Vasodilatation is obligatory for contraction-induced hyperaemia in canine skeletal muscle

• Published in: The Journal of physiology Vol. 557; no. 3; pp. 1013 - 1020
• Main Authors: Hamann, Jason J., Buckwalter, John B., Clifford, Philip S.
• Format: Journal Article
• Language: English
• Published: 9600 Garsington Road , Oxford , OX4 2DQ , UK The Physiological Society 15-06-2004; Blackwell Science Ltd; Blackwell Science Inc
• Subjects: Animals; Blood Pressure - physiology; Cell Polarity - physiology; Dogs; Electrophysiology; Female; Hindlimb - blood supply; Hyperemia - physiopathology; In Vitro Techniques; Male; Muscle Contraction - physiology; Muscle, Skeletal - blood supply; Muscle, Skeletal - physiopathology; Potassium - pharmacology; Regional Blood Flow - physiology; Research Papers; Vasodilation - physiology
• ISSN: 0022-3751; 1469-7793
• DOI: 10.1113/jphysiol.2004.062836

There is a rapid increase in blood flow to active skeletal muscle with the onset of exercise, but the mechanism(s) eliciting
this increase remains elusive. We hypothesized that the rapid increase in blood flow to active skeletal muscle with the onset
of exercise is attributable to vasodilatation as a consequence of smooth muscle hyperpolarization. To test this hypothesis
we examined the blood flow response to a brief tetanic contraction in which potassium (K + ) was infused intra-arterially to elevate the [K + ] o and clamp the smooth muscle membrane potential within the skeletal muscle vascular bed. In six anaesthetized beagle dogs
control contractions increased hindlimb blood flow by 97 ± 14 ml min −1 . During K + infusion the hyperaemic response to contraction was 8 ± 3 ml min −1 . Since the hindlimb blood flow was reduced during K + infusion, a similar reduction in baseline blood flow was produced with phenylephrine infusion. During phenylephrine infusion
the hyperaemic response to contraction was preserved (89 ± 23 ml min −1 ). Recovery contractions performed after the discontinuation of the K + infusion elicited blood flow responses similar to control (100 ± 11 ml min −1 ). In a separate experimental protocol using the isolated gastrocnemius muscle of mongrel dogs ( n = 6) K + infusion did not alter force production by the skeletal muscle. Our data indicate that in the absence of vasodilatation,
there is virtually no change in blood flow. One implication of this finding is that the muscle pump cannot be responsible
for the initial contraction-induced hyperaemia. We conclude that the increase in blood flow immediately following a single
muscle contraction is due to vasodilatation, presumably as a consequence of smooth muscle hyperpolarization.