School of Health Sciences, College of Health and Medicine, University of Tasmania, Hobart, AUSTRALIA.
Human and Environmental Physiology Research Unit, School of Human Kinetics, University of Ottawa, Ottawa, ON, CANADA.
Med Sci Sports Exerc. 2020 Feb;52(2):362-369. doi: 10.1249/MSS.0000000000002136.
Sweat-induced fluid loss during prolonged exercise-heat stress can compromise cardiovascular and thermoregulatory function, although its effects on cardiac autonomic modulation remain unclear. We therefore examined heart rate variability (HRV) and recovery (HRRec), as surrogates of cardiac autonomic modulation, during and after prolonged exercise in the heat with and without fluid replacement.
Eleven young and healthy men performed 90 min of semi-recumbent cycling in dry heat (40°C; 20% relative humidity) at a fixed rate of metabolic heat production (600 W; ~46% V˙O2peak) followed by 40-min resting recovery without fluid replacement (No-FR; ~3.4% reduction in body mass). On a separate day, participants completed the same protocol with fluid replacement (FR; 500-700 mL timed boluses) to offset sweat losses. Esophageal temperature and ECG were recorded throughout, with measurements analyzed over 10-min averaged epochs during baseline, each 30-min interval during exercise and 20-min interval during recovery.
Esophageal temperature and heart rate were elevated in No-FR relative to FR throughout exercise (all P ≤ 0.02). The HRV indices reflecting vagal influence of heart rate including the cardiac vagal index (CVI = log10[16 × SD1 × SD2]) and root-mean-square of successive differences were attenuated throughout exercise relative to baseline in both conditions (all P < 0.05), with the magnitude of the reduction greater in the No-FR condition (all P < 0.05). Further, sample entropy was reduced throughout all time points measured during exercise in the No-FR relative to FR condition (all P ≤ 0.03).
Our unique observations indicate that while prolonged exercise heat stress attenuates the vagal influence and complexity of cardiac rhythms, that reduction is further exacerbated by fluid loss, highlighting the importance of fluid replacement in such conditions.
在长时间运动-热应激下，出汗导致的液体流失会损害心血管和体温调节功能，尽管其对心脏自主神经调节的影响尚不清楚。因此，我们研究了在有和没有液体补充的情况下，长时间运动-热应激期间和之后的心率变异性（HRV）和恢复（HRRec），作为心脏自主神经调节的替代指标。
11 名年轻健康男性在干热（40°C；20%相对湿度）下以固定代谢产热率（600 W；46%最大摄氧量）进行半卧位自行车运动 90 分钟，随后在没有液体补充的情况下进行 40 分钟休息恢复（No-FR；3.4%体重减轻）。在另一天，参与者完成了相同的方案，用液体补充（FR；500-700 mL 定时滴注）来弥补汗液流失。整个过程中记录食管温度和心电图，分析基线、运动中每 30 分钟间隔和恢复中 20 分钟间隔的 10 分钟平均时段的测量结果。
在整个运动过程中，No-FR 组的食管温度和心率均高于 FR 组（所有 P ≤ 0.02）。反映心率迷走神经影响的 HRV 指数，包括心脏迷走神经指数（CVI = log10[16 × SD1 × SD2]）和连续差异的均方根，在两种情况下均较基线降低（所有 P < 0.05），No-FR 条件下的降低幅度更大（所有 P < 0.05）。此外，在 No-FR 条件下，样本熵在运动期间所有测量的时间点均降低（所有 P ≤ 0.03）。
我们的独特观察结果表明，虽然长时间运动-热应激会削弱迷走神经对心脏节律的影响和复杂性，但在液体流失的情况下，这种降低会进一步加剧，这凸显了在这种情况下补充液体的重要性。
