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J Appl Physiol 77: 671-678, 1994;
8750-7587/94 $5.00
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Journal of Applied Physiology, Vol 77, Issue 2 671-678, Copyright © 1994 by American Physiological Society

ARTICLES

Exercise O2 transport model assuming zero cytochrome PO2 at VO2 max

J. W. Severinghaus
Cardiovascular Research Institute, San Francisco, California 94143.

An analogy is drawn between cytochrome aa3 function and a polarographic cathode at which the potential of -0.6 V captures all O2 diffusing to the surface, achieving maximal O2 consumption (VO2max) by eliminating O2 backpressure and outward diffusion from the surface, defined herein as zero surface PO2. The relationship of O2 consumption (as %VO2max) to muscle venous, myoglobin, and cytochrome PO2 is modeled assuming that cytochrome aa3 PO2 reaches zero at VO2max, incorporating published data on the profile of leg venous PO2, pH, and blood lactate vs. work. Equations describe hemoglobin and myoglobin O2 dissociation and the Bohr effect of acid on O2 unloading. The O2 gradient from capillary blood to cytochrome aa3 is assumed to be proportional to O2 consumption. The model suggests that 1) to extract 75% of the O2 from myoglobin at VO2max, myoglobin must lie 90% down the O2 gradient from capillary to cytochrome; 2) the Bohr effect adds 15-30% to VO2max and keeps venous PO2 almost constant as work rises from 60 to 100% of VO2max; and 3) in steady heavy work, the rising arterial lactate may impede lactate excretion from muscle, reduce anaerobic ATP generation, and shift the energy balance toward aerobic metabolism. The zero PO2 hypothesis facilitates modeling and may be the key to understanding the physiological limitation of work.


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