Physical inactivity

Physical inactivity (sedentary lifestyle) has become a major public health concern. Physical inactivity and obesity are modifiable risk factors for many chronic diseases, including cardiovascular disease, type 2 diabetes mellitus (T2DM), osteoporosis and cancer. Both physical inactivity and obesity produces an increment in total blood volume and cardiac output that is caused in part by the increased metabolic demand induced by excess body weight. Obesity is an independent risk factor for cardiovascular diseases and its risks have been shown a correlation between BMI in adolescence and all-cause mortality. The association between obesity, fasting insulin, insulin sensitivity, and blood pressure may be explained by phenomena related to the concomitant variation in the amount of abdominal fat. Obesity and oxidative stress is associated with low-grade systemic inflammation that may contribute to the inflammatory processes present in many chronic diseases. The relationship between obesity and systemic inflammation state may provide one other mechanism for an increase in blood pressure. Like physical evaluation, the electrocardiogram (ECG) is influenced by morphological changes induced by obesity, including displacement of the heart, increased cardiac workload with associated cardiac hypertrophy and the potential associated chronic lung disease. Several changes in the ECG occur with increasing obesity (QRS voltage, ST-segment depression). One of the most studied non-pharmacological therapy in CV disease for weight reduction is the physical exercise training, which resulted in a 37% reduction in the prevalence of metabolic disorders. The regular practice of moderate intensity physical exercise also showed capacity to improve insulin sensitivity, increase circulating levels of HDL, decrease triglyceride levels and normalize blood pressure.

Exercise training may improve endothelial function by up-regulating endothelial nitric oxide synthase (eNOS) protein expression and phosphorylation, which augment endothelial, NO-dependent vasodilatation. The enhanced NO bioavailability shows protective effects on endothelial dysfunction.