Effects of arterial hypotension on microvascular oxygen exchange in contracting skeletal muscle

In healthy animals under normotensive conditions (N), contracting skeletal muscle perfusion is regulated to maintain microvascular O-2 pressures (PmvO(2)) at levels commensurate with O-2 demands. Hypovolemic hypotension (H) impairs muscle contractile function; we tested whether this condition would alter the matching of O-2 delivery (Qo(2)) to O-2 utilization (Vo(2)), as determined by PmvO(2) at the onset of muscle contractions. PmvO(2) in the spinotrapezius muscles of seven female Sprague-Dawley rats ( 280 +/- 6 g) was measured every 2 s across the transition from rest to 1-Hz twitch contractions. Measurements were made under N ( mean arterial pressure, 97 +/- 4 mmHg) and H ( induced by arterial section; mean arterial pressure, 58 +/- 3 mmHg, P < 0.05) conditions; PmvO(2) profiles were modeled using a multicomponent exponential fitted with independent time delays. Hypotension reduced muscle blood flow at rest ( 24 +/- 8 vs. 6 +/- 1 ml(-1) (.) min(-1) (.) 100 g(-1) for N and H, respectively; P < 0.05) and during contractions ( 74 +/- 20 vs. 22 +/- 4 ml(-1) (.) min(-1) (.) 100 g(-1) for N and H, respectively; P < 0.05). H significantly decreased resting PmvO(2) and steady-state contracting PmvO2 (19.4 +/- 2.4 vs. 8.7 +/- 1.6 Torr for N and H, respectively, P < 0.05). At the onset of contractions, H reduced the time delay ( 11.8 +/- 1.7 vs. 5.9 +/- 0.9 s for N and H, respectively, P < 0.05) before the fall in PmvO(2) and accelerated the rate of PmvO(2) decrease ( time constant, 12.6 +/- 1.4 vs. 7.3 +/- 0.9 s for N and H, respectively, P < 0.05). Muscle V. O-2 was reduced by 71% at rest and 64% with contractions in H vs. N, and O-2 extraction during H averaged 78% at rest and 94% during contractions vs. 51 and 78% in N. These results demonstrate that H constrains the increase of skeletal muscle Qo(2) relative to that of Vo(2) at the onset of contractions, leading to a decreased PmvO(2). According to Fick's law, this scenario will decrease blood-myocyte O-2 flux, thereby slowing Vo(2) kinetics and exacerbating the O-2 deficit generated at exercise onset.