Exercise training alters skeletal muscle mitochondrial morphometry in heart failure patients

J Cardiovasc Risk. 2002 Dec;9(6):377-81. doi: 10.1097/01.hjr.0000049243.21319.ee.


Background: Previous research has demonstrated that exercise intolerance in heart failure patients is associated with significant alterations in skeletal muscle ultrastructure and oxidative metabolism that may be more consequential than cardiac output.

Design: To examine the effect of exercise training on skeletal muscle mitochondrial size in chronic heart failure patients.

Methods: Six heart failure patients participated in 16-weeks of supervised upper and lower extremity exercise training. At the conclusion of training, percutaneous needle biopsies of the vastus lateralis were taken and electron microscopy was used to assess mitochondrial sizes.

Results: The exercise programme resulted in a significant increase in peak maximal oxygen consumption ( P< 0.05) and anaerobic threshold (P < 0.04). Knee extension muscle force increased following training ( P< 0.02). After exercise training, the average size of the mitochondria increased by 23.4% (0.036 to 0.046 mu(2), P< 0.015) and the average shape was unaltered.

Conclusion: Exercise training with heart failure patients alters skeletal muscle morphology by increasing mitochondrial size, with no change in shape. This may enhance oxidative metabolism resulting in an increased exercise tolerance.

MeSH terms

  • Aged
  • Aged, 80 and over
  • Anaerobic Threshold / physiology
  • Biopsy / methods
  • Exercise / physiology*
  • Exercise Tolerance / physiology
  • Female
  • Heart Failure / physiopathology*
  • Humans
  • Knee Joint / physiology
  • Linear Models
  • Male
  • Mitochondria, Muscle / ultrastructure*
  • Myocardium / ultrastructure*
  • Oxygen Consumption / physiology
  • Range of Motion, Articular / physiology
  • Regression Analysis