title: Skeletal muscle lactate accumulation and creatine phosphate depletion during heavy exercise in congestive heart failure. Cause of limited exercise capacity?
abstract: OBJECTIVE
  To study the mechanisms of limited exercise capacity and skeletal muscle energy production in male patients with congestive heart failure.
  
  
  METHODS
  Muscle biopsy study.
  
  
  METHODS
  Skeletal muscle metabolic response to maximal bicycle exercise was studied in 10 patients with chronic congestive heart failure (ejection fraction 0.22 +/- 0.05; peak oxygen consumption, VO2 15.1 +/- 4.9 ml.min-1.kg-1) and in nine healthy subjects (peak VO2 33.5 +/- 6.7 ml.min-1.kg-1). Activities of skeletal muscle enzymes were measured from the vastus lateralis muscle of 48 patients (ejection fraction 0.24 +/- 0.06, peak VO2 17.4 +/- 5.4 ml.min-1.kg-1) and 36 healthy subjects (peak VO2 38.3 +/- 8.4 ml.min-1.kg-1).
  
  
  RESULTS
  Although blood lactate levels were lower in patients than in healthy subjects (2.2 +/- 0.3 vs 5.2 +/- 0.6 mmol.l-1; P < 0.001) at peak exercise (96 +/- 11 W for patients and 273 +/- 14 W for controls), skeletal muscle lactate was similarly elevated (25.6 +/- 3.2 vs 22.7 +/- 2.7 mmol.kg-1) and creatine phosphate was equally depressed (P < 0.02) to low levels (7.0 +/- 1.9 vs 6.7 +/- 0.9 mmol.kg-1). The muscle ATP decreased by 21% (P < 0.05) and 8% (P < 0.01) in the patients and controls, respectively. Activities of rate limiting enzymes of the citric acid cycle (alpha-ketoglutarate dehydrogenase) and oxidation of free fatty acids (carnitine palmitoyltransferase II) were 48% and 21% lower than in controls, but the mean phosphofructokinase activity was unchanged in congestive heart failure.
  
  
  CONCLUSIONS
  It seems that the main limiting factor of exercise performance during heavy exercise is the same in congestive heart failure and healthy subjects, a high rate of skeletal muscle lactate accumulation and high-energy phosphate depletion. In congestive heart failure, the low activity of aerobic enzymes is likely to impair energy production and lead to lactate acidosis at low workloads.
authors.affiliation: Department of Medicine, Helsinki University Central Hospital, Finland.
authors.forename: H K
authors.initials: HK
authors.lastname: Näveri
authors.forename: H
authors.initials: H
authors.lastname: Leinonen
authors.forename: K
authors.initials: K
authors.lastname: Kiilavuori
authors.forename: M
authors.initials: M
authors.lastname: Härkönen
mesh_terms: D000255:Adenosine Triphosphate / Q000032:analysis; D000328:Adult; D002908:Chronic Disease; D004837:Epinephrine / Q000097:blood; D015444:Exercise / Q000502:physiology*; D005080:Exercise Test; D017079:Exercise Tolerance / Q000502:physiology*; D006333:Heart Failure / Q000378:metabolism*; D006801:Humans; D007773:Lactates / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000737:chemistry / Q000378:metabolism*; D009638:Norepinephrine / Q000097:blood; D010725:Phosphocreatine / Q000031:analogs & derivatives / Q000032:analysis
chemical_list: D007773:Lactates; D010725:Phosphocreatine; C025403:phosphocreatinine; D000255:Adenosine Triphosphate; D009638:Norepinephrine; D004837:Epinephrine