Modulation of rat skeletal muscle microvascular O2 pressure via KATP channel inhibition following the onset of contractions.

Vascular hyperpolarization mediated, in part, by the ATP-sensitive K(+) (KATP) channel contributes to exercise-induced increases in skeletal muscle O2 delivery. We hypothesized that KATP channel inhibition via glibenclamide (GLI) would speed the fall of microvascular O2 driving pressure (PO2mv; set by the O2 delivery-O2 utilization ratio), during muscle contractions. Spinotrapezius muscle PO2mv (phosphorescence quenching) was measured in 12 adult Sprague Dawley rats during 180s of 1-Hz twitch contractions (∼ 6 V) under control and GLI (5mg/kg) conditions. The total mean PO2mv response time was greater with GLI (i.e., slowed; control: 42.0 ± 14.2, GLI: 79.5 ± 14.7s, p<0.05). A clear undershoot of the contracting steady-state PO2mv was evident with GLI (15.6 ± 5.3%, p<0.05) but not control (2.3 ± 1.6%, p>0.05). This indicates that KATP channel inhibition does not speed PO2mv kinetics per se during small muscle mass contraction. However, it does induce a transient mismatch of O2 delivery-O2 utilization, lowers PO2mv, and delays attainment of the contracting steady-state.