title: Skeletal muscle abnormalities in chronic heart failure patients: relation to exercise capacity and therapeutic implications.
abstract: Recent studies suggest that changes in the periphery, like those occurring in the skeletal muscles of patients with chronic heart failure, might play an important role in the origin of symptoms and exercise intolerance in this condition. Biochemical and histologic changes in the skeletal muscles of chronic heart failure patients relate with the degree of exercise intolerance better than hemodynamics parameters. A reduction in skeletal muscle mass represents another important determinant of exercise intolerance in chronic heart failure patients. The relationship between skeletal muscle changes and exercise intolerance suggests the possibility of modifying the peripheral changes in order to improve functional capacity in chronic heart failure patients. Recent studies have shown that the administration of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers can improve the properties of the skeletal muscles. Similarly, exercise training allows improvement in peak oxygen consumption, which parallels important biochemical and histologic changes in the skeletal muscles.
authors.affiliation: Dipartimento di Scienze Biomediche e Chirurgiche, Sezione di Cardiologia, Universita degli Studi di Verona, Verona, Italy.
authors.forename: Ilaria
authors.initials: I
authors.lastname: Nicoletti
authors.forename: Mariaantoinetta
authors.initials: M
authors.lastname: Cicoira
authors.forename: Luisa
authors.initials: L
authors.lastname: Zanolla
authors.forename: Lorenzo
authors.initials: L
authors.lastname: Franceschini
authors.forename: Giovanna
authors.initials: G
authors.lastname: Brighetti
authors.forename: Maria
authors.initials: M
authors.lastname: Pilati
authors.forename: Piero
authors.initials: P
authors.lastname: Zardini
mesh_terms: D015444:Exercise / Q000502:physiology; D017079:Exercise Tolerance; D006333:Heart Failure / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology*; D006801:Humans; D018482:Muscle, Skeletal / Q000378:metabolism / Q000473:pathology* / Q000648:ultrastructure; D010101:Oxygen Consumption