Rapid vasodilation within contracted skeletal muscle in humans: new insight from concurrent use of diffuse correlation spectroscopy and Doppler ultrasound.

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. Through the concurrent use of diffuse correlation spectroscopy and Doppler ultrasound, we provide the first evidence in humans that a single brief muscle contraction evokes rapid, intensity-dependent hyperemia within the contracted skeletal muscle microvasculature and the upstream conduit artery. We also show that the magnitude and time course of the contraction-induced rapid hyperemia and vasodilatory responses within skeletal muscle microvessels significantly differ from those in the conduit artery.