标题:Ventilatory responses to constant load exercise following the inhalation of a short-acting ß2-agonist in a laboratory-controlled diesel exhaust exposure study in individuals with exercise-induced bronchoconstriction
摘要:Objective Individuals with exercise-induced bronchoconstriction (EIB) use ß 2 -agonists to reduce respiratory symptoms during acute exercise. The resulting bronchodilation could increase the dose of inhaled pollutants and impair respiratory function when exercise is performed in air pollution . We aimed to assess respiratory responses in individuals with EIB when completing a cycling bout while being exposed to diesel exhaust (DE) or filtered air (FA) with and without the inhalation of salbutamol (SAL), a short-acting ß 2 -agonist. Methods In a double-blind, repeated-measures design, 19 participants with EIB (22-33 years of age) completed four visits: FA-placebo (FA-PLA), FA-SAL, DE-PLA, DE-SAL. After the inhalation of either 400 µg of SAL or PLA, participants sat in the exposure chamber for 60 min, breathing either FA or DE (PM 2.5 = 300 μg/m 3 ). Participants then cycled for 30 min at 50 % of peak work rate while breathing FA or DE. Respiratory responses were assessed via spirometry, work of breathing (WOB), fractional use of ventilatory capacity ( V ̇ E / V ̇ E,CAP ), area under the maximal expiratory flow-volume curve (MEFV AUC ), and dyspnea during and following cycling. Results Bronchodilation in response to SAL and acute cycling was observed, independent of FA/DE exposure. Specifically, FEV 1 was increased by 7.7 % (confidence interval (CI): 7.2–8.2 %; p < 0.01) in response to SAL, and MEFV AUC was increased after cycling by 1.1 % (0.9–1.3 %; p = 0.03). Despite a significant decrease in total WOB by 6.2 J/min (4.7–7.5 J/min; p = 0.049) and a reduction in V ̇ E / V ̇ E,CAP by 5.8 % (5–6 %, p < 0.01) in the SAL exposures, no changes were observed in dyspnea. The DE exposure significantly increased V ̇ E / V ̇ E,CAP by 2.4 % (0.9–3.9 %; p < 0.01), but this did not affect dyspnea. Discussion Our findings suggest that the use of SAL prior to moderate-intensity exercise when breathing high levels of DE, does not reduce respiratory function or exercise ventilatory responses for up to 60 min following exercise.