Searching for a mitochondrial root to the decline in muscle function with ageing

Journal of Cachexia, Sarcopenia and Muscle

Ruin Moaddel¹  Marta Gonzalez‐Freire²  Luigi Ferrucci²  Fatemeh Adelnia² 

[1] Diabetes Section, Laboratory of Clinical Investigation, National Institute on Aging National Institutes of Health Baltimore MD USA;Longitudinal Studies Section, Translational Gerontology Branch, National Institute on Aging National Institutes of Health Baltimore MD USA;

关键词: Mitochondria;    Aging;    Skeletal muscle;    Sarcopenia;    Branched chain amino acids;    Muscle quality;   

DOI  :  10.1002/jcsm.12313

来源: DOAJ

【 摘 要 】

Abstract Sarcopenia, the age‐related loss of muscle mass and strength, is linked to a range of adverse outcomes, such as impaired physical performance, cognitive function, and mortality. Preventing sarcopenia may reduce the burden of functional decline with aging and its impact on physiological and economic well‐being in older adults. Mitochondria in muscle cells lose their intrinsic efficiency and capacity to produce energy during aging, and it has been hypothesized that such a decline is the main driver of sarcopenia. Oxidative phosphorylation becomes impaired with aging, affecting muscle performance, and contributing to an age‐associated decline in mobility. However, it is unclear whether this deterioration is due to a reduced mitochondria population, decreased mitochondrial energetic efficiency, or a reduced capacity to dynamically transport oxygen and nutrients into the mitochondria, and addressing these questions is an active area of research. Further research in humans will require use of new “omics” technologies, progress in neuroimaging techniques that permit energy production assessment, and visualization of molecules critical for energetic metabolism, as well as proxy biomarkers of muscle perfusion.

【 授权许可】

Unknown