title: Alterations of skeletal muscle in chronic heart failure.
abstract: BACKGROUND
  The present study was designed to define the prevalence and characteristics of skeletal muscle alterations in patients with chronic heart failure (CHF) and their relation to exercise capacity.
  
  
  RESULTS
  The ultrastructure of skeletal muscle was analyzed by ultrastructural morphometry in 57 patients with CHF and 18 healthy controls. The volume density of mitochondria (Vvm) and the surface density (Svmc) of mitochondrial cristae were evaluated as a structural correlate of oxidative capacity of skeletal muscle. Vvm and Svmc were reduced by approximately 20% in patients with severe CHF irrespective of age and etiology. The cytochrome oxidase activity in mitochondria as determined by cytochemistry and subsequent morphometry in a subset of patients (n = 10) was significantly decreased in heart failure (p less than 0.01). The capillary length density of skeletal muscle was reduced in CHF (n = 12, p less than 0.05), and the fiber type distribution was shifted to type II fibers (n = 15, p less than 0.05). Vvm and Svmc were significantly related to peak exercise VO2 (r = 0.56, p less than 0.001, n = 60) and to VO2 at anaerobic threshold (r = 0.535, p less than 0.0001, n = 60). In 16 patients with severe heart failure, Vvm was inversely related to the duration of heart failure (r = 0.545, p less than 0.03). In 11 patients who underwent repeat biopsies after 4 months, a correlation was observed between the change in Vvm and the change in peak exercise VO2 (r = 0.89, p less than 0.001).
  
  
  CONCLUSIONS
  These findings indicate that patients with CHF develop significant ultrastructural abnormalities of skeletal muscle reflecting a depressed oxidative capacity of working muscle. It appears that these alterations of skeletal muscle contribute to the decreased exercise capacity of these patients but are, in principle, reversible by an effective treatment regimen.
authors.affiliation: Medizinische Klinik III, Universität Freiburg, FRG.
authors.forename: H
authors.initials: H
authors.lastname: Drexler
authors.forename: U
authors.initials: U
authors.lastname: Riede
authors.forename: T
authors.initials: T
authors.lastname: Münzel
authors.forename: H
authors.initials: H
authors.lastname: König
authors.forename: E
authors.initials: E
authors.lastname: Funke
authors.forename: H
authors.initials: H
authors.lastname: Just
mesh_terms: D000375:Aging / Q000502:physiology; D001706:Biopsy; D002196:Capillaries / Q000473:pathology; D002303:Cardiac Output, Low / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology; D003576:Electron Transport Complex IV / Q000378:metabolism; D005080:Exercise Test; D006651:Histocytochemistry; D006801:Humans; D008297:Male; D008875:Middle Aged; D008931:Mitochondria, Muscle / Q000201:enzymology / Q000648:ultrastructure; D009132:Muscles / Q000098:blood supply / Q000473:pathology / Q000648:ultrastructure*; D015388:Organelles / Q000648:ultrastructure; D010807:Physical Endurance
chemical_list: D003576:Electron Transport Complex IV