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

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.