Peçanha Tiago, Forjaz Cláudia L de Moraes, Low David A
Exercise Hemodynamic Laboratory, School of Physical Education and Sport, University of São Paulo, São Paulo, Brazil.
Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, Liverpool, United Kingdom.
Front Neurosci. 2017 Dec 21;11:727. doi: 10.3389/fnins.2017.00727. eCollection 2017.
Post-exercise heart rate (HR) recovery (HRR) presents a biphasic pattern, which is mediated by parasympathetic reactivation and sympathetic withdrawal. Several mechanisms regulate these post-exercise autonomic responses and thermoregulation has been proposed to play an important role. The aim of this study was to test the effects of heat stress on HRR and HR variability (HRV) after aerobic exercise in healthy subjects. Twelve healthy males (25 ± 1 years, 23.8 ± 0.5 kg/m) performed 14 min of moderate-intensity cycling exercise (40-60% HR) followed by 5 min of loadless active recovery in two conditions: heat stress (HS) and normothermia (NT). In HS, subjects dressed in a whole-body water-perfused tube-lined suit to increase internal temperature (T) by ~1°C. In NT, subjects did not wear the suit. HR, core and skin temperatures (T and T), mean arterial pressure (MAP) skin blood flow (SKBF), and cutaneous vascular conductance (CVC) were measured throughout and analyzed during post-exercise recovery. HRR was assessed through calculations of HR decay after 60 and 300 s of recovery (HRR60s and HRR300s), and the short- and long-term time constants of HRR (T30 and HRRt). Post-exercise HRV was examined via calculations of RMSSD (root mean square of successive RR intervals) and RMS (root mean square residual of RR intervals). The HS protocol promoted significant thermal stress and hemodynamic adjustments during the recovery (HS-NT differences: T = +0.7 ± 0.3°C; T = +3.2 ± 1.5°C; MAP = -12 ± 14 mmHg; SKBF = +90 ± 80 a.u; CVC = +1.5 ± 1.3 a.u./mmHg). HRR and post-exercise HRV were significantly delayed in HS (e.g., HRR60s = 27 ± 9 vs. 44 ± 12 bpm, < 0.01; HRR300s = 39 ± 12 vs. 59 ± 16 bpm, < 0.01). The effects of heat stress (e.g., the HS-NT differences) on HRR were associated with its effects on thermal and hemodynamic responses. In conclusion, heat stress delays HRR, and this effect seems to be mediated by an attenuated parasympathetic reactivation and sympathetic withdrawal after exercise. In addition, the impact of heat stress on HRR is related to the magnitude of the heat stress-induced thermal stress and hemodynamic changes.
运动后心率（HR）恢复（HRR）呈现双相模式，这是由副交感神经再激活和交感神经撤离介导的。有几种机制调节这些运动后的自主反应，并且有人提出体温调节起着重要作用。本研究的目的是测试热应激对健康受试者有氧运动后HRR和心率变异性（HRV）的影响。12名健康男性（25±1岁，体重指数23.8±0.5kg/m²）在两种条件下进行了14分钟的中等强度骑行运动（心率40-60%），随后进行5分钟的无负荷主动恢复：热应激（HS）和正常体温（NT）。在HS组，受试者穿着全身水灌注管衬套装，以使体内温度（T）升高约1°C。在NT组，受试者不穿该套装。在运动后恢复期间全程测量并分析心率、核心温度和皮肤温度（Tₑ和Tₛ）、平均动脉压（MAP）、皮肤血流量（SKBF）和皮肤血管传导率（CVC）。通过计算恢复60秒和300秒后的心率下降（HRR60s和HRR300s）以及HRR的短期和长期时间常数（T₃₀和HRRt）来评估HRR。通过计算RMSSD（连续RR间期的均方根）和RMS（RR间期的均方根残差）来检查运动后HRV。HS方案在恢复期间促进了显著的热应激和血流动力学调整（HS与NT的差异：Tₑ = +0.7±0.3°C；Tₛ = +3.2±1.5°C；MAP = -12±14mmHg；SKBF = +90±80任意单位；CVC = +1.5±1.3任意单位/mmHg）。HS组的HRR和运动后HRV明显延迟（例如，HRR60s = 27±9对44±12次/分钟，P < 0.01；HRR300s = 39±12对59±16次/分钟，P < 0.01）。热应激（例如HS与NT的差异）对HRR的影响与其对热和血流动力学反应的影响相关。总之，热应激会延迟HRR，这种影响似乎是由运动后副交感神经再激活减弱和交感神经撤离介导的。此外，热应激对HRR的影响与热应激诱导的热应激和血流动力学变化的程度有关。
