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J Appl Physiol 87: 325-331, 1999;
8750-7587/99 $5.00
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Vol. 87, Issue 1, 325-331, July 1999

Cellular PO2 as a determinant of maximal mitochondrial O2 consumption in trained human skeletal muscle

R. S. Richardson1, J. S. Leigh2, P. D. Wagner1, and E. A. Noyszewski2

1 Department of Medicine, University of California San Diego, La Jolla, California 92093; and 2 Department of Radiology, University of Pennsylvania, Philadelphia, Pennsylvania 19104-6021

Previously, by measuring myoglobin-associated PO2 (PMbO2) during maximal exercise, we have demonstrated that 1) intracellular PO2 is 10-fold less than calculated mean capillary PO2 and 2) intracellular PO2 and maximum O2 uptake (VO2 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 (VO2) was calculated from arterial and venous blood O2 concentrations 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 PMbO2 from saturation. Skeletal muscle VO2 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. PMbO2 values 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, VO2 and PMbO2 were again proportionately related. However, 100% O2 increased VO2 max relatively less than PMbO2, suggesting an approach to maximal mitochondrial capacity with 100% O2. These data 1) again demonstrate very low cytoplasmic PO2 at VO2 max, 2) are consistent with supply limitation of VO2 max of trained skeletal muscle, even in hyperoxia, and 3) reveal a disproportionate increase in intracellular PO2 in hyperoxia, which may be interpreted as evidence that, in trained skeletal muscle, very high mitochondrial metabolic limits to muscle VO2 are being approached.

blood flow; oxygen transport; myoglobin; magnetic resonance spectroscopy


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