Department of Radiology, 667, Radboud University Nijmegen Medical Centre, P.O. box 9101, 6500 HB, Nijmegen, The Netherlands.
Eur J Appl Physiol. 2011 Feb;111(2):275-83. doi: 10.1007/s00421-010-1650-0. Epub 2010 Sep 24.
In obesity, insulin-stimulated glucose uptake in skeletal muscle is decreased. We investigated whether the stimulatory effect of acute exercise on glucose uptake and subsequent glycogen synthesis was normal. The study was performed on 18 healthy volunteers, 9 obese (BMI = 32.6 ± 1.2 kg/m(2), mean ± SEM) and 9 lean (BMI = 22.0 ± 0.9 kg/m(2)), matched for age and gender. All participants underwent a euglycemic hyperinsulinemic clamp, showing reduced glucose uptake in the obese group (P = 0.01), during which they performed a short intense local exercise (single-legged toe lifting). Dynamic glucose incorporation into glycogen in the gastrocnemius muscle before and after exercise was assessed by (13)C magnetic resonance spectroscopy combined with infusion of [1-(13)C]glucose. Blood flow was measured to investigate its potential contribution to glucose uptake. Before exercise, glycogen synthesis rate tended to be lower in obese subjects compared with lean (78 ± 14 vs. 132 ± 24 μmol/kg muscle/min; P = 0.07). Exercise induced highly significant rises in glycogen synthesis rates in both groups, but the increase in obese subjects was reduced compared with lean (112 ± 15 vs. 186 ± 27 μmol/kg muscle/min; P = 0.03), although the relative increase was similar (184 ± 35 vs. 202 ± 51%; P = 0.78). After exercise, blood flow increased equally in both groups, without a temporal relationship with the rate of glycogen synthesis. In conclusion, this study shows a stimulatory effect of a short bout of acute exercise on insulin-induced glycogen synthesis rate that is reduced in absolute values but similar in percentages in obese subjects. These results suggest a shared pathway between insulin- and exercise-induced glucose uptake and subsequent glycogen synthesis.
在肥胖症中，骨骼肌对胰岛素刺激的葡萄糖摄取减少。我们研究了急性运动对葡萄糖摄取和随后的糖原合成的刺激作用是否正常。这项研究在 18 名健康志愿者中进行，9 名肥胖者（BMI=32.6±1.2kg/m²，平均值±SEM）和 9 名瘦者（BMI=22.0±0.9kg/m²），年龄和性别相匹配。所有参与者都接受了正常血糖高胰岛素钳夹实验，结果显示肥胖组的葡萄糖摄取减少（P=0.01），在此期间，他们进行了短暂而剧烈的局部运动（单腿脚趾抬起）。通过 13C 磁共振波谱与 [1-(13)C]葡萄糖输注相结合，评估腓肠肌在运动前后的动态葡萄糖掺入糖原的情况。测量血流量以研究其对葡萄糖摄取的潜在贡献。在运动前，与瘦者相比，肥胖者的糖原合成率趋于较低（78±14 与 132±24μmol/kg 肌肉/min；P=0.07）。运动引起两组的糖原合成率显著升高，但肥胖组的增加幅度低于瘦者（112±15 与 186±27μmol/kg 肌肉/min；P=0.03），尽管相对增加相似（184±35 与 202±51%；P=0.78）。运动后，两组的血流量均等增加，与糖原合成率没有时间关系。总之，这项研究表明，短暂的急性运动对胰岛素诱导的糖原合成率有刺激作用，在绝对值上减少，但在百分比上与肥胖者相似。这些结果表明，胰岛素和运动诱导的葡萄糖摄取以及随后的糖原合成之间存在共同途径。
