Recent advances in the understanding of exercise-induced asthma.
Most asthmatic patients have less exercise-induced asthma (EIA) after a second challenge. However, the degree to which a patient becomes refractory is variable. The mechanism of refractoriness is unknown. Heat loss from the airways, the initiating stimulus in EIA, remains unchanged on repeated challenge. It is unlikely that bronchial smooth muscle becomes refractory, or that residual catecholamines induce protection since histamine sensitivity remains relatively unchanged during a refractory period. Histamine release has been measured in some patients during EIA, but further studies are needed to elucidate the role of histamine in EIA and the refractory period. In patients who do not become refractory, EIA may be induced by stimuli independent of mediator release and perhaps vagal in origin. In some patients EIA may be blocked by small doses of anticholinergic agents while, in others, these drugs have no effect. Similar observations have been made with sodium cromoglycate. The superiority of aerosols in preventing EIA suggests that exercise induces changes in the airways mucosa. The loss of water during exercise may change the osmotic environment of irritant receptors or mast cells triggering bronchoconstriction.
D001249:Asthma / Q000503:physiopathology*; D001250:Asthma, Exercise-Induced / Q000503:physiopathology*; D001980:Bronchi / Q000503:physiopathology; D002395:Catecholamines / Q000097:blood; D006636:Histamine Release; D006801:Humans; D009130:Muscle, Smooth / Q000503:physiopathology; D012129:Respiratory Function Tests
D002395:Catecholamines