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PRIOR SARS-COV-2 INFECTION DOES NOT INCREASE RISK OF EXERTIONAL HEAT STROKE OR CAUSE DETRIMENTAL CHANGES IN PLASMA CYTOKINES

Abstract

Rachel Kowis, Rachael Badeau, Matthew Kuennen. High Point University, High Point, NC.

Background. SARS-CoV-2 is a viral infection that can cause systemic inflammation with fever symptoms and impaired respiration. Data from animal models suggest that some forms of viral infection can increase risk for exertional heatstroke (EHS), possibly via reductions in the cellular stress response that lead to impaired stress tolerance.Purpose. To determine if persons with prior clinical diagnosis of SARS-CoV-2 infection exhibit any differences in thermoregulatory or cardiopulmonary responses to 60min of cycling exercise in hot, dry ambient conditions. Methods. Nine participants (Age: 22 ± 2 years, Stature: 1.74 ± 0.02 m, Mass: 71.3 ± 3.9 kg, VO2max: 46 ± 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. Four participants had been previously diagnosed with SARS-CoV-2, and the other five participants served as the Control group. Heart rate (HR), esophageal temperature (Tc), mean body temperature (Tb), physiological strain index (PSI), minute ventilation (VE), and oxygen consumption (VO2) were examined throughout exercise. Interleukin 1 Receptor Antagonist (IL-1RA) and Interleukin 6 (IL-6) were assayed from plasma samples that were collected before (Pre), after (Post), and 1h after (1-Post) exercise. Differences between group data were determined with Two-Way RM-ANOVA with Tukey Post Hocs. Results: As compared to the Control group, persons with prior SARS-CoV-2 infection did not exhibit greater elevations in HR (84 ± 4% of HRmax vs 87 ± 2% of HRmax), Tc (1.4 ± 0.3 °C vs 1.1 ± 0.2 °C), Tb (1.2 ± 0.3 °C vs1.1 ± 0.2 °C), PSI (6.9 ± 1.0 vs 6.7 ± 0.6), VE (38.8 ± 4.3 L/min vs 40.5 ± 0.3 L/min) or VO2 (23.8 ± 1.1 ml/kg/min vs 21.0 ± 1.4 ml/kg/min) during 1hr of cycling exercise at a fixed rate of heat production in hot/dry ambient conditions [all P > 0.05]. There were no differences in plasma IL-1RA between the two groups at any time-point [all P > 0.05]. Despite having similar plasma IL-6 concentrations at baseline (0.5 ± 0.2 pg/ml vs 0.6 ± 0.3 pg/ml), the increase in IL-6 post-exercise was more than two-fold greater in the Control group (5.9 ±1.6 pg/ml vs 2.8 ± 0.6 pg/ml; P = 0.04). Conclusions. As compared to Control, we see no evidence of greater thermal or cardiovascular strain during 1hr of exertional heat stress in persons with prior SARS-CoV-2 infection. We also see no difference between groups in plasma IL-RA (which is anti-inflammatory), whereas the plasma IL-6 response to exercise appears to be diminished in persons with prior SARS-CoV-2 infection. While the exact physiologic relevance of this change remains to be determined, 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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