Journal
AGING CELL
Volume 17, Issue 1, Pages -Publisher
WILEY
DOI: 10.1111/acel.12697
Keywords
aging; exercise; mitochondria; motor function; PGC-1 alpha; sarcopenia; skeletal muscle
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Funding
- Swiss National Science Foundation
- European Research Council (ERC) [616830-MUSCLE_NET]
- Swiss Cancer Research [KFS-3733-08-2015]
- Swiss Society for Research on Muscle Diseases (SSEM)
- SystemsX.ch
- Novartis Stiftung fur Medizinisch-Biologische Forschung
- University of Basel
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The age-related impairment in muscle function results in a drastic decline in motor coordination and mobility in elderly individuals. Regular physical activity is the only efficient intervention to prevent and treat this age-associated degeneration. However, the mechanisms that underlie the therapeutic effect of exercise in this context remain unclear. We assessed whether endurance exercise training in old age is sufficient to affect muscle and motor function. Moreover, as muscle peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1 alpha) is a key regulatory hub in endurance exercise adaptation with decreased expression in old muscle, we studied the involvement of PGC-1 alpha in the therapeutic effect of exercise in aging. Intriguingly, PGC-1 alpha muscle-specific knockout and overexpression, respectively, precipitated and alleviated specific aspects of aging-related deterioration of muscle function in old mice, while other muscle dysfunctions remained unchanged upon PGC-1 alpha modulation. Surprisingly, we discovered that muscle PGC-1 alpha was not only involved in improving muscle endurance and mitochondrial remodeling, but also phenocopied endurance exercise training in advanced age by contributing to maintaining balance and motor coordination in old animals. Our data therefore suggest that the benefits of exercise, even when performed at old age, extend beyond skeletal muscle and are at least in part mediated by PGC-1 alpha.
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