ABNORMALITIES IN EXERCISING SKELETAL-MUSCLE IN CONGESTIVE-HEART-FAILURE CAN BE EXPLAINED IN TERMS OF DECREASED MITOCHONDRIAL ATP SYNTHESIS,REDUCED METABOLIC EFFICIENCY, AND INCREASED GLYCOGENOLYSIS

Objective-To distinguish between the effects of reduced oxidative capa city and reduced metabolic efficiency on skeletal muscle bioenergetics during exercise in patients with congestive heart failure. Design and patients-Patients were studied by P-31 magnetic resonance spectroscop y during aerobic exercise and recovery, and results compared with cont rols. Results-In flexor digitorum superficialis muscle (26 patients) t here was a 30% decrease in oxidative capacity compared with control (m ean (SE) 36 (2) v 51 (4) mM/min) and also a 40% decrease in ''effectiv e muscle mass'' (5 (1) v 9 (1) arbitrary units), probably at least par tly the result of reduced metabolic efficiency. Both contribute to inc reased phosphocreatine depletion and intracellular acidosis during exe rcise. However, an increased concentration of ADP (an important mitoch ondrial regulator) during exercise permitted near-normal rates of oxid ative ATP synthesis. Results were similar in gastrocnemius muscle (20 patients), with a 30% decrease in maximum oxidative capacity (29 (4) v 39 (3) mM/min) and a 65% decrease in effective muscle mass (5 (1) v 1 3 (2) arbitrary units). Exercise training improved maximum oxidative c apacity in both muscles, and in gastrocnemius effective muscle mass al so. Conclusions-Skeletal muscle exercise abnormalities in patients wit h congestive heart failure result more from decreased metabolic effici ency than from the abnormalities in mitochondrial oxidation. Both decr eased efficiency and defective mitochondrial oxidation result in an in creased activation of glycogen phosphorylase, and may be improved by e xercise training.