thma (Randolph, 1997). The results of these studies provided the basis on which to classify EIA. This basis includes airway constriction within the first 6-12 minutes of vigorous exercise, a peak at about 5-10 minutes after exercise, and recovery that is usually spontaneous and within 60 minutes, except in severe cases where it may require up to 3 hours (Enright, 1996; Spector, 1993). The exact causes of EIA are unknown, but according to Storms (1999), there are two theories of the possible pathogenesis of EIA: The first is the water loss theory which states that the hyperventilation associated with strenuous exercise leads to loss of water through the epithelium of the bronchial mucosa. This loss of water leads to changes in intracellular osmolarity, pH, and temperature through mechanisms currently unknown, producing the signs and symptoms of EIA. (p. S35) This theory states that as exercise begins, rate of breathing increases rapidly, and in order for the air to be warmed and saturated with water as it is inhaled, water vapor from the respiratory epithelium must be contributed. This contribution leads to hyperosmolarity of the epithelium, which causes bronchoconstriction through a series of undetermined events. This can be supported by the fact that inhaling hyperosmolar saline at rest will cause bronchoconstriction. Storms (1999) states the following: The second hypothesis, the thermal expenditure or respiratory heat exchange theory, states that EIA results from heat transfer from the bronchiolar blood vessels in the pulmonary vascular bed with heat loss during exercise; after the exercise, the heat transfer is followed by a rewarming of the bronchiolar blood vessels, which causes dilation and hyperemia of the vessels; this then leads to EIA by mechanisms unknown. (p. S35) This theory states that heat is lost from the upper and lower airways during exercise, and this...
