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Objective: To determine whether caffeine consumption affects bronchoprovocation challenge (BPC)., Design: A prospective, double-blind, placebo-controlled, randomized, crossover trial., Patients: Eleven nonsmoking men, aged 18 to 42 years, with normal baseline spirometry and evidence of exercise-induced bronchospasm., Intervention: On three separate test days, each individual received, in random order, either placebo, 5 mg/kg caffeine, or 10 mg/kg caffeine, and then underwent BPC with eucapnic voluntary hyperventilation (EVH)., Results: Caffeine (10 mg/kg) significantly reduced bronchoconstriction compared to placebo (p = 0.02). The reduction in bronchoconstriction correlated with the serum level of caffeine (p = 0.014)., Conclusions: Caffeine decreases bronchoconstriction due to EVH. Caffeine should be eliminated from diet prior to BPC.

Airflow limitation in exercise-induced asthma is related to the thermal events in the intrathoracic airways. This article reviews the present knowledge about the exchange of respiratory heat and water. The evidence for the various theories proposed for the basic mechanisms involved in exercise-induced asthma are discussed. The evidence suggests that exercise-induced airways obstruction may be a vascular phenomenon dependent on the rapidity and magnitude of airway rewarming. Obstruction is induced if a thermal gradient exists at the end of exercise and the greater the gradient the greater the resultant hyperemia and edema. The basic mechanism of control of reactivity is still not known and directions for future research are outlined.

The possibility that sympathoadrenal activity is altered in asthma was examined in eight patients with a history of exercise-induced asthma (EIA), eight matched patients with nonexercise induced asthma (NEIA), and eight matched healthy control subjects. No medication was allowed for at least one week before examination. In a pretrial exercise test diagnosis of EIA was confirmed and each individual's work capacity (Vo2 max) was determined. The trial consisted of an orthostatic test and a standardized exercise test at 80 to 90 percent of VO2 max on a treadmill. The trial exercise test caused a decrease in FEV1 in EIA patients only, whereas measurements of Sgaw revealed a significant but less pronounced postexercise bronchoconstriction in NEIA-patients as well. Basal plasma catecholamine levels were similar in all groups. Noradrenaline and adrenaline levels were approximately doubled by the orthostatic test and increased approximately ten-fold following exercise, with no differences between the groups. Plasma cAMP levels were approximately doubled by the exercise test. In the EIA patients there was an inverse correlation between increases in plasma cAMP and decreases in Sgaw. Our study does not support earlier claims that exaggerated catecholamine response to exercise causes postexercise bronchoconstriction by alpha-adrenoceptor stimulation in EIA. Differences in study results appear to have methodologic explanations.