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Strength Training Increases Insulin-Mediated Glucose Uptake, GLUT4 Content, and Insulin Signaling in Skeletal Muscle in Patients With Type 2 Diabetes

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TLDR
It is found that strength training for 30 min three times per week increases insulin action in skeletal muscle in both groups, and the adaptation is attributable to local contraction-mediated mechanisms involving key proteins in the insulin signaling cascade.
Abstract
Strength training represents an alternative to endurance training for patients with type 2 diabetes. Little is known about the effect on insulin action and key proteins in skeletal muscle, and the necessary volume of strength training is unknown. A total of 10 type 2 diabetic subjects and 7 healthy men (control subjects) strength-trained one leg three times per week for 6 weeks while the other leg remained untrained. Each session lasted no more than 30 min. After strength training, muscle biopsies were obtained, and an isoglycemic-hyperinsulinemic clamp combined with arterio-femoral venous catheterization of both legs was carried out. In general, qualitatively similar responses were obtained in both groups. During the clamp, leg blood flow was higher (P < 0.05) in trained versus untrained legs, but despite this, arterio-venous extraction glucose did not decrease in trained legs. Thus, leg glucose clearance was increased in trained legs (P < 0.05) and more than explained by increases in muscle mass. Strength training increased protein content of GLUT4, insulin receptor, protein kinase B-alpha/beta, glycogen synthase (GS), and GS total activity. In conclusion, we found that strength training for 30 min three times per week increases insulin action in skeletal muscle in both groups. The adaptation is attributable to local contraction-mediated mechanisms involving key proteins in the insulin signaling cascade.

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Exercise and type 2 diabetes: the American College of Sports Medicine and the American Diabetes Association: joint position statement.

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Effects of Aerobic Training, Resistance Training, or Both on Glycemic Control in Type 2 Diabetes: A Randomized Trial

TL;DR: In this paper, the authors evaluated the effects of combined aerobic and resistance training compared with either type of exercise alone on hemoglobin A1c values in patients with type 2 diabetes.
References
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Journal ArticleDOI

Effects of Exercise on Glycemic Control and Body Mass in Type 2 Diabetes Mellitus: A Meta-analysis of Controlled Clinical Trials

TL;DR: Exercise training reduces HbA1c by an amount that should decrease the risk of diabetic complications, but no significantly greater change in body mass was found when exercise groups were compared with control groups.
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A rapid filter paper assay for UDPglucose-glycogen glucosyltransferase, including an improved biosynthesis of UDP-14C-glucose.

TL;DR: A modified method for enzymic synthesis of UDP-14C-glucose in high yield is described, and it was found that stopping the transferase-catalyzed reaction by precipitation of trichloroacetic acid insoluble protein resulted in a loss of radioactive glucose.
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A randomized controlled trial of resistance exercise training to improve glycemic control in older adults with type 2 diabetes.

TL;DR: PRT as an adjunct to standard of care is feasible and effective in improving glycemic control and some of the abnormalities associated with the metabolic syndrome among high-risk older adults with type 2 diabetes.
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High-intensity resistance training improves glycemic control in older patients with type 2 diabetes.

TL;DR: High-intensity progressive resistance training, in combination with moderate weight loss, was effective in improving glycemic control in older patients with type 2 diabetes.
Journal ArticleDOI

Normal insulin-dependent activation of Akt/protein kinase B, with diminished activation of phosphoinositide 3-kinase, in muscle in type 2 diabetes

TL;DR: In lean subjects only, insulin-stimulated Akt1/2 activity correlated with glucose disposal rate, and it is unlikely that Akt plays a major role in the resistance to insulin action on glucose disposal or GS activation that is observed in muscle of obese type 2 diabetic subjects.
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