Models of Steady-State Control of Skeletal Muscle $\rm\dot{v}$O₂ Evaluation Using Tissue Data

Abstract

Oxygen delivered to the skeletal muscle ultimately serves as a substrate for mitochondrial oxidative phosphorylation. All models dealing with oxygen delivery to the mitochondria must include some quantitative description of oxygen consumption ($\rm\dot{v}$ O₂) • Although a number of proposals for the regulation of mitochondrial VO₂ have been made and tested with isolated mitochondria, there is still considerable uncertainty as to the best way of relating changes in $\rm\dot{v}$ O₂ in vivo to measurable changes in tissue metabolites. In a recent report (Connett, 1987) we demonstrated that during a rest-work transition in dog skeletal muscle, neither adenosine diphosphate concentration [ADP] nor inorganic phosphate [Pi] alone appeared to be rate-limiting and, therefore, regulating substrates. It was found that the best description of the changes in VO₂ with time was obtained by relating $\rm\dot{v}$ O₂ to the phosphorylation potential with the charge balance of adenosine triphosphate [ATP] hydrolysis taken into account. This report deals with a preliminary evaluation of the same models using data from various rates of steady-state energy turnover.