This paper describes a model of skeletal muscle metabolism and local control of vascular resistance. The model predicts changes in tissue PO2 and interstitial K+ concentration associated with muscle activity and the effects of these alterations on vascular resistance. We have attempted to use physiologically sound relationships, parameters and constant values throughout. Predictions based on the model match the experimentally determined responses of venous O2 saturation, venous K+ concentration, and vascular resistance to brief tetanus at both high and low constant flow. Model simulations of brief tetanus indicate that the resistance response at high flow is caused almost entirely by changes in interstitial K+, whereas the vascular response observed at low flow has a fast component due to K+ and a slow component caused by low tissue PO2. Our study supports the hypothesis that local vascular control involves more than one substance but that the relative importance of each influence on vascular resistance depends upon the experimental conditions.

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