Laboratoire J. A. Dieudonné, UMR CNRS 7351, Université Côte d'Azur, Nice, France.
Centre VADER, Université Côte d'Azur, Nice, France.
J Appl Physiol (1985). 2022 Apr 1;132(4):1031-1040. doi: 10.1152/japplphysiol.00520.2021. Epub 2022 Feb 24.
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 () and five did not (). Compared with post warm-up, the increase in cc16/cr postexercise was significant (mean increase ± SE: 0.48 ± 0.08 ng·L only in but not in (mean difference ± SE: 0.10 ± 0.04 ng·L). This corresponds to an increase of 101 ± 32% [range: 16%-367%] in (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. 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.
在健康受试者中,在低分钟通气量(V̇e)下进行体力活动时,气道的水分和温度得到很好的调节。然而,随着 V̇e 的增加,支气管黏膜会脱水,上皮细胞受损。我们的目标是证明实验测量的诱导上皮损伤的通气阈与数值估计的脱水阈之间的对应关系。在 16 名健康成年人中,我们通过测量血清 club 细胞蛋白(cc16/cr)在运动前后的变化来评估运动 30 分钟后上皮损伤情况,运动方案为 70%最大工作率的持续踏车运动。在休息时、标准 10 分钟热身结束时以及运动后 30 分钟和 60 分钟采集血液样本。分析时保持运动过程中的平均 V̇e。使用适应实验条件的计算模型来估计气道水和热损失,并将其与基于文献的支气管脱水阈值进行比较。11 名参与者在运动过程中超过了支气管脱水的阈值(),而 5 名参与者没有()。与热身结束时相比,运动后 cc16/cr 的增加在中显著(仅中平均增加 ± SE:0.48±0.08ng·L,而中没有显著增加(平均差异 ± SE:0.10±0.04ng·L)。这相当于(平均值 ± SE)中增加 101±32%[范围:16%-367%]。我们的研究结果表明,使用计算模型可能有助于估计与体力活动中上皮损伤相关的气道个体脱水阈值。通过使用计算模型来模拟热和水在支气管中的转移,我们确定了一个在运动中发生气道脱水的通气阈值。当超过该阈值时,就会出现上皮损伤。因此,该阈值可能代表易感个体在运动中的通气上限。我们的研究结果可能有助于防止慢性运动适应性不良,如运动性支气管收缩或哮喘。