Bogardus C, Thuillez P, Ravussin E, Vasquez B, Narimiga M, Azhar S
J Clin Invest. 1983 Nov;72(5):1605-10. doi: 10.1172/JCI111119.
In rats, muscle glycogen depletion has been associated with increased insulin action. Whether this also occurs in man has not been reported. After 4 d rest, 13 males (E Group) had a percutaneous muscle biopsy of the vastus lateralis muscle followed by a euglycemic clamp at plasma insulin congruent to 100 microU/ml and congruent to 1,900 microU/ml, with simultaneous indirect calorimetry. This was repeated 1 wk later, but after glycogen-depleting exercise the night before the euglycemic clamp. Seven subjects underwent the same protocol but were also re-fed 100 g carbohydrate (CHO) after the exercise (EF group). In both groups, the mean muscle glycogen content was approximately 40% lower (P less than 0.01) after exercise compared with the muscle glycogen content measured after rest. In the E group, the mean muscle glycogen synthase activity (percent independent of glucose-6-phosphate) increased threefold (P less than 0.001) after exercise, but increased only twofold in the EF group (P less than 0.02 between groups). In both groups, the mean basal and insulin-stimulated CHO oxidation rates were lower in the post-exercise, glycogen-depleted condition compared with the rested, glycogen-replete condition. The mean insulin-stimulated CHO storage rate increased significantly in the E group after exercise but not in the EF group. In the E group, the total insulin-stimulated CHO disposal rate (M) was 17 (P less than 0.04) and 10% (P less than 0.03) higher after exercise during the low and high dose insulin infusion, respectively. No significant changes in M were observed in the EF group. For all subjects, after rest and exercise, the M correlated with the CHO storage rates during the low (r = 0.80, P less than 0.001) and high dose (r = 0.77, P less than 0.001) insulin infusions. After exercise, the muscle glycogen synthase activity correlated with the CHO storage rate (r = 0.73, P less than 0.002; r = 0.75, P less than 0.002) during the low and high dose insulin infusions, respectively, and also with M (r = 0.64, P less than 0.008; r = 0.57; P less than 0.02).
在大鼠中,肌肉糖原耗竭与胰岛素作用增强有关。这种情况在人类中是否也会发生尚无报道。在休息4天后,13名男性(E组)接受了股外侧肌的经皮肌肉活检,随后在血浆胰岛素浓度分别为100微单位/毫升和1900微单位/毫升时进行正常血糖钳夹试验,并同时进行间接测热法。1周后重复上述操作,但在正常血糖钳夹试验前一晚进行了消耗糖原的运动。7名受试者接受相同方案,但在运动后还重新摄入了100克碳水化合物(CHO)(EF组)。在两组中,运动后平均肌肉糖原含量比休息后测得的肌肉糖原含量低约40%(P<0.01)。在E组中,运动后平均肌肉糖原合酶活性(与6-磷酸葡萄糖无关的百分比)增加了三倍(P<0.001),但在EF组中仅增加了两倍(两组间P<0.02)。在两组中,与休息、糖原充足状态相比,运动后、糖原耗竭状态下的平均基础和胰岛素刺激的CHO氧化率均较低。E组运动后胰岛素刺激的CHO储存率显著增加,而EF组未增加。在E组中,运动后在低剂量和高剂量胰岛素输注期间,胰岛素刺激的总CHO处置率(M)分别高出17%(P<0.04)和10%(P<0.03)。EF组未观察到M有显著变化。对于所有受试者,休息和运动后,M与低剂量(r = 0·80,P<0.001)和高剂量(r = 0·77,P<0.001)胰岛素输注期间的CHO储存率相关。运动后,低剂量和高剂量胰岛素输注期间肌肉糖原合酶活性分别与CHO储存率相关(r = 0·73,P<0.002;r = 0·75,P<0.002),也与M相关(r = 0·64,P<0.008;r = 0·57;P<0.02)。