Exercise-Released Myokines in the Control of Energy Metabolism

Abstract

Physical activity reduces cardiometabolic risk, while physical inactivity increases chronic diseases risk. This led to the idea that exercise-induced muscle contraction contributes to metabolic regulation and health. It is now well established that skeletal muscle, through the release of endocrine factors, i.e., so-called myokines, crosstalk with metabolic organs such as adipose tissue, liver and pancreas. Recent advances suggested that a number of myokines are able to modulate adipose tissue metabolism and thermogenic activity, liver endogenous glucose production and β-cell insulin secretion. This novel paradigm offers a compelling hypothesis and molecular basis to explain the link between physical inactivity and chronic diseases. Herein, we review major findings and recent advances linking exercise, myokines secretion and inter-organ crosstalk. Identifying the molecular mediators linking physical activity to metabolic health could open the path toward novel therapeutic targets in metabolic diseases.

Keywords: crosstalk; exercise; exerkine; metabolism; skeletal muscle.

FIGURE 1

Skeletal muscle as an endocrine organ. Interleukin-15 (IL-15), brain-derived neurotrophic factor (BDNF) and interleukin-6 (IL-6) stimulate lipid oxidation and oxidative metabolism in an autocrine fashion. IL-6 also stimulates intramyocellular triacylglycerol lipolysis and glucose uptake. IL-6 stimulates pancreatic insulin secretion and exercise-induced hepatic neoglucogenesis through an endocrine communication. Myostatin inhibits muscle hypertrophy. Finally, fibroblast growth factor-21 (FGF-21) stimulates white adipose tissue lipolysis and brown adipose tissue thermogenesis.