目的:评估抗阻运动训练(RET)和/或补充谷氨酰胺(GS)对成年大鼠骨骼肌信号蛋白合成的影响。
方法:对以下各组进行了研究:(1)对照组,无运动(C);(2)运动,肥大阻力运动训练方案(T);(3)不运动,补充有谷氨酰胺(G);和(4)运动并补充有谷氨酰胺(GT)。大鼠进行肥大训练,相对于水平面倾斜80°,爬上高度为1.1m的垂直梯子,尾巴上有额外的重量。RET一周三天,持续五周。每个培训课程包括六个梯子爬升。在每次训练期间,每只动物的额外重量负荷逐渐增加。G组通过管饲法每天接受L-谷氨酰胺(每天每公斤体重1克),持续五周。C组在同一时期接受相同体积的水。老鼠被安乐死,取出来自两个后肢的指长伸肌(EDL)并立即称重。测量了谷氨酰胺和谷氨酸的浓度,和组织学,信号蛋白含量,并进行mRNA表达分析。
结果:补充游离L-谷氨酰胺可增加C组EDL肌肉中的谷氨酰胺浓度。T大鼠的EDL肌肉中的谷氨酸浓度增加。EDL肌肉质量没有改变,但在三个实验组中,据报道纤维的横截面积(CSA)显著增加.磷酸化蛋白的水平(pAkt/Akt,pp70S6K/p70S6K,在G大鼠的EDL肌肉中,p4E-BP1/4E-BP1和pS6/S6比率)显着增加,T大鼠存在p4E-BP1的激活。T中EDL肌肉的纤维CSA,G,与C组相比,GT年夜鼠均增高。这些变化伴随着来自T大鼠的EDL肌肉的26个蛋白酶体活性的降低。
结论:五周GS和/或RET诱导肌肉肥大,如EDL肌纤维的CSA增加所示。CSA的增加是通过Akt的上调磷酸化介导的,4E-BP1,p70S6k,G动物中的S6和T动物中的4E-BP1。在来自T动物的EDL肌肉中,蛋白酶体活性的减少,有利于进一步增加肌肉纤维的CSA,已报告。
OBJECTIVE: To evaluate the effects of resistance exercise training (RET) and/or glutamine supplementation (GS) on signaling protein synthesis in adult rat skeletal muscles.
METHODS: The following groups were studied: (1) control, no exercise (C); (2) exercise, hypertrophy resistance exercise training protocol (T); (3) no exercise, supplemented with glutamine (G); and (4) exercise and supplemented with glutamine (GT). The rats performed hypertrophic training, climbing a vertical ladder with a height of 1.1 m at an 80° incline relative to the horizontal with extra weights tied to their tails. The RET was performed three days a week for five weeks. Each training session consisted of six ladder climbs. The extra weight load was progressively increased for each animal during each training session. The G groups received daily L-glutamine by gavage (one g per kilogram of body weight per day) for five weeks. The C group received the same volume of water during the same period. The rats were euthanized, and the extensor digitorum longus (EDL) muscles from both hind limbs were removed and immediately weighed. Glutamine and glutamate concentrations were measured, and histological, signaling protein contents, and mRNA expression analyses were performed.
RESULTS: Supplementation with free L-glutamine increased the glutamine concentration in the EDL muscle in the C group. The glutamate concentration was augmented in the EDL muscles from T rats. The EDL muscle mass did not change, but a significant rise was reported in the cross-sectional area (CSA) of the fibers in the three experimental groups. The levels of the phosphorylated proteins (pAkt/Akt, pp70S6K/p70S6K, p4E-BP1/4E-BP1, and pS6/S6 ratios) were significantly increased in EDL muscles of G rats, and the activation of p4E-BP1 was present in T rats. The fiber CSAs of the EDL muscles in T, G, and GT rats were increased compared to the C group. These changes were accompanied by a reduction in the 26 proteasome activity of EDL muscles from T rats.
CONCLUSIONS: Five weeks of GS and/or RET induced muscle hypertrophy, as indicated by the increased CSAs of the EDL muscle fibers. The increase in CSA was mediated via the upregulated phosphorylation of Akt, 4E-BP1, p70S6k, and S6 in G animals and 4E-BP1 in T animals. In the EDL muscles from T animals, a decrease in proteasome activity, favoring a further increase in the CSA of the muscle fibers, was reported.