NADPH oxidase and exercise

The combination of a sedentary lifestyle and high-caloric intake disturbs metabolic processes. Accumulation of visceral fat and the consequent activation of a network of inflammatory pathways and oxidative stress cascades that promote the development of some pathological disorders (e.g. atherosclerosis) and consequently

clinical events (e.g. myocardial infarction and stroke). Clinical and experimental evidence show that chronic physical exercise prevents the progression of atherosclerotic cardiovascular diseases and reduces cardiovascular morbidity. Dysfunction of vascular cells, especially endothelial cells, is one of the earliest events in the development of the pathogenesis of atherosclerosis and atherosclerotic cardiovascular diseases, and mortality. In obese patients, increased NADPH oxidase

activity, along with expression of specific subunits, such as p47phox, leads to excessive production of superoxide anions and rapid inactivation of nitric oxide (NO) by ROS, thereby causing endothelial oxidative stress and endothelial dysfunction.