Document Detail

Skeletal muscle lactate accumulation and creatine phosphate depletion during heavy exercise in congestive heart failure. Cause of limited exercise capacity?
MedLine Citation:
PMID:  9447322     Owner:  NLM     Status:  MEDLINE    
OBJECTIVE: To study the mechanisms of limited exercise capacity and skeletal muscle energy production in male patients with congestive heart failure. DESIGN: Muscle biopsy study. PATIENTS: 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 and in nine healthy subjects (peak VO2 33.5 +/- 6.7 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 and 36 healthy subjects (peak VO2 38.3 +/- 8.4 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 and creatine phosphate was equally depressed (P < 0.02) to low levels (7.0 +/- 1.9 vs 6.7 +/- 0.9 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.
H K Näveri; H Leinonen; K Kiilavuori; M Härkönen
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  European heart journal     Volume:  18     ISSN:  0195-668X     ISO Abbreviation:  Eur. Heart J.     Publication Date:  1997 Dec 
Date Detail:
Created Date:  1998-03-18     Completed Date:  1998-03-18     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  8006263     Medline TA:  Eur Heart J     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  1937-45     Citation Subset:  IM; S    
Department of Medicine, Helsinki University Central Hospital, Finland.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Adenosine Triphosphate / analysis
Chronic Disease
Epinephrine / blood
Exercise / physiology*
Exercise Test
Exercise Tolerance / physiology*
Heart Failure / metabolism*
Lactates / metabolism*
Middle Aged
Muscle, Skeletal / chemistry,  metabolism*
Norepinephrine / blood
Phosphocreatine / analogs & derivatives,  analysis
Reg. No./Substance:
0/Lactates; 51-41-2/Norepinephrine; 51-43-4/Epinephrine; 56-65-5/Adenosine Triphosphate; 5786-71-0/phosphocreatinine; 67-07-2/Phosphocreatine

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Improvement in lower limb vasodilatory reserve and exercise capacity in patients with chronic heart ...
Next Document:  Syncope and ventricular arrhythmias in hypertrophic cardiomyopathy are not related to the derangemen...