Sarcopenia is the decline of muscle mass and strength with age. Sarcopenia leads to significant impairment in the ability to carry out normal daily function and thus there is a great need for interventions that will lead to muscle regeneration and repair in the aging population. Age-related sarcopenia in humans, characterized by loss of type I and type II muscle fibers and a decrease in fiber cross-sectional area primarily in type II fibers, can be attenuated by mechanical load on the muscle, which increases cross-sectional area of the remaining fibers, but does not restore fiber numbers characteristic of young muscle. Considerable evidence also implicates age-related declines in muscle insulin-like growth factor action in sarcopenia. IGF-I promotes myoblast proliferation, differentiation, and protein accretion in muscle through multiple signaling mechanisms, including the PI3-kinase, MAP kinase and calcineurin pathways. Exercise and injury induce increases in IGF-I, IGF-I receptors and IGF-I-activated signaling pathways. Although there is evidence that aging muscle retains the ability to synthesize IGF-I, there is also evidence that aging may be associated with attenuation of the ability of exercise to induce an isoform of IGF-I that promotes satellite cell proliferation. Moreover, aging muscle may be resistant to IGF-I, an effect that is reversed by exercise. However, it is clear that over-expression of IGF-I in muscle can protect against age-related sarcopenia.