Endurance Exercise, Mitochondrial Rejuvenescence and Aging: On Your Mark, Get Set, GO!
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abstract
The role of mitochondrial abnormalities has been extensively characterized in the etiology of systemic decline with aging. A causal role for mitochondrial DNA (mtDNA) mutagenesis in mammalian ageing is supported by recent studies demonstrating that the polymerase gamma (PolG) mutator mouse, harbouring a proofreading‐deficient copy of PolG, exhibits an accelerated aging phenotype, systemic mitochondrial dysfunction, multisystem failure, and reduced lifespan. Longitudinal studies in humans have demonstrated that endurance training reduces the risk of chronic diseases and extends life expectancy. We aimed to delineate if endurance training can prevent the premature aging, and reverse and/or attenuate systemic mitochondrial decline in PolG mice. At 3 months of age, 36 PolG mice (♀ = ♂) were randomly assigned to a sedentary (SED) or forced‐endurance training (END; 15m/min for 45 min, 3x/week for 5 months) group. END induced systemic mitochondrial biogenesis, increased oxidative capacity, restored mitochondrial morphology, and prevented mtDNA depletion in multiple tissues in PolG mice. These adaptations synergistically conferred complete phenotypic protection, rescued multisystem pathology (sarcopenia, cardiac hypertrophy, macrocytic anemia and splenomegaly), and increased lifespan of these mice. We conclude that endurance exercise promotes systemic mitochondrial oxidative capacity, contributing to the complete rejuvenation of PolG mice. However, it seems unlikely that the multi‐organ mitochondrial biogenesis observed is attributable to a single factor which can be mimicked by an “exercise pill.” (Funded by CIHR, and Mr. Warren Lammert and family)
