Journal of Applied Physiology
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J Appl Physiol 76: 1512-1519, 1994;
8750-7587/94 $5.00
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Journal of Applied Physiology, Vol 76, Issue 4 1512-1519, Copyright © 1994 by American Physiological Society


ARTICLES

Contribution of arterial feed vessels to skeletal muscle functional hyperemia

J. M. Lash
Department of Physiology and Biophysics, Indiana University School of Medicine, Indianapolis 46202.

The purpose of this study was to determine whether dilation of arterial vessels preceding the microcirculation contributes differentially to increases in skeletal muscle blood flow during contractions in anesthetized sedentary (SED) or trained (TR) rats. Experiments were performed in the spinotrapezius muscle of adult male Sprague-Dawley rats. Before and immediately after muscle contractions (2, 4, or 8 Hz), intravascular pressures, red blood cell velocities, and vessel diameters were measured in terminal feed arteries at a site before penetration into the tissue. Pressure was also measured in the accompanying vein. Contraction-induced changes in vascular resistance were calculated for upstream (Rup), spinotrapezius muscle microvascular (Rst), and downstream segments. At rest, Rup accounted for less (32 vs. 40%) and Rst for more (59 vs. 47%) of total resistance in TR than in SED rats. At 8 Hz, contractions produced significantly greater functional dilation (SED, 138 +/- 14 microns; TR, 178 +/- 12 microns) and hyperemia (SED, 11.9 +/- 3.2 x control; TR, 16.8 +/- 3.1 x control) in TR than in SED rats. Inflow pressures did not change, and outflow pressures increased significantly with contractions. Rup and Rst each decreased 60-80% after 2-Hz contractions and > 90% after 8-Hz contractions. Therefore, feed artery dilation contributes significantly to functional hyperemia in the rat spinotrapezius muscle. Furthermore, it appears that aerobic exercise training results in a redistribution of segmental vascular resistance between feed vessels and the microcirculation.


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