The function and regulation of myogenic progenitor populations in aging and exercise

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Aging is associated with a loss of skeletal muscle mass, and strength, which is collectively referred to as sarcopenia.  Common consequences of sarcopenia include bone fractures due to falls, a loss of independence and institutionalization, ultimately leading to a reduced quality of life.  Despite many theories regarding the fundamental mechanism(s) underlying sarcopenia, none is entirely acceptable or explains all aspects of the sarcopenic process. Skeletal muscle is a unique tissue that is associated with a population of cells (satellite cells and stem cells) with the ability to make new muscle.  The maintenance of skeletal muscle mass is dependent on the sustained operation of these cells throughout life.  My research program proposes to examine the abundance of satellite cell and stem cells with aging as well as the regulatory pathways that govern satellite cell and stem cell function, as I believe that these myogenic progenitor populations may be a component of the fundamental mechanism(s) of age-related sarcopenia.  In addition, to better understand the signals that may influence satellite and stem cell regulatory pathways my research program will examine exercise training in older adults as a strategy to maintain efficient satellite cell and stem cell function.  We will identify whether the machinery necessary to keep these cells functioning is maintained during aging, and if not, what exactly is going wrong during the aging process.  . Ultimately, improved quality of life, with prolonged independent living is the goal for our aging population.  My research program is aimed at unraveling the mysteries of skeletal muscle aging, and providing others with the direction (by providing intriguing molecular, cellular, and biochemical data) to extend these results for the development of countermeasures for age-related sarcopenia.