Publication date: May 26, 2025

Prior viral infection has been suggested to increase exertional heatstroke (EHS) risk. This study examined physiological and immune responses in persons with prior clinical diagnosis of SARS-CoV-2 infection, who were challenged with 1 h of cycling exercise in hot, moderately humid ambient conditions. Fourteen men and six women (age: 21 +/- 1 years, stature: 1. 7 +/- 0. 1 m, mass: 70. 7 +/- 2. 6 kg, VO: 47 +/- 1 mL kg lbm min) completed 1 h of cycling exercise at an intensity that elicited 7. 0 W/kg of metabolic heat production in an environmental chamber (35 ^0C/35% RH). Ten participants had been previously diagnosed with SARS-CoV-2 and ten participants served as CONTROL. Physiological parameters including heart rate (HR), esophageal temperature (T), mean body temperature (T), minute ventilation (V), and oxygen consumption (VO) were measured throughout exercise. Blood samples collected at Pre, Post, 1 h-Post, and 3 h-Post exercise were assayed for immune markers including Interleukin 1 receptor antagonist (IL-1RA) and interferon gamma (IFN-γ). As compared to CONTROL, prior SARS-CoV-2 infection did not cause greater elevations in HR, T, T, V or VO during 1 h of cycling exercise [all p > 0. 05]. The increase in IL-1RA at 1 h-Post exercise in SARS-CoV-2 (195 +/- 104%, p = 0. 012) was greater than the increase in CONTROL (44 +/- 18%, p = 0. 002). IFN-y was elevated at 1 h-Post exercise in SARS-CoV-2 (105 +/- 50%, p = 0. 021) but did not increase following exercise in CONTROL (p > 0. 05). Prior SARS-CoV-2 infection did not alter metabolic responses or increase the rate of rise in HR, T or T during matched workload cycling exercise under hot, moderately humid ambient conditions. IL-1RA is an anti-inflammatory cytokine and IFN-y exhibits direct anti-viral activity, suggesting that immunocompetence was maintained during exertional heat stress.

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