Exercise, Advanced Glycation End Products, and Their Effects on Cardiovascular Disorders: A Narrative Review

Abstract

Lifelong accumulation of advanced glycation end products (AGEs) is linked to cardiovascular disease (CVD). As a result of AGEs, cardiovascular dysfunction develops and progresses via two main mechanisms: cross-linking AGEs with tissue proteins and binding of AGEs to their receptor for AGE (RAGE). In addition, the formation of atherosclerotic plaques in these patients may be due to increased oxidative stress, leading to an elevation in blood circulation and tissue AGEs. Increasing physical activity is a critical approach among the different strategies to manage the deleterious effects of these changes caused by disease. Exercise prevents the accumulation of AGEs and slows the progression of chronic disease sequels. Exercise reduces AGE levels through a reduction of insulin sensitivity, fat mass, inflammation, and RAGE expression. An improvement in glucose metabolism and glycemic control are also other possible explanations. Reduced peripheral insulin resistance may attenuate AGE accumulation. Physical exercise causes more antioxidant enzyme secretion and reduces oxidative stress. Antioxidant and anti-inflammatory endothelial function is improved by exercise. After exercise, subendothelial matrix stiffness decreases, and endothelial function is improved. In this current study, the association between AGEs and exercise and their interaction effects on CVD are discussed.