BackgroundUrsolic acid altered muscle protein metabolism in normal and resting conditions after acute resistance exercise, suggesting that eating fruits rich in ursolic acid could enhance muscle protein synthesis and decrease muscle degradation. Aronia melanocarpa, a member of the family Rosaceae and native to North America and Eastern Canada, is rich in ursolic acid. In this study, we examined the effects of A. melanocarpa extract (AME) supplementation on the mTORC1 signaling pathway and muscle degradation-related factors in rats, both alone and in combination with resistance exercise.MethodsMale Sprague-Dawley rats were divided into AME and normal chow (NOR) groups. AME group was fed chow providing a dose of 3 g/kg of AME and 115 mg/kg of ursolic acid for 7 days, whereas NOR rats were fed normal powder chow. The right gastrocnemius muscle of each animal was isometrically exercised (5 sets of ten 3-s contractions, with a 7-s interval between contractions and 3-min rest intervals between sets), while the left gastrocnemius muscle served as an internal control. Western blotting and real-time polymerase chain reaction were used to assess expression of factors involved in the mTORC1 signaling pathway and muscle degradation.ResultsAt 1 h after resistance exercise, phosphorylation of ERK1/2 was significantly increased by AME consumption. At 6 h after resistance exercise, AME consumption significantly increased the phosphorylation of Akt, p70S6K, rpS6, and AMPK. It also increased MAFbx expression. Furthermore, AME significantly increased the phosphorylation of p70S6K and rpS6 in response to resistance exercise. However, AME did not increase muscle protein synthesis (MPS) after resistance exercise. AME did not affect the expression of any of the mediators of protein degradation, with the exception of MAFbx.ConclusionsDietary AME enhanced mTORC1 activation in response to resistance exercise without increasing MPS. Moreover, it neither accelerated muscle protein degradation nor otherwise negatively affected protein metabolism. Further study is needed to clarify the effect of the combination of AME and chronic resistance training on muscle hypertrophy.

中文翻译：

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膳食 Aronia melanocarpa 提取物增强 mTORC1 信号，但对蛋白质合成和蛋白质分解相关信号没有影响，以响应大鼠骨骼肌的抗阻运动

背景熊果酸在急性抗阻运动后的正常和休息条件下改变了肌肉蛋白质代谢，表明食用富含熊果酸的水果可以增强肌肉蛋白质合成并减少肌肉降解。Aronia melanocarpa 是蔷薇科的一员，原产于北美和加拿大东部，富含熊果酸。在这项研究中，我们检查了黑果树提取物 (AME) 补充剂对大鼠 mTORC1 信号通路和肌肉降解相关因子的影响，单独和与阻力运动相结合。 方法雄性 Sprague-Dawley 大鼠分为 AME 和正常食物 (NOR) 组。AME 组喂食提供 3 g/kg AME 和 115 mg/kg 熊果酸的饲料，持续 7 天，而 NOR 大鼠喂食正常粉末饲料。每只动物的右腓肠肌进行等长锻炼（5 组，每组 10 次 3 秒收缩，收缩间隔为 7 秒，组间休息间隔为 3 分钟），而左腓肠肌作为内部对照。Western印迹和实时聚合酶链反应用于评估参与mTORC1信号通路和肌肉降解的因子的表达。结果在抗阻运动后1小时，消耗AME显着增加ERK1/2的磷酸化。在抗阻运动后 6 小时，AME 消耗显着增加 Akt、p70S6K、rpS6 和 AMPK 的磷酸化。它还增加了 MAFbx 表达。此外，AME 显着增加 p70S6K 和 rpS6 的磷酸化以响应抗阻运动。然而，抗阻运动后，AME 不会增加肌肉蛋白质合成 (MPS)。除 MAFbx 外，AME 不影响任何蛋白质降解介质的表达。结论饮食 AME 增强了 mTORC1 激活以响应抗阻运动而不增加 MPS。此外，它既不会加速肌肉蛋白质降解，也不会对蛋白质代谢产生负面影响。需要进一步的研究来阐明 AME 和慢性阻力训练相结合对肌肉肥大的影响。它既不会加速肌肉蛋白质降解，也不会对蛋白质代谢产生负面影响。需要进一步的研究来阐明 AME 和慢性阻力训练相结合对肌肉肥大的影响。它既不会加速肌肉蛋白质降解，也不会对蛋白质代谢产生负面影响。需要进一步的研究来阐明 AME 和慢性阻力训练相结合对肌肉肥大的影响。