Key result
Previous symptomatic COVID-19 infection significantly reduced heart rate variability (SDNN 77.7 ms vs 138 ms in controls) and blood pressure variability during acute submaximal exercise.
Why the study?
Cardiovascular defects have been observed after SARS-CoV-2 infection, but little is known about how prior infection alters cardiovascular responses to exercise or differs between previously symptomatic and asymptomatic individuals.
Does a previous symptomatic COVID-19 infection alter heart rate and blood pressure variability during acute exercise in young adults?
Cross-Sectional (n=27)
No
Does a previous symptomatic COVID-19 infection alter heart rate and blood pressure variability during acute exercise in young adults?
Absolute Event Rate: 77.7% vs 138%
p-value: p=<0.05
A previous symptomatic COVID-19 infection is associated with altered autonomic regulation during exercise, evidenced by reduced heart rate and blood pressure variability, which may contribute to post-COVID exercise intolerance.
May link prior symptomatic COVID-19 to exercise intolerance via autonomic changes; hypothesis-generating and requires prospective confirmation before practice implications.
Introduction: As the number of COVID-19 cases begin to diminish it is important to turn our attention to any long-term issues that may be associated with a prior infection. Cardiovascular defects have been noted following prior SARS-CoV-2 infections. However, less is known about how a previous infection alters the cardiovascular response to exercise. Further, differences may exist during exercise between previously SARS-CoV-2 positive individuals who had symptoms (symptomatic) relative to those who did not have symptoms (asymptomatic). We hypothesized that previously symptomatic (S) COVID-19 recoveries have an altered cardiovascular response to acute exercise relative to both control (CON; never infected), and previously COVID-19 positive asymptomatic (AS) individuals. Methods: Twenty-seven subjects (CON = 9; AS = 9; S = 9) underwent 30 min of submaximal treadmill exercise. During exercise, blood pressure was recorded on the brachial artery every 5 min and 3-lead electrocardiography was measured continuously. Indirect indicators of autonomic nervous system health: heart rate variability and blood pressure variability were measured during each session. Baseline mean arterial pressure (MAP) was taken prior to exercise in seated, standing and supine positions. Results: Blood pressure was similar (p > 0.05) amongst all three groups. There were no differences between average heart rate (HR; CON = 104 ± 4 BPM vs AS = 118 ± 6 BPM vs. S = 112 ± 3 BPM), mean arterial pressure (MAP; CON = 108 ± 4 mmHg vs. AS = 105 ± 13 mmHg vs. S = 108 ± 7 mmHg) or oxygen consumption (VO2) between groups during a bout of exercise. However, the standard deviation of the inter beat intervals of normal sinus beats, a measure of heart rate variability (HRV) (CON = 138 ± 2.8 m vs. AS = 156 ± 6 m vs. S = 77.7 ± 11 m; p < 0.05) and blood pressure variability (BPV; CON = 5.18 ± 1.1 vs. AS = 12.1 ± 0.88 mmHg vs. S = 10.2 ± 10.7 mmHg; p < 0.05) were different in our S group. Further, when HRV was assessed in the frequency domain the very low frequency was different during exercise in the S group relative to the other groups. Discussion: Collectively, these data suggest that a previous symptomatic SARS-CoV-2 infection may alter heart rate and blood pressure regulation during exercise.
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Chan et al. (2023) conducted a cross-sectional in COVID-19 (n=27). Previous symptomatic COVID-19 infection vs. Previous asymptomatic COVID-19 infection and uninfected controls was evaluated on Heart rate variability (SDNN) during exercise (p=<0.05). Previous symptomatic COVID-19 infection significantly reduced heart rate variability (SDNN 77.7 ms vs 138 ms in controls) and blood pressure variability during acute submaximal exercise.
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