Implications of exercise-induced adipo-myokines in bone metabolism

Abstract

Physical inactivity has been recognized, by the World Health Organization as the fourth cause of death (5.5 % worldwide). On the contrary, physical activity (PA) has been associated with improved quality of life and decreased risk of several diseases (i.e., stroke, hypertension, myocardial infarction, obesity, malignancies). Bone turnover is profoundly affected from PA both directly (load degree is the key determinant for BMD) and indirectly through the activation of several endocrine axes. Several molecules, secreted by muscle (myokines) and adipose tissues (adipokines) in response to exercise, are involved in the fine regulation of bone metabolism in response to the energy availability. Furthermore, bone regulates energy metabolism by communicating its energetic needs thanks to osteocalcin which acts on pancreatic β-cells and adipocytes. The beneficial effects of exercise on bone metabolism depends on the intermittent exposure to myokines (i.e., irisin, IL-6, LIF, IGF-I) which, instead, act as inflammatory/pro-resorptive mediators when chronically elevated; on the other hand, the reduction in the circulating levels of adipokines (i.e., leptin, visfatin, adiponectin, resistin) sustains these effects as well as improves the whole-body metabolic status. The aim of this review is to highlight the newest findings about the exercise-dependent regulation of these molecules and their role in the fine regulation of bone metabolism.

Exercise-induced circulating extracellular vesicles protect against cardiac ischemia–reperfusion injury

“…Exercise is able to trigger the release of a variety of “exerkines” into the circulation that can be contained within EVs [20, 35]. Exercise-derived EVs are hypothesized to be released from cells to the blood and can confer the systemic benefits of exercise to distal organs, including the heart [40].…”

Measuring myokines with cardiovascular functions: pre-analytical variables affecting the analytical output

“…Circulating irisin is affected by acute exercise [for review (57)], particularly, resistance training more than endurance training (58), although chronic exercising decreases irisin (59). Circulating irisin levels are predicted by biceps circumference, and they correlate with BMI, glucose, ghrelin, and IGF-1 and negatively with age, insulin, cholesterol, and adiponectin levels (60).…”

Serum sclerostin decreases following 12months of resistance- or jump-training in men with low bone mass

“…Exercise also increases circulating IGF-I, the source of which is the liver or extrahepatic tissues. In particular, in response to exercise, skeletal muscle releases “myokines,” including IGF-I, which can have systemic and local effects on other tissues, including bone [19, 23, 30]. The osteoblast response to endogenous IGF-I is dependent on mechanical strain, thus, IGF-I is needed to optimize response to exercise [14, 31].…”