ORCID
- Affourtit, Charles: 0000-0003-1776-9943
- Carre, Jane: 0000-0002-0699-104X
Abstract
Sarcopenia lowers the quality-of-life for millions of people across the world, as accelerated loss of skeletal muscle mass and function contributes to both age- and disease-related frailty. Physical activity remains the only proven therapy for sarcopenia to date, but alternatives are much sought after to manage this progressive muscle disorder in individuals who are unable to exercise. Mitochondria have been widely implicated in the etiology of sarcopenia and are increasingly suggested as attractive therapeutic targets to help restore the perturbed balance between protein synthesis and breakdown that underpins skeletal muscle atrophy. Reviewing current literature, we note that mitochondrial bioenergetic changes in sarcopenia are generally interpreted as intrinsic dysfunction that renders muscle cells incapable of making sufficient ATP to fuel protein synthesis. Based on the reported mitochondrial effects of therapeutic interventions, however, we argue that the observed bioenergetic changes may instead reflect an adaptation to pathologically decreased energy expenditure in sarcopenic muscle. Discrimination between these mechanistic possibilities will be crucial for improving the management of sarcopenia.
DOI
10.1111/apha.14107
Publication Date
2024-02-02
Publication Title
Acta Physiologica
Volume
240
Issue
3
ISSN
1748-1708
Organisational Unit
School of Biomedical Sciences
Recommended Citation
Affourtit, C., & Carré, J. (2024) 'Mitochondrial involvement in sarcopenia', Acta Physiologica, 240(3). Available at: https://doi.org/10.1111/apha.14107