Sanchez Otto A, Snow LeAnn M, Lowe Dawn A, Serfass Robert C, Thompson LaDora V
School of Kinesiology, University of Minnesota Medical School, 420 Delaware Street, Minneapolis, MN 55455, USA.
J Appl Physiol (1985). 2005 Aug;99(2):472-8. doi: 10.1152/japplphysiol.01233.2004. Epub 2005 Apr 14.
The purpose of this study was to characterize the contractile properties of individual skinned muscle fibers from insulin-treated streptozotocin-induced diabetic rats after an endurance exercise training program. We hypothesized that single-fiber contractile function would decrease in the diabetic sedentary rats and that endurance exercise would preserve the function. In the study, 28 rats were assigned to either a nondiabetic sedentary, a nondiabetic exercise, a diabetic sedentary, or a diabetic exercise group. Rats in the diabetic groups received subcutaneous intermediate-lasting insulin daily. The exercise-trained rats ran on a treadmill at a moderate intensity for 60 min, five times per week. After 12 wk, the extensor digitorum longus and soleus muscles were dissected. Single-fiber diameter, Ca(2+)-activated peak force, specific tension, activation threshold, and pCa(50) as well as the myosin heavy chain isoform expression (MHC) were determined. We found that in MHC type II fibers from extensor digitorum longus muscle, diameters were significantly smaller from diabetic sedentary rats compared with nondiabetic sedentary rats (P < 0.001). Among the nondiabetic rats, fiber diameters were smaller with exercise (P = 0.038). The absolute force-generating capacity of single fibers was lower in muscles from diabetic rats. There was greater specific tension (force normalized to cross-sectional area) by fibers from the rats that followed an endurance exercise program compared with sedentary. From the results, we conclude that alterations in the properties of contractile proteins are not implicated in the decrease in strength associated with diabetes and that endurance-exercise training does not prevent or increase muscle weakness in diabetic rats.
本研究的目的是在耐力运动训练计划后,对胰岛素治疗的链脲佐菌素诱导的糖尿病大鼠的单个去皮肤肌纤维的收缩特性进行表征。我们假设,糖尿病久坐大鼠的单纤维收缩功能会下降,而耐力运动将保留该功能。在该研究中,28只大鼠被分配到非糖尿病久坐组、非糖尿病运动组、糖尿病久坐组或糖尿病运动组。糖尿病组的大鼠每天接受皮下注射中效胰岛素。运动训练的大鼠在跑步机上以中等强度跑步60分钟,每周5次。12周后,解剖趾长伸肌和比目鱼肌。测定单纤维直径、Ca(2+)激活的峰值力、比张力、激活阈值和pCa(50)以及肌球蛋白重链同工型表达(MHC)。我们发现,在趾长伸肌的MHC II型纤维中,糖尿病久坐大鼠的纤维直径明显小于非糖尿病久坐大鼠(P < 0.001)。在非糖尿病大鼠中,运动后纤维直径较小(P = 0.038)。糖尿病大鼠肌肉中单个纤维的绝对力量产生能力较低。与久坐大鼠相比,进行耐力运动训练的大鼠的纤维具有更大的比张力(力量除以横截面积)。从结果来看,我们得出结论,收缩蛋白特性的改变与糖尿病相关的力量下降无关,并且耐力运动训练不能预防或增加糖尿病大鼠的肌肉无力。