APPS November 2002 Meeting Abstract 2407


SHORT-TERM EXERCISE TRAINING SUPPRESSES INCREASES IN HUMAN SKELETAL MUSCLE AMPK ACTIVITY DURING PROLONGED EXERCISE

G.K. McConell1, N.K. Stepto1, Z-P. Chen2, T.J. Stephens1, N.N. Huynh1, B.J. Canny1, B.E. Kemp2, 1 Department of Physiology, Monash University, Clayton, Victoria, 3800, 2 St. Vincent's Institute of Medical Research, Fitzroy, Victoria, 3065.

AMP-activated protein kinase (AMPK) is activated by increases in skeletal muscle free AMP:ATP ratio. Two isoforms of AMPK are expressed in skeletal muscle (AMPK α1 and α2). There is evidence for a role for AMPK α2 in the regulation of skeletal muscle glucose uptake during exercise. Short-term exercise training attenuates the exercise-induced increases in skeletal muscle free AMP:ATP ratio and glucose uptake. The aim of this study was to determine the effect of short-term exercise training on AMPK (α1 and α2) activity, tracer-determined glucose disappearance (glucose Rd) and muscle energy balance during exercise. Five untrained male subjects completed 120 min of cycling at 64 2 % VO2 peak, and then trained for 10 days, before repeating the exercise bout at the same absolute workload. Subjects rested for 72 hr before each trial while ingesting a high carbohydrate diet. Training increased (P<0.05) VO2 peak by 5% from 3.66 0.3 to 3.83 0.3 L.min-1. Pre-exercise muscle glycogen content was significantly higher after training (103 21% increase, P<0.05). Training significantly attenuated the exercise-induced increases in glucose Rd (by 33% at 120 min, P<0.05) and skeletal muscle free AMP:ATP ratio (by 63% at 120 min, P<0.05). The rate of muscle glycogen utilization during exercise was unaffected by exercise training. AMPK α1 and α2 activity increased significantly (9.8 2.5 and 13.2 2.4 fold, respectively) during exercise before training. Following training the significant increase in AMPK α1 activity during exercise was significantly attenuated (1.8-fold above rest), while no significant increase in AMPK α2 activity during exercise was observed. These findings suggest a dissociation between skeletal muscle AMPK α2 activity and skeletal muscle glucose uptake during exercise since glucose Rd was only partially reduced during exercise after exercise training, whereas no increase in AMPK α2 activity was observed. It is unclear whether the lack of increase in AMPK α2 activity during exercise after training was due to the training effect alone or whether the higher pre-exercise muscle glycogen levels also played a role.


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