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AJP - Heart and Circulatory Physiology, Vol 246, Issue 1 120-H128, Copyright © 1984 by American Physiological Society
ARTICLES |
R. J. Connett, T. E. Gayeski and C. R. Honig
Tissue lactate was measured in dog gracilis muscles frozen at rest and during phasic twitch contractions, which evoked 10-100% of maximum O2 consumption (VO2 max). Myoglobin cryomicrospectroscopy was used to obtain the distribution of PO2 in subcellular volumes. Tissue sampling was designed to estimate lactate concentration in the population of cells used for spectroscopy. Covariates included vascular resistance, functional capillary density, VO2, tissue pyruvate, ATP, phosphocreatine, and creatine, as well as lactate efflux. Myoglobin saturation did not decrease in the first seconds of stimulation at 1 or 4/s. In the steady state, muscle lactate accumulation was linear with stimulation rate and VO2. At 1 and 4/s the minimum PO2 found was greater than 5 Torr during the rest-work transition and greater than 2 Torr in the steady state. VO2 did not increase when flow was increased during contraction at 1/s, although the minimum PO2 found rose to approximately 10 Torr. If flow was restricted during stimulation, PO2 was 0 at many loci, and lactate concentration was elevated above the value predicted by its linear relationship with twitch rate. We conclude that fully aerobic lactate accumulation occurs in this pure red muscle. This accumulation results from causes other than a simple O2 limit on mitochondrial ATP production.
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