Exercise effects on muscle β-adrenergic signaling for MAPK-dependent NKCC activity are rapid and persistent

Aidar R. Gosmanov, Nicholas C. Nordtvedt, Richard Brown, Donald Thomason

Research output: Contribution to journalArticle

21 Citations (Scopus)

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 86Rb 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 86Rb 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 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.

Original languageEnglish (US)
Pages (from-to)1457-1465
Number of pages9
JournalJournal of applied physiology
Volume93
Issue number4
DOIs
StatePublished - Jan 1 2002

Fingerprint

Extracellular Signal-Regulated MAP Kinases
Adrenergic Agents
Skeletal Muscle
Isoproterenol
Muscles
Phosphorylation
Exercise
Proto-Oncogene Proteins c-akt
Signal Transduction
Potassium
Up-Regulation

All Science Journal Classification (ASJC) codes

  • Physiology
  • Physiology (medical)

Cite this

Exercise effects on muscle β-adrenergic signaling for MAPK-dependent NKCC activity are rapid and persistent. / Gosmanov, Aidar R.; Nordtvedt, Nicholas C.; Brown, Richard; Thomason, Donald.

In: Journal of applied physiology, Vol. 93, No. 4, 01.01.2002, p. 1457-1465.

Research output: Contribution to journalArticle

Gosmanov, Aidar R. ; Nordtvedt, Nicholas C. ; Brown, Richard ; Thomason, Donald. / Exercise effects on muscle β-adrenergic signaling for MAPK-dependent NKCC activity are rapid and persistent. In: Journal of applied physiology. 2002 ; Vol. 93, No. 4. pp. 1457-1465.
@article{09d51b15a9864e19ad2888dfe815091a,
title = "Exercise effects on muscle β-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 86Rb 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 86Rb 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 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.",
author = "Gosmanov, {Aidar R.} and Nordtvedt, {Nicholas C.} and Richard Brown and Donald Thomason",
year = "2002",
month = "1",
day = "1",
doi = "10.1152/japplphysiol.00440.2002",
language = "English (US)",
volume = "93",
pages = "1457--1465",
journal = "Journal of Applied Physiology",
issn = "8750-7587",
publisher = "American Physiological Society",
number = "4",

}

TY - JOUR

T1 - Exercise effects on muscle β-adrenergic signaling for MAPK-dependent NKCC activity are rapid and persistent

AU - Gosmanov, Aidar R.

AU - Nordtvedt, Nicholas C.

AU - Brown, Richard

AU - Thomason, Donald

PY - 2002/1/1

Y1 - 2002/1/1

N2 - 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 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 86Rb 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 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.

AB - 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 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 86Rb 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 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.

UR - http://www.scopus.com/inward/record.url?scp=0036785032&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0036785032&partnerID=8YFLogxK

U2 - 10.1152/japplphysiol.00440.2002

DO - 10.1152/japplphysiol.00440.2002

M3 - Article

VL - 93

SP - 1457

EP - 1465

JO - Journal of Applied Physiology

JF - Journal of Applied Physiology

SN - 8750-7587

IS - 4

ER -