Meeting Abstract
Muscles adapt quickly to perturbations such as exercise training, disuse, or aging. Advanced aging is associated with a decline of muscle performance , whereas training results in enhanced contractile properties of muscle and metabolic changes that benefit performance. While numerous studies have documented age-related declines in muscle and locomotor performance, it is still unclear how factors such as extreme, lifelong aerobic training and genetics can impact the timing and trajectory of muscle aging. Here we use mice from two genetic lines (control and mice selected for high levels of wheel running over 70 generations, or HR mice) to better understand the effect of high levels of aerobic activity on age-related declines in muscle performance. Mice were divided into four cohorts (Ctrl/wheel access, Ctrl/no wheel access, HR/wheel access, HR/no wheel access) and muscle contractile properties were obtained from mice at time points spanning two years for each cohort. In order to characterize contractile performance we used an in situ preparation to measure the force, velocity, power, and passive properties of the triceps surae complex. We found that, without training, control mice had significantly higher shortening velocities than HR mice, regardless of age. There were no significant differences in power production, force, or resilience across any line or treatment cohort. We found that passive stiffness significantly declined across all mice with wheel access in late ontogeny. This study informs our understanding the role of endurance training in preserving a healthy muscle phenotype throughout ontogeny. Our results may also provide insight into relative contributions of genotype and phenotypic plasticity as mechanisms that determine how muscles respond to training and aging.
