Alterations in mitochondria and their impact in aging skeletal muscle

Abstract

There is an abundance of studies examining the involvement of mitochondria in aging, including their role in the functional and structural deterioration of skeletal muscle with aging. Despite years of study, the precise involvement of mitochondria in the aging of skeletal muscle remains to be fully understood. This chapter provides some context for the current knowledge in this area and areas that will be refined through further study. It will examine the issue of mitochondrial dysfunction in aging; why it occurs and the functional consequences. The potential impact of three important age-related changes in mitochondria will be considered here: a reduced capacity for generating cellular energy in the form of adenosine triphosphate (ATP); an increased susceptibility to apoptosis; and an increase in reactive oxygen species (ROS) production with aging. The chapter considers the extent to which the mitochondrial content may be up-regulated in response to muscle activity as a means of assessing the malleability of the age-related impairments in mitochondria. Given the central importance of mitochondrial biology to so many facets of normal cell function, particularly in tissues with a wide metabolic scope like skeletal muscle, new discoveries about the significance of changes in mitochondria for aging skeletal muscles, and their potential remedy through lifestyle modification (e.g., exercise training, diet) and/or medical intervention (e.g., pharmaceuticals, gene therapy), will remain at the forefront of our quest to promote healthy aging.