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Physiological responses to exercise-heat stress arise from accumulated body heat and the metabolic demands of exercise. Muscle heat production and restricted heat loss determine how rapidly core temperature rises, its peak, and the time spent at an elevated temperature; these features shape heat shock protein 70/72 (HSP70/HSP72) transcription, intracellular accumulation, and release into the circulation. Interleukin-6 (IL-6) released by contracting muscle rises during exercise. Reduced splanchnic perfusion and disruption of the intestinal barrier can accompany nuclear factor κB (NF-κB) activation and modulate tumor necrosis factor α (TNF-α) and interleukin-1β (IL-1β), while interleukin-10 (IL-10) and interleukin-1 receptor antagonist (IL-1ra) contribute to regulation during recovery; C-reactive protein (CRP) generally rises later. This review considers acute exercise-heat stress and repeated heat adaptation along a common physiological trajectory. During acute exposure, heat shock protein (HSP) responses to endurance exercise largely follow cumulative internal heat load, whereas local metabolic stress and mechanical injury may also contribute during resistance and eccentric exercise. Clothing, precooling, intermittent recovery, and superimposed hypoxia alter heat accumulation and circulatory demand, producing different magnitudes of HSP and inflammatory responses. After heat acclimation, the same exercise task produces less thermal and circulatory strain; basal intracellular HSP72 (iHSP72) may increase while the increment induced by a subsequent challenge becomes smaller. Some postexercise inflammatory responses are attenuated, whereas resting concentrations and responses to ex vivo lipopolysaccharide (LPS) stimulation may remain stable. Relating the core-temperature trajectory to HSP70/HSP72 and inflammatory responses helps clarify how acute cellular protection and adaptive reserve develop with repeated heat exposure.
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Jiang et al. (2026) studied this question.
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