Late-life exercise mitigates skeletal muscle epigenetic aging

K. A. Murach, A. L. Dimet-Wiley, Y. Wen, C. R. Brightwell, C. M. Latham, C. M. Dungan, C. S. Fry, S. J. Watowich

Research output: Contribution to journalArticlepeer-review


There are functional benefits to exercise in muscle, even when performed late in life, but the contributions of epigenetic factors to late-life exercise adaptation are poorly defined. Using reduced representation bisulfite sequencing (RRBS), ribosomal DNA (rDNA) and mitochondrial-specific examination of methylation, targeted high-resolution methylation analysis, and DNAge epigenetic aging clock analysis with a translatable model of voluntary murine endurance/resistance exercise training (progressive weighted wheel running, PoWeR), we provide evidence that exercise may mitigate epigenetic aging in skeletal muscle. Late-life PoWeR from 22-24 months of age modestly but significantly attenuates an age-associated shift toward promoter hypermethylation. The epigenetic age of muscle from old mice that PoWeR-trained for eight weeks was approximately eight weeks younger than 24-month-old sedentary counterparts, which represents ~8% of the expected murine lifespan. These data provide a molecular basis for exercise as a therapy to attenuate skeletal muscle aging.
Original languageAmerican English
Pages (from-to)e13527
JournalAging Cell
StatePublished - 2021

Bibliographical note

Murach, Kevin A Dimet-Wiley, Andrea L Wen, Yuan Brightwell, Camille R Latham, Christine M Dungan, Cory M Fry, Christopher S Watowich, Stanley J eng R00 AG063994/AG/NIA NIH HHS/ AG063994/AG/NIA NIH HHS/ AG063056/AG/NIA NIH HHS/ England 2021/12/22 Aging Cell. 2021 Dec 21:e13527. doi: 10.1111/acel.13527.


  • Rbm10 Timm8a1 Horvath clock PoWeR rDNA


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