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Previous studies showed that conduit artery blood flow rapidly increases after even a brief contraction of muscles within the dependent limb. Whether this rapid hyperemia occurs within contracted skeletal muscle in humans has yet to be confirmed, however. We therefore used diffuse correlation spectroscopy (DCS) to characterize the rapid hyperemia and vasodilatory responses within the muscle microvasculature induced by single muscle contractions in humans. Twenty-five healthy male volunteers performed single 1-s isometric handgrips at 20%, 40%, 60%, and 80% of maximum voluntary contraction. DCS probes were placed on the flexor digitorum superficialis muscle, and a skeletal muscle blood flow index (SMBFI) was derived continuously. At the same time, brachial artery blood flow (BABF) responses were measured using Doppler ultrasound. Single muscle contractions evoked rapid, monophasic increases in both SMBFI and BABF that occurred within 3 s after release of contraction. The initial and peak responses increased with increases in contraction intensity and were greater for BABF than for SMBFI at all intensities. BABF reached its peak within 5 to 8 s after the end of contraction. The SMBFI continued to increase after the BABF passed its peak and was decreasing toward the resting level and peaked about 10 to 15 s after completion of the contraction. We conclude that single muscle contractions induce rapid, intensity-dependent hyperemia within the contracted skeletal muscle microvasculature. Moreover, the characteristics of the rapid hyperemia and vasodilatory responses of skeletal muscle microvessels differ from those simultaneously evaluated in the upstream conduit artery. [ABSTRACT FROM AUTHOR]

We used diffuse correlation spectroscopy to investigate sympathetic vasoconstriction, local vasodilation, and integration of these two responses in the skeletal muscle microvasculature of 20 healthy volunteers. Diffuse correlation spectroscopy probes were placed on the flexor carpi radialis muscle or vastus lateralis muscle, and a blood flow index was derived continuously. We measured hemodynamic responses during sympathoexcitation induced by forehead cooling, after which the effects of the increased sympathetic tone on vasodilatory responses during postocclusive reactive hyperemia (PORH) were examined. PORH was induced by releasing arterial occlusion (3 min) in an arm or leg. To increase sympathetic tone during PORH, forehead cooling was begun 60 s before the occlusion release and ended 60 s after the release. During forehead cooling, mean arterial pressure rose significantly and was sustained at an elevated level. Significant vasoconstriction and decreases in blood flow index followed by gradual blunting of the vasoconstriction also occurred. The time course of these responses is in good agreement with previous observations in animals. The acute sympathoexcitation diminished the peak vasodilation during PORH only in the vastus lateralis muscle, but it hastened the decline in vasodilation after the peak in both the flexor carpi radialis muscle and vastus lateralis muscle. Consequently, the total vasodilatory response assessed as the area of the vascular conductance during the first minute of PORH was significantly diminished in both regions. We conclude that, in humans, the integrated effects of sympathetic vasoconstriction and local vasodilation have an important role in vascular regulation and control of perfusion in the skeletal muscle microcirculation. NEW & NOTEWORTHY We used diffuse correlation spectroscopy to demonstrate that acute sympathoexcitation constrains local vasodilation in the human skeletal muscle microvasculature during postocclusive reactive hyperemia. This finding indicates that integration of sympathetic vasoconstriction and local vasodilation is importantly involved in vascular regulation and the control of perfusion of the skeletal muscle microcirculation in humans. [ABSTRACT FROM AUTHOR]