PURPOSE To determine the acute effects of carbohydrate (CHO) ingestion following a bout of maximal eccentric resistance exercise on key anabolic kinases of mammalian target of rapamycin and extracellular signal-regulated kinase (ERK) pathways. The authors' hypothesis was that the activation of anabolic signaling pathways known to be upregulated by resistance exercise would be further stimulated by the physiological hyperinsulinemia resulting from CHO supplementation. METHODS Ten resistance-trained men were randomized in a crossover, double-blind, placebo (PLA)-controlled manner to ingest either a noncaloric PLA or 3 g/kg of CHO beverage throughout recovery from resistance exercise. Muscle biopsies were collected at rest, immediately after a single bout of intense lower body resistance exercise, and after 3 hr of recovery. RESULTS CHO ingestion elevated plasma glucose and insulin concentrations throughout recovery compared with PLA ingestion. The ERK pathway (phosphorylation of ERK1/2 [Thr202/Tyr204], RSK [Ser380], and p70S6K [Thr421/Ser424]) was markedly activated immediately after resistance exercise, without any effect of CHO supplementation. The phosphorylation state of AKT (Thr308) was unchanged postexercise in the PLA trial and increased at 3 hr of recovery above resting with ingestion of CHO compared with PLA. Despite stimulating-marked phosphorylation of AKT, CHO ingestion did not enhance resistance exercise-induced phosphorylation of p70S6K (Thr389) and rpS6 (Ser235/236 and Ser240/244). CONCLUSION CHO supplementation after resistance exercise and hyperinsulinemia does not influence the ERK pathway nor the mTORC1 target p70S6K and its downstream proteins, despite the increased AKT phosphorylation.

中文翻译：

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离心阻力运动后摄入碳水化合物对 AKT/mTOR 和 ERK 通路的影响：一项随机、双盲、交叉研究。

目的 确定碳水化合物 (CHO) 摄入对哺乳动物雷帕霉素靶标和细胞外信号调节激酶 (ERK) 通路的关键合成代谢激酶进行一次最大离心阻力运动后的急性影响。作者的假设是，已知由抗阻运动上调的合成代谢信号通路的激活将受到补充 CHO 引起的生理性高胰岛素血症的进一步刺激。方法 10 名接受过阻力训练的男性以交叉、双盲、安慰剂 (PLA) 控制的方式随机分组，在阻力运动恢复期间摄入无热量 PLA 或 3 g/kg CHO 饮料。肌肉活组织检查是在休息时、在一次剧烈的下肢抵抗运动后和恢复 3 小时后立即收集的。结果 与 PLA 摄入相比，CHO 摄入在整个恢复过程中升高了血浆葡萄糖和胰岛素浓度。ERK 通路（ERK1/2 [Thr202/Tyr204]、RSK [Ser380] 和 p70S6K [Thr421/Ser424] 的磷酸化）在抗阻运动后立即显着激活，补充 CHO 没有任何影响。AKT (Thr308) 的磷酸化状态在 PLA 试验中在运动后没有变化，与 PLA 相比，在摄入 CHO 后恢复 3 小时以上时增加。尽管刺激标记的 AKT 磷酸化，CHO 摄入并没有增强抗阻运动诱导的 p70S6K（Thr389）和 rpS6（Ser235/236 和 Ser240/244）磷酸化。结论 抗阻运动和高胰岛素血症后补充 CHO 不影响 ERK 通路，也不影响 mTORC1 靶标 p70S6K 及其下游蛋白，