Athletes, Exercise Induced Asthma and Optimal Medication

Abstract

Exercise-induced asthma (EIA) affects ∼20% of athletes. The British Thoracic Society guidelines recommend that individuals with mild EIA should be managed using a short-acting Beta 2-agonist. However, this treatment does little to attenuate the underlying inflammatory and remodelling processes that may occur in athletes with EIA. PURPOSE: To examine the effects of a combined corticosteroid/ long-acting Beta 2-agonist (fluticasone propionate/salmeterol) in the control of mild EIA in athletes. METHODS: Following approval from Harrow Local ethics committee, 7 athletes (mean±SD; age 21.3±4.1years; height 172.8±11.8cm; body mass 67.1±12.9kg), who had previous diagnosis of EIA, volunteered and provide written informed consent. Each athlete was prescribed the following inhaled pharmaceutical therapies, in a randomised double blind design, for a three week period with a two week wash between each: 200mcg fluticasone propionate (FLU), 50mcg Salmeterol (SAL), 250mcg fluticasone propionate and salmeterol in combination (FXS) or placebo (PLA). Following each three week period the athlete completed a 6 minute eucapnic voluntary hyperventilation (EVH) challenge with voluntary flow volume loops and exhaled nitric oxide (eNO) analysis measured before and 3, 5, 10 and 15 minutes after the EVH challenge. Throughout the study, athletes were prescribed inhaled salbutamol to use when required. Repeated measures ANOVA were used to compare the means of resting FEV1 and eNO and percent changes in FEV1 and eNO following the EVH challenge. RESULTS: The difference between baseline FEV1 for FXS (4.3±0.9l) and PLA (4.2±1.01) approached significance (p=0.07). However, there was no significant difference in falls of FEV1 following EVH challenge between any of the therapies (FLU=−13±11.1%;SAL=−20.4±15.2%;FXS=−12.2±6.8%;PLA=−20.0±17.7%). The VE during each EVH challenge was not significantly different. Baseline eNO for both FXS (21.5±8.2ppb) and FLU (21.3±8.9ppb) were significantly (p=0.02) lower than SAL (44.3±25.4ppb) or PLA (50.6±26.5ppb). There was no difference in the fall of eNO following EVH between any of the therapies. CONCLUSOON: The reduction in baseline eNO following three weeks treatment of using either FLU or FXS suggests that athletes with EIA have underlying inflammation that benefits from treatment with an inhaled corticosteroid. Response to EVH challenge suggested that a long-acting Beta 2-agonist is insufficient to control EIA in this group. Further, the measurement of eNO may provide a greater insight into the control of inflammatory processes occurring in EIA than the FEV1 response to bronchoprovocation challenges.