Effect of birth weight and 12 weeks of exercise training on exercise-induced AMPK signaling in human skeletal muscle.
Citat:
Abstract:
Subjects with a low birth weight (LBW) display increased risk of developing type 2 diabetes (T2D). We hypothesized that this is associated with defects in muscle adaptations following acute and regular physical activity, evident by impairments in the exercise-induced activation of AMPK signaling.
We investigated 21 LBW and 21 normal birth weight (NBW) subjects during 1 hour of acute exercise performed at the same relative workload before and after 12 weeks of exercise training. Multiple skeletal muscle biopsies were obtained before and after exercise. Protein levels and phosphorylation status were determined by Western blotting. AMPK activities were measured using activity assays.
Protein levels of AMPK isoforms α1 and γ1 were significantly increased while γ3 levels decreased with training independent of group. The LBW group had higher exercise-induced AMPK Thr172 phosphorylation before training and higher exercise-induced ACC2 Ser221 phosphorylation both before and after training compared with NBW. Despite exercise being performed at the same relative intensity (65% of VO2peak), the acute exercise response on AMPK Thr172, ACC2 Ser221, AMPK α2β2γ1 and α2β2γ3- activities, GS activity, adenine nucleotides as well as Hexokinase II mRNA levels were all reduced after exercise training.
Increased exercise-induced muscle AMPK activation and ACC2 Ser221 phosphorylation in LBW subjects may indicate a more sensitive AMPK system in this population. Long term exercise training may reduce the need for AMPK to control energy turnover during exercise.
Thus, the remaining γ3-associated AMPK activation by acute exercise after exercise training might be sufficient to maintain cellular energy balance.
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http://www.ncbi.nlm.nih.gov/pubmed/23612997
Am J Physiol Endocrinol Metab. 2013 Apr 23
2013-04-25, 15:51
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