title: Contribution of skeletal muscle atrophy to exercise intolerance and altered muscle metabolism in heart failure.
abstract: BACKGROUND
  The purpose of this study was to investigate the prevalence of skeletal muscle atrophy and its relation to exercise intolerance and abnormal muscle metabolism in patients with heart failure (HF).
  
  
  RESULTS
  Peak VO2, percent ideal body weight (% IBW), 24-hour urine creatinine (Cr), and anthropometrics were measured in 62 ambulatory patients with HF. 31P magnetic resonance spectroscopy (MRS) and imaging (MRI) of the calf were performed in 15 patients with HF and 10 control subjects. Inorganic phosphorus (Pi), phosphocreatine (PCr), and intracellular pH were measured at rest and during exercise. Calf muscle volume was determined from the sum of the integrated area of muscle in 1-cm-thick contiguous axial images from the patella to the calcaneus. A reduced skeletal muscle mass was noted in 68% of patients, as evidenced by a decrease in Cr-to-height ratio of less than 7.4 mg/cm and/or upper arm circumference of less than 5% of normal. Calf muscle volume (MRI) was also reduced in the patients with HF (controls, 675 +/- 84 cm3/m2; HF, 567 +/- 112 cm3/m2; p less than 0.05). Fat stores were largely preserved with triceps skinfold of less than 5% of normal and/or IBW of less than 80% in only 8% of patients. Modest linear correlations were observed between peak VO2 and both calf muscle volume per meter squared (r = 0.48) and midarm muscle area (r = 0.36) (both p less than 0.05). 31P metabolic abnormalities during exercise were observed in the patients with HF, which is consistent with intrinsic oxidative abnormalities. The metabolic changes were weakly correlated with muscle volume (r = -0.42, p less than 0.05).
  
  
  CONCLUSIONS
  These findings indicate that patients with chronic HF frequently develop significant skeletal muscle atrophy and metabolic abnormalities. Atrophy contributes modestly to both the reduced exercise capacity and altered muscle metabolism.
authors.affiliation: Department of Medicine, University of Pennsylvania, Philadelphia.
authors.forename: D M
authors.initials: DM
authors.lastname: Mancini
authors.forename: G
authors.initials: G
authors.lastname: Walter
authors.forename: N
authors.initials: N
authors.lastname: Reichek
authors.forename: R
authors.initials: R
authors.lastname: Lenkinski
authors.forename: K K
authors.initials: KK
authors.lastname: McCully
authors.forename: J L
authors.initials: JL
authors.lastname: Mullen
authors.forename: J R
authors.initials: JR
authors.lastname: Wilson
mesh_terms: D015444:Exercise / Q000502:physiology*; D005080:Exercise Test; D005260:Female; D006333:Heart Failure / Q000150:complications* / Q000503:physiopathology; D006801:Humans; D008279:Magnetic Resonance Imaging; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D008875:Middle Aged; D009132:Muscles / Q000378:metabolism*; D009133:Muscular Atrophy / Q000150:complications* / Q000175:diagnosis / Q000453:epidemiology; D010725:Phosphocreatine / Q000378:metabolism; D010758:Phosphorus / Q000378:metabolism; D015995:Prevalence
chemical_list: D010725:Phosphocreatine; D010758:Phosphorus