Sarcopenia refers to age-related loss of muscle mass and function.
Several age-related changes occur in skeletal muscle including a decrease in myofiber size and number and a diminished ability of satellite cells to activate and proliferate upon injury leading to impaired muscle remodeling.
Although the molecular mechanisms underlying sarcopenia are unknown, it is tempting to hypothesize that interplay between biological and environmental factors cooperate in a positive feedback cycle contributing to the progression of sarcopenia.
Indeed many essential biological mechanisms such as apoptosis and autophagy and critical signaling pathways involved in skeletal muscle homeostasis are altered during aging and have been linked to loss of muscle mass.
Moreover, the environmental effects of the sedentary lifestyle of older people further promote and contribute the loss of muscle mass.
There are currently no widely accepted therapeutic strategies to halt or reverse the progression of sarcopenia.
Caloric restriction has been shown to be beneficial as a sarcopenia and aging antagonist.
Such results have made the search for caloric restriction mimetics (CRM) a priority.
However given the mechanisms of action, some of the currently investigated CRMs may not combat sarcopenia.
Thus, sarcopenia may represent a unique phenotypic feature of aging that requires specific and individually tailored therapeutic strategies.
Synergistic Interplay between Biological and Environmental Factors Contribute to Sarcopenia
With an increase in age, people are subjected to environmental changes such as inactivity and malnutrition, which leads to an increased susceptibility to injury and disuse atrophy.
When skeletal muscles incur such challenges, alterations to signaling pathways promote inefficient muscle regeneration and protein degradation resulting in a loss of muscle mass.
This loss of muscle mass and other biological changes are concurrent with a loss of muscle function.