Fuel for the work required: a practical approach to amalgamating train-low paradigms for endurance athletes.
Fuel for the work required: a practical approach to amalgamating train-low paradigms for endurance athletes.
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DOI：
10.14814/phy2.12803
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发表时间：
2016-05
影响因子：
2.5
通讯作者：
Morton JP
中科院分区：
文献类型：
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作者：
Impey SG;Hammond KM;Shepherd SO;Sharples AP;Stewart C;Limb M;Smith K;Philp A;Jeromson S;Hamilton DL;Close GL;Morton JP
使用先前研究的“低训练”范例的合并，我们测试了减少碳水化合物（CHO）但高亮氨酸可用性对与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传导反应的影响。在重复测量交叉设计中，11名男性在运动前、运动中和运动后完成了具有高CHO可用性（HIGH）或低CHO但高蛋白质（富含亮氨酸）可用性（LOW + LEU）的极限循环方案。运动前的肌糖原不同（高：583 ± 158，低+ LEU：271 ± 85 mmol kg−1 dw），但在力竭时（<100 mmol kg −1 dw）降低（P < 0.05）至相当水平。尽管存在分歧运动能力（P < 0.05）（高：158 ± 29，低+亮：100 ± 17 min），运动诱导（P < 0.05）可比AMPK α2（3-4倍）活性，PGC-1α（13倍），p53（2倍），Tfam（1.5倍），SIRT 1（1.5倍），Atrogin 1（2倍）和MuRF 1（5倍）基因表达。力竭运动抑制p70 S6 K活性至运动后即刻的相当水平（<20 fmol min−1 mg−1）。尽管运动后亮氨酸利用率升高，但在LOW + LEU（28 ± 14 fmol min−1 mg−1）中运动后3 h，p70 S6 K活性仍受到抑制（P < 0.05），而在HIGH（53 ± 30 fmol min−1 mg −1）中，肌糖原再合成（40 mmol kg−1 dw h−1）与p70 S6 K活性升高（P < 0.05）相关。我们得出结论：（1）运动前和运动期间限制CHO可诱导“工作效率”线粒体相关细胞信号传导，但（2）运动后限制CHO和能量可使p70 S6 K活性维持在基础水平，尽管喂食富含亮氨酸的蛋白质。我们的数据支持“为所需工作加油”的实用概念，作为将低训练模式合并到周期性培训计划中的潜在策略。
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 MuRF1 (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 LOW + 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 HIGH (53 ± 30 fmol min−1 mg−1). We conclude: (1) CHO restriction before and during exercise induces “work‐efficient” mitochondrial‐related cell signaling but; (2) post‐exercise 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.