Exercise-induced dehydration alters pulmonary function but does not modify airway responsiveness to dry air in athletes with mild asthma

Abstract

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_CO), were conducted before and after three conditions: 1) 2 h of exercise in the heat with no fluid intake (dehydration), 2) 2 h of exercise with ad libitum fluid intake (control), and 3) 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, P = 0.001) and concomitant increases in residual volume (260 ± 180 ml, P = 0.001) and functional residual capacity (260 ± 250 ml, P = 0.011), with no change in Dl_CO Mild exercise-induced dehydration does not exaggerate airway responsiveness to dry air in athletes with mild asthma/EIB but may affect small airway function.NEW & NOTEWORTHY 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.

Keywords: airway hyperresponsiveness; eucapnic voluntary hyperpnea; exercise-induced asthma; exercise-induced bronchoconstriction; whole body dehydration.

Fig. 1.

Schematic of protocol to assess changes in airway responsiveness and pulmonary function in a dehydration condition (2 h of exercise in the heat with fluid restriction), a control condition (2 h of exercise in ambient conditions with voluntary fluid consumption), and a time-matched rest condition (2 h of rest with voluntary fluid consumption). EVH, eucapnic voluntary hyperpnea; Dl_CO, diffusing capacity of the lung for carbon monoxide; V̇_E, ventilation; HR, heart rate.

Fig. 2.

Change in forced expiratory volume in 1 s (FEV₁) after exercise in a dehydrated state (dehydration), exercise in a euhydrated state (control), and a time-matched rest period (rest). Values are medians and interquartile ranges for 10 recreational athletes with mild asthma and/or exercise-induced bronchoconstriction.

Fig. 3.

Change in forced vital capacity (FVC) after exercise in a dehydrated state (dehydration), exercise in a euhydrated state (control), and a time-matched rest period (rest). Values are means ± 95% confidence interval for 10 recreational athletes with mild asthma and/or exercise-induced bronchoconstriction. *P ≤ 0.05; **P ≤ 0.01 vs. control and rest. Reduction in FVC >200 ml (dashed lines) is considered clinically meaningful (28).

Fig. 4.

Change in functional residual capacity (FRC) and residual volume (RV) after exercise in a dehydrated state (dehydration), exercise in a euhydrated state (control), and a time-matched rest period (rest). Values are means ± 95% confidence intervals for 10 recreational athletes with mild asthma and/or exercise-induced bronchoconstriction.

Fig. 5.

Relationship between change in body mass and change in residual volume (RV) after 2 h of exercise with fluid restriction.