Oxygen dynamics in microcirculation of skeletal muscle

Capillaries were believed to be the sole source of O₂ supply to tissue. However, the recent studies have demonstrated a longitudinal PO₂ drop in arterioles, suggesting the possibility of O₂ supply from arterioles. Furthermore, analysis of the diffusion process based on the PO₂ drop has shown that the O₂ diffusivity in the arteriolar wall was dramatically greater than in the tissue; thus, such a large O₂ loss from arterioles seemed unlikely to be solely attributable to simple diffusion. To explain this discrepancy we hypothesized the O₂ consumption by arteriolar walls was much higher than previously thought. In this study, we quantified the O₂ consumption rate in arteriolar walls to evaluate its impact on the PO₂ drop in the arterioles. Phosphorescence quenching microscopy was used to determine the intra- and perivascular PO₂ values of rat cremaster arterioles both under normal condition and during vasodilation. Using the measured PO₂ values, we calculated the O₂ consumption rate of the arteriolar wall. Our results showed that 100 times more O₂ is consumed by arteriolar walls, compared with in vitro vascular segments; consequently, O₂ consumption by arteriolar walls could be the main cause of the PO₂ drop in arterioles. Furthermore, we found the O₂ consumption rate of the arteriolar walls under normal condition to be higher than during vasodilation and the O₂ consumption to be dependent on the mechanical work of vascular smooth muscle. These findings suggested important roles of arterioles for O₂ transport to tissue. Under resting skeletal muscle, to ensure blood supply to other organs with low systemic blood flow, the arterioles consume a large amount of O₂ to restrict blood flow into skeletal muscle. While During exercise, arteriolar O₂ consumption decreases as a result of vasodilation, thereby efficiently supplying O₂ to the skeletal muscle of high O₂ demand.