TRAINING PARTIALLY REVERSES SKELETAL-MUSCLE METABOLIC ABNORMALITIES DURING EXERCISE IN HEART-FAILURE

Using P-31-magnetic resonance spectroscopy during and after exercise, we studied whether forearm metabolic responses to exercise were improv ed by 1 mo of training in 10 males with heart failure. In the control (untrained) arm, there were no changes in any of the measured variable s. In the trained arm, maximal voluntary contraction increased 6% (P = 0.05). During incremental exercise, duration increased 19% (P < 0.05) and submaximal responses improved for pH (6.78 +/- 0.13 pretraining v s. 6.85 +/- 0.17 posttraining; P < 0.01) and PCr/(PCr +/- P-i) (where PCr is phosphocreatine; 0.48 +/- 0.09 pretraining vs. 0.52 +/- 0.07 po sttraining; P < 0.01). The PCr resynthesis rate increased by 48% (P < 0.01), and estimated effective maximal rate of mitochondrial ATP synth esis increased by 37% (P < 0.05). Endurance exercise duration increase d by 67% (P < 0.01), and submaximal levels of PCr/(PCr + P-i) (P < 0.0 5) and pH (P = 0.07) improved. The PCr resynthesis rate (P < 0.01) and the effective maximal rate of mitochondrial ATP synthesis (P < 0.05) also improved. These findings document that impaired oxidative capacit y of skeletal muscle can be improved by local muscle training in heart failure, which is compatible with the hypothesis that a part of the a bnormality present in heart failure may be due to inactivity.