Author + information
- Received February 28, 1992
- Revision received October 5, 1992
- Accepted October 6, 1992
- Published online April 1, 1993.
- Stamatis Adamopoulos, MD∗∗,†,
- Andrew J.S. Coats, DM, FRACP∗,†,
- François Brunotte, MD‡,
- Leonard Arnolda, MB, PhD‡,
- Theo Meyer, MB, DPhil∗,
- Campbell H. Thompson, MB, FRACP‡,
- Jeff F. Dunn, DPhil‡,
- John Stratton, MD, FACC‡,
- Graham J. Kemp, BM, BCh‡,
- George K. Radda, DPhiL, FRS‡ and
- Bheeshma Rajagopalan, DPhiL, FRCP‡
- ↵∗Address for correspondence: Stamatis Adamopoulos, MD, Cardiac Department, National Heart and Lung Institute, Dovehouse Street, London SW3 6LY, England, United Kingdom.
Objectives. This study investigated the effects of physical training on skeletal muscle metabolism in patients with chronic heart failure.
Background. Skeletal muscle metabolic abnormalities in patients with chronic heart failure have been associated with exercise intolerance. Muscle deconditioning is a possible mechanism for the intrinsic skeletal muscle metabolic changes seen in chronic heart failure.
Methods. We used phosphorus-31 nuclear magnetic resonance spectroscopy to study muscle metabolism during exercise in 12 patients with stable ischemic chronic heart failure undergoing 8 weeks of home-based bicycle exercise training in a randomized crossover controlled trial. Changes in muscle pH and concentrations of phosphocreatine and adenosine diphosphate (ADP) were measured in phosphorus-31 spectra of calf muscle obtained at rest, throughout incremental work load plantar flexion until exhaustion and during recovery from exercise. Results were compared with those in 15 age-matched control subjects who performed a single study only.
Results. Before training, phosphocreatine depletion, muscle acidification and the increase in ADP during the 1st 4 min of plantar flexion exercise were all increased (p < 0.04) compared with values in control subjects. Training produced an increase (p < 0.002) in incremental plantar flexion exercise tolerance. After training, phosphocreatine depletion and the increase in ADP during exercise were reduced significantly (p < 0.003) at all matched submaximal work loads and at peak exercise, although there was no significant change in the response of muscle pH to exercise. After training, changes in ADP were not significantly different from those in control subjects, although phosphocreatine depletion was still greater (p < 0.05) in trained patients than in control subjects. The phosphocreatine recovery half-time was significantly (p < 0.05) shorter after training, althrough there was no significant change in the half-time of adenosine diphosphate recovery. In untrained subjects, the initial rate of phosphocreatine resynthesis after exercise (a measure of the rate of oxidative adenosine triphosphate [ATP]synthesis) and the inferred maximal rate of mitochondrial ATP synthesis were reduced compared with rates in control subjects (p < 0.003) and both were significantly increased (p < 0.05) by training, so that they were not significantly different from values in control subjects.
Conclusions. The reduction in phosphocreatine depletion and in the increase in ADP during exercise, and the enhanced rate of phosphocreatine resynthesis in recovery (which is independent of muscle mass) indicate that a substantial correction of the impaired oxidative capacity of skeletal muscle in chronic heart failure can be achieved by exercise training.
☆ This study was supported by the British Heart Foundation, London. Medical Research Council London, and Eli Lilly Pharmaceutical Company, Basingsloke, England.
- Received February 28, 1992.
- Revision received October 5, 1992.
- Accepted October 6, 1992.