Rapid Effects Of Inhaled Beclomethasone On Hyperpnea-Induced Bronchoconstriction And Mast Cell Mediator Release In Athletes

Abstract

Exercise provokes bronchoconstriction in most asthmatics. Asymptomatic elite athletes also report exercise-induced bronchoconstriction (EIB). Although the bronchial response following exercise is similar in these two groups, the underlying mechanism responsible for the transient airway narrowing might differ. Whilst an inflammatory process is involved in asthmatics, non-inflammatory mediated vascular engorgement and mucosal oedema may mediate EIB in athletes. PURPOSE: To determine if a single dose of inhaled beclomethasone diproprionate (BDP), through its acute vasoconstrictive and antioedematous properties, has a protective effect on EIB in athletes. METHODS: 6 trained athletes with EIB and 8 untrained mild asthmatics performed two eucapnic voluntary hyperpnea (EVH) tests (a surrogate for exercise) at 41/2h interval on the same day, the first 0.25h after placebo, and the second 3h after BDP (1500jj.g). Pulmonary function was recorded and urine was collected 60min before and for 90min after EVH for measurements by immunoassay of the mast cell marker 9?,11?-prostaglandin (PG)F2. RESULTS: BDP provided significant protection against post-EVH bronchoconstriction in both groups (P=0.0001): mean FEV1 fall (±SEM) in athletes 21.5±4.9% after placebo vs 14.3±2.8% after BDP; in untrained asthmatics 23.3±3.7% after placebo vs 14.0±3.2% after BDP. Urinary 9α, 11β-PGF2 increased post-EVH after placebo only (P=0.0462) with no significant difference between groups (Fig. 1).Fig 1: Mean ± SEM urinary excretion of 9α, 11β-PGF2 in asthmatics (o) and athletes (δ) at baseline and during the 90min period after EVH after administration of placebo (closed black symbols) or BDP (open grey symbols).CONCLUSIONS: A single dose of BDP has an acute protective effect on the bronchial response to hyperpnea in both untrained asthmatics and trained athletes with EIB. This effect seems at least partly mediated by an inhibition of the release of mast cell mediators.