Altered purine and glycogen metabolism in skeletal muscle during exercise in patients with heart failure

Plasma levels of ammonia and hypoxanthine (HX) can be indices of purine nucleotide degradation. The present study determined if patients with heart failure (HF) have altered exercise plasma ammonia and HX levels relative to the peak work rate performed. Blood lactate, plasma ammonia, and plasma HX levels were measured in 59 patients with HF (New York Heart Association [NYHA] classes I:20, II:21, and III:18) and 21 controls at test and after a maximal cardiopulmonary exercise test. The peak work rate (normal and NYHA I, II, and III, 163 +/- 11, 152 +/- 9, 94 +/- 5, and 69 +/- 5 W) and peak oxygen uptake ([VO2] 32.3 +/- 1.7, 25.1 +/- 0.9, 18.6 +/- 0.5, and 14.1 +/- 0.6 ml/min/kg) decreased as the NYHA functional class increased. The increment from rest to peak exercise (Delta) for lactate ([Delta lactate] 6.1 +/- 0.3, 4.8 +/- 0.4, 4.6 +/- 0.3, and 2.9 +/- 0.3 mmol/L), Delta ammonia (132 +/- 14, 119 +/- 20, 94 +/- 13, and 32 +/- 6 mu g/dL), and Delta HX (33.5 +/- 3.4 24.9 +/- 4.7, 20,6 +/- 3.0, and 9.9 +/- 1.2 mu mol/L) was progressively smaller as HF worsened. The ratio for Delta lactate to peak work rate (0.037 +/- 0.003, 0.032 +/- 0.004, 0.049 +/- 0.003, and 0.042 +/- 0.005) was higher in classes II to III HF, while the ratio for Delta ammonia to peak work rate (0.81 +/- 0.14, 0.78 +/- 0.16, 0.99 +/- 0.11, and 0.47 +/- 0.11) was significantly lower in class III HF. In summary, patients with HF exhibited a smaller ammonia response with a higher lactate response to exercise when normalized with the peak work rate. These results suggest there may be an altered purine and glycogen metabolism during exercise in skeletal muscle in patients with HF. Copyright (C) 1999 by W.B. Saunders Company.