Physical Exercise Potentially Targets Epicardial Adipose Tissue to Reduce Cardiovascular Disease Risk in Patients with Metabolic Diseases: Oxidative Stress and Inflammation Emerge as Major Therapeutic Targets

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  Figure 1. An overview of pathological mechanisms linking increased epicardial adipose tissue (EAT) with the detrimental effects of oxidative stress and inflammation. Briefly, the expansion of EAT is consistent with raised heart weight, and this may be associated with free fatty acid (FFA) overload and impaired lipid metabolism and mitochondrial dysfunction, as evident in some preclinical and clinical studies summarized in the current review. As such, prominent markers of oxidative stress and inflammation that are consistently altered within EAT and that are also detected in the myocardial tissue and in circulation, include glutathione peroxidase (GPx), heme oxygenase 1 (HO-1), superoxide dismutase (SOD), C-reactive protein (CRP), interleukin (IL)-6, and tumor necrosis factor alpha (TNF-α). Notably, the expression levels of some antioxidant genes such as GPx, HO-1, and SOD were increased within EAT in some patients at risk of cardiovascular disease (CVD), indicating a possible adaptive response against oxidative damage. Overall, beyond the detrimental effects of oxidative stress and inflammation, other factors that may be induced through high fat diet feeding, such as dysfunctional adipose…

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  Figure 2. An overview of how physical exercise may contribute to lowered cardiovascular disease (CVD) risk by improving metabolic function and myocardial maximal oxygen uptake, especially by reducing epicardial adipose tissue (EAT) thickness in correlation with markers of inflammation in patients with obesity or metabolic syndrome. Briefly, physical exercise can reduce EAT volume to improve myocardial aerobic capacity, lower blood pressure, and reverse the myocardial remodeling process, in part by blocking low-density lipoprotein (LDL) and enhancing high-density lipoprotein (HDL) levels. This is also consistent with decreasing markers of inflammation such as high sensitivity-C-reactive protein (hs-CRP), interleukin (IL)-6, and tumor necrosis factor alpha (TNF-α).