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Significant bronchoconstriction, comparable in severity to that observed after moderate treadmill exercise, was induced in asthmatic children by voluntary isocapnic hyperventilation of 3-min and 10-min duration. In both hyperventilation and exercise, nasal breathing inhibited the bronchoconstrictive responses, whereas mouth breathing potentiated the bronchoconstrictive response. In the asthmatic children, 10 min of voluntary isocapnic hyperventilation did not represent a greater bronchoconstrictive stimulus than did 10 min of exercise or 3 min of isocapnic hyperventilation. This study also showed that in normal children there was no measurable airway response after either voluntary isocapnic hyperventilation or moderate exercise. Finally, this study indicates that it is the stimulation of upper airway receptors by relatively cold and dry air, rather than hyperventilation per se, that provokes exercise-induced bronchoconstriction.
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