[Metabolic, morpho-histologic and biochemical changes in skeletal muscles in chronic cardiac failure]

The study of skeletal muscle by nuclear magnetic resonance (NMR) 31p in patients with chronic heart failure (CHF) or in experimental animal models has not shown metabolic abnormalities under basal conditions. However, during exercise, phosphocreatinine (PCr) depletion is increased and early intracellular acidosis has been demonstrated. These changes contribute to deterioration of exercise capacity as they are related to peak VO2 and exercise duration. Other metabolites may play an important role. The depletion of ATP at maximal exercise may be observed in some patients with severe CCF. The results of PCr recovery kinetics are contradictory. Apparently, its recovery rate is unchanged. Most biochemical and histological abnormalities are represented by a decrease in oxidative structure (type I muscular fibres, mitochondria) and in enzymatic oxidative capacity. These changes are related to the metabolic abnormalities and exercise capacity. Muscular hypotrophy alone cannot explain the metabolic changes observed in CHF. Several mechanisms could be involved, physical deconditioning probably being the most pertinent. Other factors such as neurohormonal activation and insulin resistance should be investigated. Physical training improves exercise capacity and may reverse these muscular abnormalities. A long-term benefit of physical training on morbidity and mortality should be demonstrated.