Effect of birth weight and 12 weeks of exercise training on exercise-induced AMPK signaling in human skeletal muscle
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Effect of birth weight and 12 weeks of exercise training on exercise-induced AMPK signaling in human skeletal muscle. / Mortensen, Brynjulf; Hingst, Janne Rasmuss; Frederiksen, Nicklas; Hansen, Rikke W W; Christiansen, Caroline S; Iversen, Ninna; Friedrichsen, Martin; Birk, Jesper Bratz; Pilegaard, Henriette; Hellsten, Ylva; Vaag, Allan; Wojtaszewski, Jørgen F.P.
I: American Journal of Physiology: Endocrinology and Metabolism, Bind 304, Nr. 12, 2013, s. E1379-E1390.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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TY - JOUR
T1 - Effect of birth weight and 12 weeks of exercise training on exercise-induced AMPK signaling in human skeletal muscle
AU - Mortensen, Brynjulf
AU - Hingst, Janne Rasmuss
AU - Frederiksen, Nicklas
AU - Hansen, Rikke W W
AU - Christiansen, Caroline S
AU - Iversen, Ninna
AU - Friedrichsen, Martin
AU - Birk, Jesper Bratz
AU - Pilegaard, Henriette
AU - Hellsten, Ylva
AU - Vaag, Allan
AU - Wojtaszewski, Jørgen F.P.
N1 - CURIS 2013 NEXS 088
PY - 2013
Y1 - 2013
N2 - 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 a1 and ¿1 were significantly increased while ¿3 levels decreased with training independent of group. The LBW group had higher exercise-induced AMPK Thr(172) phosphorylation before training and higher exercise-induced ACC2 Ser(221) 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 Ser(221), AMPK a2ß2¿1 and a2ß2¿3- 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 Ser(221) 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 ¿3-associated AMPK activation by acute exercise after exercise training might be sufficient to maintain cellular energy balance.
AB - 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 a1 and ¿1 were significantly increased while ¿3 levels decreased with training independent of group. The LBW group had higher exercise-induced AMPK Thr(172) phosphorylation before training and higher exercise-induced ACC2 Ser(221) 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 Ser(221), AMPK a2ß2¿1 and a2ß2¿3- 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 Ser(221) 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 ¿3-associated AMPK activation by acute exercise after exercise training might be sufficient to maintain cellular energy balance.
U2 - 10.1152/ajpendo.00295.2012
DO - 10.1152/ajpendo.00295.2012
M3 - Journal article
C2 - 23612997
VL - 304
SP - E1379-E1390
JO - American Journal of Physiology - Endocrinology and Metabolism
JF - American Journal of Physiology - Endocrinology and Metabolism
SN - 0193-1849
IS - 12
ER -
ID: 45694823