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J Appl Physiol (July 5, 2002). doi:10.1152/japplphysiol.00440.2002
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Articles in PresS, published online ahead of print July 5, 2002
J Appl Physiol, 10.1152/jap.00440.2002
Submitted on May 17, 2002
Accepted on June 28, 2002

Rapid and persistent exercise adaptation of ß-adrenergic signaling for MAPK-dependent NKCC activity in muscle

Aidar R Gosmanov1, Nicholas C Nordtvedt1, Richard Brown1, and Donald B Thomason1*

1 Department of Physiology, The University of Tennessee Health Science Center, Memphis, TN, USA

* To whom correspondence should be addressed. E-mail: thomason{at}physio1.utmem.edu.

This study investigated exercise adaptation of signaling mechanisms that control Na+-K+-2Cl- cotransporter (NKCC) activity in rat skeletal muscle. An acute bout of exercise increased total and NKCC-mediated 86Rb influx. Inhibition of ERK activation abolished the exercise-induced NKCC upregulation. Treadmill training (20m/min, 20% grade, 30 min/d, 5d./wk) stimulated the total 86Rb influx and increased NKCC activity in the soleus muscle after 2 wks and in the plantaris muscle after 4 wks. Exercise-induced NKCC activity was associated with a 1.4-2-fold increase in ERK phosphorylation. Isoproterenol, which activates ERK and NKCC in sedentary muscle, caused a remarkable inhibition of the exercise-induced NKCC activity. Furthermore, isoproterenol inhibition of exercise-induced NKCC activity was accompanied with decreased ERK phosphorylation in the plantaris muscle. Akt phosphorylation on both Thr308 and Ser473, which activates Akt and inhibits NKCC activity in sedentary muscle, was stimulated by acute and chronic exercise. This Akt activation was unaffected by isoproterenol. These results indicate an immediate and persistent exercise adaptation of the signal pathways that participate in the control of potassium transport.




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