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

  • Richard J. Connett
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 227)


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.


Creatine Kinase Adenosine Diphosphate Mitochondrial Oxidative Phosphorylation Adenine Nucleotide Translocase Mitochondrial Redox 
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Copyright information

© Plenum Press, New York 1988

Authors and Affiliations

  • Richard J. Connett
    • 1
  1. 1.School of Medicine and DentistryUniversity of RochesterRochesterUSA

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