Carlos E. Negrão

Our group studies the relationship between physical activity and an improved health, especially in relation to the metabolic syndrome. Here are some topics of great interest to us. The way they all interrelate is also listed below. Metabolic syndrome (MetS) Patients with metabolic syndrome have changes in chemoreflex control of sympathetic nerve activity and breathing pattern. Diet and exercise improve sleep patterns in patients with metabolic syndrome. Hypertension (HBP) Physical activities reduce the sympathetic nerve activity that is associated with improvement in arterial baroreflex sensitivity. Coronary Artery Disease (CAD) Exercise training improves cardiac autonomic modulation and neurovascular control in patients with acute myocardial infarction. Swimming training restores miRNA-29 (both a and c) levels and prevents the expression of collagen around the edges of the infarcted region, which may contribute to the improvement of ventricular function after myocardial infarction. Heart failure (HF) The decrease in sympathetic nerve activity in patients with heart failure undergoing exercise is related to the improvement of the Meccan control and muscle metaboreflex. Skeletal muscle biopsies show that the molecular basis for this improvement are decreases in gene expression and in protein COX2, NFkB and increase in miRNA146, expression of TRPV1 receptors and CB1 skeletal muscle. The improved ubiquitin-proteasome pathway related to muscle protein degradation after physical training in heart failure depends on reducing muscle angiotensin II, since the infusion of this peptide abolishes the effects of physical exercise on the expression of atrogina, MURF1 and E3? ligase, and the expression of ubiquitinated proteins and carbonyl proteins. Physical activities lower the expression of angiotensin II and angiotensin AT1 receptors. Moreover, exercise increases the expression of angiotensin 1-7 and MAS receptors in skeletal muscle in the presence of heart failure. Hyperactivation of NADPH oxidase is a major source of production of reactive oxygen species associated with muscle atrophy in heart failure.