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首页> 外文期刊>Journal of applied physiology >Resistance exercise load does not determine training-mediated hypertrophic gains in young men
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Resistance exercise load does not determine training-mediated hypertrophic gains in young men

机译:抵抗运动负荷不能确定年轻男子训练介导的肥厚性增高

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摘要

We have reported that the acute postexercise increases in muscle protein synthesis rates, with differing nutritional support, are predictive of longer-term traininginduced muscle hypertrophy. Here, we aimed to test whether the same was true with acute exercise-mediated changes in muscle protein synthesis. Eighteen men (21 ± 1 yr, 22.6 ± 2.1 kg/m 2; means ± SE) had their legs randomly assigned to two of three training conditions that differed in contraction intensity [% of maximal strength (1 repetition maximum)] or contraction volume (1 or 3 sets of repetitions): 30%-3, 80%-1, and 80%-3. Subjects trained each leg with their assigned regime for a period of 10 wk, 3 times/wk. We made pre- and posttraining measures of strength, muscle volume by magnetic resonance (MR) scans, as well as pre- and posttraining biopsies of the vastus lateralis, and a single postexercise (1 h) biopsy following the first bout of exercise, to measure signaling proteins. Training-induced increases in MR-measured muscle volume were significant (P 0.01), with no difference between groups: 30%-3 = 6.8 ± 1.8%, 80%-1 = 3.2 ± 0.8%, and 80%-3= 7.2 ± 1.9%, P = 0.18. Isotonic maximal strength gains were not different between 80%-1 and 80%-3, but were greater than 30%-3 (P = 0.04), whereas training-induced isometric strength gains were significant but not different between conditions (P 0.92). Biopsies taken 1 h following the initial resistance exercise bout showed increased phosphorylation (P 0.05) of p70S6K only in the 80%-1 and 80%-3 conditions. There was no correlation between phosphorylation of any signaling protein and hypertrophy. In accordance with our previous acute measurements of muscle protein synthetic rates a lower load lifted to failure resulted in similar hypertrophy as a heavy load lifted to failure.
机译:我们已经报道,运动后肌肉蛋白质合成速率的急性增加,具有不同的营养支持,可以预测长期训练引起的肌肉肥大。在这里,我们旨在测试急性运动介导的肌肉蛋白质合成变化是否同样如此。 18名男性(21±1岁,22.6±2.1 kg / m 2;均值±SE)将他们的腿随机分配到三种训练条件中的两种中,其中两种训练条件的收缩强度[最大力量的百分比(最大1次重复)]或收缩量不同(1或3组重复):30%-3、80%-1和80%-3。受试者以其指定的方案训练每条腿,为期10周,每周3次。我们通过磁共振(MR)扫描对力量,肌肉体积进行了训练前和训练后的测量,以及股外侧肌的训练前和训练后的活检,以及在首次运动后进行了一次运动后(1 h)的活检,测量信号蛋白。训练导致的MR测量的肌肉体积显着增加(P <0.01),两组之间无差异:30%-3 = 6.8±1.8%,80%-1 = 3.2±0.8%和80%-3 = 7.2±1.9%,P = 0.18。等渗最大强度增加在80%-1和80%-3之间没有差异,但大于30%-3(P = 0.04),而训练引起的等距强度增加显着,但在不同情况下无差异(P <0.92 )。最初的抗性锻炼后1小时进行的活检显示,仅在80%-1和80%-3的条件下,p70S6K的磷酸化增强(P <0.05)。任何信号蛋白的磷酸化与肥大之间均无相关性。根据我们先前对肌肉蛋白质合成率的急性测量,较低的负荷解除失败会导致与肥大相似的肥大。

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