Skeletal Muscle Metabolic Alternation Develops Sarcopenia

Abstract

Sarcopenia is a new type of senile syndrome with progressive skeletal muscle mass loss with age, accompanied by decreased muscle strength and/or muscle function. Sarcopenia poses a serious threat to the health of the elderly and increases the burden of family and society. The underlying pathophysiological mechanisms of sarcopenia are still unclear. Recent studies have shown that changes of skeletal muscle metabolism are the risk factors for sarcopenia. Furthermore, the importance of the skeletal muscle metabolic microenvironment in regulating satellite cells (SCs) is gaining significant attention. Skeletal muscle metabolism has intrinsic relationship with the regulation of skeletal muscle mass and regeneration. This review is to discuss recent findings regarding skeletal muscle metabolic alternation and the development of sarcopenia, hoping to contribute better understanding and treatment of sarcopenia.

Keywords: Sarcopenia; metabolic alternation; regeneration; signaling pathways.

Figure 1.

Overview of the underlying causes of sarcopenia. Decreased neuro-muscular function, Pro-inflammatory cytokines, imbalance of calcium homeostasis, imbalance in protein synthesis and decomposition, changes in caloric and protein intake, changes in hormone levels, mitochondrial dysfunction, free radical oxidative damage, skeletal muscle regeneration damage and muscle cell apoptosis. The mechanism that causes sarcopenia is the metabolic microenvironmental change in skeletal muscle.

Figure 2.

Skeletal muscle fiber type in Young-Healthy muscle and old-Atrophy muscle. Different types of skeletal muscle fibers can be converted to each other.

Figure 3.

The model of signaling pathways and transcription factors that regulate metabolic microenvironment in skeletal muscle. AMPK/PGC-1α signaling, MAPK signaling, Calcium-NFAT/MEF2 and Calcium-CaMK/MEF2 signaling, WNT signaling, miRNA and lncRNA and other transcription factors.