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Exercise and Cardiovascular Risk Modulation in Post-COVID Syndrome.

Created on 13 Aug 2026

Authors

Cássia da Luz Goulart, Leandro Tolfo Franzoni, Filipe Ferrari, Ananda Silveira Cardoso, Natália Bittencourt, Ricardo Stein

Published in

Current atherosclerosis reports. Volume 28. Issue 1. Aug 13, 2026. Epub Aug 13, 2026.

Abstract

Post-COVID syndrome (PASC) has emerged as a multisystem condition associated with persistent cardiovascular abnormalities, including endothelial dysfunction, arterial stiffness, chronic inflammation, metabolic disturbances, autonomic imbalance, and increased atherosclerotic risk. This review summarizes the current evidence regarding the pathophysiological mechanisms linking PASC to cardiovascular disease and discusses the potential role of exercise training as a strategy to mitigate vascular dysfunction and cardiovascular risk.
Recent studies demonstrate that individuals with PASC exhibit persistent low-grade inflammation, impaired endothelial function, accelerated vascular aging, platelet hyperreactivity, insulin resistance, sarcopenia, and autonomic dysfunction. These alterations contribute to a pro-atherogenic phenotype that may persist months to years after SARS-CoV-2 infection. Emerging evidence indicates that exercise training improves inflammatory status, endothelial function, arterial stiffness, metabolic health, autonomic regulation, and functional capacity in post-COVID patients, potentially attenuating mechanisms involved in atherosclerotic progression. Post-COVID syndrome is associated with multiple interconnected biological pathways that increase long-term cardiovascular risk. Exercise training appears to be a promising non-pharmacological intervention capable of targeting several of these mechanisms simultaneously. Although further randomized controlled trials are needed, current evidence supports the integration of individualized exercise-based rehabilitation into the management of patients with PASC to promote vascular recovery and reduce cardiovascular risk.

PMID:
42593604
Bibliographic data and abstract were imported from PubMed on 13 Aug 2026.

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