Sarcopenia: Molecular Pathways and Potential Targets for Intervention

Abstract

Aging is associated with sarcopenia. The loss of strength results in decreased muscle mass and motor function. This process accelerates the progressive muscle deterioration observed in older adults, favoring the presence of debilitating pathologies. In addition, sarcopenia leads to a decrease in quality of life, significantly affecting self-sufficiency. Altogether, these results in an increase in economic resources from the National Health Systems devoted to mitigating this problem in the elderly, particularly in developed countries. Different etiological determinants are involved in the progression of the disease, including: neurological factors, endocrine alterations, as well as nutritional and lifestyle changes related to the adoption of more sedentary habits. Molecular and cellular mechanisms have not been clearly characterized, resulting in the absence of an effective treatment for sarcopenia. Nevertheless, physical activity seems to be the sole strategy to delay sarcopenia and its symptoms. The present review intends to bring together the data explaining how physical activity modulates at a molecular and cellular level all factors that predispose or favor the progression of this deteriorating pathology.

Keywords: aging; inflammation; oxidative stress; physical activity; sarcopenia; satellite cells.

Figure 1

Scheme of the main factors predisposing to sarcopenia and the role of physical activity in delaying this process. See text for more details. Abbreviations and symbols used: BDNF, brain-derived neurotrophic factor; HGF, hepatic growth factor; NO, nitric oxide; NOS, nitric oxide synthase; RONS, reactive oxygen and nitrogen species; (↑) increased; (↓) decreased.