The development of drugs to inhibit exercise induced bronchoconstriction (EIB) helped to understand the mechanisms underlying EIB.
The site of action for EIB being close to the airway surface was established by the inhibitory effects of breathing warm humid air during exercise. These studies provided evidence for dehydration of the airways being the stimulus to EIB. It was, however, the finding that inhaled drugs such as DSCG and the beta2-agonists could inhibit EIB by preventing the release of mast cell mediators that finally indicated the mechanism for the transient airway narrowing in response to exercise.