Pathophysiology of human heart failure: importance of skeletal muscle myopathy and reflexes

New Findings: What is the topic of this review? This article reviews the role played by reflexes arising from muscle metaboreceptors in the pathophysiology of exercise intolerance in chronic heart failure (CHF). These receptors trigger the metaboreflex, which is likely to play an important role in the genesis of exercise intolerance in CHF. What advances does it highlight? This article highlights that, in CHF, the target blood pressure response during muscle metaboreflex activation is achieved mainly by vasoconstriction, whereas in healthy individuals the main mechanism is an increase in cardiac output. In the last 20 years there has been mounting evidence that chronic heart failure (CHF) has a complex pathophysiology, which begins with an abnormality of the heart as a 'primum movens', but involves adaptive changes in many body parts, including the cardiovascular, musculoskeletal, renal, neuroendocrine, haemostatic, immune and inflammatory systems. Alterations in skeletal muscle are also of importance in limiting functional capacity in patients with CHF, because reduced physical activity plays some part in the muscle alterations in CHF. On the whole, these abnormalities resemble those induced by physical deconditioning. Moreover, the overactivation of signals originating from skeletal muscle receptors (mechano-metaboreceptors) is an intriguing hypothesis proposed to explain the origin of symptoms and the beneficial effect of exercise training in the CHF syndrome. These reflexes may contribute to sympathetic overactivation, to exercise intolerance and to the progression of CHF syndrome. The so-called metaboreflex has been reported to be hyperactive in CHF and to be responsible for a paradoxical increase in systemic vascular resistance and decrease in cardiac output whenever activated in these patients. This report is a brief summary of the latest news in this area of research