title: Strength training increases insulin-mediated glucose uptake, GLUT4 content, and insulin signaling in skeletal muscle in patients with type 2 diabetes.
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.
authors.affiliation: Department of Medical Physiology, the Panum Institute, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark.
authors.forename: Mads K
authors.initials: MK
authors.lastname: Holten
authors.forename: Morten
authors.initials: M
authors.lastname: Zacho
authors.forename: Michael
authors.initials: M
authors.lastname: Gaster
authors.forename: Carsten
authors.initials: C
authors.lastname: Juel
authors.forename: Jørgen F P
authors.initials: JF
authors.lastname: Wojtaszewski
authors.forename: Flemming
authors.initials: F
authors.lastname: Dela
mesh_terms: D001692:Biological Transport / Q000187:drug effects; D002196:Capillaries / Q000502:physiology / Q000503:physiopathology; D003718:Denmark; D003924:Diabetes Mellitus, Type 2 / Q000503:physiopathology*; D015444:Exercise / Q000502:physiology*; D005947:Glucose / Q000378:metabolism*; D051275:Glucose Transporter Type 4; D006003:Glycogen / Q000378:metabolism; D006801:Humans; D007328:Insulin / Q000494:pharmacology* / Q000502:physiology*; D007866:Leg; D008297:Male; D009004:Monosaccharide Transport Proteins / Q000378:metabolism*; D018485:Muscle Fibers, Skeletal / Q000187:drug effects / Q000502:physiology; D009124:Muscle Proteins; D018482:Muscle, Skeletal / Q000187:drug effects / Q000502:physiology / Q000503:physiopathology*; D010809:Physical Fitness; D012016:Reference Values; D013718:Tensile Strength / Q000502:physiology*; D044465:White People
chemical_list: D051275:Glucose Transporter Type 4; D007328:Insulin; D009004:Monosaccharide Transport Proteins; D009124:Muscle Proteins; C495692:SLC2A4 protein, human; D006003:Glycogen; D005947:Glucose