| Impaired Muscle AMPK Activation in the Metabolic Syndrome May Attenuate Improved Insulin Action after Exercise Training. | |
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MedLine Citation:
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PMID: 21508135 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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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 α coactivator γ (57%),and ATPsynthase (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. |
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Authors:
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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:
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Type: JOURNAL ARTICLE Date: 2011-4-20 |
Journal Detail:
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Title: The Journal of clinical endocrinology and metabolism Volume: - ISSN: 1945-7197 ISO Abbreviation: - Publication Date: 2011 Apr |
Date Detail:
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Created Date: 2011-4-21 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0375362 Medline TA: J Clin Endocrinol Metab Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Affiliation:
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The Center of Excellence for Sport Science and Coach Education (A.S.L., M.A.S., M.W.R., M.H.S.), Department of Kinesiology, Leisure, and Sports Science, Clemmer College of Education, and Department of Internal Medicine (S.N., M.E.A.H., M.P.M., C.A.S.), Quillen College of Medicine, East Tennessee State University, Johnson City, Tennessee 37614. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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