Sepsis-induced skeletal muscle atrophy and mitochondrial dysfunction: The beneficial effects of exercise
Gokhan Burcin Kubat1
, Ibrahim Turkel2, Fırat Akat3
1Mitochondria and Cellular Research Unit, Gulhane Health Sciences Institute, University of Health Sciences, Ankara, Turkiye
2Department of Exercise and Sport Sciences, Faculty of Sport Sciences, Hacettepe University, Ankara, Turkiye
3Department of Physiology, Faculty of Medicine, Ankara University, Ankara, Turkiye
Keywords: Sepsis, skeletal muscle atrophy, mitochondria, exercise
Abstract
Sepsis can lead to a wide range of clinical symptoms due to a dysregulated immune response to infection. It remains a major cause of morbidity and mortality in hospitalized patients, particularly those in intensive care units. The association between sepsis and skeletal muscle atrophy is primarily due to inflammation and immobilization during prolonged sepsis. In addition, the physical inactivity caused by sepsis accelerates skeletal muscle atrophy. Sepsis-induced skeletal muscle atrophy is primarily caused by mitochondrial dysfunction, which is recognized as a major contributing factor. Moreover, oxidative stress is implicated in the etiology of sepsis-induced muscle atrophy by contributing to the functional loss of mitochondria. Numerous studies have demonstrated the positive impact of regular exercise on the overall health of patients with various conditions, including sepsis, by modulating mitochondrial health and quality control pathways. This review will explore the role of mitochondria and the potential benefits of exercise in mitigating sepsis-induced skeletal muscle atrophy.
Cite this article as: Kubat GB, Turkel I, Akat F. Sepsis-induced skeletal muscle atrophy and mitochondrial dysfunction: The beneficial effects of exercise.. Turk J Sports Med. 2025;60(1):25-31; https://doi.org/10.47447/tjsm.0872
Concept: GBK, IT, FA Design: GBK, IT, FA Supervision: GBK,FA Data Collection and/or Processing: GBK, IT Analysis and Interpretation: GBK, IT, FA Literature Review: GBK, IT, FA Writing Manuscript: GBK, IT, FA Critical Reviews: GBK, IT, FA. All authors contributed to the final version of the manuscript and discussed the results and contributed to the final manuscript.
The authors declared no conflicts of interest with respect to authorship and/or publication of the article.
The authors received no financial support for the research and/or publication of this article.
