Muscle metabolism assessed by phosphorus-31 nuclear magnetic resonance spectroscopy after myocardial infarction in rehabilitated patients: a 1-year follow-up

Abstract

Background: The most common effect of postmyocardial infarction (post MI) rehabilitation is an increase of peak maximal oxygen consumption correlated with changes in calf muscle metabolism, but there are few data on follow-up after rehabilitation on skeletal muscle and maximal oxygen consumption. The purpose of this study was to investigate the respective modifications in skeletal muscle metabolism and peak oxygen consumption (VO2) occurring during a supervised rehabilitation program and 1 year after MI in patients free of heart failure.

Methods: Fifteen outpatients were studied prospectively after the acute phase of the MI, at the end of the rehabilitation program (2 months after the MI), and 1 year after. The rehabilitation comprised 20 sessions with three sessions per week. The program consisted of exercise training with bicycle, arm ergometer, and treadmill. The program also included respiratory exercises, psychological support, and counseling for secondary prevention of cardiovascular diseases. At each visit, a stress test on a bicycle ergometer was performed and the peak VO2 was measured. Phosphorus magnetic resonance spectroscopy of the gastrocnemius muscle was performed at rest and during a plantar flexion-type exercise against an adjustable load. Data were analyzed using analysis of variance and post-hoc test when appropriate.

Results: The mechanical power output measured during the bicycle exercise increased from 111 +/- 28 watts at the post MI test to 136 +/- 40 watts after rehabilitation (post rehab) and decreased to 125 +/- 36 watts at 1 year. The peak VO2 increased significantly (P < 0.05) from 22 +/- 7 ml/kg-1/min-1 (post MI) to 27 +/- 9 ml/kg-1/min-1 (post rehab), and decreased significantly to 24 +/- 8 ml/kg-1/min-1 (1 year). The mechanical power output measured in the magnet during the stress test increased from 2.22 +/- 0.13 watts (post MI) to 2.85 +/- 1.24 (post rehab), and stabilized at 2.78 +/- 1.10 watts at 1 year. At the highest workload attained in the three successive tests, the phosphocreatine/(phosphocreatine + inorganic phosphate) ratio rose significantly (P < 0.05) from 0.46 +/- 0.13 (post MI) to 0.51 +/- 0.13 (post rehab) and remained at 0.51 +/- 0.13 at 1 year.

Conclusion: The improvement of the peak VO2 after training post MI is not maintained 1 year later. This decline is not accompanied by muscular metabolic abnormalities. This suggests that the muscle metabolism after MI remains normal, and that the long-term decrease of the peak VO2 reflects a global deconditioning that should be avoided by maintaining a long-term phase III rehabilitation program.