Strength training increases insulin-mediated glucose uptake, GLUT4 content, and insulin signaling in skeletal muscle in patients with type 2 diabetes

被引:407
作者
Holten, MK
Zacho, M
Gaster, M
Juel, C
Wojtaszewski, JFP
Dela, F
机构
[1] Univ Copenhagen, Panum Inst, Dept Med Physiol, Fac Hlth Sci, DK-2200 Copenhagen N, Denmark
[2] Rigshosp, Copenhagen Muscle Res Ctr, DK-2100 Copenhagen, Denmark
[3] Odense Univ Hosp, Dept Endocrinol, DK-5000 Odense, Denmark
[4] Odense Univ Hosp, Dept Pathol, DK-5000 Odense, Denmark
[5] Univ Copenhagen, August Krogh Inst, DK-2100 Copenhagen, Denmark
[6] Univ Copenhagen, Fac Nat Sci, Inst Exercise & Sport Sci, DK-1168 Copenhagen, Denmark
关键词
D O I
10.2337/diabetes.53.2.294
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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.
引用
收藏
页码:294 / 305
页数:12
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