Dynamics of microvascular oxygen pressure across the rest-exercise transition in rat skeletal muscle

There exists substantial controversy as to whether muscle oxygen (O-2) delivery ((Q) over dot o(2)) or muscle mitochondrial O-2 demand determines the profile of pulmonary (V) over dot o(2) kinetics in the rest-exercise transition. To address this issue, we adapted intravascular phosphorescence quenching techniques for measurement of rat spinotrapezius microvascular O-2 pressure (P(o2)m) The spinotrapezius muscle intravital microscopy preparation is used extensively for investigation of muscle microcirculatory control. The phosphor palladium-meso-tetra(4-carboxyphenyl)porphyrin dendrimer (R2) at 15 mg/kg was bound to albumin within the blood of female Sprague-Dawley rats (similar to 250 g). Spinotrapezius blood flow (radioactive microspheres) and P(o2)m profiles were determined in situ across the transition from rest to 1 Hz twitch contractions. Stimulation increased muscle blood flow by 240% from 16.6 +/- 3.0 to 56.2 +/- 8.3 (SE) ml/min per 100 g (P < 0.05). Muscle contractions reduced P(o2)m from a baseline of 31.4 +/- 1.6 to a steady-state value of 21.0 +/- 1.7 mmHg (n = 24, P < 0.01). The response profile of P(o2)m was well fit by a time delay of 19.2 +/- 2.8 sec (P < 0.05) followed by a monoexponential decline (time constant, 21.7 +/- 2.1 sec) to its steady state level. The absence of either an immediate and precipitous fall in microvascular P-o2 at exercise onset or any P(o2)m undershoot prior to achievement of steady-state values, provides compelling evidence that O-2 delivery is not limiting under these conditions. (C) 2001 Elsevier Science B.V. All rights reserved.