranted to confirm these results and to obtain more information about sport-specific effects of β2 treatment and to identify possible ergogenic mechanisms. In addition, all studies to date have used the recommended therapeutic doses of the β2 agonists. It is also possible that higher doses, which could be used by athletes attempting to obtain performance advantage, may be more effective ergogenic aids.

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The results of these studies raise some critical issues related to regulation of drug use among athletes. A key question for sports governing bodies will be the need to develop standard screening tests to diagnose EIA so that those athletes who need treatment can obtain it without compromising their eligibility. Additionally, it might also be reasonable to develop standard protocols to determine whether a given asthma drug is “ergogenic” in athletes without asthma. Such standard protocols could be used to avoid unnecessary regulation of substances that give no objective benefit to the nonasthmatic athlete.

In conclusion, asthma can affect lung function during as well as after athletic events. It is possible that certain sports can cause airway injury by repeated exposure to high ventilations with cold air or noxious agents. Untreated asthma can adversely affect long-term trends in lung function. Current therapeutic agents can control symptoms and eliminate or reduce airway inflammation. These agents have minimal adverse effects that are well tolerated by most asthmatic athletes. For these reasons, effective therapy is recommended for asthmatic athletes to control airway inflammation and to avoid spontaneous or exercise-induced bronchospasms. Data on practical improvement in exercise capacity with β2 agonist use in nonasthmatics suggest the biggest benefit is in short-term anaerobic power output rather than aerobic capacity or endurance.

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© 2002 Lippincott Williams & Wilkins, Inc.