Exercise training increases ERK2 activity in skeletal muscle of obese Zucker rats

Acute exercise and training increase insulin action in skeletal muscle, but the mechanism responsible for this effect is unknown. Activation of the in sulin receptor initiates signaling through both the phosphatidylinositol (P I) 3-kinase and the mitogen-activated protein kinase [MAPK, also referred t o as extracellular signal-regulated kinases (ERK1/2)] pathways. Acute exerc ise has no effect on the PI3-kinase pathway signaling elements but does act ivate the MAPK pathway, which may play a role in the adaptation of muscle t o exercise. It is unknown whether training produces a chronic effect on bas al activity or insulin response of the MAPK pathway. The present study was undertaken to determine whether exercise training improves the activity of the MAPK pathway or its response to insulin in obese Zucker rats, a well-ch aracterized model of insulin resistance. To accomplish this, obese Zucker r ats were studied by using the hindlimb perfusion method with or without 7 w k of treadmill training. Activation of the MAPK pathway was determined in g astrocnemius muscles exposed in situ to insulin. Compared with lean Zucker rats, untrained obese Zucker rats had reduced basal and insulin-stimulated activities of ERK2 and its downstream target p90 ribosomal S6 kinase (RSK2) . Seven weeks of training significantly increased basal and insulin-stimula ted ERK2 and RSK2 activities, as well as insulin stimulation of MAPK kinase activity. This effect was maintained for at least 96 h in the case of ERK2 . The training-induced increase in basal ERK2 activity was correlated with the increase in citrate synthase activity. Therefore, 7 wk of training incr eases basal and insulin-stimulated ERK2 activity. The increase in basal ERK 2 activity may be related to the response of muscle to training.