HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) All Versions of this Article: db06-1698v1 56/8/2093    most recent Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Frøsig, C. Articles by Wojtaszewski, J. F. P. Search for Related Content PubMed PubMed Citation Articles by Frøsig, C. Articles by Wojtaszewski, J. F. P. Social Bookmarking                What's this?

Effects of endurance exercise training on insulin signalling in human skeletal muscle - Interactions at the level of PI3-K, Akt and AS160.

Copenhagen Muscle Research Centre, Section of Human Physiology, Department of Exercise and Sport Sciences, University of Copenhagen, Copenhagen, Denmark

Correspondence: Jwojtaszewski{at}ifi.ku.dk

Objective:To investigate the mechanisms explaining improved insulin stimulated glucose uptake after exercise training in human skeletal muscle.

Research design and methods:Eight healthy men performed three weeks of one-legged knee extensor endurance exercise training. 15 hours after the last exercise bout, insulin-stimulated glucose uptake was 60% higher (p<0.01) in the trained compared with the untrained leg during a euglycemic hyperinsulinemic clamp. Muscle biopsies were obtained before and after training as well as after 10 and 120 min of insulin stimulation in both legs.

Results:Protein content of Akt1/2 (55±17%, P<0.05), AS160 (25±8%, P=0.08), GLUT4 (52±19%, P<0.001), HK2 (297±40%, P<0.001) and IRAP (65±15%, P<0.001) increased in muscle in response to training. During hyperinsulinemia, activities of IRS-1 associated PI3-K (P<0.005), Akt1 (P<0.05), Akt2 (P<0.005) and GS ([% I-form], P<0.05) increased similarly in both trained and untrained muscle, consistent with increased phosphorylation of Akt Thr³⁰⁸, Akt Ser⁴⁷³, AS160, GSK-3 Ser²¹ and GSK-3ß Ser⁹ and decreased phosphorylation of GS site 3a+b (all, P<0.005). Interestingly, training improved insulin action on total blood flow and furthermore in both basal and insulin stimulated muscle tissue activities of Akt1 and GS and phosphorylation of AS160 increased with training (all, P<0.05). In contrast, training reduced IRS-1 associated PI3-K activity (P<0.05) in both basal and insulin stimulated muscle tissue.

Conclusions:Our findings do not support generally improved insulin signaling after endurance training; rather it appears that improved insulin stimulated glucose uptake may result from hemodynamic adaptations as well as increased cellular protein content of individual insulin signaling components and molecules involved in glucose transport and metabolism.

CiteULike

Del.icio.us

Digg

Reddit

Technorati