Eccentric exercise induces transient insulin resistance in healthy individuals.
Eccentric exercise induces transient insulin resistance in healthy individuals.
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离心运动会导致健康个体出现短暂的胰岛素抵抗。
DOI：
10.1152/jappl.1992.72.6.2197
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发表时间：
1992
期刊：
影响因子：
--
通讯作者：
Holloszy,JO
中科院分区：
文献类型：
--
作者：
Kirwan,JP;Hickner,RC;Yarasheski,KE;Kohrt,WM;Wiethop,BV;Holloszy,JO
对6名健康的未经训练的个体进行了血糖-高胰岛素钳夹试验，以确定诱导肌肉损伤的运动是否也会导致胰岛素抵抗。在主要为1）离心运动[30 min，下坡跑，-17%等级，60 +/- 2%最大耗氧量（VO 2 max）]，2）同心运动（30 min，踏车测力计，60 +/- 2% VO 2 max）或3）未进行既往运动后48 h进行钳夹。在钳夹过程中，Euclidin维持在90 mg/dl，而胰岛素以30 mU·m-2.min-1输注120 min。使用[6，6 - 2 H]葡萄糖测定肝葡萄糖输出量（HGO）。离心运动导致明显的肌肉酸痛和显着升高肌酸激酶水平（273 +/- 73，92 +/- 27，87 +/- 25 IU/l的离心，同心，和控制条件，分别）48小时后，运动。离心运动后钳夹组胰岛素介导的葡萄糖处置率（3.47 +/- 0.51 mg.kg-1.min-1）显著低于向心运动后钳夹组（5.55 +/- 0.94 mg.kg-1.min-1）或对照组（5.48 +/- 1.0 mg.kg-1.min-1）（P <0.05）。HGO在不同条件下无显著差异（偏心夹、同心夹和对照夹分别为0.77 +/- 0.26、0.65 +/- 0.27和0.66 +/- 0.64 mg.kg-1.min-1）。离心运动后观察到的胰岛素抵抗不能归因于血浆皮质醇、胰高血糖素或儿茶酚胺浓度的改变。同样，在血清游离脂肪酸、甘油、乳酸、β-羟基丁酸或丙氨酸方面也未观察到差异。这些结果表明，运动导致肌肉损伤，反映在肌肉酸痛和酶泄漏，随后是一段时间的胰岛素抵抗。
Euglycemic-hyperinsulinemic clamps were performed on six healthy untrained individuals to determine whether exercise that induces muscle damage also results in insulin resistance. Clamps were performed 48 h after bouts of predominantly 1) eccentric exercise [30 min, downhill running, -17% grade, 60 +/- 2% maximal O2 consumption (VO2max)], 2) concentric exercise (30 min, cycle ergometry, 60 +/- 2% VO2max), or 3) without prior exercise. During the clamps, euglycemia was maintained at 90 mg/dl while insulin was infused at 30 mU.m-2.min-1 for 120 min. Hepatic glucose output (HGO) was determined using [6,6–2H]glucose. Eccentric exercise caused marked muscle soreness and significantly elevated creatine kinase levels (273 +/- 73, 92 +/- 27, 87 +/- 25 IU/l for the eccentric, concentric, and control conditions, respectively) 48 h after exercise. Insulin-mediated glucose disposal rate was significantly impaired (P less than 0.05) during the clamp performed after eccentric exercise (3.47 +/- 0.51 mg.kg-1.min-1) compared with the clamps performed after concentric exercise (5.55 +/- 0.94 mg.kg-1.min-1) or control conditions (5.48 +/- 1.0 mg.kg-1.min-1). HGO was not significantly different among conditions (0.77 +/- 0.26, 0.65 +/- 0.27, and 0.66 +/- 0.64 mg.kg-1.min-1 for the eccentric, concentric, and control clamps, respectively). The insulin resistance observed after eccentric exercise could not be attributed to altered plasma cortisol, glucagon, or catecholamine concentrations. Likewise, no differences were observed in serum free fatty acids, glycerol, lactate, beta-hydroxybutyrate, or alanine. These results show that exercise that results in muscle damage, as reflected in muscle soreness and enzyme leakage, is followed by a period of insulin resistance.