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Nathan Conrad1, Karissa Fryar1, Ben Lee2, Matthew Kuennen1. 1High Point University, High Point, NC. 2Coventry University, Coventry, United Kingdom.

BACKGROUND: Persons with a compromised cellular stress response are more susceptible to exertional heat stroke. The present study examined the cellular stress response in persons with prior clinical diagnosis of SARS-CoV-2 infection, who were challenged with 60min of cycling exercise in hot, dry ambient conditions. METHODS: Eighteen participants (Age: 21±1 years, Stature: 1.7±0.1 m, Mass: 70.3±2.7 kg, VO2max: 47±2 mL-1kg lean body mass-1.min-1) completed 1hr of cycling exercise in an environmental chamber (35°C/35% RH) at an intensity that elicited 9.0 W/kg of metabolic heat production. Ten participants had been previously diagnosed with SARS-CoV-2, and the other eight participants served as the Control group. Heart rate (HR), esophageal temperature (Tc), mean body temperature (Tb), minute ventilation (VE), and oxygen consumption (VO2) were examined throughout exercise. Leukocytes were isolated from blood samples collected before (Pre), after (Post), 1h after (1-Post), and 3h after (3-Post) exercise. Western blot was used to quantify the protein content of markers along the TLR signaling pathway (TLR4, pNFKB, NFKB) and mediators of the cellular stress response (HSP90, HSP70, HSP60, HSP32). Between group differences were examined using RM-ANOVA with Bonferroni Post Hocs. RESULTS: As compared to Control, persons with prior SARS-CoV-2 infection did not exhibit greater elevations in HR (87±5% vs 82±8% of HRmax), Tc (1.27±0.50 vs 1.25±0.63 °C), Tb (1.21±0.41 vs 1.12±0.47 °C), VE (40.7±7.0 vs 36.8±7.8 L/min) or VO2 (22.9±2.7 vs 24.3±2.4 mL-1kg lean body mass-1.min-1) during 1hr of cycling exercise at a fixed rate of heat production in hot/dry ambient conditions [all p>0.05]. Participants in the Control group exhibited a 57± 27% increase in TLR4 content at 1-Post (p< 0.05), whereas TLR4 content did not increase following exercise in SARS CoV-2. HSP90 content was increased by 83±39% at 3-Post exercise in the SARS CoV-2 group (p<0.05), whereas HSP90 content did not increase following exercise in the Control group. HSP70, HSP60, HSP32, and the pNFKB/NFKB ratio were all increased following exercise, but there were no differences between the SARS-CoV-2 and Control groups [all p>0.05]. CONCLUSIONS: As compared to Control, persons with prior SARS-CoV-2 infection do not exhibit greater thermal or cardiovascular strain during 1hr of exertional heat stress. Increased HSP90 and diminished TLR4 content in leukocytes following exercise suggest that persons with prior SARS-CoV-2 infection may experience reduced inflammation, which might be attributable to superior activation of the cellular stress response. While the exact physiologic relevance of these adjustments remains to be determined, the present study data do not provide any evidence of an adverse response to exertional heat stress in persons with prior SARS-CoV-2 infection.

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