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首页> 外文学位 >Skeletal muscle eukaryotic elongation factor 2 (eEF2) response to acute resistance exercise in young and old men and women: Relationship to muscle glycogen content and 5'-AMP-activated protein kinase (AMPK) activity.
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Skeletal muscle eukaryotic elongation factor 2 (eEF2) response to acute resistance exercise in young and old men and women: Relationship to muscle glycogen content and 5'-AMP-activated protein kinase (AMPK) activity.

机译：骨骼肌真核伸长因子2（eEF2）对男女青年急性抵抗运动的反应：与肌肉糖原含量和5'-AMP激活的蛋白激酶（AMPK）活性的关系。

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摘要

Sarcopenia is associated with an age-related decrease in skeletal muscle mass, which can result in decreases in strength and physical functioning in the older population. Resistance training interventions are not completely effective in stimulating muscle protein synthesis in aged muscle and thus do not completely combat age-related atrophy. Phosphorylation (and thus theoretically activation) of the energy-sensing molecule 5'-AMP-activated protein kinase (AMPK, known to inhibit the muscle protein synthesis pathway) has been shown to be elevated for up to three hours in response to a resistance training bout in the muscles of older, but not younger individuals. Data in rats indicate that, in response to muscle contractions, elevated AMPK activity can accentuate the inhibitory phosphorylation (and thus deactivation) of its downstream intermediate, eukaryotic elongation factor 2 (eEF2, which normally stimulates protein translation and synthesis). AMPK activity is inhibited by high muscle glycogen levels. Interestingly, older individuals exhibit a lower muscle glycogen content compared to younger individuals, which may account for the greater AMPK phosphorylation response to resistance exercise in older individuals. The relationship between muscle glycogen content, AMPK activity, and eEF2 phosphorylation in response to an acute bout of resistance exercise has not yet been examined in young or old individuals. We hypothesized that inhibitory eEF2 phosphorylation would be higher in response to an acute resistance exercise bout in the skeletal muscles of older versus younger individuals. We further hypothesized that this higher eEF2 phosphorylation response would be related to a higher AMPK activation, and that higher AMPK activation would be related to lower glycogen content, in the skeletal muscles of older versus younger individuals. Seven young (21.7 +/- 0.8 yrs) and 10 old (67.0 +/- 2.6 yrs) untrained but physically active men and women performed 3 sets of leg extensions at a 10-repetition maximum resistance until failure after an overnight fast. Muscle biopsies were obtained from the vastus lateralis pre-exercise (PRE), immediately post exercise (0P), 1-hour post exercise (1P), and 2-hours post exercise (2P). Glycogen content was measured in muscle samples, as were the phosphorylations, by western blot, of AMPK (Thr172), acetyl-CoA carboxylase (ACC, a marker of in vivo AMPK activity) (Ser79), and eEF2 (Thr56). Muscle glycogen content was significantly lower in the old vs. young subjects at the PRE time point and decreased in response to exercise in both age groups; however, glycogen content decreased to a greater degree in young subjects such that it was equal between young and old at all post-exercise timepoints. As expected, AMPK phosphorylation was significantly increased in the old subjects immediately post exercise, but no such response was noted in the young. However, no age-related differences were observed in AMPK activity as measured by ACC phosphorylation, which was significantly elevated at 0P and 1P in both age groups. Similarly, the eEF2 phosphorylation response (elevated vs. PRE at 0P and decreased vs. PRE at 1P and 2P in both age groups) was also not affected by age. Regardless of age, higher muscle glycogen content was associated with lower AMPK activity (as assessed by phospho-ACC content) at 0P and 1P, and this lower AMPK activity was associated with lower inhibitory phosphorylation of eEF2 at those same timepoints. These findings indicate the possibility that higher muscle glycogen content may result in lower AMPK activation and consequently lower inhibitory eEF2 phosphorylation in response to a resistance training session in the muscles of both younger and older individuals, thereby potentially enabling greater translation elongation, protein synthesis, and muscle growth regardless of age.
机译：肌肉减少症与年龄相关的骨骼肌质量下降有关，这可能导致老年人口力量和身体机能下降。阻力训练干预措施不能完全有效地刺激老年肌肉的肌肉蛋白质合成，因此不能完全对抗与年龄有关的萎缩。能量敏感分子5'-AMP激活的蛋白激酶（AMPK，已知抑制肌肉蛋白合成途径）的磷酸化作用（因此理论上被激活）已被证明在抵抗训练中可升高多达三个小时在较老但较年轻的人的肌肉中运动。大鼠的数据表明，响应肌肉收缩，AMPK活性升高可加剧其下游中间体真核生物延伸因子2（eEF2，通常刺激蛋白质翻译和合成）的抑制性磷酸化作用（并因此使其失活）。 AMPK活性受到肌肉糖原水平高的抑制。有趣的是，与年轻个体相比，老年个体表现出较低的肌肉糖原含量，这可能解释了老年个体对抵抗运动的更大的AMPK磷酸化反应。尚未在年轻或老年人中检查肌肉糖原含量，AMPK活性和eEF2磷酸化对急性抵抗运动的反应之间的关系。我们假设抑制eEF2的磷酸化会响应于老年人与年轻人的骨骼肌中的急性抵抗性运动而更高。我们进一步假设，较高的eEF2磷酸化反应将与较高的AMPK激活有关，而较高的AMPK激活将与较低个体的骨骼肌中较低的糖原含量有关。七名年轻（21.7 +/- 0.8岁）和10岁（67.0 +/- 2.6岁）未经训练但身体活跃的男性和女性以10次重复的最大阻力进行了三组腿伸，直到过夜禁食后失败。从运动前的股外侧肌（PRE），运动后立即（0P），运动后1小时（1P）和运动后2小时（2P）获得肌肉活检。肌肉样品中的糖原含量以及AMPK（Thr172），乙酰辅酶A羧化酶（ACC，体内AMPK活性的标志物）（Ser79）和eEF2（Thr56）的磷酸化通过蛋白质印迹法进行了测量。在PRE时间点，老年受试者的肌肉糖原含量显着降低，而青年受试者的肌肉糖原含量降低。然而，年轻受试者中的糖原含量降低的程度更大，以至于在运动后的所有时间点，年轻人与老人之间的糖原含量均相等。正如预期的那样，运动后立即出现的老年受试者中AMPK磷酸化显着增加，但在年轻受试者中未发现这种反应。但是，通过ACC磷酸化检测到的AMPK活性未发现与年龄相关的差异，这两个年龄组的0P和1P均显着升高。同样，两个年龄组的eEF2磷酸化反应（在0P时相对于PRE升高，在1P和2P时相对于PRE降低）也不受年龄影响。无论年龄大小，在0P和1P时较高的肌肉糖原含量与较低的AMPK活性（通过磷酸ACC含量评估）相关，而在相同的时间点，较低的AMPK活性与eEF2的抑制性磷酸化较低相关。这些发现表明，较高的肌肉糖原含量可能会导致较低的AMPK活化并因此降低较低的抑制性eEF2磷酸化，这可能是对年轻人和老年人的肌肉进行抵抗训练所致，从而有可能实现更大的翻译延伸，蛋白质合成和肌肉生长，不分年龄。

著录项

  • 作者

    Macesich, Jennifer Lea.;

  • 作者单位

    East Carolina University.;

  • 授予单位 East Carolina University.;
  • 学科 Health Sciences Recreation.
  • 学位 M.S.
  • 年度 2010
  • 页码 115 p.
  • 总页数 115
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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