Impaired muscle oxygen transfer in patients with chronic renal failure

Abstract

We hypothesized that impaired O2 transport plays a role in limiting exercise in patients with chronic renal failure (CRF). Six CRF patients (25 ± 6 yr) and six controls (24 ± 6 yr) were examined twice during incremental single-leg isolated quadriceps exercise. Leg O2 delivery (Q˙o 2leg) and leg O2 uptake (V˙o 2leg) were obtained when subjects breathed gas of three inspired O2 fractions (Fi O2 ) (0.13, 0.21, and 1.0). On a different day, myoglobin O2 saturation and muscle bioenergetics were measured by proton and phosphorus magnetic resonance spectroscopy. CRF patients, but not controls, showed O2supply dependency of peak V˙o 2(V˙o 2peak) by a proportional relationship between peak V˙o 2leg at each inspired O2 fraction (0.59 ± 0.20, 0.47 ± 0.10, 0.43 ± 0.10 l/min, respectively) and 1) work rate (933 ± 372, 733 ± 163, 667 ± 207 g), 2) Q˙o 2leg (0.80 ± 0.20, 0.64 ± 0.10, 0.59 ± 0.10 l/min), and 3) cell Po 2 (6.3 ± 5.4, 1.7 ± 1.3, 1.2 ± 0.7 mmHg). CRF patients breathing 100% O2 and controls breathing 21% O2 had similar peakQ˙o 2leg (0.80 ± 0.20 vs. 0.79 ± 0.10 l/min) and similar peak V˙o 2leg(0.59 ± 0.20 vs. 0.57 ± 0.10 l/min). However, mean capillary Po 2 (47.9 ± 4.0 vs. 38.2 ± 4.6 mmHg) and the capillary-to-myocite gradient (40.7 ± 6.2 vs. 34.4 ± 4.0 mmHg) were both higher in CRF patients than in controls ( P < 0.03 each). We conclude that low muscle O2 conductance, but not limited mitochondrial oxidative capacity, plays a role in limiting exercise tolerance in these patients.