Objective

Individuals with exercise-induced bronchoconstriction (EIB) use ß₂-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 ß₂-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/m³). 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 ($\dot{\text{V}}$_E/$\dot{\text{V}}$_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, FEV₁ 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 $\dot{\text{V}}$_E/$\dot{\text{V}}$_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 $\dot{\text{V}}$_E/$\dot{\text{V}}$_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.

中文翻译：

---

通气反应恒定负荷运动的吸入以下短效ß ₂与运动诱发的支气管收缩个人激动剂在实验室控制柴油车尾气暴露研究

目的

与SS运动诱发支气管收缩（EIB）使用个人₂激动剂急性运动过程中，以减少呼吸道症状。在有空气污染的运动中进行支气管扩张可能增加吸入污染物的剂量并损害呼吸功能。我们的目的是在完成一个循环的较量，同时暴露于柴油废气（DE）或过滤空气（FA）时，为了评估与EIB个人呼吸的反应与不沙丁胺醇吸入（SAL），短效ß ₂激动剂。

方法

在一项双盲，重复测量设计中，EIB（22-33岁）的19位参与者完成了四次访问：FA-安慰剂（FA-PLA），FA-SAL，DE-PLA和DE-SAL。吸入400 µg SAL或PLA后，参与者坐在暴露室中60分钟，呼吸FA或DE（PM _2.5   = 300μg/ m ³）。然后，参与者在呼吸FA或DE时以峰值工作率的50％循环30分钟。通过肺活量测定，呼吸功（WOB），部分使用通气量（$\dot{\text{V}}$_E /$\dot{\text{V}}$_E，CAP），最大呼气流量曲线下的面积（MEFV _AUC），以及骑车期间和之后的呼吸困难。

结果

观察到响应SAL和急性循环的支气管扩张，与FA / DE暴露无关。具体而言，响应SAL ，FEV ₁增加7.7％（置信区间（CI）：7.2–8.2％； p <0.01），而骑自行车后MEFV _AUC增加1.1％（0.9–1.3％； p = 0.03）。 。尽管总WOB显着下降了6.2 J / min（4.7–7.5 J / min； p = 0.049），并且$\dot{\text{V}}$_E /$\dot{\text{V}}$在SAL暴露中，_E，CAP降低了5.8％（5–6％，p <0.01），呼吸困难未见变化。DE暴露量显着增加$\dot{\text{V}}$_E /$\dot{\text{V}}$_E，CAP降低了2.4％（0.9-3.9％； p <0.01），但这并不影响呼吸困难。

讨论区

我们的研究结果表明，在中等强度运动之前呼吸高水平的DE时使用SAL，在运动后长达60分钟的时间内不会降低呼吸功能或运动通风反应。