• T K Roy and A S Popel.
• Department of Biomedical Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.
• Am. J. Physiol. 1996 Aug 1;271(2 Pt 2):H721-37.

AbstractCharacterizing the resistances to O2 transport from the erythrocyte to the mitochondrion is important in understanding potential transport limitations. A steady-state model of this process was developed to predict the minimum (critical) end-capillary PO2 required to prevent hypoxia at maximal O2 consumption (VO2max) in a circular region of tissue surrounding the venular end of a capillary. Capillary density was used as a measure of O2 delivery, and mitochondrial density was used as a measure of O2 consumption. The effects of oxyhemoglobin dissociation kinetics and diffusion facilitation by hemoglobin in the erythrocytes and facilitation by myoglobin in the tissue were taken into account. Calculations made for selected skeletal muscles, diaphragm, and myocardium in three adaptive animal pairs (dog and goat, horse and cow, and pony and calf) yielded values of end-capillary PO2 that were consistent with measured values of mixed venous PO2 in maximally working animals. Values of end-capillary PO2 were found to be uncorrelated with values of VO2max in different muscles. No significant difference in end-capillary PO2 was found between similar muscles of athletic versus nonathletic animals. Predicted intracapillary O2 transport resistance ranged from 18 to 54% of the total transport resistance in the O2 pathway. Further investigation is required to explore the extent to which spatial and temporal heterogeneities in O2 delivery and consumption play a role in O2 transport.

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