Abstract

Obesity and intermittent hypoxia (IH) occurring during obstructive sleep apnea (OSA) are two independent risk factors for impaired ventricular function; cardiac dysfunction is exacerbated when the two factors co-occur. Regular exercise provides beneficial effects to attenuate cardiac fibrosis by reducing body fat percentage and preventing adipokine dysregulation. However, the mechanisms by which myokines, muscle-derived factors released during exercise, play a role in the prevention of IH-induced cardiac dysfunction, are still unclear. This study investigates the effects of myokines on ventricular dysfunction. The important role that myokines play in cardiac function in patients with OSA is discussed in the literature review. The conclusion of this study is that in obese individuals, excess adipose tissues trigger the dysregulation of adipokines. This dysregulation leads to myocardial inflammation, resulting in left ventricular dysfunction. Physical activity induces an increase in energy expenditure and triggers the release of myokines into the circulation by skeletal muscles, accelerating lipid metabolism, and improving the altered secretion profiles of adipokines. This process helps to alleviate myocardial inflammation and prevents the impairment of ventricular function. The paper suggests that future studies can investigate the effects of myokines on lipid metabolism, including how to reduce fat deposition and alleviate inflammation efficiently. In effect, muscle-derived cytokines (myokines) can be considered as anti-inflammatory mediators. This similarity provides support for advocating that regular exercise provides cardioprotective effects against cardiac function impairment in obese patients with OSA.