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

Abstract

There exists substantial controversy as to whether muscle oxygen (O 2) delivery ( Q ̇ O 2 ) or muscle mitochondrial O 2 demand determines the profile of pulmonary V ̇ 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 O 2 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 (∼250 g). Spinotrapezius blood flow (radioactive microspheres) and P O 2 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 l00 g ( P<0.05). Muscle contractions reduced P O 2 m from a baseline of 31.4±1.6 to a steady-state value of 21.0±1.7 mmHg ( n=24, P<0.0l). The response profile of P O 2 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 O 2 at exercise onset or any P O 2 m undershoot prior to achievement of steady-state values, provides compelling evidence that O 2 delivery is not limiting under these conditions.