Age-induced muscle atrophy and increase in fatigue resistance

Abstract

A number of changes occur with aging in skeletal muscles including a reduction in muscle fiber size and fiber number. However, recent studies have indicated that the elderly tend to be more resistant to fatigue than the young, particularly during prolonged isometric muscle contraction. In this review, we explore the molecular mechanisms in muscle cells that are involved in this phenomenon. Aging has been thought to induce preferential loss of fast-type fibers. However, previous studies have shown that a fiber-type shift with aging is specific to the region, type and/or function of the muscles. Aging promotes the production of reactive oxygen species (ROS) in skeletal muscle, and ROS is suggested to activate AMP-activated protein kinase (AMPK). AMPK signaling is involved in muscle atrophy, and it activates peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α). PGC-1α is considered a key regulator of mitochondrial biogenesis, and furthermore, it could be involved in the reinnervation of muscle fibers that have been denervated due to aging. Thus, the balance between AMPK and PGC-1α could play an important role in increasing fatigue resistance in aged skeletal muscle.