Is airway damage during physical exercise related to airway dehydration? Inputs from a computational model.

Abstract

In healthy subjects, at low minute ventilation (V̇e) during physical exercise, the water content and temperature of the airways are well regulated. However, with the increase in V̇e, the bronchial mucosa becomes dehydrated and epithelial damage occurs. Our goal was to demonstrate the correspondence between the ventilatory threshold inducing epithelial damage, measured experimentally, and the dehydration threshold, estimated numerically. In 16 healthy adults, we assessed epithelial damage before and following a 30-min continuous cycling exercise at 70% of maximal work rate, by measuring the variation pre- to postexercise of serum club cell protein (cc16/cr). Blood samples were collected at rest, just at the end of the standardized 10-min warm-up, and immediately, 30 min and 60 min postexercise. Mean V̇e during exercise was kept for analysis. Airway water and heat losses were estimated using a computational model adapted to the experimental conditions and were compared with a literature-based threshold of bronchial dehydration. Eleven participants exceeded the threshold for bronchial dehydration during exercise (group A) and five did not (group B). Compared with post warm-up, the increase in cc16/cr postexercise was significant (mean increase ± SE: 0.48 ± 0.08 ng·L-1 only in group A but not in group B (mean difference ± SE: 0.10 ± 0.04 ng·L-1). This corresponds to an increase of 101 ± 32% [range: 16%-367%] in group A (mean ± SE). Our findings suggest that the use of a computational model may be helpful to estimate an individual dehydration threshold of the airways that is associated with epithelial damage during physical exercise.NEW & NOTEWORTHY Using a computational model for heat and water transfers in the bronchi, we identified a threshold in ventilation during exercise above which airway dehydration is thought to occur. When this threshold was exceeded, epithelial damage was found. This threshold might therefore represent the ventilation upper limit during exercise in susceptible individuals. Our results might help to prevent maladaptation to chronic exercise such as exercise-induced bronchoconstriction or asthma.