There is a direct correlation between an increase in insulin sensitivity and increased cell surface GLUT4 content. Acute exercise promotes glucose-transport stimulation that is independent of AMPK and CaMKII insulin-signaling. In turn, post-exercise glucose uptake occurs through changes in components of the insulin signaling cascade involving alterations in downstream mediators such as TBC1D1, TBC1D4/AS160 and p38 MAPK. However, the effects of acute exercise can be reversed within 18–24 hours and appear to be dependent on muscle glycogen levels. Exercise training results in adaptations that facilitate insulin-mediated glucose uptake and are regulated by different mechanisms. It leads to changes in gene expression and greater blood flow and signaling and changes in GLUT4 protein exocytosis and endocytosis. But when exercise training is discontinued GLUT4 tend to return to baseline levels. We have demonstrated in our laboratory that one-week detraining is sufficient to reduce GLUT4 in the heart and adipocytes while this same effect was seen in the gastrocnemius muscle within 2 weeks of training. The present study aimed to review how acute exercise, exercise training, and detraining affect mainly GLUT4 translocation to the insulin-sensitive cell surface.
M Lehnen, A. (2013). Changes in the GLUT4 Expression by Acute Exercise, Exercise Training and Detraining in Experimental Models. Journal of Diabetes & Metabolism, 01(S10). https://doi.org/10.4172/2155-6156.s10-002