INTRODUCTION: Current studies in the general population provide evidence that persisting symptoms after SARS-CoV-2 infection may relate to a dysfunction in the autonomic nervous system regarding blood pressure (BP) and heart rate (HR) regulation (1,2,3). In many studies, the measurements have been performed in resting state or with the tilt table test (TTT). In the absence of definitive data, there is ongoing uncertainty about how the autonomic nervous system adapts to physical stress in elite athletes. The aim of the study was to evaluate the dynamics of BP and HR and physical performance during exercise test in elite athletes before and after SARS-CoV-2 infection. METHODS: 17 German Olympic Sports Confederation athletes (15 men, 2 women; mean age 23 years ± 5) aged between 20 and 35 with laboratory-confirmed SARS-CoV-2 infection were included in this panel study, which was implemented from December 2020 to September 2021 at the Institute of Cardiology and Sports medicine of the German Sport University Cologne (DSHS). SARS-CoV-2 infection as determined by reverse transcription-polymerase chain reaction (PCR) or serum immune globulin G antibody against the SARS-CoV-2 virus. To evaluate autonomic regulation of systolic BP and HR including rate pressure-product (HR × BPsyst.) incremental exercise test was conducted as soon as possible, after initial SARS-CoV-2 infection (t0) and 16 weeks later (t1). Physical performance was determined by peak power output (Wpeak). All results were compared with existing pre-covid data (t-1) of the athletes. RESULTS: Our analysis showed a significant increase in HR at 250 Watt (p=0.035) at t0.The mean Wpeak (t-1: 261,06 ± 64,61, t0: 257,20 ± 69,44, t1: 256,64 ± 55,38), BPsyst. and rate pressure - product (p>0.05) showed no significant difference between all time points of measurement. CONCLUSION: In conclusion, the study indicates that the autonomic regulation of BP and HR was not critically altered by SARS-CoV-2 infection in elite athletes. Although significant increases in HR at the pre maximum intensity levels were observed 4 weeks after acute infection, no limitations in HR regulation could be identified. Further long-term research including spiroergometry data is needed to draw reliable conclusions.
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