Abstract
When acute SARS-CoV-2 infections cause symptoms that persist longer than 3 months, this condition is termed long COVID. Symptoms experienced by patients often include myalgia, fatigue, brain fog, cognitive impairments, and post-exertional malaise (PEM), which is the worsening of symptoms following mental or physical exertion. There is little consensus on the pathophysiology of exercise-induced PEM and skeletal-muscle-related symptoms. In this opinion article we highlight intrinsic mitochondrial dysfunction, endothelial abnormalities, and a muscle fiber type shift towards a more glycolytic phenotype as main contributors to the reduced exercise capacity in long COVID. The mechanistic trigger for physical exercise to induce PEM is unknown, but rapid skeletal muscle tissue damage and intramuscular infiltration of immune cells contribute to PEM-related symptoms.
Original language | English |
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Journal | Trends in Endocrinology and Metabolism |
Early online date | 17 Dec 2024 |
DOIs |
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Publication status | E-pub ahead of print - 17 Dec 2024 |
Bibliographical note
Copyright © 2024 The Author(s). Published by Elsevier Ltd.. All rights reserved.Funding
This study was supported the Patient-Led Research Collaborative for Long COVID, ZonMw Onderzoeksprogramma ME/CVS, the Solve ME 2022 Ramsay Grant Program, ME Research UK, ME Stars of Tomorrow Scholarship award from the ICanCME Research Network (to B.T.C.), and Stichting Long COVID Nederland. The authors want to thank our patient representatives for insightful discussions. The authors declare no conflicts of interest.
Funders | Funder number |
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Center for Visual Science, University of Rochester | |
ME Research UK | |
ZonMw Onderzoeksprogramma ME | |
Patient-Led Research Collaborative for Long COVID | |
ICanCME Research Network | |
Stichting Long COVID |