Heat stress, gastrointestinal permeability and interleukin-6 signaling — Implications for exercise performance and fatigue

N. Vargas, F. Marino
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引用次数: 33

Abstract

ABSTRACT Exercise in heat stress exacerbates performance decrements compared to normothermic environments. It has been documented that the performance decrements are associated with reduced efferent drive from the central nervous system (CNS), however, specific factors that contribute to the decrements are not completely understood. During exertional heat stress, blood flow is preferentially distributed away from the intestinal area to supply the muscles and brain with oxygen. Consequently, the gastrointestinal barrier becomes increasingly permeable, resulting in the release of lipopolysaccharides (LPS, endotoxin) into the circulation. LPS leakage stimulates an acute-phase inflammatory response, including the release of interleukin (IL)-6 in response to an increasingly endotoxic environment. If LPS translocation is too great, heat shock, neurological dysfunction, or death may ensue. IL-6 acts initially in a pro-inflammatory manner during endotoxemia, but can attenuate the response through signaling the hypothalamic pituitary adrenal (HPA)-axis. Likewise, IL-6 is believed to be a thermoregulatory sensor in the gut during the febrile response, hence highlighting its role in periphery – to – brain communication. Recently, IL-6 has been implicated in signaling the CNS and influencing perceptions of fatigue and performance during exercise. Therefore, due to the cascade of events that occur during exertional heat stress, it is possible that the release of LPS and exacerbated response of IL-6 contributes to CNS modulation during exertional heat stress. The purpose of this review is to evaluate previous literature and discuss the potential role for IL-6 during exertional heat stress to modulate performance in favor of whole body preservation.
热应激、胃肠通透性和白细胞介素-6信号传导——对运动表现和疲劳的影响
与常温环境相比,热应激下的运动加剧了运动能力的下降。已有文献表明,成绩下降与中枢神经系统(CNS)的传出驱动减少有关,然而,导致成绩下降的具体因素尚未完全了解。在运动性热应激时,血流优先远离肠道区域,为肌肉和大脑提供氧气。因此,胃肠道屏障变得越来越渗透性,导致脂多糖(LPS,内毒素)释放到循环中。脂多糖泄漏刺激急性期炎症反应,包括释放白介素(IL)-6,以应对日益内毒素的环境。如果LPS易位过大,可能会导致热休克、神经功能障碍或死亡。在内毒素血症中,IL-6最初以促炎方式起作用,但可以通过下丘脑垂体-肾上腺(HPA)轴信号通路减弱反应。同样,IL-6被认为是发热反应期间肠道中的温度调节传感器,因此突出了其在外周-脑通讯中的作用。最近,IL-6被认为与中枢神经系统的信号传导和运动过程中对疲劳和表现的感知有关。因此,由于在运动性热应激期间发生的一系列事件,LPS的释放和IL-6反应的加剧可能有助于运动性热应激期间中枢神经系统的调节。本综述的目的是评估先前的文献,并讨论IL-6在运动性热应激中调节性能以促进全身保存的潜在作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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