Muscle blood flow is independent of conduit artery diameter following prior vasodilation in males.

At the onset of exercise in humans, muscle blood flow (MBF) increases to a new steady-state that closely matches the metabolic demand of exercise. This increase has been attributed to "contraction-induced vasodilation," comprised of the skeletal muscle pump and rapid vasodilatory mechanisms. While most research in this area has focused on forearm blood flow (FBF) and vascular conductance, it is possible that separating FBF into diameter and blood velocity can provide more useful information on MBF regulation downstream of the conduit artery. Therefore, we attempted to dissociate the matching of oxygen delivery and oxygen demand by administering glyceryl tri-nitrate (GTN) prior to handgrip exercise. Eight healthy males (29 ± 9 years) performed two trials consisting of two bouts of rhythmic handgrip exercise (30 contractions·min-1 at 5% of maximum) for 6 min, one for each control and GTN (0.4 mg sublingual) condition. Administration of GTN resulted in a 12% increase in resting brachial artery diameter that persisted throughout the duration of exercise (CON: 0.50 ± 0.01 cm; GTN: 0.56 ± 0.01 cm, p < 0.05). Resting FBF was greater following GTN administration compared to control (p < 0.05); however, differences in FBF disappeared following the onset of muscle contractions. Our results indicate that the matching of FBF to oxygen demand during exercise is not affected by prior vasodilation, so that any over-perfusion is corrected at the onset of exercise. Additionally, our findings provide further evidence that the regulation of vascular tone within the microvasculature is independent of the conduit artery diameter.