In this study, disodium cromoglycate and Sch 1000 were found to be effective in the prevention of exercise-induced asthma in the majority of patients. While most studies agree that disodium cromoglycate is partially effective in the prevention of exercise-induced asthma, the reports on the effectiveness of administration of atropine are conflicting. The finding of this study that inhalation of Sch 1000 prevents exercise-induced asthma in the majority of patients is in agreement with the results reported by Simonsson et al but at variance with the observation of Sly et al and of Poppius and his co-workers.The mechanism of exercise-induced asthma is unknown.
Several factors, such as hyperventilation, hypocapnia, and acidosis, have been postulated, but there is no substantial evidence that any one of them explains the underlying mechanism. In our previous study, we found that patients with exercise-induced asthma developed bronchoconstriction following voluntary hyperventilation; however, Silverman et al and Allen et al reported that some patients with exercise-induced asthma failed to develop bronchoconstriction following hyperventilation at a level similar to that maintained during exercise. Hypocapnia has been quoted as the cause of increased airway resistance following exercise, since the administration of carbon dioxide prevented such occurrence. Other studies failed to find any relationship between the level of carbon dioxide tension and hyperventilation asthma. Metabolic acidosis has been thought to induce asthma after exercise; however, treatment with bicarbonate corrected the metabolic acidosis but failed to prevent exercise-induced asthma. About airway resistance syndrome during insomnia see on article: “Insomnia not always a clear-cut diagnosis“.
The study of the influence of drugs on exercise-induced asthma is useful in furthering our understanding of the mechanism of the disease. Since disodium cromoglycate acts by stabilizing the mast cell membrane and inhibits the release of chemical mediators, its effectiveness in preventing exercise-induced asthma suggests that the release of chemical mediators may be an important mechanism in some patients. The fact that Sch 1000 is effective in preventing exercise-induced asthma indicates that reflex mechanism via the vagal pathways is also important In a few patients (eg, patients 5 and 6), vagal reflex may be the sole mechanism involved. In the majority of patients, vagal reflex may be the triggering event leading to the release of chemical mediators; in such patients, both Sch 1000 and disodium cromoglycate are effective.
In allergen-induced bronchoconstriction, there is some evidence that vagal reflex is necessary. Gold and associates found that in dogs sensitized to parasites and grass pollen, section or cooling of the vagus nerve could reverse bronchoconstriction; however, in man the effect of administration of atropine on allergen-induced bronchoconstriction varied in different studies, as is the case with exercise-induced bronchoconstriction. While Altounyan found that administration of atropine had little or no protective effect, Yu and co-workers showed that it reduced the allergen-induced bronchoconstriction.
In conclusion, Sch 1000 and disodium cromoglycate are found to be effective in the prevention of exercise-induced asthma in the majority of patients. The fact that in some patients, one drug is more effective than another suggests that the mechanism of exercise-induced asthma may be multifactorial, and the relative important of each factor may vary in different patients.
Previously published articles on the topic: