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Updated: Sep 5, 2026

A Preclinical Model of Exertional Heat Stroke in Mice
Published on: July 1, 2021
Acute exertional heat stress alters both pro- and anti-inflammatory blood markers: A meta-analysis
Albertas Klugas1, Christiana Donkor2, Rachael Nelson2
1School of Medicine, Central Michigan University, Mt. Pleasant, MI, USA.
Abstract:
Exertional heat stress (ExHS) has a significant impact on human health and performance in various occupational and athletic sectors. While exercise is known to affect cytokine levels, there is limited information quantifying the circulating inflammatory response to acute exercise in the heat. This meta-analysis aims to quantify acute changes in circulating pro- and anti-inflammatory markers in response to ExHS among nonacclimatized humans and to determine if these responses are moderated by peak core temperature, heat exposure duration, or exercise intensity. Following PRISMA guidelines, four databases were searched for studies measuring cytokines IL-1β, IL-6, TNF-α, IL-8, IL-10, IL-1ra, and IFN-γ after exercise in temperatures ≥26°C (universal thermal climate index). Random-effects meta-analyses and meta-regressions were performed. Thirty‑six studies (N = 498, 86% male) were included. Acute ExHS induced significant immediate increase in IL-6, TNF-α, IL-8, IL-10, and IL-1ra (all p < 0.05). Both IL-6 and IL-10 remained significantly elevated 1-h post‑ExHS with IL-6 significant at 2 h post. Peak core temperature was a significant moderator for TNF-α and IL-10, and trended for IL-6 at immediate post-ExHS. No significant effects were observed for IL-1β or IFN-γ. Thermal strain in ExHS causes an abrupt disruption of immune homeostasis. The response shifts toward an anti-inflammatory state in early recovery, mirroring the cytokine profile of exertional heat stroke but at a lower magnitude. However, substantial heterogeneity makes future predictions from the model challenging and possibly unreliable.
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