Figure 1. A hypothetical view of the etiology and therapy of sarcopenia. mTORC1 activity increases during aging, starting from middle age, resulting in progressively altered mitochondria, leading to mitochondrial oxidative stress and thus catabolism including protein degradation, apoptosis, and necrosis. This elevated catabolic activity results in muscle fiber loss, atrophy, and damage. Therefore, inhibition of mTORC1 activity with rapamycin may rescue skeletal muscle during aging. mTORC1-selective inhibitors and optimized treatment protocols may maximize the beneficial effect of rapalog treatment.