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Strength Training Increases Insulin Action in Type 2
Diabetes
posted 03/31/04
Strength training improves the effect of insulin in
skeletal muscle of patients with type 2 diabetes.
Dr. Flemming Dela from the University of Copenhagen stated that "physical inactivity is becoming close to the number-one leading cause of death in the US." "Our study is one which shows how to fight this trend."
Earlier research demonstrated the value of aerobic endurance training in increasing insulin action in type 2 diabetes, the authors explain in the February issue of Diabetes, but most patients with type 2 diabetes are overweight and unlikely to take up endurance training.
Dr. Dela and colleagues, therefore, investigated the impact of strength training three times weekly for 6 weeks on insulin action in the skeletal muscle of 10 type 2 diabetics and 7 healthy controls.
Strength training resulted in an increased insulin-mediated blood flow that was not accompanied by an increase in glucose extraction, the authors report. Glucose clearance was, however, increased in the trained muscles.
Strength training significantly increased muscle mass, the report indicates, as well as GLUT4 protein content, insulin receptor protein content, and glycogen synthase protein content and total activity in skeletal muscle biopsies.
"The increases in muscle GLUT4 content and in various insulin signaling protein expressions and/or activity are part of the mechanism behind the improvement in insulin action," the researchers note, "but each of them should probably not be attributed a single effect, but rather be looked on in concert."
"Strength training is a realistic and effective alternative to endurance training and probably much more attractive to the 'average' type 2 diabetic patient," Dr. Dela concluded.
"We have followed up on this study by exploring the molecular mechanisms in the muscle that lies behind the effect," Dr. Dela added. In particular, they have examined the effects of resistance training on monocarboxylate transporters, sodium/potassium pumps, and AMPK subunits.
Source: Diabetes In Control.com: Diabetes 2004;53:294-305.
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