Oral glucose ingestion attenuates exercise-induced activation of 5′-AMP-activated protein kinase in human skeletal muscle

Åkerström, Tobias; Birk, Jesper B.; Klein, Ditte Kjærsgaard; Erikstrup, Christian; Plomgaard, Peter; Pedersen, Bente Klarlund; Wojtaszewski, Jørgen F. P.

doi:10.1016/j.bbrc.2006.02.057

Cited by 61 publications

(66 citation statements)

References 50 publications

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“…Glucose is another nutrient that could have potentially affected the stimulation of AMPK in the type 2 diabetes group. Akerstrom et al (44) reported that ingestion of a carbohydrate-containing drink, which caused a slight increase in plasma glucose levels, attenuated exercise-induced AMPK activation; yet, this finding was not confirmed by other investigators (45). We previously reported that lean type 2 diabetic subjects with elevated fasting plasma glucose concentrations achieve normal AMPK stimulation with exercise (18).…”

Section: Discussionmentioning

confidence: 86%

Effect of Acute Exercise on AMPK Signaling in Skeletal Muscle of Subjects With Type 2 Diabetes

et al. 2007

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Activation of AMP-activated protein kinase (AMPK) by exercise induces several cellular processes in muscle. Exercise activation of AMPK is unaffected in lean (BMI ϳ25 kg/m 2 ) subjects with type 2 diabetes. However, most type 2 diabetic subjects are obese (BMI >30 kg/m 2 ), and exercise stimulation of AMPK is blunted in obese rodents. We examined whether obese type 2 diabetic subjects have impaired exercise stimulation of AMPK, at different signaling levels, spanning from the upstream kinase, LKB1, to the putative AMPK targets, AS160 and peroxisome proliferator-activated receptor coactivator (PGC)-1␣, involved in glucose transport regulation and mitochondrial biogenesis, respectively. Twelve type 2 diabetic, eight obese, and eight lean subjects exercised on a cycle ergometer for 40 min. Muscle biopsies were done before, during, and after exercise. Subjects underwent this protocol on two occasions, at low (50% VO 2max ) and moderate (70% VO 2max ) intensities, with a 4 -6 week interval. Exercise had no effect on LKB1 activity. Exercise had a time-and intensity-dependent effect to increase AMPK activity and AS160 phosphorylation. Obese and type 2 diabetic subjects had attenuated exercise-stimulated AMPK activity and AS160 phosphorylation. Type 2 diabetic subjects had reduced basal PGC-1 gene expression but normal exercise-induced increases in PGC-1 expression. Our findings suggest that obese type 2 diabetic subjects may need to exercise at higher intensity to stimulate the AMPK-AS160 axis to the same level as lean subjects. Diabetes 56:836 -848, 2007

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Section: Discussionmentioning

confidence: 86%

Effect of Acute Exercise on AMPK Signaling in Skeletal Muscle of Subjects With Type 2 Diabetes

et al. 2007

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“…Because of this subjects often had trouble Wnishing the trials despite the moderate intensity. It has previously been shown that exogenous carbohydrate may blunt the upregulation of oxidative enzyme expression during aerobic exercise (Akerstrom et al 2006;Civitarese et al 2005;Cluberton et al 2005). This may be a result of reduced PGC-1 protein expression upon carbohydrate ingestion (Mathai et al 2008).…”

