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热环境中运动时,蛋白酶激活受体 2 的外源性激活可减轻老年男性的皮肤血管扩张和出汗。

Exogenous Activation of Protease-Activated Receptor 2 Attenuates Cutaneous Vasodilatation and Sweating in Older Men Exercising in the Heat.

机构信息

Human and Environmental Physiology Research Unit, University of Ottawa, Ottawa, Ontario, Canada,

Faculty of Health and Sport Sciences, University of Tsukuba, Tsukuba, Japan,

出版信息

Skin Pharmacol Physiol. 2019;32(5):235-243. doi: 10.1159/000500643. Epub 2019 Jun 20.

Abstract

BACKGROUND

Protease-activated receptor 2 (PAR2) exists in the cutaneous vasculature and eccrine sweat glands. We previously showed that in young habitually active men, exogenous PAR2 activation via the agonist SLIGKV-NH2 had no effect on heat loss responses of cutaneous vasodilatation and sweating during rest or exercise in the heat. However, ageing is associated with altered mechanisms governing these responses. Thus, the effect of exogenous PAR2 activation on cutaneous vasodilatation and sweating in older individuals may differ from that in young adults.

METHODS

Local cutaneous vascular conductance (CVC) and sweat rate were measured in 9 older males (62 ± 4 years) at four forearm skin sites treated with the following: (1) lactated Ringer solution (control), (2) 0.05 mM, (3) 0.5 mM, or (4) 5 mM SLIGKV-NH2. Measurements were performed while participants rested in a non-heat-stress environment (25°C) for ∼60 min and an additional 50 min thereafter in the heat (40°C). Participants then performed 50 min of cycling at a fixed metabolic heat load of 200 W/m2 (to maintain the same thermal drive for heat loss between participants) followed by a 30-min recovery.

RESULTS

CVC during non-heat-stress resting was elevated from the control site with 5 mM SLIGKV-NH2 (p ≤ 0.05), but this response was not observed during ambient heat exposure. By contrast, 5 mM SLIGKV-NH2 lowered CVC during the early stage (10 and 20 min) of exercise compared to the control site (all p ≤ 0.05). Although sweating during non-heat-stressed and heat-stressed resting was not affected by any dose of SLIGKV-NH2, it was reduced with all SLIGKV-NH2 doses relative to the control site during and following exercise (all p ≤ 0.05).

CONCLUSION

We show that while exogenous PAR2 activation induces cutaneous vasodilatation at rest under non-heat-stressed conditions, it attenuates cutaneous vasodilatation and sweating during and following an exercise-induced heat stress in older men.

摘要

背景

蛋白酶激活受体 2(PAR2)存在于皮肤血管和外分泌汗腺中。我们之前的研究表明,在年轻、习惯性活跃的男性中,通过激动剂 SLIGKV-NH2 对 PAR2 的外源性激活对休息或热环境下运动时皮肤血管扩张和出汗的热损失反应没有影响。然而,衰老与这些反应的调节机制改变有关。因此,外源性 PAR2 激活对老年人皮肤血管扩张和出汗的影响可能与年轻人不同。

方法

在 9 名老年男性(62±4 岁)的四个前臂皮肤部位进行局部皮肤血管传导(CVC)和出汗率测量,分别接受以下处理:(1)乳酸林格溶液(对照)、(2)0.05mM、(3)0.5mM 或(4)5mM SLIGKV-NH2。在参与者处于非热应激环境(25°C)中约 60 分钟后,以及之后在热环境(40°C)中再进行 50 分钟的测量。然后,参与者以 200W/m2 的固定代谢热负荷进行 50 分钟的自行车运动(以保持参与者之间的热损失相同的热驱动力),然后进行 30 分钟的恢复期。

结果

在非热应激休息时,用 5mM SLIGKV-NH2 处理的 CVC 从对照部位升高(p≤0.05),但在环境热暴露时未观察到这种反应。相比之下,在运动的早期(10 和 20 分钟),5mM SLIGKV-NH2 降低了与对照部位相比的 CVC(所有 p≤0.05)。尽管在非热应激和热应激休息期间,SLIGKV-NH2 的任何剂量都不会影响出汗,但在运动中和运动后,与对照部位相比,所有 SLIGKV-NH2 剂量都会减少出汗(所有 p≤0.05)。

结论

我们表明,虽然外源性 PAR2 激活在非热应激条件下休息时诱导皮肤血管扩张,但它会减弱老年人在运动引起的热应激期间和之后的皮肤血管扩张和出汗。

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