Asthma and exercise-induced bronchoconstriction in athletes.

Regular exercise is one of the most effective means to maintain good health. A substantial proportion of the general population engages in competitive sports, including many people with asthma; when controlled, asthma does not restrict exercise performance. Indeed, exercise training can improve asthma symptoms, quality of life, exercise capacity, and pulmonary function, as well as reduce airway responsiveness.1 Intense exercise imposes demands on the cardiorespiratory system. Cardiac output increases, as does minute ventilation, which can reach 200 liters per minute in high-level athletes.2 At high minute ventilations, the airways are the site of intense respiratory heat and water exchange as they condition inspired air to body temperature and humidity levels. Furthermore, because mouth breathing is common during exercise, there is an increased penetration of allergens and pollutants — such as chloramines from chlorinated pools, ozone, and particulate matter from ambient air — into the lower airways. Therefore, it is not surprising that as compared with nonathletes, high-level endurance athletes have an increased prevalence of various respiratory ailments, such as asthma and rhinitis, and related coexisting conditions.3-5 The term exercise-induced bronchoconstriction describes the transient narrowing of the airways after exercise, a phenomenon that occurs frequently among athletes who may not have a diagnosis of asthma or even have any respiratory symptoms.5-8 Exercise-induced bronchoconstriction is a distinct form of airway hyperresponsiveness, which is defined as the tendency of airways to constrict more easily and more forcefully than normal airways in response to a wide variety of bronchoconstrictor stimuli. Airway hyperresponsiveness, which is a cardinal feature of asthma, is more common among endurance athletes — particularly winter-sports athletes and swimmers — than in the general population.7,8 The mechanism of exercise-induced bronchoconstriction has not been established with certainty; both airway cooling resulting from conditioning of inspired air and postexercise rewarming of airways have been proposed as mechanisms. However, the key stimulus is probably airway dehydration as a result of increased ventilation, resulting in augmented osmolarity of the airway-lining fluid.9 This is thought to trigger the release of mediators — such as histamine, cysteinyl leukotrienes, and prostaglandins — from airway inflammatory cells, which leads to airway smooth-muscle contraction and airway edema. However, uncontrolled airway inflammation can exacerbate this process and increase exercise-induced bronchoconstriction.10 Furthermore, not only can osmotic and mechanical stress to the airways play a role in the acute response to exercise, but they may also be involved in the development of airway remodeling in athletes, probably through their effects on airway epithelial cells.4,8,9 Finally, transient immunosuppression may also develop in athletes during periods of intense training, with increased susceptibility to respiratory infections, particularly viral infections11; this may increase airway response to exercise acutely and affect overall asthma control. From the Quebec Heart and Lung Institute, Laval University, Quebec City, QC (L.-P.B.), and the Firestone Institute of Respiratory Health, Department of Medicine, McMaster University, Hamilton, ON (P.M.O.) — both in Canada. Address reprint requests to Dr. Boulet at the Institut Universitaire de Cardiologie et de Pneumologie de Québec, 2725 Chemin SainteFoy, Quebec, QC G1V 4G5, Canada, or at lpboulet@ med . ulaval . ca.