title: Pathophysiology of human heart failure: importance of skeletal muscle myopathy and reflexes.
abstract: 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.
authors.affiliation: * Department of Medical Sciences, Sports Physiology Laboratory, University of Cagliari, Via Porcell 4, 09124 Cagliari, Italy.    crisafulli@tiscali.it.
authors.forename: Massimo F
authors.initials: MF
authors.lastname: Piepoli
authors.forename: Antonio
authors.initials: A
authors.lastname: Crisafulli
mesh_terms: D000818:Animals; D018450:Disease Progression; D017079:Exercise Tolerance; D006333:Heart Failure / Q000150:complications / Q000378:metabolism / Q000503:physiopathology*; D006439:Hemodynamics; D006801:Humans; D018482:Muscle, Skeletal / Q000098:blood supply / Q000294:innervation* / Q000378:metabolism; D009135:Muscular Diseases / Q000150:complications / Q000378:metabolism / Q000503:physiopathology*; D009206:Myocardium / Q000378:metabolism; D012018:Reflex; D012307:Risk Factors; D011984:Sensory Receptor Cells / Q000378:metabolism*; D015398:Signal Transduction