Abstract
Rehabilitation after myocardial infarction produces an increased peak oxygen uptake (VO2peak). This study investigates the relationship between the modifications in skeletal muscle metabolism and the modification in VO2peak induced by a standard program of physical training following a myocardial infarction. Seventeen patients (14 male, 3 female) were studied by phosphorus 31(31P) magnetic resonance spectroscopy after the acute phase of a myocardial infarction and after 2 months of rehabilitation. Changes in calf muscle pH, phosphocreatine, and inorganic phosphates were measured at rest and during a plantar flexion-type incremental workload protocol. Calf muscle pH, phosphocreatine/(phosphocreatine + inorganic phosphates), and inorganic phosphates/phosphocreatine ratios were compared at the highest identical workload attained in both studies. The VO2peak (mL/kg/min) was determined during a cycle stress test. At the highest identical workload attained in both tests, the ratio phosphocreatine/(phosphocreatine + inorganic phosphates) was significantly higher (0.48 +/- 0.15 to 0.57 +/- 0.18: P < .001), and the ratio inorganic phosphates/phosphocreatine was lower (1.38 +/- 1.14 to 0.99 +/- 0.87: P < .01). After rehabilitation, no difference was observed for the pH at stress (6.83 +/- 0.16 to 6.91 +/- 0.14: not significant [NS]). The increase in the VO2peak was significant after rehabilitation (24 +/- 9 to 29 +/- 11 mL/kg/min: P < .001). The VO2peak improvement induced by the physical training was correlated with the increase in the phosphocreatine/(phosphocreatine + inorganic phosphates) (r = 0.818, P < .001). The reduction in phosphocreatine depletion indicated that the oxidative capacity of the skeletal muscle was improved during the rehabilitation. The good correlation between the indexes of skeletal muscle metabolism and VO2peak suggests the peripheral effect of training.
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