L-Arginine (L-Arg), the precursor of nitric oxide (NO), plays an important role in muscle function. Fast-twitch glycolytic fibres are more susceptible to age-related atrophy than slow-twitch oxidative fibres. The effect of L-Arg/NO on protein metabolism of fast- and slow-twitch muscle fibres was evaluated in chickens. In Exp. 1, 48 chicks at 1 day old were divided into 4 groups of 12 birds and subjected to 4 treatments: basal diet without supplementation or supplemented with 1% L-Arg, and water supplemented with or without L-nitro-arginine methyl ester (L-NAME, 18.5 mM). In Exp. 2, 48 chicks were divided into 4 groups of 12 birds fed with the basal diet and subjected to the following treatments: tap water (control), tap water supplemented with L-NAME (18.5 mM), or molsidomine (MS, 0.1 mM), or 18.5 mM L-NAME + 0.1 mM MS (NAMS). The regulatory effect of L-Arg/NO was further investigated in vitro with myoblasts obtained from chicken embryo pectoralis major (PM) and biceps femoris (BF). In vivo, dietary L-Arg supplementation increased breast (+14.94%, P < 0.05) and thigh muscle mass (+23.40%, P < 0.05); whereas, MS treatment had no detectable influence. However, L-NAME treatment blocked the beneficial influence of L-Arg on muscle development. L-Arg decreased (P < 0.05) protein synthesis rate, phosphorylated mTOR and ribosomal protein S6 kinase beta-1 (p70S6K) levels in breast muscle, which was recovered by L-NAME treatment. In vitro, L-Arg or sodium nitroprusside (SNP) reduced protein synthesis rate, suppressed phosphorylated mTOR/p70S6K and decreased atrogin-1 and muscle RING finger 1 (MuRF1) in myoblasts from PM muscle (P < 0.05). L-NAME abolished the inhibitory effect of L-Arg on protein synthesis and the mTOR/p70S6K pathway. However, myoblasts from BF muscle showed the weak influence. Moreover, blocking the mTOR/p70S6K pathway with rapamycin suppressed protein synthesis of the 2 types of myoblasts; whereas, the protein expression of atrogin-1 and MuRF1 levels were restricted only in myoblasts from PM muscle. In conclusion, L-Arg/NO/mTOR/p70S6K pathway enhances protein accumulation and muscle development in fast-twitch glycolytic muscle in chickens. L-Arg/NO regulates protein turnover in a muscle fibre specific way, which highlights the potential clinical application in fast-twitch glycolytic muscle fibres.

L-精氨酸 (L-Arg) 是一氧化氮 (NO) 的前体，在肌肉功能中起重要作用。快肌糖酵解纤维比慢肌氧化纤维更容易发生与年龄相关的萎缩。在鸡中评估了 L-Arg/NO 对快肌纤维和慢肌纤维蛋白质代谢的影响。在 Exp。1、48 只 1 日龄雏鸡被分为 4 组，每组 12 只鸡，接受 4 个处理：基础日粮不添加或添加 1% L-Arg，水添加或不添加 L-硝基精氨酸甲酯（L-硝基精氨酸甲酯） -名称，18.5 毫米）。在 Exp。2、将 48 只小鸡分成 4 组，每组 12 只鸡，喂以基础日粮，并接受以下处理：自来水（对照）、补充 L-NAME（18.5 mM）的自来水或 molsidomine（MS，0.1 mM） ，或 18.5 mM L-NAME + 0.1 mM MS (NAMS)。用从鸡胚胸大肌 (PM) 和股二头肌 (BF) 获得的成肌细胞在体外进一步研究了 L-Arg/NO 的调节作用。在体内，膳食 L-Arg 补充剂增加了乳房 (+14.94%,P  < 0.05) 和大腿肌肉质量 (+23.40%, P  < 0.05)；而 MS 治疗没有可检测到的影响。然而，L-NAME 治疗阻止了 L-Arg 对肌肉发育的有益影响。L-Arg 降低 ( P  < 0.05) 蛋白质合成率、磷酸化 mTOR 和核糖体蛋白 S6 激酶 beta-1 (p70S6K) 水平，通过 L-NAME 治疗恢复。在体外，L-Arg 或硝普钠 (SNP) 降低了 PM 肌肉成肌细胞中的蛋白质合成速率，抑制了磷酸化 mTOR/p70S6K 并降低了 atrogin-1 和肌肉环指 1 (MuRF1) ( P < 0.05)。L-NAME 消除了 L-Arg 对蛋白质合成和 mTOR/p70S6K 通路的抑制作用。然而，来自BF肌肉的成肌细胞显示出较弱的影响。此外，用雷帕霉素阻断mTOR/p70S6K通路抑制了2种成肌细胞的蛋白质合成；而 atrogin-1 和 MuRF1 水平的蛋白质表达仅在来自 PM 肌肉的成肌细胞中受到限制。总之，L-Arg/NO/mTOR/p70S6K 通路增强了鸡快缩糖酵解肌的蛋白质积累和肌肉发育。L-Arg/NO 以肌纤维特异性方式调节蛋白质周转，这突出了在快速收缩糖酵解肌纤维中的潜在临床应用。