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J Appl Physiol 100: 1019-1026, 2006. First published November 10, 2005; doi:10.1152/japplphysiol.00388.2005
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Effects of arterial hypotension on microvascular oxygen exchange in contracting skeletal muscle

Brad J. Behnke,1,2 Danielle J. Padilla,1 Leonardo F. Ferreira,1 Michael D. Delp,2 Timothy I. Musch,1 and David C. Poole1

1Department of Kinesiology and the Clarenburg Laboratory in the Department of Anatomy and Physiology, Kansas State University, Manhattan, Kansas; and 2Division of Exercise Physiology, West Virginia University School of Medicine, Morgantown, West Virginia

Submitted 5 April 2005 ; accepted in final form 7 November 2005

In healthy animals under normotensive conditions (N), contracting skeletal muscle perfusion is regulated to maintain microvascular O2 pressures (PmvFormula) at levels commensurate with O2 demands. Hypovolemic hypotension (H) impairs muscle contractile function; we tested whether this condition would alter the matching of O2 delivery (QO2) to O2 utilization (VO2), as determined by PmvFormula at the onset ofmuscle contractions. PmvFormula 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; PmvFormula 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 PmvFormula and steady-state contracting PmvFormula(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 andH, respectively, P < 0.05) before the fall in PmvFormula and accelerated therate of PmvFormula decrease (time constant, 12.6 ± 1.4 vs. 7.3 ± 0.9 s for N and H, respectively, P < 0.05). Muscle VO2 was reduced by 71% at rest and 64% with contractions in H vs. N, and O2 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 QO2 relative to that of VO2 at the onset of contractions,leading to a decreased PmvFormula. According to Fick's law, this scenario will decrease blood-myocyte O2 flux, thereby slowing VO2 kinetics and exacerbating the O2 deficit generated at exercise onset.

oxygen delivery; oxygen utilization; rat spinotrapezius muscle; exercise; kinetics



Address for reprint requests and other correspondence: D. C. Poole, Dept. Anatomy and Physiology, College of Veterinary Medicine, Kansas State University, Manhattan, KS 66505-5802 (e-mail: poole{at}vet.ksu.edu)




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