Introduction: A bout of vigorous endurance exercise transiently activates Toll-like receptor 4 (TLR4) and reduces TLR4 protein expressed on peripheral blood mononuclear cells (PBMCs). Endurance training, on the other hand, reduces TLR4-mediated signaling and minimizes the physiological stress imposed by exercise. Less is known about what occurs in skeletal muscle regarding TLR4 regulation and signaling.
View Article and Find Full Text PDFA rise in body temperature caused by physical work, including exercise, in a hot climate can lead to heat-related illnesses such as exertional heat exhaustion and stroke. Individuals who work physically demanding occupations in hot environments are at heightened risk of heat injury. The mechanisms that contribute to heat illness resulting from physical work in the heat are complex and include dehydration, tissue ischemia and damage, oxidative stress, and inflammatory events.
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October 2024
Purpose: Autophagy and heat shock protein (HSP) response are proteostatic systems involved in the acute and adaptive responses to exercise. These systems may upregulate sequentially following cellular stress including acute exercise, however, currently few data exist in humans. This study investigated the autophagic and HSP responses to acute intense lower body resistance exercise in peripheral blood mononuclear cells (PBMCs) with and without branched-chain amino acids (BCAA) supplementation.
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