Oxygen Dynamics in Microcirculation of Skeletal Muscle

Capillaries were believed to be the sole source of O

2

supply to tissue. However, the recent studies have demonstrated a longitudinal PO

2

drop in arterioles, suggesting the possibility of O

2

supply from arterioles. Furthermore, analysis of the diffusion process based on the PO

2

drop has shown that the O

2

diffusivity in the arteriolar wall was dramatically greater than in the tissue; thus, such a large O

2

loss from arterioles seemed unlikely to be solely attributable to simple diffusion. To explain this discrepancy we hypothesized the O

2

consumption by arteriolar than previously thought. In walls was this study, much higher we quantified the O

2

consumption rate in arteriolar walls to evaluate its impact on the PO

2

drop in the arterioles. Phosphorescence quenching microscopy was used to determine the intra- and perivascular PO

2

values of rat cremaster arterioles both under normal condition and during vasodilation. Using the measured PO

2

values, we calculated the O

2

consumption rate of the arteriolar wall. Our results showed that 100 times more O

2

is consumed by arteriolar walls, compared with

in vitro

vascular segments; consequently, O

2

consumption by arteriolar walls could be the main cause of the PO

2

drop in arterioles. Furthermore, we found the O

2

consumption rate of the arteriolar walls under normal condition to be higher than during vasodilation and the O

2

consumption to be dependent on the mechanical work of vascular smooth muscle. These findings suggested important roles of arterioles for O

2

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 O

2

to restrict blood flow into skeletal muscle. While During exercise, arteriolar O

2

consumption decreases as a result of vasodilation, thereby efficiently supplying O

2

to the skeletal muscle of high O

2

demand.