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

Abstract

BACKGROUND: SARS-CoV-2 is a viral infection that can cause systemic inflammation with fever symptoms and impaired respiration. Animal models suggest that some forms of viral infection can increase risk for exertional heatstroke (EHS), possibly via reductions in the cellular stress response. PURPOSE: To determine if persons with prior clinical diagnosis of SARS-CoV-2 infection exhibit any differences in thermoregulatory or cardiopulmonary responses to 60 min of cycling exercise in hot, dry conditions. METHODS: Nine participants (Age: 22 ± 2 years, Stature: 1.74 ± 0.02 m, Mass: 71.3 ± 3.9 kg, VO2max: 46 ± 2 mL/kg/min) completed 1 hr of cycling 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; the other five served as Control. 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 collected before (Pre), after (Post), and 1 h after (1-Post) exercise. Data were analyzed with RM-ANOVA and Tukey Post Hocs. RESULTS: As compared to Control, 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 vs 1.1 ± 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 1 hr 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 two-fold greater in Control (5.9 ± 1.6 pg/ml vs 2.8 ± 0.6 pg/ml; P = 0.04). CONCLUSIONS: Our data do not provide any evidence of an adverse response to exertional heat stress in persons with prior SARS-CoV-2 infection. Thermal and cardiovascular strain responses were not impaired. Plasma IL-6 was reduced following exercise, but the physiologic relevance of that change remains to be determined.