Mechanisms of exercise-induced muscular hypertrophy : A study with venous-occlusion models.

运动引起的肌肉肥大的机制：静脉闭塞模型的研究。

• 批准号: 16300207
• 负责人: ISHII Naokata
• 金额: $ 9.66万
• 依托单位: The University of Tokyo
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (B)
• 财政年份: 2004
• 资助国家: 日本
• 起止时间: 2004 至 2005
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-16300207/
• 关键词: Resistance training; Muscle hypertrophy; Vascular occlusion; Exercise intensity; Muscle oxygenation; DNA microarray; Growth factors; Muscle satellite cells; 運動・トレーニング; myostatin; follistatin; caveolin; 遺伝子発現; 熱ショックタンパク質

We have previously shown that low-intensity resistance training cause increases in muscular size and strength when combined with moderate vascular occlusion. Elucidating its mechanism likely contributes not only to understand the common mechanisms of exercise-induced muscular hypertrophy but also to develop new exercise methods with much reduced mechanical stress. For this purpose, we developed two types of exercise model (animal and human models). In the animal model, major veins from hindlimb muscles of the rats were surgically crush-occluded with a heated metal needle. The chronic restriction of venous blood flow for 2 weeks caused in hindlimb muscles increases in wet and dry weights and total protein content, except for the soleus muscle. In the plantaris muscle, muscle fibers of all types (types I, IIa and IIb/x) showed an increase in their cross-sectional area (CSA). In addition, transitions of muscle-fiber types directed towards faster subtypes were observed to occur. The concen … More trations of glycogen, lactate, nitric oxide (NO), HSP-72 and active form of hepatocyte growth factor (HGF) increased, whereas that of myostatin decreased. Expressions of NOS-1 increased, whereas that of IGF-I tended to increase without significance. In the human model, low-intensity resistance exercise for knee extensor muscles (30% of one-repetition maximum) was performed twice daily for 2 weeks. Even with such short period of training, increases in muscle cross-sectional area (by〜10%) and strength occurred, and analyses for biopsy samples (v.lateralis) were made in a well-matched condition. Both type I and II fibers showed hypertrophy, though type II fibers tended to show a larger increase in CSA. DNA microarray analysis showed that expressions of IGF-I/II, follistain-like peptide, caveolin and extracellular matrix-related proteins increased, whereas that of myostatin considerably decreased. The results suggest that reduced oxygen delivery during exercise plays an important part and affects the factors relating to the proliferation of muscle satellite cells. Less

我们之前的研究表明，低强度的阻力训练与适度的血管闭塞相结合，会导致肌肉大小和力量的增加。阐明其机制可能不仅有助于了解运动诱导肌肉肥大的常见机制，而且有助于开发机械应力大大降低的新运动方法。为此，我们开发了两种运动模型（动物模型和人体模型）。在动物模型中，用加热的金属针手术阻断大鼠后肢肌肉的大静脉。慢性静脉血流量限制2周后，除比目鱼肌外，后肢肌肉干、湿重及总蛋白含量均增加。在足底肌中，所有类型的肌纤维（I型、IIa型和IIb/x型）的横截面积（CSA）均增加。此外，观察到肌肉纤维类型向更快亚型的转变。糖原、乳酸、一氧化氮（NO）、热休克蛋白-72和肝细胞生长因子（HGF）活性形式的浓度升高，而肌肉生长抑制素的浓度降低。NOS-1表达升高，igf -1表达有升高趋势，但无显著性。在人体模型中，膝关节伸肌的低强度阻力运动（一次重复最大值的30%）每天进行两次，持续2周。即使在如此短的训练时间内，肌肉横截面积（约10%）和力量也有所增加，并且在良好匹配的条件下对活检样本（侧支静脉）进行了分析。I型和II型纤维均表现为肥大，但II型纤维的CSA增加幅度较大。DNA芯片分析显示，IGF-I/II、卵泡素样肽、小窝蛋白和细胞外基质相关蛋白的表达增加，而肌生长抑制素的表达明显减少。结果表明，运动过程中氧气输送的减少起着重要作用，并影响与肌肉卫星细胞增殖有关的因素。少