There has been some controversy regarding the mechanism whereby exercise can provoke an attack of asthma. It is generally agreed that heat and water are lost from the respiratory tract in bringing the air inspired to body conditions. During strenuous exercise, there is a marked increase in ventilation rate and some of the burden to heat and humidify the inspired air is transferred to the intrathoracic airways. The net effect of the air conditioning process is to cool and dehydrate these airways. There have been two hypotheses put forward to account for the mechanism whereby these events lead to exercise-induced asthma (EIA). One hypothesis proposes that cooling of the airways followed by rapid rewarming, at the end of exercise, leads to a reactive hyperemia and edema of the bronchial vascular bed "which if sufficiently severe results in the airway obstruction of EIA." The other hypothesis proposes that the rate of loss of water from the periciliary fluid during exercise exceeds the rate of return and, as a result, there is an increase in ion concentration and subsequent hyperosmolarity of the periciliary fluid. Thus the events related to drying rather than cooling are the stimulus to EIA. This paper presents the case against rapid rewarming of the bronchial vasculature as the stimulus to EIA and puts forward an argument and data in support of the case for airway drying and an increase in osmolarity being the critical event which determines the presence and severity of EIA.