Simpson A J, Romer L M, Kippelen P
Centre for Human Performance, Exercise, and Rehabilitation, Division of Sport, Health, and Exercise Sciences, College of Health and Life Sciences, Brunel University London, Uxbridge, United Kingdom
Centre for Human Performance, Exercise, and Rehabilitation, Division of Sport, Health, and Exercise Sciences, College of Health and Life Sciences, Brunel University London, Uxbridge, United Kingdom.
J Appl Physiol (1985). 2017 May 1;122(5):1329-1335. doi: 10.1152/japplphysiol.01114.2016. Epub 2017 Mar 9.
Local airway water loss is the main physiological trigger for exercise-induced bronchoconstriction (EIB). Our aim was to investigate the effects of whole body water loss on airway responsiveness and pulmonary function in athletes with mild asthma and/or EIB. Ten recreational athletes with a medical diagnosis of mild asthma and/or EIB completed a randomized, crossover study. Pulmonary function tests, including spirometry, whole body plethysmography, and diffusing capacity of the lung for carbon monoxide (Dl), were conducted before and after three conditions: ) 2 h of exercise in the heat with no fluid intake (dehydration), ) 2 h of exercise with ad libitum fluid intake (control), and ) a time-matched rest period (rest). Airway responsiveness was assessed 2 h postexercise/rest via eucapnic voluntary hyperpnea (EVH) to dry air. Exercise in the heat with no fluid intake induced a state of mild dehydration, with a body mass loss of 2.3 ± 0.8% (SD). After EVH, airway narrowing was not different between conditions: median (interquartile range) maximum fall in forced expiratory volume in 1 s was 13 (7-15)%, 11 (9-24)%, and 12 (7-20)% in dehydration, control, and rest conditions, respectively. Dehydration caused a significant reduction in forced vital capacity (300 ± 190 ml, = 0.001) and concomitant increases in residual volume (260 ± 180 ml, = 0.001) and functional residual capacity (260 ± 250 ml, = 0.011), with no change in Dl Mild exercise-induced dehydration does not exaggerate airway responsiveness to dry air in athletes with mild asthma/EIB but may affect small airway function. This study is the first to investigate the effect of whole body dehydration on airway responsiveness. Our data suggest that the airway response to dry air hyperpnea in athletes with mild asthma and/or exercise-induced bronchoconstriction is not exacerbated in a state of mild dehydration. On the basis of alterations in lung volumes, however, exercise-induced dehydration appears to compromise small airway function.
局部气道水分流失是运动诱发支气管收缩(EIB)的主要生理触发因素。我们的目的是研究全身水分流失对轻度哮喘和/或EIB运动员气道反应性和肺功能的影响。10名经医学诊断为轻度哮喘和/或EIB的休闲运动员完成了一项随机交叉研究。在三种情况下前后进行了肺功能测试,包括肺活量测定、全身体积描记法和肺一氧化碳弥散量(Dl):)在炎热环境中进行2小时无液体摄入的运动(脱水),)进行2小时随意摄入液体的运动(对照),以及)一个时间匹配的休息期(休息)。运动/休息2小时后,通过对干燥空气进行等碳酸自主过度通气(EVH)评估气道反应性。在炎热环境中无液体摄入的运动导致轻度脱水状态,体重减轻2.3±0.8%(标准差)。EVH后,各情况下气道狭窄情况无差异:脱水、对照和休息情况下,1秒用力呼气量的最大下降中位数(四分位间距)分别为13(7 - 15)%、11(9 - 24)%和12(7 - 20)%。脱水导致用力肺活量显著降低(300±190毫升,P = 0.001),同时残气量(260±180毫升,P = 0.001)和功能残气量(260±250毫升,P = 0.011)增加,而Dl无变化。轻度运动诱发的脱水不会夸大轻度哮喘/EIB运动员对干燥空气的气道反应性,但可能会影响小气道功能。本研究首次调查了全身脱水对气道反应性的影响。我们的数据表明,轻度哮喘和/或运动诱发支气管收缩的运动员在轻度脱水状态下,对干燥空气过度通气的气道反应不会加剧。然而,基于肺容积的改变,运动诱发的脱水似乎会损害小气道功能。