The skeletal muscle pump does not appear to be a major contributor to the hyperemic response to skeletal muscle contraction in this canine model.
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May not implicate muscle pump in canine contraction hyperemia; hypothesis-generating for human exercise physiology and requires translational confirmation.
The skeletal muscle pump is thought to be at least partially responsible for the immediate muscle hyperemia seen with exercise. We hypothesized that increases in venous pressure within the muscle would enhance the effectiveness of the muscle pump and yield greater postcontraction hyperemia. In nine anesthetized beagle dogs, arterial inflow and venous outflow of a single hindlimb were measured with ultrasonic transit-time flow probes in response to 1-s tetanic contractions evoked by electrical stimulation of the sciatic nerve. Venous pressure in the hindlimb was manipulated by tilting the upright dogs to a 30 degrees angle in the head-up or head-down positions. The volume of venous blood expelled during contractions was 2.2 +/- 0.2, 1.6 +/- 0.2, and 1.4 +/- 0.2 ml with the head-up, horizontal, and head-down positions, respectively. Although altering hindlimb venous pressure influenced venous expulsion during contraction, the increase in arterial inflow was similar regardless of position. Moreover, the volume of blood expelled was a small fraction of the cumulative arterial volume after the contraction. These results suggest that the muscle pump is not a major contributor to the hyperemic response to skeletal muscle contraction.
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Valić et al. (2004) studied this question.
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