Skeletal muscle microvascular and interstitial PO2 from rest to contractions

Abstract

Oxygen pressure (PO₂) gradients across the blood-myocyte interface are required for diffusive O₂ transport thereby supporting oxidative metabolism. The greatest resistance to O₂ flux into skeletal muscle is considered to reside between the erythrocyte surface and adjacent sarcolemma, although this has not been measured during contractions. We tested the hypothesis that O₂ gradients between skeletal muscle microvascular (PO₂mv) and interstitial (PO₂is) spaces would be present at rest and maintained or increased during contractions. PO₂mv and PO₂is were determined via phosphorescence quenching (Oxyphor probes G2 and G4, respectively) in the exposed rat spinotrapezius during the rest-contraction transient (1 Hz, 6 V; n = 8). PO₂mv was higher than PO₂is in all instances from rest (34.9 ± 6.0 vs. 15.7 ± 6.4) to contractions (28.4 ± 5.3 vs. 10.6 ± 5.2 mmHg; respectively) such that the mean PO₂ gradient throughout the transient was 16.9 ± 6.6 mmHg (P < 0.05 for all). No differences in the amplitude of PO₂ fall with contractions were observed between the microvasculature and interstitium (10.9 ± 2.3 vs. 9.0 ± 3.5 mmHg, respectively; P > 0.05). However, the speed of the PO₂is fall during contractions was slower than that of PO₂mv (time constant: 12.8 ± 4.7 vs. 9.0 ± 5.1 s, respectively; P < 0.05). Consistent with our hypothesis, a significant transmural gradient was sustained (but not increased) from rest to contractions. This supports that the blood-myocyte interface is the site of a substantial PO₂ gradient driving O₂ diffusion during metabolic transients. Based on Fick's law, elevated O₂ flux with contractions must thus rely primarily on modulations in effective diffusing capacity (mainly erythrocyte hemodynamics and distribution) as the PO₂ gradient is not increased.

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