Abstract
The rate of O2 consumption (V̇O2) may increase 100-fold between rest and steady work in red skeletal muscles (1,2). Does hyperemia supply O2 at a rate which keeps pace with this massive increase in O2 demand, or is an O2 debt incurred? Does exercise hyperemia depend on O2 lack (3), a redox signal (4), or cytosolic energy charge (5)? To answer these questions we related the time course of exercise hyperemia to myoglobin (Mb) saturation in subcellular volumes (6,7). ATP, creatine phosphate (PCr), lactate (LA), and pyruvate (Pyr) concentrations were co-variates.
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© 1984 Plenum Press, New York
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Honig, C.R., Gayeski, T.E.J., Connett, R.J. (1984). Balance between O2 Availability and V̇O2 in Rest-Work Transition as Measured by Myoglobin Saturation in Subcellular Volumes. In: Bruley, D., Bicher, H.I., Reneau, D. (eds) Oxygen Transport to Tissue—VI. Advances in Experimental Medicine and Biology, vol 180. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-4895-5_63
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DOI: https://doi.org/10.1007/978-1-4684-4895-5_63
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