The "Relocalization of Chromatin Modifiers" theory postulates that aging and age-associated tissue degeneration results from a lifetime of accumulation of epigenetic noise, which transcriptionally dysregulates cellular signaling, triggering the symptoms of tissue dysfunction and health deterioration. Evidence suggests that DNA methylation may set the pace of the aging clock in several mammalian tissues, yet it is unclear whether these changes are reversible. Skeletal muscle is of particular interest because of its high metabolic load, biomass, and susceptibility to age-related dysfunction, termed sarcopenia. Using my background in studies of muscular dystrophies, my research focuses on testing if partial epigenetic reprogramming can prevent or reverse aging in vivo, using muscle as a model tissue. I aim to define and reverse the transcriptional, epigenomic, and functional changes that occur in sarcopenia, in addition to determining the impact of partial reprogramming on the aged satellite cell niche.