title: Exercise effects on muscle beta-adrenergic signaling for MAPK-dependent NKCC activity are rapid and persistent.
abstract: 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 (86)Rb influx. Inhibition of extracellular signal-regulated kinase (ERK) activation abolished the exercise-induced NKCC upregulation. Treadmill training (20 m/min, 20% grade, 30 min/day, 5 days/wk) stimulated total (86)Rb influx and increased NKCC activity in the soleus muscle after 2 wk and in the plantaris muscle after 4 wk. Exercise-induced NKCC activity was associated with a 1.4- to 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 (protein kinase B) phosphorylation on both Thr(308) and Ser(473), 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.
authors.affiliation: Department of Physiology, College of Medicine, University of Tennessee Health Science Center, Memphis, Tennessee 38163, USA.
authors.forename: Aidar R
authors.initials: AR
authors.lastname: Gosmanov
authors.forename: Nicholas C
authors.initials: NC
authors.lastname: Nordtvedt
authors.forename: Richard
authors.initials: R
authors.lastname: Brown
authors.forename: Donald B
authors.initials: DB
authors.lastname: Thomason
mesh_terms: D000818:Animals; D001835:Body Weight; D002950:Citrate (si)-Synthase / Q000378:metabolism; D004789:Enzyme Activation / Q000502:physiology; D005260:Female; D007545:Isoproterenol / Q000494:pharmacology; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism / Q000502:physiology*; D009043:Motor Activity / Q000502:physiology*; D018482:Muscle, Skeletal / Q000378:metabolism*; D010766:Phosphorylation / Q000187:drug effects; D010805:Physical Conditioning, Animal / Q000502:physiology; D017346:Protein Serine-Threonine Kinases; D011518:Proto-Oncogene Proteins / Q000378:metabolism; D051057:Proto-Oncogene Proteins c-akt; D051381:Rats; D017207:Rats, Sprague-Dawley; D011943:Receptors, Adrenergic, beta / Q000502:physiology*; D012413:Rubidium / Q000493:pharmacokinetics; D015398:Signal Transduction / Q000502:physiology*; D049994:Sodium Potassium Chloride Symporter Inhibitors; D028021:Sodium-Potassium-Chloride Symporters / Q000378:metabolism*; D013997:Time Factors; D048051:p38 Mitogen-Activated Protein Kinases
chemical_list: D011518:Proto-Oncogene Proteins; D011943:Receptors, Adrenergic, beta; D049994:Sodium Potassium Chloride Symporter Inhibitors; D028021:Sodium-Potassium-Chloride Symporters; D002950:Citrate (si)-Synthase; C494920:Akt1 protein, rat; D017346:Protein Serine-Threonine Kinases; D051057:Proto-Oncogene Proteins c-akt; D020928:Mitogen-Activated Protein Kinases; D048051:p38 Mitogen-Activated Protein Kinases; D007545:Isoproterenol; D012413:Rubidium