GLUT4 is not essential for exercise-induced exaggerated muscle glycogen degradation in AMPKα2 knockout mice

The purpose of this study was to explore the effects of AMPKα2 knockout on expression of GLUT4 after exercise with different intensities. This was investigated in the quadriceps femoris muscle from control, lower intensity (12 m/minute) and higher intensity (20 m/minute) running groups of wild-type (WT) and AMPKα2 knockout (KO) mice. The skeletal muscle glycogen content was also measured to investigate the role of AMPK in regulation of glycogen metabolism. GLUT4 mRNA was increased immediately at the end of 60 minutes of running, but there were no differences between WT and KO mice, and between lower intensity and higher intensity groups. Pre-exercise muscle glycogen levels were not different between WT and KO; however, the lack of the α2-isoform was associated with a generally lower level of muscle glycogen after 60 minutes of running either with lower intensity or higher intensity. The finding that KO of the AMPKα2 isoform had no effect on expressions of GLUT4 mRNA and protein expression in mouse skeletal muscle and that muscle glycogen degradation was greater in AMPKα2 KO mice than that in WT mice after different intensity exercises, provides further evidence that AMPK is dispensable in exercise-induced expression of GLUT4, and suggests alternative pathways other than GLUT4 being involved in the regulation of muscle glycogen degradation by AMPK. Also, the present investigation demonstrated that higher intensity (20 m/minute) treadmill running, lasting 1 h, increased GLUT4 mRNA in mice skeletal muscle to a level similar to that attained after 1 h of lower intensity (12 m/minute) treadmill running.