Open AccessSearching for a mitochondrial root to the decline in muscle function with ageing
Author(s) -
GonzalezFreire Marta,
Adelnia Fatemeh,
Moaddel Ruin,
Ferrucci Luigi
Publication year - 2018
Publication title -
journal of cachexia, sarcopenia and muscle
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.803
H-Index - 66
eISSN - 2190-6009
pISSN - 2190-5991
DOI - 10.1002/jcsm.12313
Subject(s) - sarcopenia , ageing , mitochondrion , oxidative phosphorylation , skeletal muscle , cognitive decline , senescence , population , population ageing , oxidative stress , biology , gerontology , physical medicine and rehabilitation , microbiology and biotechnology , medicine , endocrinology , biochemistry , environmental health , dementia , disease
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.