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运动恢复期间摄入酮酯饮料可促进人体肌肉中的mTORC1信号传导,但不能促进糖原再合成。

Intake of a Ketone Ester Drink during Recovery from Exercise Promotes mTORC1 Signaling but Not Glycogen Resynthesis in Human Muscle.

作者信息

Vandoorne Tijs, De Smet Stefan, Ramaekers Monique, Van Thienen Ruud, De Bock Katrien, Clarke Kieran, Hespel Peter

机构信息

Exercise Physiology Research Group, Department of Kinesiology, KU LeuvenLeuven, Belgium.

Laboratory of Exercise and Health, Department of Health Sciences and Technology, ETH ZurichZurich, Switzerland.

出版信息

Front Physiol. 2017 May 23;8:310. doi: 10.3389/fphys.2017.00310. eCollection 2017.

Abstract

Ketone bodies are energy substrates produced by the liver during prolonged fasting or low-carbohydrate diet. The ingestion of a ketone ester (KE) rapidly increases blood ketone levels independent of nutritional status. KE has recently been shown to improve exercise performance, but whether it can also promote post-exercise muscle protein or glycogen synthesis is unknown. Eight healthy trained males participated in a randomized double-blind placebo-controlled crossover study. In each session, subjects undertook a bout of intense one-leg glycogen-depleting exercise followed by a 5-h recovery period during which they ingested a protein/carbohydrate mixture. Additionally, subjects ingested a ketone ester (KE) or an isocaloric placebo (PL). KE intake did not affect muscle glycogen resynthesis, but more rapidly lowered post-exercise AMPK phosphorylation and resulted in higher mTORC1 activation, as evidenced by the higher phosphorylation of its main downstream targets S6K1 and 4E-BP1. As enhanced mTORC1 activation following KE suggests higher protein synthesis rates, we used myogenic CC cells to further confirm that ketone bodies increase both leucine-mediated mTORC1 activation and protein synthesis in muscle cells. Our results indicate that adding KE to a standard post-exercise recovery beverage enhances the post-exercise activation of mTORC1 but does not affect muscle glycogen resynthesis in young healthy volunteers. , we confirmed that ketone bodies potentiate the increase in mTORC1 activation and protein synthesis in leucine-stimulated myotubes. Whether, chronic oral KE intake during recovery from exercise can facilitate training-induced muscular adaptation and remodeling need to be further investigated.

摘要

酮体是肝脏在长期禁食或低碳水化合物饮食期间产生的能量底物。摄入酮酯(KE)可迅速提高血酮水平,且与营养状况无关。最近有研究表明KE可改善运动表现,但它是否还能促进运动后肌肉蛋白质或糖原合成尚不清楚。八名健康的受过训练的男性参与了一项随机双盲安慰剂对照交叉研究。在每个试验阶段,受试者进行一轮高强度的单腿糖原消耗运动,随后是5小时的恢复期,在此期间他们摄入蛋白质/碳水化合物混合物。此外,受试者摄入酮酯(KE)或等热量安慰剂(PL)。摄入KE并不影响肌肉糖原的再合成,但能更快地降低运动后AMPK的磷酸化水平,并导致更高的mTORC1激活,其主要下游靶点S6K1和4E-BP1的磷酸化水平升高证明了这一点。由于KE后增强的mTORC1激活表明蛋白质合成速率更高,我们使用成肌CC细胞进一步证实酮体可增加亮氨酸介导的mTORC1激活和肌肉细胞中的蛋白质合成。我们的结果表明,在标准的运动后恢复饮料中添加KE可增强运动后mTORC1的激活,但不影响年轻健康志愿者的肌肉糖原再合成。我们证实,酮体可增强亮氨酸刺激的肌管中mTORC1激活和蛋白质合成的增加。运动恢复期间长期口服KE是否能促进训练诱导的肌肉适应和重塑有待进一步研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6cfd/5440563/f7f5abf7e741/fphys-08-00310-g0001.jpg

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