Please use this identifier to cite or link to this item: https://doi.org/10.1186/s12967-021-02737-1.
Title: Exercise rescues mitochondrial coupling in aged skeletal muscle: a comparison of different modalities in preventing sarcopenia
Authors: Harper, Colin
Gopalan, Venkatesh
Goh, Jor Ming 
Keywords: Skeletal muscle
Mitochondria
Aging
Exercise
Issue Date: 16-Feb-2021
Publisher: Springer Nature
Citation: Harper, Colin, Gopalan, Venkatesh, Goh, Jor Ming (2021-02-16). Exercise rescues mitochondrial coupling in aged skeletal muscle: a comparison of different modalities in preventing sarcopenia. Journal of Translational Medicine 19 (71). ScholarBank@NUS Repository. https://doi.org/10.1186/s12967-021-02737-1.
Abstract: Skeletal muscle aging is associated with a decline in motor function and loss of muscle mass- a condition known as sarcopenia. The underlying mechanisms that drive this pathology are associated with a failure in energy generation in skeletal muscle, either from age-related decline in mitochondrial function, or from disuse. To an extent, lifelong exercise is efcacious in preserving the energetic properties of skeletal muscle and thus may delay the onset of sarcopenia. This review discusses the cellular and molecular changes in skeletal muscle mitochondria during the aging process and how diferent exercise modalities work to reverse these changes. A key factor that will be described is the efciency of mitochondrial coupling—ATP production relative to O2 uptake in myocytes and how that efciency is a main driver for age-associated decline in skeletal muscle function. With that, we postulate the most efective exercise modality and protocol for reversing the molecular hallmarks of skeletal muscle aging and staving of sarcopenia. Two other concepts pertinent to mitochondrial efciency in exercise-trained skeletal muscle will be integrated in this review, including- mitophagy, the removal of dysfunctional mitochondrial via autophagy, as well as the implications of muscle fber type changes with sarcopenia on mitochondrial function.
Source Title: Journal of Translational Medicine
URI: https://scholarbank.nus.edu.sg/handle/10635/191000
ISSN: 14795876
DOI: 10.1186/s12967-021-02737-1.
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