Asthma is a disease of airways where there is inflammation of the airways and reversible obstruction. There are different types of asthma like allergic asthma, non allergic asthma, exercise induced asthma, occupational asthma, cough variant asthma and steroid resistant asthma. Understanding the type of asthma is very important to achieve most effective treatment. Exercise induced asthma (EIA) is a term often used to describe episodic bronchoconstriction triggered by exercise and lasts through aerobic exercise. Exercise induced bronchoconstriction (EIB) sometimes used instead of EIA as EIB is a more accurate reflection of underlying pathophysiology.
EIA affects 12-15% of the population. 80% of symptomatic asthma has some degree of EIB. Even when those with rhinitis and allergic asthma are excluded, a 3-10% incidence of EIA is seen in the general population. The magnitude of EIA is strongly correlated with the underlying degree of airway hyper responsiveness and the presence of airway inflammation, as measured by the number of airway eosinophils. Thus in many patients with mild episodic asthma, minimally increased airway responsiveness, and mild airway inflammation, even strenuous exercise does not cause clinically significant bronchoconstriction. EIA seems to be more prevalent in some winter or sold weather sports. Some studies have demonstrated rates as high as 35% in competitive-caliber figure skaters, ice hockey players, and cross country skiers.
EIA usually affect individuals who participate in sports that include an aerobic component. This condition can be seen in any sport, but EIA is much less common in predominantly anaerobic activities. EIA is probably triggered by the large volume of relatively cool, dry air inhaled during vigorous activity. This is supported by the fact that EIA is attenuated when the inspired air is more fully humidified and closer to body temperature. Certain sports played in cold and dry environments usually result in more symptoms manifestation for athletes with this condition. On the other hand when environment is warm and humid, the incidence and severity of EIA decrease. The biochemical and or physical pathways that mediate these responses are not clear. Evidence may even exist to support the idea that the resulting cascades are not the inflammatory pathways to which we attribute the allergic asthma. Large dry and cold air movement results in drying and cooling of the airway may be primary stimulus responsible for bronchoconstriction. 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 drying and an effort to heat the airway. Other relevant observations regarding EIA include levels of bronchoconstrictive and inflammatory mediators like Leukotriene LTC4 and LTD4 are increased, peripheral TH2 lymphocytes are activated, eosinophils activation and influx is present. In contrast exhaled nitric oxide levels, which generally reflect airway inflammation, do not appear to correlate with development or severity of EIA.
The patients with EIA have bronchoconstriction which begins by 3 minutes and generally peaks within 10-15 minutes and resolves by 60 minutes. Typical symptoms are shortness of breath, chest tightness and cough. In most patients with EA, bronchoconstriction if followed by a refractory period, during which repeated exertion causes less bronchoconstriction. Refractory period is less than 4 hours. Inhibitory prostaglandins released during the refractory period probably protect against repeated episodes of EIA. Chemicals used in certain sports for environmental maintenance can predispose to EIA symptoms. These chemicals include chlorination to pools, insecticide and pesticide used in the fields, fertilizer used to maintain field. Certain medications can provoke or exacerbate bronchial reactivity in EIA as B blocker, Aspirin, NSAID, Diuretics, and Zanamivir.
In patients with well documented asthma with typical asthma symptoms following exercise, formal exercise testing is not needed. In patients without documented asthma further assessment is needed if exercise induced asthma is suspected. An exercise challenge test is the most direct way to establish diagnosis of EIA. This usually involves 6-8 minute of ergometer or treadmill exercise, sufficient to raise the heart rate to 85% of the predicted maximum. A test is generally considered positive if the FEV1 falls by 10% or more. Although a fall of 15% is more diagnostic of EIA. Alternatively, surrogate tests to assess bronchial hyperresponsive, e.g., cold air hyperventilation, methacholine, histamine, Mannitol inhalation challenge may be performed, but not always correlate with the presence of EIB.
Patient education is crucial in the management of EIA. A major goal is ensure that exercise is not avoided by patients with 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 from aggravating activity and initiate treatment as necessary. This includes education about the proper choice of agents to abort an acute attack i.e., short acting beta agonist but not Leukotriene, receptor blocker, LABA or inhaled corticosteroid. Asthmatics should exercise as much as desired. Improved understanding of the pathophysiology of EIB has resulted in general recommendations than can help reduce its severity. Improving cardiovascular fitness reduce the minute ventilation required for a given level of exercise, thereby decreasing the stimulus for bronchoconstriction. Similarly bronchorestriction is lessened when the inspired gas is warmer and more humid.
All patients with EIA should be instructed to use short acting Beta agonist 10 minutes before exercise. An alternative approach is prophylactic use of inhaled Cromolyn sodium 2-4 puffs taken 15-20 minutes before exercise. Equipotent doses of Formoterol, Sametrol appears to be effective in providing short term control of EIA. Long acting beta agonist and regular use of short acting beta agonist provide less effective protection against EIA than does intermittent use of short acting beta agonist. When poor control of asthma is the cause of exercise induced bronchospasm, the most effective method of achieving asthma control involves use of inhaled glucocorticoids. Studies have shown that inhaled glucocorticoid do not decrease exercise induced bronchospasm in a dose related manner. These findings indicate mechanism of EIA distinct from allergic asthma. Leukotriene modifying agents provide a therapeutic alternative in the setting of chronic asthma complicated by EIA. Leukotriene modifying agents appear superior to long acting beta agonist when treating asthmatics with EIA. In patients who require daily therapy for EIA it is suggested to use anti-Leukotriene agent or inhaled glucocorticoid rather than regular daily use of beta agonist alone. When exercise is unpredictable or repeated during the day, daily morning dose of Leukotriene receptor antagonist rather than a pre exercise inhaler is recommended. The prognosis for athletes with asthma is excellent. With proper interventions, most symptoms can be prevented and performance should not be limited for 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.
By Syed L. Mobin, M.D.
Syed L. Mobin, MD, completed his Fellowship at Mayo Clinic Rochester, MN and Mayo Clinic Jacksonville, FL and is board certified in Pulmonary Medicine, Critical Care Medicine and Sleep Medicine.
He has been elected the Internal Medicine Department Chairperson for Florida Hospital Medical Staff and is Director of CFPG Institute of Sleep Medicine. Dr. Mobin is also the clinical assistant professor at University of Central Florida School of Medicine, a member of the American Academy of Sleep Medicine, the American College of Chest Physicians, the Society of Critical Care Medicine and a Mayo alumni. Dr. Mobin is practicing with the Central Florida Pulmonary Group and can be contacted at (407) 841-1100 or by visiting cfpulmonary.com.