Sarcomere Length-Induced Alterations of Capillary Hemodynamics in Rat Spinotrapezius Muscle: Vasoactive vs Passive Control

Abstract

Skeletal muscle blood flow is reduced as fibers are stretched longitudinally. Neither the underlying cause(s) of this decrement in blood flow nor the consequences in terms of capillary red blood cell (rbc) hemodynamics has been established clearly within the physiological range of muscle sarcomere length. Using intravital microscopy, this investigation determined arteriolar diameter and capillary rbc velocity (Vrbc), flux (Frbc), and hematocrit (Hctt) in the rat spinotrapezius muscle at shortened/resting (2.6 μm) and physiological extended (3.2 μm) sarcomere lengths under control (c) and local maximally vasodilated (v, phentolamine, 1 μmol/L; prazosin, 0.1 μmol/L; nitroprusside, 10 μmol/L) conditions. The hypothesis tested was that muscle stretch would reduce Vrbc and Frbc proportionally such that Hctt would remain unchanged and that these reductions in Vrbc and Frbc would be attenuated following maximal vasodilation. Vrbc and Frbc were increased significantly following maximal vasodilation at 2.6-μm (59 and 84%) and 3.2-μm (64 and 104%) sarcomere lengths, respectively. Irrespective of sarcomere length, Hctt was elevated significantly following vasodilation (c, 0.20 ± 0.01; v, 0.27 ± 0.01). At 3.2 μm compared with the 2.6-μm sarcomere length, Vrbc and Frbc were both reduced significantly under control and vasodilated conditions as expected. However, the percent reduction in either Vrbc (c, 27%, and v, 29%) or Frbc (c, 26%, and v, 33%) was not significantly different between the 2.6- and 3.2-μm sarcomere lengths. In addition, arteriolar diameter was not altered discernably as sarcomere length was increased from 2.7 μm (c, 29.0 ± 4.5; v, 37.9 ± 6.7 μm) to 3.2 μm (c, 29.4 ± 4.5; v, 37.3 ± 6.2 μm). These data suggest that increasing sarcomere length from resting to the upper extreme of the physiological range in the rat spinotrapezius muscle reduces Vrbc and Frbc (at constant hematocrit) by a mechanism that is independent of stretch-activated arteriolar vasoconstriction.