Document Detail

Impaired muscle AMPK activation in the metabolic syndrome may attenuate improved insulin action after exercise training.
MedLine Citation:
PMID:  21508135     Owner:  NLM     Status:  MEDLINE    
CONTEXT: Strength training induces muscle remodeling and may improve insulin responsiveness.
OBJECTIVE: This study will quantify the impact of resistance training on insulin sensitivity in subjects with the metabolic syndrome and correlate this with activation of intramuscular pathways mediating mitochondrial biogenesis and muscle fiber hypertrophy.
DESIGN: Ten subjects with the metabolic syndrome (MS) and nine sedentary controls underwent 8 wk of supervised resistance exercise training with pre- and posttraining anthropometric and muscle biochemical assessments.
SETTING: Resistance exercise training took place in a sports laboratory on a college campus.
MAIN OUTCOME MEASURES: Pre- and posttraining insulin responsiveness was quantified using a euglycemic clamp. Changes in expression of muscle 5-AMP-activated protein kinase (AMPK) and mammalian target of rapamycin (mTOR) pathways were quantified using immunoblots.
RESULTS: Strength and stamina increased in both groups. Insulin sensitivity increased in controls (steady-state glucose infusion rate = 7.0 ± 2.0 mg/kg · min pretraining training vs. 8.7 ± 3.1 mg/kg · min posttraining; P < 0.01) but did not improve in MS subjects (3.3 ± 1.3 pre vs. 3.1 ± 1.0 post). Muscle glucose transporter 4 increased 67% in controls and 36% in the MS subjects. Control subjects increased muscle phospho-AMPK (43%), peroxisome proliferator-activated receptor γ coactivator 1α (57%), and ATP synthase (60%), more than MS subjects (8, 28, and 21%, respectively). In contrast, muscle phospho-mTOR increased most in the MS group (57 vs. 32%).
CONCLUSION: Failure of resistance training to improve insulin responsiveness in MS subjects was coincident with diminished phosphorylation of muscle AMPK, but increased phosphorylation of mTOR, suggesting activation of the mTOR pathway could be involved in inhibition of exercise training-related increases in AMPK and its activation and downstream events.
Andrew S Layne; Sami Nasrallah; Mark A South; Mary E A Howell; Melanie P McCurry; Michael W Ramsey; Michael H Stone; Charles A Stuart
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2011-04-20
Journal Detail:
Title:  The Journal of clinical endocrinology and metabolism     Volume:  96     ISSN:  1945-7197     ISO Abbreviation:  J. Clin. Endocrinol. Metab.     Publication Date:  2011 Jun 
Date Detail:
Created Date:  2011-05-23     Completed Date:  2011-08-05     Revised Date:  2013-06-30    
Medline Journal Info:
Nlm Unique ID:  0375362     Medline TA:  J Clin Endocrinol Metab     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1815-26     Citation Subset:  AIM; IM    
Center of Excellence for Sport Science and Coach Education, Department of Kinesiology, Leisure, and Sports Science, Clemmer College of Education, East Tennessee State University, Johnson City, Tennessee 37614, USA.
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MeSH Terms
Adenylate Kinase / metabolism*
Analysis of Variance
Exercise / physiology*
Glucose Clamp Technique
Glucose Transporter Type 4 / metabolism
Glucose Transporter Type 5 / metabolism
Insulin / metabolism*
Insulin Resistance / physiology
Metabolic Syndrome X / metabolism*
Middle Aged
Mitochondria / metabolism
Muscle, Skeletal / metabolism*
Phosphorylation / physiology
Sedentary Lifestyle
Signal Transduction / physiology
TOR Serine-Threonine Kinases / metabolism
Grant Support
Reg. No./Substance:
0/Glucose Transporter Type 4; 0/Glucose Transporter Type 5; 0/Insulin; 0/SLC2A4 protein, human; 0/SLC2A5 protein, human; EC Serine-Threonine Kinases; EC Kinase

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