An Upper Bound on the Minimum PO2 for O2 Consumption in Red Muscle
At a certain PO2 the rate of O2 consumption (VO2) becomes limited by O2 availability rather than energy demand. This PO2 may be defined as the critical PO2 (PcritO2) for the corresponding rate of cytochrome turnover. PcritO2 sets the minimum PO2 which convective and diffusive transport must defend. To date there have been no estimates of PcritO2 for VO2 in vivo, though the influence of O2 on redox ratios has been studied extensively in heart, liver and brain. Some contend that cytochrome a,a3 is highly reduced in tissue over the entire physiologic range of O2 tensions.1,2 Such reduction implies that tissue respiration should be strongly O2 dependent and that there should be no PcritO2 for VO2 in vivo. Chance and associates studied O2 binding to cytochrome a, a3 in brain in the presence and absence of CO.3 They interpret their data to mean that cytochrome a, a3 is almost fully oxidized in vivo and in vitro. Lubbers and associates found cytochrome a, a3 more than 95% oxidized in rat heart (personal communication). Highly oxidized a, a3 suggests that VO2 depends solely on redox and phosphorylation potentials above a PO2 negligible for O2 transport.
KeywordsGracilis Muscle Redox Ratio Glycolytic Fiber Reflectance Spectrophotometry Cytosolic Redox
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