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Medicine & Science in Sports & Exercise:
May 2005 - Volume 37 - Issue 5 - p S222
D-21: Free Communication/Poster - Circulation: Blood Flow Control: THURSDAY, JUNE 2,2005 2:00 PM - 5:00 PM ROOM: Ryman C2

Is Potassium Responsible for Contraction-Induced Hyperemia?: 1174 Board #29 2:00 PM - 3:30 PM

Hamann, Jason J. FACSM; DeLorey, Darren S.; Buckwalter, John B. FACSM; Kluess, Heidi A.; Clifford, Philip S. FACSM

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Medical College of Wisconsin and VA Medical Center, Milwaukee, WI

Email: hamannj@mcw.edu

One theory that has been proposed to explain exercise hyperemia is that vasodilation in contracting skeletal muscle is due to rapid accumulation of K+ in the interstitium. Previous descriptive studies have shown that the time course of increased [K+] in venous blood following muscle contraction correlates well with the observed time course of changes in blood flow. Interestingly, the vascular smooth muscle response to K+ is biphasic, with hyperpolarization and dilation at low concentrations and depolarization and constriction at high concentrations. Theoretically, it should be possible to infuse K+ at a concentration which would not change the smooth muscle membrane potential nor blood flow. We reasoned that if K+ release from muscle plays a substantive role in contraction-induced hyperemia, imposing a contraction during K+ infusion would further elevate interstitial [K+] which would cause constriction.

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PURPOSE

We hypothesized that contraction during K+ infusion would further increase the interstitial [K+] causing vasoconstriction.

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METHODS

In anesthetized dogs (n=5) hindlimb blood flow was monitored with transit time ultrasonic flowprobes placed around the external iliac arteries. A femoral artery catheter was placed for K+infusion. Brief tetanic contractions were evoked by stimulation of the sciatic nerve for 1 sec (50Hz, 0.2ms).

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RESULTS

As anticipated, intraarterial infusion of low doses of K+ produced dilation, high doses produced constriction, and intermediate doses produced no change in blood flow. Under control conditions, a single titanic contraction increased hindlimb blood flow by 113±15 ml/min. However, at an intermediate infusion rate of K+ that did not change blood flow from the baseline, a single contraction evoked an increase in hindlimb blood flow of 43±19 ml/min. In none of the experiments was vasoconstriction observed in response to contraction.

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CONCLUSIONS

These data do not support the notion that K+ is an important contributor to vasodilation evoked by muscle contraction.

Supported by NIH and VA Medical Research.

©2005The American College of Sports Medicine