患有运动诱发的支气管收缩(EIB)的个体使用β2-激动剂减轻急性运动期间的呼吸道症状。在空气污染中进行运动时,结果支气管扩张会增加吸入污染物的剂量并损害呼吸功能。我们的目的是评估EIB患者在暴露于柴油废气(DE)或过滤空气(FA)的同时完成自行车比赛时的呼吸反应,有或没有吸入沙丁胺醇(SAL)。短效β2激动剂。
在双盲中,重复措施设计,19名EIB(22-33岁)参与者完成了四次访问:FA-安慰剂(FA-PLA),FA-SAL,DE-PLA,DE-SAL.吸入400微克SAL或PLA后,参与者在暴露室中坐了60分钟,呼吸FA或DE(PM2.5=300μg/m3)。然后,参与者在呼吸FA或DE时以50%的峰值工作速率循环30分钟。通过肺活量测定法评估呼吸反应,呼吸功(WOB),部分使用通气能力(V^E/V^E,CAP),最大呼气流量-容积曲线下面积(MEFVAUC),以及骑自行车期间和之后的呼吸困难。
观察到响应SAL和急性循环的支气管扩张,独立于FA/DE暴露。具体来说,FEV1增加了7.7%(置信区间(CI):7.2-8.2%;p<0.01)响应SAL,MEFVAUC在循环后增加了1.1%(0.9-1.3%;p=0.03)。尽管总WOB显著降低了6.2J/min(4.7-7.5J/min;p=0.049),V^E/V^E降低,CAP下降5.8%(5-6%,p<0.01)在SAL暴露中,没有观察到呼吸困难的变化。DE暴露显著增加了V^E/V^E,CAP下降2.4%(0.9-3.9%;p<0.01),但这并不影响呼吸困难。
我们的研究结果表明,当呼吸高水平的DE时,在中等强度运动之前使用SAL,运动后60分钟内不会降低呼吸功能或运动通气反应。
Individuals with exercise-induced
bronchoconstriction (EIB) use ß2-agonists to reduce respiratory symptoms during acute exercise. The resultingbronchodilation could increase the dose of inhaled pollutants and impair respiratory function when exercise is performedin 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.
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 (PM2.5 = 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 (V̇E/V̇E,CAP), area under the maximal expiratory flow-volume curve (MEFVAUC), and dyspnea during and following cycling.
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 MEFVAUC 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 V̇E/V̇E,CAP by 5.8 % (5-6 %, p < 0.01) in the SAL exposures, no changes were observed in dyspnea. The DE exposure significantly increased V̇E/V̇E,CAP by 2.4 % (0.9-3.9 %; p < 0.01), but this did not affect dyspnea.
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.