Impaired Muscle AMPK Activation in the Metabolic Syndrome May Attenuate Improved Insulin Action after Exercise Training
| Autor: | Mary E. A. Howell, Charles A. Stuart, Michael H. Stone, Mark A. South, Melanie P. McCurry, Sami Nasrallah, Michael W. Ramsey, Andrew S. Layne |
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| Rok vydání: | 2011 |
| Předmět: |
Adult
Male medicine.medical_specialty Strength training Endocrinology Diabetes and Metabolism medicine.medical_treatment Clinical Biochemistry Physical exercise Biology Biochemistry Muscle hypertrophy Endocrinology Internal medicine medicine Endocrine Research Humans Insulin Phosphorylation Exercise physiology Muscle Skeletal Exercise Metabolic Syndrome Analysis of Variance Glucose Transporter Type 4 Glucose Transporter Type 5 TOR Serine-Threonine Kinases Adenylate Kinase Biochemistry (medical) AMPK Middle Aged Glucose clamp technique medicine.disease Mitochondria Glucose Clamp Technique Female Insulin Resistance Sedentary Behavior Metabolic syndrome Signal Transduction |
| Zdroj: | The Journal of Clinical Endocrinology & Metabolism. 96:1815-1826 |
| ISSN: | 1945-7197 0021-972X |
| DOI: | 10.1210/jc.2010-2532 |
| Popis: | Strength training induces muscle remodeling and may improve insulin responsiveness.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.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.Resistance exercise training took place in a sports laboratory on a college campus.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.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; P0.01) 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%).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. |
| Databáze: | OpenAIRE |
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