The loss of skeletal muscle is one of the most dramatic changes in the human body consequent to advancing age and is referred to as sarcopenia. It is a primary cause of age-related changes in muscle performance, functional status and metabolic homeostasis. In an effort to counter sarcopenia and its consequences, we have studied strategies to inhibit the muscle-enriched TGF-β superfamily member, myostatin. The purpose of this seminar is to demonstrate how antibody-directed approaches to myostatin have not only increased muscle mass in mouse models of aging and disease, but improved physical function and whole-body metabolism. Ultimately, strategies to disrupt myostatin may provide a means to extend healthspan.