加压力量训练的研究评述
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  • 英文篇名:Review on the Effect of KAATUS Training
  • 作者:彭一腾 ; 黄骅
  • 英文作者:Peng Yiteng;Huang Hua;Haibin College, Beijing Jiaotong University;
  • 关键词:加压力量训练 ; 低强度阻力训练 ; 肌肉适能
  • 英文关键词:KAATUS training;;Low intensity resistance training;;Muscle fitness
  • 中文刊名:GXNB
  • 英文刊名:Genomics and Applied Biology
  • 机构:北京交通大学海滨学院;
  • 出版日期:2018-12-25
  • 出版单位:基因组学与应用生物学
  • 年:2018
  • 期:v.37
  • 基金:北京交通大学海滨学院资助
  • 语种:中文;
  • 页:GXNB201812080
  • 页数:16
  • CN:12
  • ISSN:45-1369/Q
  • 分类号:478-493
摘要
加压力量训练是指在加压限制或短时间断性阻断静脉血流量的情况下,以较小的练习强度刺激肌肉生长、改善肌肉功能的训练方法。为探讨加压力量训练促进肌肉肥大、肌肉量增加的可能机制,本研究通过研究加压力量训练对肌肉适能即时性、短期、中长期影响以及该影响的生理机制,发现加压力量训练可显著刺激体内性激素合成与代谢压力提升,产生加剧性反应,对加速肌肉蛋白合成有良好效果;6 d至16周的加压力量训练均有助于MVC、1RM及CSA的提升,效果与高强度阻力训练类似。训练的强度在20%~50%1RM、加压压力在50~250 mmHg范围内,可适用于大部分的人群。加压力量训练生理机制尚不十分明确,可能的途径包括:肌肉在缺血状态下招募更多Ⅱ型肌纤维,并增加代谢压力物质,进而刺激GH的释放;mTOR路径的活化与泛素-蛋白水解酶复合通路的抑制;热激蛋白与神经性一氧化氮合成酶-1活性的增加;肌肉生成抑制素浓度降低与肌肉干细胞数量增加等。
        KAATUS training is a training method to simulate muscle growth and improve muscle function with a relative small amount of exercise intensity in the case of pressure limitation or short-term interruption of venous blood flow. To explore the possible mechanisms for KAATSU training to promote muscle hypertrophy and increase in muscle mass, in the study, the real-term, short-term, medium and long-term influences of KAATUS training on muscle fitness, as well as its physiological mechanism were analyzed. We could draw the following conclusions: KAATUS training could significantly stimulate the synthesis of sexhormone and the promotion of metabolic stress, resulting in intensified reaction which would have a good effect on accelerating the synthesis of intramuscular protein. KAATUS training in 6 days to 16 weeks could help promoting MVC, 1 RM and CSA, and the effect resembled the effect of high intensity resistance training. The intensity of training was between 20%~50% 1 RM, and the intensity of pressure was between 50~250 mm Hg, which could be applied to most of the people. The physiological mechanism of KAATUS training remained unclear. There were several possible pathways, including additional recruitment of type II fibers in a ischemia condition; the increase in intramuscular metabolic stress substances so as to stimulate GH release; activation of mTOR pathway and inhibition of the ubiquitin-proteolytic enzyme complex pathway; increased activity of heat shock proteins and Nitric oxide synthase-1, as well as the decreased myostatin concentration and increased number of muscle stem cells.
引文
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