Wilkinson Sarah B, Phillips Stuart M, Atherton Philip J, Patel Rekha, Yarasheski Kevin E, Tarnopolsky Mark A, Rennie Michael J
Exercise Metabolism Research Group, Department of Kinesiology, McMaster University, 1280 Main Street West, Hamilton, ON, Canada L8S 4K1.
J Physiol. 2008 Aug 1;586(15):3701-17. doi: 10.1113/jphysiol.2008.153916. Epub 2008 Jun 12.
Resistance (RE) and endurance (EE) exercise stimulate mixed skeletal muscle protein synthesis. The phenotypes induced by RE (myofibrillar protein accretion) and EE (mitochondrial expansion) training must result from differential stimulation of myofibrillar and mitochondrial protein synthesis. We measured the synthetic rates of myofibrillar and mitochondrial proteins and the activation of signalling proteins (Akt-mTOR-p70S6K) at rest and after an acute bout of RE or EE in the untrained state and after 10 weeks of RE or EE training in young healthy men. While untrained, RE stimulated both myofibrillar and mitochondrial protein synthesis, 67% and 69% (P < 0.02), respectively. After training, only myofibrillar protein synthesis increased with RE (36%, P = 0.05). EE stimulated mitochondrial protein synthesis in both the untrained, 154%, and trained, 105% (both P < 0.05), but not myofibrillar protein synthesis. Acute RE and EE increased the phosphorylation of proteins in the Akt-mTOR-p70S6K pathway with comparatively minor differences between two exercise stimuli. Phosphorylation of Akt-mTOR-p70S6K proteins was increased after 10 weeks of RE training but not by EE training. Chronic RE or EE training modifies the protein synthetic response of functional protein fractions, with a shift toward exercise phenotype-specific responses, without an obvious explanatory change in the phosphorylation of regulatory signalling pathway proteins.
抗阻（RE）运动和耐力（EE）运动可刺激混合性骨骼肌蛋白质合成。RE训练（肌原纤维蛋白增加）和EE训练（线粒体扩张）所诱导的表型必定源于对肌原纤维蛋白和线粒体蛋白合成的不同刺激。我们测量了年轻健康男性在未训练状态下以及进行10周RE或EE训练后，静息时和急性一次RE或EE运动后肌原纤维蛋白和线粒体蛋白的合成速率以及信号蛋白（Akt-mTOR-p70S6K）的激活情况。在未训练时，RE刺激肌原纤维蛋白和线粒体蛋白合成，分别增加67%和69%（P<0.02）。训练后，只有RE能使肌原纤维蛋白合成增加（36%，P=0.05）。EE在未训练时刺激线粒体蛋白合成增加154%，训练后增加105%（均P<0.05），但不刺激肌原纤维蛋白合成。急性RE和EE可增加Akt-mTOR-p70S6K信号通路中蛋白的磷酸化，两种运动刺激之间的差异相对较小。RE训练10周后Akt-mTOR-p70S6K蛋白的磷酸化增加，但EE训练未使其增加。慢性RE或EE训练改变了功能性蛋白组分的蛋白质合成反应模式，向运动表型特异性反应转变，而调节信号通路蛋白的磷酸化没有明显可解释的变化。
