Impaired muscle oxygen transfer in patients with chronic renal failure

We hypothesized that impaired O-2 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 O-2 delivery ((Q) over dot O-2leg) and leg O-2 uptake ((V) over dot O-2leg) were obtained when subjects breathed gas of three inspired O-2 fractions (FIO2) (0.13, 0.21, and 1.0). On a different day, myoglobin O-2 saturation and muscle bioenergetics were measured by proton and phosphorus magnetic resonance spectroscopy. CRF patients, but not controls, showed O-2 supply dependency of peak (V) over dot O-2 ((V) over dot O-2peak) by a proportional relationship between peak (V) over dot O-2leg at each inspired O-2 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) over dot O-2leg (0.80 +/- 0.20, 0.64 +/- 0.10, 0.59 +/- 0.10 l/min), and 3) cell PO2 (6.3 +/- 5.4, 1.7 +/- 1.3, 1.2 +/- 0.7 mmHg). CRF patients breathing 100% O-2 and controls breathing 21% O-2 had similar peak (Q) over dot O-2leg (0.80 +/- 0.20 vs. 0.79 +/- 0.10 l/min) and similar peak (V) over dot O-2leg (0.59 +/- 0.20 vs. 0.57 +/- 0.10 l/min). However, mean capillary PO2 (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 O-2 conductance, but not limited mitochondrial oxidative capacity, plays a role in limiting exercise tolerance in these patients.