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Fuel for the work required: a practical approach to amalgamating train‐low paradigms for endurance athletes

机译:所需工作的燃料:为耐力运动员融合低火车范式的实用方法

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摘要

Using an amalgamation of previously studied “train‐low” paradigms, we tested the effects of reduced carbohydrate (CHO) but high leucine availability on cell‐signaling responses associated with exercise‐induced regulation of mitochondrial biogenesis and muscle protein synthesis (MPS). In a repeated‐measures crossover design, 11 males completed an exhaustive cycling protocol with high CHO availability before, during, and after exercise (HIGH) or alternatively, low CHO but high protein (leucine enriched) availability (LOW + LEU). Muscle glycogen was different (P < 0.05) pre‐exercise (HIGH: 583 ± 158, LOW + LEU: 271 ± 85 mmol kg−1 dw) but decreased (P < 0.05) to comparable levels at exhaustion (≈100 mmol kg−1 dw). Despite differences (P < 0.05) in exercise capacity (HIGH: 158 ± 29, LOW + LEU: 100 ± 17 min), exercise induced (P < 0.05) comparable AMPK α2 (3–4‐fold) activity, PGC‐1α (13‐fold), p53 (2‐fold), Tfam (1.5‐fold), SIRT1 (1.5‐fold), Atrogin 1 (2‐fold), and Mu style="fixed-case">RF1 (5‐fold) gene expression at 3 h post‐exercise. Exhaustive exercise suppressed p70S6K activity to comparable levels immediately post‐exercise (≈20 fmol min−1 mg−1). Despite elevated leucine availability post‐exercise, p70S6K activity remained suppressed (P < 0.05) 3 h post‐exercise in style="fixed-case">LOW +  style="fixed-case">LEU (28 ± 14 fmol min−1 mg−1), whereas muscle glycogen resynthesis (40 mmol kg−1 dw h−1) was associated with elevated (P < 0.05) p70S6K activity in style="fixed-case">HIGH (53 ± 30 fmol min−1 mg−1). We conclude: (1) style="fixed-case">CHO restriction before and during exercise induces “work‐efficient” mitochondrial‐related cell signaling but; (2) post‐exercise style="fixed-case">CHO and energy restriction maintains p70S6K activity at basal levels despite feeding leucine‐enriched protein. Our data support the practical concept of “fuelling for the work required” as a potential strategy for which to amalgamate train‐low paradigms into periodized training programs.
机译:通过合并使用先前研究的“低训练”范式,我们测试了碳水化合物减少(CHO)但亮氨酸利用率高对运动诱导的线粒体生物发生和肌肉蛋白合成(MPS)调节相关的细胞信号反应的影响。在重复测量的交叉设计中,有11名男性在运动前,运动中和运动后(HIGH)或CHO较低但蛋白(亮氨酸丰富)较高(LOW + LEU)较高的情况下完成了详尽的循环方案,具有较高的CHO利用率。锻炼前的肌肉糖原含量不同(P <0.05)(HIGH:583±158,LOW + LEU:271±85 mmol kg -1 dw),但在相同水平下降低(P <0.05)耗尽(≈100mmol kg -1 dw)。尽管运动能力(HIGH:158±29,LOW + LEU:100±17 min)有差异(P <0.05),但运动诱导(P <0.05)的AMPKα2(3-4倍)活性,PGC-1α( 13倍),p53(2倍),Tfam(1.5倍),SIRT1(1.5倍),Atrogin 1(2倍)和Mu style =“ fixed-case”> RF 1(5倍)。运动后立即用力竭运动将p70S6K活性抑制到可比水平(≈20fmol·min -1 mg -1 )。尽管运动后亮氨酸的可用性升高,但在 style =“ fixed-case”> LOW + style =“ fixed-case”> LEU的运动后3小时,p70S6K活性仍然受到抑制(P <0.05) (28±14 fmol·min −1 mg -1 ),而肌肉糖原再合成(40 mmol kg −1 dw·h -1 )与 style =“ fixed-case”> HIGH (53±30 fmol·min -1 )中的p70S6K活性升高(P <0.05)相关sup> mg -1 )。我们得出以下结论:(1)运动前后的 style =“ fixed-case”> CHO 限制会诱导“工作效率高”的线粒体相关细胞信号传导,但; (2)运动后 style =“ fixed-case”> CHO 和能量限制使p70S6K活性维持在基础水平,尽管饲喂富含亮氨酸的蛋白质。我们的数据支持“为所需工作加油”的实际概念,这是一种将低培训范式合并到定期培训计划中的潜在策略。

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