Respiratory water loss as a stimulus to exercise-induced bronchoconstriction.
Exercise and the resultant hyperpnea increase the magnitude of many stimuli delivered to the airways. Thus clinical "exercise-induced" bronchoconstriction can probably be initiated by a number of stimuli including, for example, sulfur dioxide, which is present in polluted air. In the laboratory, when subjects perform exercise breathing clean air, the water content of the inspired air is a major determinant of the bronchoconstriction induced, whereas in our hands, the temperature of the inspired air is of little or no importance, even over a range associated with significant differences in airway cooling. These observations support the view that water loss is an important stimulus to exercise-induced bronchoconstriction, perhaps as a result of a transient increase in the osmolarity of airway surface liquid.
D001249:Asthma / Q000209:etiology*; D001250:Asthma, Exercise-Induced / Q000209:etiology*; D001833:Body Temperature Regulation; D005260:Female; D006801:Humans; D008297:Male; D009994:Osmolar Concentration; D012119:Respiration; D012965:Sodium Chloride; D014870:Water Loss, Insensible
D012965:Sodium Chloride