Farrell P A, Fedele M J, Hernandez J, Fluckey J D, Miller J L, Lang C H, Vary T C, Kimball S R, Jefferson L S
Noll Physiological Research Center and Department of Kinesiology, University Park, Pennsylvania 16802, USA.
J Appl Physiol (1985). 1999 Sep;87(3):1075-82. doi: 10.1152/jappl.1999.87.3.1075.
This study had the following objectives: 1) to determine whether diabetic rats could increase muscle mass due to a physiological manipulation (chronic resistance exercise), 2) to determine whether exercise training status modifies the effect of the last bout of exercise on elevations in rates of protein synthesis, and 3) to determine whether chronic resistance exercise alters basal glycemia. Groups consisted of diabetic or nondiabetic rats that performed progressive resistance exercise for 8 wk, performed acute resistance exercise, or remained sedentary. Arterial plasma insulin in diabetic groups was reduced by about one-half (P < 0.05) compared with nondiabetic groups. Soleus and gastrocnemius-plantaris complex muscle wet weights were lower because of diabetes, but in response to chronic exercise these muscles hypertrophied in diabetic (0.028 +/- 0.003 vs. 0.032 +/- 0.0015 g/cm for sedentary vs. exercised soleus and 0.42 +/- 0.068 vs. 0.53 +/- 0.041 g/cm for sedentary vs. exercised gastrocnemius-plantaris, both P < 0.05) but not in nondiabetic (0.041 +/- 0.0026 vs. 0.042 +/- 0.003 g/cm for sedentary vs. exercised soleus and 0.72 +/- 0.015 vs. 0.69 +/- 0.013 g/cm for sedentary vs. exercised gastrocnemius-plantaris) rats when muscle weight was expressed relative to tibial length or body weight (data not shown). Another group of diabetic rats that lifted heavier weights showed muscle hypertrophy. Rates of protein synthesis were higher in red gastrocnemius in chronically exercised than in sedentary rats: 155 +/- 11 and 170 +/- 7 nmol phenylalanine incorporated x g muscle(-1) x h(-1) in exercised diabetic and nondiabetic rats vs. 110 +/- 14 and 143 +/- 7 nmol phenylalanine incorporated x g muscle(-1) x h(-1) in sedentary diabetic and nondiabetic rats. These elevations, however, were lower than in acutely exercised (but untrained) rats: 176 +/- 15 and 193 +/- 8 nmol phenylalanine incorporated x g muscle(-1) x h(-1) in diabetic and nondiabetic rats. Finally, chronic exercise training in diabetic rats was associated with reductions in basal glycemia, and such reductions did not occur in sedentary diabetic groups. These data demonstrate that, despite lower circulating insulin concentrations, diabetic rats can increase muscle mass in response to a physiological stimulus.
1)确定糖尿病大鼠是否可因生理干预(慢性抗阻运动)而增加肌肉量;2)确定运动训练状态是否会改变最后一次运动 bout 对蛋白质合成速率升高的影响;3)确定慢性抗阻运动是否会改变基础血糖水平。实验分组包括进行 8 周渐进性抗阻运动、进行急性抗阻运动或保持久坐的糖尿病或非糖尿病大鼠。与非糖尿病组相比,糖尿病组的动脉血浆胰岛素降低了约一半(P < 0.05)。由于糖尿病,比目鱼肌和腓肠肌 - 跖肌复合体的肌肉湿重较低,但对慢性运动的反应是,这些肌肉在糖尿病大鼠中肥大(久坐组与运动组比目鱼肌分别为 0.028 ± 0.003 与 0.032 ± 0.0015 g/cm,久坐组与运动组腓肠肌 - 跖肌分别为 0.42 ± 0.068 与 0.53 ± 0.041 g/cm,均 P < 0.05),而在非糖尿病大鼠中未出现肥大(久坐组与运动组比目鱼肌分别为 0.041 ± 0.0026 与 0.042 ± 0.003 g/cm,久坐组与运动组腓肠肌 - 跖肌分别为 0.72 ± 0.015 与 0.69 ± 0.013 g/cm),当肌肉重量相对于胫骨长度或体重表示时(数据未显示)。另一组举起更重重量的糖尿病大鼠出现了肌肉肥大。长期运动的糖尿病大鼠比久坐大鼠的红腓肠肌蛋白质合成速率更高:运动的糖尿病和非糖尿病大鼠中分别为 155 ± 11 和 170 ± 7 nmol 苯丙氨酸掺入 x g 肌肉(-1) x h(-1),而久坐的糖尿病和非糖尿病大鼠中分别为 110 ± 14 和 143 ± 7 nmol 苯丙氨酸掺入 x g 肌肉(-1) x h(-1)。然而这些升高幅度低于急性运动(但未训练)的大鼠:糖尿病和非糖尿病大鼠中分别为 176 ± 15 和 193 ± 8 nmol 苯丙氨酸掺入 x g 肌肉(-1) x h(-1)。最后,糖尿病大鼠的慢性运动训练与基础血糖降低有关,而久坐的糖尿病组未出现这种降低。这些数据表明,尽管循环胰岛素浓度较低,但糖尿病大鼠可因生理刺激而增加肌肉量。