Effect of voluntary hypocapnic hyperventilation on the relationship between core temperature and heat loss responses in exercising humans
Effect of voluntary hypocapnic hyperventilation on the relationship between core temperature and heat loss responses in exercising humans
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DOI：
10.1152/japplphysiol.00334.2014
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发表时间：
2014-12-01
影响因子：
3.3
通讯作者：
Nishiyasu, Takeshi
中科院分区：
文献类型：
--
作者：
Fujii, Naoto;Honda, Yasushi;Nishiyasu, Takeshi
当核心温度达到临界阈值时，两种体温调节反应，皮肤血管舒张和出汗，开始，之后反应幅度随着核心温度的增加而线性增加;因此斜率表示反应灵敏度。我们评估了自主过度通气引起的低碳酸血症对核心温度阈值和体温调节反应敏感性的影响。10名健康男性在三种呼吸条件下以117 W（29.5 ℃，50%RH）进行15分钟的自行车运动：1）自主通气，2）自愿正常碳酸过度通气，3）自愿低碳酸过度通气。在低碳酸血症过度通气试验中，潮气末CO2压力在整个运动过程中降低，而在其他两项试验中，潮气末CO2压力维持在正常碳酸血症水平附近。前臂和前额的皮肤血管传导率被评估为激光多普勒信号/平均动脉血压，前臂出汗率使用通气胶囊法测量。在前臂（36.88 +/- 0.36 vs. 36.68 +/-0.34 ℃，P < 0.05）和前额（36.89 +/- 0.31 vs. 36.75 +/-0.31 ℃，P < 0.05），低碳酸血症患者皮肤血管传导性增加的食管温度阈值高于正常碳酸血症过度通气试验。在低碳酸血症过度通气试验中，与正常碳酸血症过度通气试验相比，前臂（302 +/- 177 vs. 420 +/- 178%基线/℃，P < 0.05）和前额（236 +/- 164 vs. 358 +/- 221%基线/℃，P < 0.05）处食管温度与皮肤血管传导性相关的斜率降低。在低碳酸血症或正常碳酸血症过度通气试验中，前臂出汗率的阈值和斜率均无显著差异。这些研究结果表明，在行使人类，由自愿过度换气引起的低碳酸血症不影响出汗，但它减弱了皮肤血管舒张反应，增加其阈值和降低其敏感性。
Two thermolytic thermoregulatory responses, cutaneous vasodilation and sweating, begin when core temperature reaches a critical threshold, after which response magnitudes increase linearly with increasing core temperature; thus the slope indicates response sensitivity. We evaluated the influence of hypocapnia induced by voluntary hyperventilation on the core temperature threshold and sensitivity of thermoregulatory responses. Ten healthy males performed 15 min of cycling at 117 W (29.5 degrees C, 50% RH) under three breathing conditions: 1) spontaneous ventilation, 2) voluntary normocapnic hyperventilation, and 3) voluntary hypocapnic hyperventilation. In the hypocapnic hyperventilation trial, end-tidal CO2 pressure was reduced throughout the exercise, whereas it was maintained around the normocapnic level in the other two trials. Cutaneous vascular conductances at the forearm and forehead were evaluated as laser-Doppler signal/mean arterial blood pressure, and the forearm sweat rate was measured using the ventilated capsule method. Esophageal temperature threshold was higher for the increase in cutaneous vascular conductance in the hypocapnic than normocapnic hyperventilation trial at the forearm (36.88 +/- 0.36 vs. 36.68 +/- 0.34 degrees C, P < 0.05) and forehead (36.89 +/- 0.31 vs. 36.75 +/- 0.31 degrees C, P < 0.05). The slope relating esophageal temperature to cutaneous vascular conductance was decreased in the hypocapnic than normocapnic hyperventilation trial at the forearm (302 +/- 177 vs. 420 +/- 178% baseline/degrees C, P < 0.05) and forehead (236 +/- 164 vs. 358 +/- 221% baseline/degrees C, P < 0.05). Neither the threshold nor the slope for the forearm sweat rate differed significantly between the hypocapnic or normocapnic hyperventilation trials. These findings indicate that in exercising humans, hypocapnia induced by voluntary hyperventilation does not influence sweating, but it attenuates the cutaneous vasodilatory response by increasing its threshold and reducing its sensitivity.