Cellular P O 2 as a determinant of maximal mitochondrial O2consumption in trained human skeletal muscle

Abstract

Previously, by measuring myoglobin-associated [Formula: see text](PMb o 2) during maximal exercise, we have demonstrated that 1) intracellular[Formula: see text] is 10-fold less than calculated mean capillary [Formula: see text] and 2) intracellular[Formula: see text] and maximum O2 uptake (V˙o 2 max) fall proportionately in hypoxia. To further elucidate this relationship, five trained subjects performed maximum knee-extensor exercise under conditions of normoxia (21% O2), hypoxia (12% O2), and hyperoxia (100% O2) in balanced order. Quadriceps O2 uptake (V˙o 2) was calculated from arterial and venous blood O2concentrations and thermodilution blood flow measurements. Magnetic resonance spectroscopy was used to determine myoglobin desaturation, and an O2 half-saturation pressure of 3.2 Torr was used to calculate PMb o 2from saturation. Skeletal muscleV˙o 2 max at 12, 21, and 100% O2 was 0.86 ± 0.1, 1.08 ± 0.2, and 1.28 ± 0.2 ml ⋅ min−1 ⋅ ml−1, respectively. The 100% O2 values approached twice that previously reported in human skeletal muscle. PMb o 2values were 2.3 ± 0.5, 3.0 ± 0.7, and 4.1 ± 0.7 Torr while the subjects breathed 12, 21, and 100% O2, respectively. From 12 to 21% O2,V˙o 2 and PMb o 2were again proportionately related. However, 100% O2 increasedV˙o 2 max relatively less than PMb o 2, suggesting an approach to maximal mitochondrial capacity with 100% O2. These data 1) again demonstrate very low cytoplasmic [Formula: see text] atV˙o 2 max, 2) are consistent with supply limitation of V˙o 2 maxof trained skeletal muscle, even in hyperoxia, and 3) reveal a disproportionate increase in intracellular [Formula: see text] in hyperoxia, which may be interpreted as evidence that, in trained skeletal muscle, very high mitochondrial metabolic limits to muscleV˙o 2 are being approached.