L-Arginine (L-Arg), the precursor of nitric oxide (NO), plays an important role in muscle function. Fasttwitchglycolytic fibres are more susceptible to age-related atrophy than slow-twitch oxidative fibres.The effect ...L-Arginine (L-Arg), the precursor of nitric oxide (NO), plays an important role in muscle function. Fasttwitchglycolytic 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 inchickens. In Exp. 1, 48 chicks at 1 day old were divided into 4 groups of 12 birds and subjected to 4treatments: basal diet without supplementation or supplemented with 1% L-Arg, and water supplementedwith or without L-nitro-arginine methyl ester (L-NAME, 18.5 mM). In Exp. 2, 48 chicks weredivided into 4 groups of 12 birds fed with the basal diet and subjected to the following treatments: tapwater (control), tap water supplemented with L-NAME (18.5 mM), or molsidomine (MS, 0.1 mM), or18.5 mM L-NAME t 0.1 mM MS (NAMS). The regulatory effect of L-Arg/NO was further investigatedin vitro with myoblasts obtained from chicken embryo pectoralis major (PM) and biceps femoris (BF).In vivo, dietary L-Arg supplementation increased breast (t14.94%, P < 0.05) and thigh muscle mass(t23.40%, P < 0.05);whereas, MS treatment had no detectable influence. However, L-NAME treatmentblocked the beneficial influence of L-Arg on muscle development. L-Arg decreased (P < 0.05) proteinsynthesis rate, phosphorylated mTOR and ribosomal protein S6 kinase beta-1 (p70S6K) levels in breastmuscle, 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 andmuscle RING finger 1 (MuRF1) in myoblasts from PM muscle (P < 0.05). L-NAME abolished the inhibitoryeffect of L-Arg on protein synthesis and the mTOR/p70S6K pathway. However, myoblasts from BF muscleshowed the weak influence. Moreover, blocking the mTOR/p70S6K pathway with rapamycin suppressedprotein synthesis of the 2 types of myoblasts;whereas, the protein expression of atrogin-1 and MuRF1levels were restricted only in myoblasts from PM muscle. In conclusion, L-Arg/NO/mTOR/p70S6Kpathway enhances protein accumulation and muscle development in fast-twitch glycolytic muscle inchickens. L-Arg/NO regulates protein turnover in a muscle fibre specific way, which highlights the potentialclinical application in fast-twitch glycolytic muscle fibres.展开更多
基金the Key Technologies Research and Development Programof China(2021YFD1300405)the Earmarked Fund for China Agriculture Research System(CARS-40-K09)+1 种基金National Natural Science Foundation of China(31772619)Key Technology Research and Development Program of Shandong Province(2019JZZY020602).
文摘L-Arginine (L-Arg), the precursor of nitric oxide (NO), plays an important role in muscle function. Fasttwitchglycolytic 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 inchickens. In Exp. 1, 48 chicks at 1 day old were divided into 4 groups of 12 birds and subjected to 4treatments: basal diet without supplementation or supplemented with 1% L-Arg, and water supplementedwith or without L-nitro-arginine methyl ester (L-NAME, 18.5 mM). In Exp. 2, 48 chicks weredivided into 4 groups of 12 birds fed with the basal diet and subjected to the following treatments: tapwater (control), tap water supplemented with L-NAME (18.5 mM), or molsidomine (MS, 0.1 mM), or18.5 mM L-NAME t 0.1 mM MS (NAMS). The regulatory effect of L-Arg/NO was further investigatedin vitro with myoblasts obtained from chicken embryo pectoralis major (PM) and biceps femoris (BF).In vivo, dietary L-Arg supplementation increased breast (t14.94%, P < 0.05) and thigh muscle mass(t23.40%, P < 0.05);whereas, MS treatment had no detectable influence. However, L-NAME treatmentblocked the beneficial influence of L-Arg on muscle development. L-Arg decreased (P < 0.05) proteinsynthesis rate, phosphorylated mTOR and ribosomal protein S6 kinase beta-1 (p70S6K) levels in breastmuscle, 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 andmuscle RING finger 1 (MuRF1) in myoblasts from PM muscle (P < 0.05). L-NAME abolished the inhibitoryeffect of L-Arg on protein synthesis and the mTOR/p70S6K pathway. However, myoblasts from BF muscleshowed the weak influence. Moreover, blocking the mTOR/p70S6K pathway with rapamycin suppressedprotein synthesis of the 2 types of myoblasts;whereas, the protein expression of atrogin-1 and MuRF1levels were restricted only in myoblasts from PM muscle. In conclusion, L-Arg/NO/mTOR/p70S6Kpathway enhances protein accumulation and muscle development in fast-twitch glycolytic muscle inchickens. L-Arg/NO regulates protein turnover in a muscle fibre specific way, which highlights the potentialclinical application in fast-twitch glycolytic muscle fibres.
