Recent studies have reported an impaired exercise response at cardiopulmonary exercise testing (CPET) during convalescence from coronavirus disease 2019 (COVID-19). In detail, these previous reports suggest the presence of functional limitations in a consistent proportion of COVID-19 survivors, in the absence of relevant alterations of ventilatory and gas exchange parameters at CPET. Therefore, deconditioning has been proposed as the main mechanism of the reduced peak oxygen uptake in this clinical setting. This interpretation of the results is supported by the evidence that deconditioning is a recognized aspect of the post-intensive care syndrome, with acute sarcopenia being frequently observed among COVID-19 survivors. Here, we hypothesized the role of endothelial dysfunction as a key pathogenic mechanism of the functional limitations of COVID-19, including multisystem deconditioning and subsequent exercise intolerance.
Deconditioning in COVID-19 survivors with reduced exercise performance: A role for endothelial dysfunction? / Ambrosino, Pasquale; Maniscalco, Mauro. - In: MEDICAL HYPOTHESES. - ISSN 0306-9877. - 163:(2022), p. 110847. [10.1016/j.mehy.2022.110847]
Deconditioning in COVID-19 survivors with reduced exercise performance: A role for endothelial dysfunction?
Ambrosino, Pasquale;Maniscalco, Mauro
2022
Abstract
Recent studies have reported an impaired exercise response at cardiopulmonary exercise testing (CPET) during convalescence from coronavirus disease 2019 (COVID-19). In detail, these previous reports suggest the presence of functional limitations in a consistent proportion of COVID-19 survivors, in the absence of relevant alterations of ventilatory and gas exchange parameters at CPET. Therefore, deconditioning has been proposed as the main mechanism of the reduced peak oxygen uptake in this clinical setting. This interpretation of the results is supported by the evidence that deconditioning is a recognized aspect of the post-intensive care syndrome, with acute sarcopenia being frequently observed among COVID-19 survivors. Here, we hypothesized the role of endothelial dysfunction as a key pathogenic mechanism of the functional limitations of COVID-19, including multisystem deconditioning and subsequent exercise intolerance.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
