During periods of elevated metabolism, muscles of different fiber type and oxidative capacity must overcome the resistance to oxygen flux inherent in the capillary-myocyte interface and extract O2 to meet tissue metabolic needs. As the microvasculature is the predominant site of cellular gas exchange, the kinetic profile of microvascular PO2 provides unique insights into the exchange of oxygen between blood and tissue. Specifically, microvascular PO2 kinetics allows determination of the degree to which O2 extraction compensates for reduced bulk flow (QO2) as found in CHF & diabetes. As muscle is composed of fibers differing in size, contractile speed and oxidative capacity, manipulation of these characteristics will allow direct quantification of their effect upon the both the microvascular driving pressure for oxygen at rest (baseline PO2) from the blood to the mitochondria and the """"""""speed"""""""" of the response, which is indicative of the dynamic balance between VO2 and QO2. The following hypotheses are proposed. 1) Baseline PO2 will be reduced in fast-twitch glycolytic fibers due to an elevated VO2/QO2 ratio. 2) The temporal delay preceding the initial fall in PO2 will be correlated with the reduction in baseline PO2. 3) Due to hypotheses 1 & 2, the """"""""speed' with which PO2 falls after the initial delay will be dependent upon both fiber type and oxidative capacity. 4) Recovery PO2 kinetics will be determined by both the degree of metabolic perturbation and oxidative capacity.
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