Faculty of Health and Sport Sciences, University of Tsukuba, Tsukuba City, Ibaraki , Japan.
Department of Health Sciences, Prefectural University of Hiroshima , Hiroshima , Japan.
J Appl Physiol (1985). 2018 Jan 1;124(1):225-233. doi: 10.1152/japplphysiol.00232.2017. Epub 2017 Sep 28.
Elevating core temperature at rest causes increases in minute ventilation (V̇e), which lead to reductions in both arterial CO partial pressure (hypocapnia) and cerebral blood flow. We tested the hypothesis that in resting heated humans this hypocapnia diminishes the ventilatory sensitivity to rising core temperature but does not explain a large portion of the decrease in cerebral blood flow. Fourteen healthy men were passively heated using hot-water immersion (41°C) combined with a water-perfused suit, which caused esophageal temperature (T) to reach 39°C. During heating in two separate trials, end-tidal CO partial pressure decreased from the level before heating (39.4 ± 2.0 mmHg) to the end of heating (30.5 ± 6.3 mmHg) ( P = 0.005) in the Control trial. This decrease was prevented by breathing CO-enriched air throughout the heating such that end-tidal CO partial pressure did not differ between the beginning (39.8 ± 1.5 mmHg) and end (40.9 ± 2.7 mmHg) of heating ( P = 1.00). The sensitivity to rising T (i.e., slope of the T - V̇ relation) did not differ between the Control and CO-breathing trials (37.1 ± 43.1 vs. 16.5 ± 11.1 l·min·°C, P = 0.31). In both trials, middle cerebral artery blood velocity (MCAV) decreased early during heating (all P < 0.01), despite the absence of hyperventilation-induced hypocapnia. CO breathing increased MCAV relative to Control at the end of heating ( P = 0.005) and explained 36.6% of the heat-induced reduction in MCAV. These results indicate that during passive heating at rest ventilatory sensitivity to rising core temperature is not suppressed by hypocapnia and that most of the decrease in cerebral blood flow occurs independently of hypocapnia. NEW & NOTEWORTHY Hyperthermia causes hyperventilation and concomitant hypocapnia and cerebral hypoperfusion. The last may underlie central fatigue. We are the first to demonstrate that hyperthermia-induced hyperventilation is not suppressed by the resultant hypocapnia and that hypocapnia explains only 36% of cerebral hypoperfusion elicited by hyperthermia. These new findings advance our understanding of the mechanisms controlling ventilation and cerebral blood flow during heat stress, which may be useful for developing interventions aimed at preventing central fatigue during hyperthermia.
在休息时升高核心温度会导致分钟通气量（V̇e）增加，从而导致动脉 CO 分压（低碳酸血症）和脑血流量降低。我们检验了这样一个假设，即在休息时受热的人体中，这种低碳酸血症会降低对核心温度升高的通气敏感性，但不能解释脑血流量下降的大部分原因。14 名健康男性通过热水浸泡（41°C）和水灌注服被动加热，使食管温度（T）达到 39°C。在两次单独的加热试验中，与加热前（39.4±2.0mmHg）相比，潮气末 CO 分压在加热结束时（30.5±6.3mmHg）下降（P=0.005）在对照试验中。通过在整个加热过程中呼吸富含 CO 的空气，防止了这种下降，从而使潮气末 CO 分压在加热开始（39.8±1.5mmHg）和结束（40.9±2.7mmHg）时没有差异（P=1.00）。在对照和 CO 呼吸试验中，升高 T 的敏感性（即 T-V̇关系的斜率）没有差异（37.1±43.1 与 16.5±11.1l·min·°C，P=0.31）。在这两个试验中，尽管没有因过度通气引起的低碳酸血症，但大脑中动脉血流速度（MCAV）在加热早期就下降了（所有 P<0.01）。CO 呼吸在加热结束时使 MCAV 相对于对照升高（P=0.005），并解释了 MCAV 因发热而降低的 36.6%。这些结果表明，在休息时被动加热时，升高核心温度的通气敏感性不受低碳酸血症的抑制，而脑血流量的大部分下降与低碳酸血症无关。新发现和值得注意的发现 体温升高会导致过度通气和随之而来的低碳酸血症和脑灌注不足。后者可能是中枢疲劳的基础。我们是第一个证明发热引起的过度通气不受由此产生的低碳酸血症抑制的人，而且低碳酸血症仅解释了发热引起的脑灌注减少的 36%。这些新发现增进了我们对热应激期间控制通气和脑血流机制的理解，这可能有助于开发旨在预防发热时中枢疲劳的干预措施。
