Effect of heart failure on skeletal muscle in dogs

Abstract

To investigate the effect of heart failure (HF) on skeletal muscle, gracilis, gastrocnemius, and triceps muscle histochemistry and enzyme activity, gracilis muscle performance, and gracilis muscle 31P magnetic resonance spectroscopy (MRS) metabolic responses to exercise were compared in six sham-operated control dogs (C) and seven dogs with HF produced by 3 mo of rapid ventricular pacing. HF reduced skeletal muscle weights and decreased type II fiber area (3,315 +/- 996 to 1,750 +/- 638 microns 2; P less than 0.01). Citrate synthase and beta-hydroxyacyl CoA dehydrogenase activity also tended to decrease. Gracilis muscle inorganic phosphate-to-phosphocreatine ratios, oxygen uptake (VO2), and pH responses to exercise using supramaximal twitch stimulation, a form of exercise that produces maximal stimulation of all muscle fibers and therefore is independent of muscle mass, were similar in both groups. There was no significant difference in developed tension per gram muscle during stimulation at 0.5-200 Hz, maximal developed tension (C: 177 +/- 32 vs. HF: 173 +/- 44 g/g muscle), or muscle fatigability as assessed by percent of initial tension observed at the end of 2 min of 20 Hz stimulation (C: 52 +/- 17% vs. HF: 52 +/- 11%; all P = NS). These data suggest that HF produces skeletal muscle atrophy but that the remaining muscle exhibits normal performance and metabolism.