COVID‐19 is getting on our nerves: sympathetic neural activity and haemodynamics in young adults recovering from SARS‐CoV‐2

Key points The impact of SARS‐CoV‐2 infection on autonomic and cardiovascular function in otherwise healthy individuals is unknown. For the first time it is shown that young adults recovering from SARS‐CoV‐2 have elevated resting sympathetic activity, but similar heart rate and blood pressure, compa...

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Published inThe Journal of physiology Vol. 599; no. 18; pp. 4269 - 4285
Main Authors Stute, Nina L., Stickford, Jonathon L., Province, Valesha M., Augenreich, Marc A., Ratchford, Stephen M., Stickford, Abigail S. L.
Format Journal Article
LanguageEnglish
Published London Wiley Subscription Services, Inc 01.09.2021
John Wiley and Sons Inc
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Summary:Key points The impact of SARS‐CoV‐2 infection on autonomic and cardiovascular function in otherwise healthy individuals is unknown. For the first time it is shown that young adults recovering from SARS‐CoV‐2 have elevated resting sympathetic activity, but similar heart rate and blood pressure, compared with control subjects. Survivors of SARS‐CoV‐2 also exhibit similar sympathetic nerve activity and haemodynamics, but decreased pain perception, during a cold pressor test compared with healthy controls. Further, these individuals display higher sympathetic nerve activity throughout an orthostatic challenge, as well as an exaggerated heart rate response to orthostasis. If similar autonomic dysregulation, like that found here in young individuals, is present in older adults following SARS‐CoV‐2 infection, there may be substantial adverse implications for cardiovascular health. The novel severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) can elicit systemic adverse physiological effects. However, the impact of SARS‐CoV‐2 on autonomic and cardiovascular function in otherwise healthy individuals remains unclear. Young adults who tested positive for SARS‐CoV‐2 (COV+; n = 16, 8 F) visited the laboratory 35 ± 16 days following diagnosis. Muscle sympathetic nerve activity (MSNA), systolic (SBP) and diastolic (DBP) blood pressure, and heart rate (HR) were measured in participants at rest and during a 2 min cold pressor test (CPT) and 5 min each at 30° and 60° head‐up tilt (HUT). Data were compared with age‐matched healthy controls (CON; n = 14, 9 F). COV+ participants (18.2 ± 6.6 bursts min−1) had higher resting MSNA burst frequency compared with CON (12.7 ± 3.4 bursts min−1) (P = 0.020), as well as higher MSNA burst incidence and total activity. Resting HR, SBP and DBP were not different. During CPT, there were no differences in MSNA, HR, SBP or DBP between groups. COV+ participants reported less pain during the CPT compared with CON (5.7 ± 1.8 vs. 7.2 ± 1.9 a.u., P = 0.036). MSNA was higher in COV+ compared with CON during HUT. There was a group‐by‐position interaction in MSNA burst incidence, as well as HR, in response to HUT. These results indicate resting sympathetic activity, but not HR or BP, may be elevated following SARS‐CoV‐2 infection. Further, cardiovascular and perceptual responses to physiological stress may be altered, including both exaggerated (orthostasis) and suppressed (pain perception) responses, compared with healthy young adults. Key points The impact of SARS‐CoV‐2 infection on autonomic and cardiovascular function in otherwise healthy individuals is unknown. For the first time it is shown that young adults recovering from SARS‐CoV‐2 have elevated resting sympathetic activity, but similar heart rate and blood pressure, compared with control subjects. Survivors of SARS‐CoV‐2 also exhibit similar sympathetic nerve activity and haemodynamics, but decreased pain perception, during a cold pressor test compared with healthy controls. Further, these individuals display higher sympathetic nerve activity throughout an orthostatic challenge, as well as an exaggerated heart rate response to orthostasis. If similar autonomic dysregulation, like that found here in young individuals, is present in older adults following SARS‐CoV‐2 infection, there may be substantial adverse implications for cardiovascular health.
Bibliography:This is an Editor's Choice article from the 15 September 2021 issue.
The peer review history is available in the Supporting Information section of this article
Edited by: Harold Schultz & Vaughan Macefield
https://doi.org/10.1113/JP281888#support‐information‐section
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The peer review history is available in the Supporting Information section of this article (https://doi.org/10.1113/JP281888#support‐information‐section).
ISSN:0022-3751
1469-7793
1469-7793
DOI:10.1113/JP281888