You might recall that in some ways muscle tissue shows a surprising lack of degeneration associated with aging. Not every measure and biological mechanism declines greatly. It's not all that comforting, as evidently we're all still aging into frailty regardless, but it does suggest that perhaps a larger fraction of muscle aging than previously thought is under our control, the result of poor lifestyle choices such as sedentary behavior.
While the general understanding of muscle regenerative capacity is that it declines with increasing age due to impairments in the number of muscle progenitor cells and interaction with their niche, studies vary in their model of choice, indices of myogenic repair, muscle of interest and duration of studies.
We focused on the net outcome of regeneration, functional architecture, compared across three models of acute muscle injury to test the hypothesis that satellite cells maintain their capacity for effective myogenic regeneration with age. Muscle regeneration in extensor digitorum longus muscle (EDL) of young (3 mo-old), old (22 mo-old) and senescent female mice (28 mo-old) was evaluated for architectural features, fiber number and central nucleation, weight, collagen and fat deposition.
Histological analyses revealed successful architectural regeneration following [injury] with negligible fibrosis and fully restored function, regardless of age. In comparison, the regenerative response to injuries that damaged the neurovascular supply [was] less effective, but similar across the ages. The focus on net regenerative outcome demonstrated that old and senescent muscle has a robust capacity to regenerate functional architecture.