The Role of Exercise on L-Arginine Nitric Oxide Pathway in Chronic Heart Failure

Abstract

Chronic heart failure (CHF) is a pathological state with high morbidity and mortality and the full understanding of its genesis remain to be elucidated. In this syndrome, a cascade of neurohormonal and hemodynamic mechanisms, as well as inflammatory mediators, are activated to improve the impaired cardiac function. Clinical and experimental observations have shown that CHF is associated with a generalized disturbance in endothelium-dependent vasodilation, which may contribute to the progression of ventricular and vascular remodelling in this syndrome. There is also accumulating evidence that disturbances in nitric oxide (NO) availability is involved in the development of heart failure at the systemic and cardiac levels. NO is a ubiquitous signalling molecule which causes potent vasodilation, inhibits platelet activation and regulates the contractile properties of cardiac myocytes. It is generated from the amino acid L-arginine via constitutive and inducible isoforms of the enzyme NO synthase (NOS). There is evidence that exercise, a nonpharmacological tool, improves symptoms, fitness (VO2peak), quality of life and NO bioavailability in CHF population. This review examines different aspects of the L-arginine-NO pathway and inflammation in the physiopathology of CHF and highlights the important beneficial effects of exercise in this disease.

Coordination Between Nitric Oxide and Superoxide Anion Radical During Progressive Exercise in Elite Soccer Players

“…So, we confirmed the assumption that long-term training induces increase in NO bioavailability, whilst training cessations, i. e. physical inactivity, have negative effect – it leads to reversible changes and preclude the increase in NO bioavailability. That is in accordance with studies that showed that physically active people have greater basal NO production than sedentary population [27-29], as well as that exercise induces increase in basal NO production [30-32], especially in sedentary [33] and people with some kind of endothelial dysfunction [34-37]. However, it should be emphasized that these exercise-induced changes in NO bioavailabilty are transitory and can be lost during inactivity period [32].…”

Comparison of blood pro/antioxidant levels before and after acute exercise in athletes and non-athletes

“…It is in accordance with numerous previous studies that showed that regular physical activity increases the bioavailibity of NO (Jungersten et al 1997;Kingwell et al 1997;Lewis et al 1999;Maeda et al 2001;Maiorana et al 2003;Mendes-Ribeiro et al 2009) and that physically active people have greater basal NO production compared with a sedentary population (Poveda et al 1997;Green et al 2004;Banfi et al 2006). Studies that investigated the effects of acute exercise on NO production yielded various results.…”

Increased NT-proANP predicts risk of congestive heart failure in Cavalier King Charles spaniels with mitral regurgitation caused by myxomatous valve disease

“…In the progression of heart failure NO may therefore mediate either essential vasodilation or cell death, via its toxic effects. 21,22 In healthy dogs plasma NOx levels correlate with NT-proANP concentrations and increases with age. 15 Indices of increased tissue activity have been reported in the mitral valves in dogs with MMVD, 23 and signs of endothelial dysfunction have been observed in dogs with MMVD through necropsy material, 24,25 by peripheral blood flow measurements, 26,27 and through analysis of plasma cGMP or precursors 28 and end-products 29 to NO.…”