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Am J Physiol Regul Integr Comp Physiol 258: R1192-R1200, 1990;
0363-6119/90 $5.00
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AJP - Regulatory, Integrative and Comparative Physiology, Vol 258, Issue 5 1192-R1200, Copyright © 1990 by American Physiological Society

ARTICLES

Beta 2-adrenergic stimulation does not prevent potassium loss from exercising quadriceps muscle

E. L. Rolett, S. Strange, G. Sjogaard, B. Kiens and B. Saltin
August Krogh Institute, University of Copenhagen, Denmark.

During exercise K+ is released from contracting muscle and plasma K+ concentration rises. Because beta 2-adrenergic agonists stimulate K+ uptake by skeletal muscle in vitro, we tested whether terbutaline, a selective beta 2-agonist, would reduce the loss of K+ from working muscle. Dynamic quadriceps muscle exercise was performed by 12 healthy male volunteers for 50 or 80 min at an average workload of 38 W. A steady K+ loss estimated at 0.16 +/- 0.02 mmol.min-1.kg working muscle-1 and a 0.30 +/- 0.05 mM elevation of arterial plasma K+ concentration were observed. The addition of terbutaline during exercise caused leg blood flow to increase 13% from 5.10 +/- 0.16 to 5.75 +/- 0.13 l/min and arterial K+ concentration to fall monoexponentially by 0.90 +/- 0.05 mM with a rate constant of 0.26 min-1. Terbutaline increased, rather than decreased, the washout of K+ from working quadriceps by 40% to an average value of 0.23 +/- 0.02 mmol.min-1.kg muscle-1. In an additional subject who exercised to exhaustion, terbutaline failed to diminish muscle K+ loss. We conclude that terbutaline does not augment Na(+)-K+ pump activity to a degree sufficient to prevent K+ loss from exercising muscle in humans. On the other hand, the rapid reduction in plasma K+ concentration observed with beta 2-adrenergic stimulation is compatible with an uptake of K+ by nonexercising tissue at an estimated maximal rate of 0.5 micromol.g-1.min-1.


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