Farrell P A, Fedele M J, Vary T C, Kimball S R, Lang C H, Jefferson L S
Noll Physiological Research Center and Department of Kinesiology, University Park 16802; and Department of Cellular and Molecular Physiology, Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033, USA.
Am J Physiol. 1999 Apr;276(4):E721-7. doi: 10.1152/ajpendo.1999.276.4.E721.
These studies determined whether insulin-like growth factor-I (IGF-I) involvement in exercise-stimulated anabolic processes becomes more evident during hypoinsulinemia. Male Sprague-Dawley rats (n = 6-12/group) were made diabetic (blood glucose congruent with 300 mg/dl) by partial pancreatectomy (PPX) or remained nondiabetic (glucose congruent with 144 mg/dl). Rats performed acute resistance exercise by repetitive standing on the hindlimbs with weighted backpacks (ex), or they remained sedentary (sed). Resistance exercise caused increases in rates of protein synthesis (nmol Phe incorporated. g muscle-1. h-1, measured for gastrocnemius muscle in vivo 16 h after exercise) for both nondiabetic [sed = 154 +/- 6 (SE) vs. ex = 189 +/- 7] and diabetic rats (PPXsed = 152 +/- 11 vs. PPXex = 202 +/- 14, P < 0.05). Arterial plasma insulin concentrations in diabetic rats, congruent with180 pM, were less than one-half those found in nondiabetic rats, congruent with444 pM, (P < 0.05). The activity of eukaryotic initiation factor 2B (eIF2B; pmol GDP exchanged/min) was higher (P < 0.05) in ex rats (sed = 0.028 +/- 0.006 vs. ex = 0.053 +/- 0.015; PPXsed = 0.033 +/- 0.013 vs. PPXex = 0.047 +/- 0.009) regardless of diabetic status. Plasma IGF-I concentrations were higher in ex compared with sed diabetic rats (P < 0.05). In contrast, plasma IGF-I was not different in nondiabetic ex or sed rats. Muscle IGF-I (ng/g wet wt) was similar in ex and sed nondiabetic rats, but in diabetic rats was 2- to 3-fold higher in ex (P < 0.05) than in sed rats. In conclusion, moderate hypoinsulinemia that is sufficient to alter glucose homeostasis does not inhibit an increase in rates of protein synthesis after acute moderate-intensity resistance exercise. This preserved response may be due to a compensatory increase in muscle IGF-I content and a maintained ability to activate eIF2B.
这些研究确定了在低胰岛素血症期间，胰岛素样生长因子-I（IGF-I）参与运动刺激的合成代谢过程是否会变得更加明显。通过部分胰腺切除术（PPX）使雄性Sprague-Dawley大鼠（每组n = 6 - 12只）患糖尿病（血糖相当于300 mg/dl），或保持非糖尿病状态（血糖相当于144 mg/dl）。大鼠通过背负重物后肢重复站立进行急性抗阻运动（ex），或保持久坐不动（sed）。抗阻运动使非糖尿病大鼠[sed = 154 ± 6（SE） vs. ex = 189 ± 7]和糖尿病大鼠（PPXsed = 152 ± 11 vs. PPXex = 202 ± 14，P < 0.05）的蛋白质合成速率（以nmol苯丙氨酸掺入量计，g肌肉-1·h-1，运动后16小时在体测量腓肠肌）均增加。糖尿病大鼠的动脉血浆胰岛素浓度相当于180 pM，不到非糖尿病大鼠（相当于444 pM）的一半（P < 0.05）。无论糖尿病状态如何，抗阻运动大鼠中真核起始因子2B（eIF2B；pmol GDP交换量/分钟）的活性均较高（P < 0.05）（sed = 0.028 ± 0.006 vs. ex = 0.053 ± 0.015；PPXsed = 0.033 ± 0.013 vs. PPXex = 0.047 ± 0.009）。与久坐的糖尿病大鼠相比，抗阻运动的糖尿病大鼠血浆IGF-I浓度更高（P < 0.05）。相比之下，非糖尿病抗阻运动大鼠和久坐大鼠的血浆IGF-I无差异。非糖尿病抗阻运动大鼠和久坐大鼠的肌肉IGF-I（ng/g湿重）相似，但在糖尿病大鼠中，抗阻运动组的肌肉IGF-I比久坐组高2至3倍（P < 0.05）。总之，足以改变葡萄糖稳态的中度低胰岛素血症不会抑制急性中度强度抗阻运动后蛋白质合成速率的增加。这种保留的反应可能是由于肌肉IGF-I含量的代偿性增加以及激活eIF2B的能力维持所致。
