Exercise-induced asthma and late phase reactions.

The hypothesis that respiratory heat loss was an initiating event in EIA was first proposed by CHEN and HoRTON [1) and later supported by McFADDEN et al. [2], who suggested that the severity of EIA is dependent upon the rapidity and magnitude of airway rewarming after exercise. It has been suggested that the airway cooling which results from hyperpnoea during exercise is followed by a rapid re-supply of heat to the airway mucosa when exercise ceases. This may cause an exaggerated rebound hyperaemia and airway oedema, thereby causing asthma. However, HAHN et al. [3] exercised asthmatic subjects under varying conditions of temperature and humidity and demonstrated that the severity of EIA did not differ even when the inspired air temperature varied by 26·c as long as the humidity was kept constant. This suggests that the response to exercise depends on the degree of respiratory water loss rather than on cooling of the airways. ANDERSON [4] has suggested that the rate of respiratory water loss caused by the hyperpnoea of exertion induces a transient hyperosmolarity of the airway epithelium and that this is the stimulus for EIA. This hypothesis is supported by several lines of evidence. Inhalation of hypertonic aerosols will induce bronchoconstriction in asthmatic subjects which is attenuated by the prior administration of sodium cromoglycate [5] and specific histamine H 1 antagonists [6] in a similar manner to that seen for inhibition of EIA [7, 8]. In the previous issue of this Journal, BELCHER and eo-workers [9] have demonstrated a correlation between airways responsiveness to inhaled hypertonic saline aerosol and to exercise in a group of ten asthmatic subjects. Asthmatic subjects demonstrate cross-refractoriness between hypertonic saline-induced bronchoconstriction and EIA [10], sug-