Cardiovascular Prevention and Rehabilitation Centre, Montreal Heart Institute, Montréal, Canada, Montréal, QC, Canada.
Department of Pharmacology and Physiology, Faculty of Medicine, Université de Montréal, Montréal, QC, Canada.
J Physiol. 2020 Mar;598(6):1223-1234. doi: 10.1113/JP279266. Epub 2020 Feb 26.
With the advent of more frequent extreme heat events, adaptability to hot environments will be crucial for the survival of many species, including humans. However, the mechanisms that mediate human heat adaptation have remained elusive. We tested the hypothesis that heat acclimation improves the neural control of body temperature. Skin sympathetic nerve activity, comprising the efferent neural signal that activates heat loss thermoeffectors, was measured in healthy adults exposed to passive heat stress before and after a 7 day heat acclimation protocol. Heat acclimation reduced the activation threshold for skin sympathetic nerve activity, leading to an earlier activation of cutaneous vasodilatation and sweat production. These findings demonstrate that heat acclimation improves the neural control of body temperature in humans.
Heat acclimation improves autonomic temperature regulation in humans. However, the mechanisms that mediate human heat adaptation remain poorly understood. The present study tested the hypothesis that heat acclimation improves the neural control of body temperature. Body temperatures, skin sympathetic nerve activity, cutaneous vasodilatation, and sweat production were measured in 14 healthy adults (nine men and five women, aged 27 ± 5 years) during passive heat stress performed before and after a 7 day heat acclimation protocol. Heat acclimation increased whole-body sweat rate [+0.54 L h (0.32, 0.75), P < 0.01] and reduced resting core temperature [-0.29°C (-0.40, -0.18), P < 0.01]. During passive heat stress, the change in mean body temperature required to activate skin sympathetic nerve activity was reduced [-0.21°C (-0.34, -0.08), P < 0.01] following heat acclimation. The earlier activation of skin sympathetic nerve activity resulted in lower activation thresholds for cutaneous vasodilatation [-0.18°C (-0.35, -0.01), P = 0.04] and local sweat rate [-0.13°C (-0.24, -0.01), P = 0.03]. These results demonstrate that heat acclimation leads to an earlier activation of the neural efferent outflow that activates the heat loss thermoeffectors of cutaneous vasodilatation and sweating.
随着极端高温事件的频繁发生，适应炎热环境对于包括人类在内的许多物种的生存至关重要。然而，介导人类热适应的机制仍然难以捉摸。我们检验了热适应改善体温神经控制的假设。在一项为期 7 天的热适应方案前后，我们测量了健康成年人在被动热应激下暴露时的皮肤交感神经活动，皮肤交感神经活动包括激活散热热敏效应器的传出神经信号。热适应降低了皮肤交感神经活动的激活阈值，导致皮肤血管舒张和出汗更早激活。这些发现表明，热适应改善了人类的体温神经控制。
热适应改善了人类的自主体温调节。然而，介导人类热适应的机制仍知之甚少。本研究检验了热适应改善体温神经控制的假设。在一项为期 7 天的热适应方案前后，我们测量了 14 名健康成年人（9 名男性和 5 名女性，年龄 27 ± 5 岁）在被动热应激期间的体温、皮肤交感神经活动、皮肤血管舒张和出汗。热适应增加了全身出汗率[+0.54 L h（0.32，0.75），P < 0.01]，降低了静息核心体温[-0.29°C（-0.40，-0.18），P < 0.01]。在被动热应激期间，皮肤交感神经活动激活所需的平均体温变化在热适应后减少[-0.21°C（-0.34，-0.08），P < 0.01]。皮肤交感神经活动的更早激活导致皮肤血管舒张和局部出汗率的更低激活阈值[-0.18°C（-0.35，-0.01），P = 0.04]和[-0.13°C（-0.24，-0.01），P = 0.03]。这些结果表明，热适应导致散热热敏效应器的神经传出输出更早激活，从而导致皮肤血管舒张和出汗。