Section: Discussionmentioning

confidence: 97%

Successive bouts of cycling stimulates genes associated with mitochondrial biogenesis

et al. 2009

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Exercise increases mRNA for genes involved in mitochondrial biogenesis and oxidative enzyme capacity. However, little is known about how these genes respond to consecutive bouts of prolonged exercise. We examined the effects of 3 h of intensive cycling performed on three consecutive days on the mRNA associated with mitochondrial biogenesis in trained human subjects. Forty trained cyclists were tested for VO(2max) (54.7 +/- 1.1 ml kg(-1) min(-1)). The subjects cycled at 57% watts(max) for 3 h using their own bicycles on CompuTrainer Pro Model trainers (RacerMate, Seattle, WA) on three consecutive days. Muscle biopsies were obtained from the vastus lateralis pre- and post-exercise on days one and three. Muscle samples were analyzed for mRNA content of peroxisome proliferator receptor gamma coactivator-1 alpha (PGC-1alpha), sirtuin 1 (Sirt-1), cytochrome c, and citrate synthase. Data were analyzed using a 2 (time) x 2 (day) repeated measures ANOVA. Of the mRNA analyzed, the following increased from pre to post 3 h rides: cytochrome c (P = 0.006), citrate synthase (P = 0.03), PGC-1alpha (P < 0.001), and Sirt-1 (P = 0.005). The following mRNA showed significant effects from days one to three: cytochrome c (P < 0.001) and citrate synthase (P = 0.01). These data show that exhaustive cycling performed on three consecutive days resulted in both acute and chronic stimuli for mRNA associated with mitochondrial biogenesis in already trained subjects. This is the first study to illustrate an increase in sirtuin-1 mRNA with acute and chronic exercise. These data contribute to the understanding of mRNA expression during both acute and successive bouts of prolonged exercise.

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“…Other variables such as exercise intensity, body composition, and sex are known to impact AMPK activity during exercise (36,38), but these are unlikely to be confounding variables because we ensured that they were similar across groups. AMPK activation is dependent on the AMP concentrations in the skeletal muscle and is altered by high glucose and free fatty acid availability (1,40). It is possible that the combination of metformin and exercise reduced intracellular AMP and/or raised substrate availability during exercise.…”

Section: Discussionmentioning

confidence: 99%

Combining short-term metformin treatment and one bout of exercise does not increase insulin action in insulin-resistant individuals

Sharoff

Hagobian

Malin

et al. 2010

American Journal of Physiology-Endocrinology and Metabolism

118

137

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Results from the Diabetes Prevention Program highlight the effectiveness of metformin or regular physical activity in the prevention of type 2 diabetes. Independently, metformin and exercise increase insulin sensitivity, but they have not been studied in combination. To assess the combined effects, insulin-resistant subjects ( n = 9) matched for weight, body fat, and aerobic fitness were studied before any treatment (B), after 2–3 wk of 2,000 mg/day metformin (MET), and after metformin plus 40 min of exercise at 65% V̇o2peak (MET + Ex). A second group ( n = 7) was studied at baseline and after an identical bout of exercise with no metformin (Ex). Biopsies of the vastus lateralis were taken at B, after MET, immediately after MET + Ex ( group 1), or immediately after Ex ( group 2). Insulin sensitivity was assessed 4 h postexercise with a euglycemic hyperinsulinemic (40 mU·m2·min−1) clamp enriched with [6,6-2H]glucose. Insulin sensitivity was 54% higher after Ex ( P < 0.01), but there was no change with Met + Ex. Skeletal muscle AMPKα2 activity was elevated threefold ( P < 0.01) after Ex, but there was no increase with MET + Ex. These findings suggest that the combination of short-term metformin treatment and an acute bout of exercise does not enhance insulin sensitivity, and the addition of metformin may attenuate the well-documented effects of exercise alone.

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Oral glucose ingestion attenuates exercise-induced activation of 5′-AMP-activated protein kinase in human skeletal muscle

Cited by 61 publications

References 50 publications

Effect of Acute Exercise on AMPK Signaling in Skeletal Muscle of Subjects With Type 2 Diabetes

Effect of Acute Exercise on AMPK Signaling in Skeletal Muscle of Subjects With Type 2 Diabetes

Successive bouts of cycling stimulates genes associated with mitochondrial biogenesis

Combining short-term metformin treatment and one bout of exercise does not increase insulin action in insulin-resistant individuals

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