Blood flow restriction in human skeletal muscle during rest periods after high-load resistance training down-regulates miR-206 and induces Pax7.

Blood flow restriction in human skeletal muscle during rest periods after high-load resistance training down-regulates miR-206 and induces Pax7.
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高载阻力训练后的休息期间,人类骨骼肌的血流限制下调了miR-206并诱导PAX7。

DOI:
10.1016/j.jshs.2019.08.004
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发表时间:
2021-07
影响因子:
11.7
通讯作者:
Radak Z
Radak Z
中科院分区:
医学1区
文献类型:
--
作者:
Torma F;Gombos Z;Fridvalszki M;Langmar G;Tarcza Z;Merkely B;Naito H;Ichinoseki-Sekine N;Takeda M;Murlasits Z;Osvath P;Radak Z

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高强度负荷运动静息期血流受限增加Pax 7表达。与对照相比,血流限制腿中的miR-206水平显著降低。从Ku 70信使RNA水平的增加来判断,血流限制会导致DNA损伤。低强度阻力训练的血流限制(BFR)已被证明会导致骨骼肌肥大。在这项研究中,我们测试了这一假设,即在急性高强度抗阻训练课程之间的休息期间的BFR(70%的1次重复最大值,7组10次重复)增强了抗阻训练的效果。共有7名健康的年轻男性进行蹲下,并在一条腿上进行BFR,而另一条腿作为对照组。由于BFR是在休息期间施加的,即使是几乎完全阻断血流的严重闭塞压力(约230 mmHg),参与者也能耐受良好。从急性训练后2小时采集的活检样品中测量了五种肌肉特异性microRNA。多普勒数据显示,血流恢复的模式在第一次和最后一次BFR之间发生了显着变化。与对照组相比,BFR腿中的microRNA-206水平显著降低。BFR腿中RAC-β丝氨酸/苏氨酸蛋白激酶v22、核呼吸因子1、血管内皮生长因子、狼疮Ku自身抗原蛋白p70基因(p < 0.05)和配对盒7(p < 0.01)的mRNA水平增加。BFR腿和对照腿之间配对盒7、核呼吸因子1和过氧化物酶体增殖物激活受体γ共激活因子1α的蛋白水平没有差异。在高负荷抗阻训练的休息期间,BFR可导致调节血管生成、线粒体生物合成以及肌肉肥大和修复的那些蛋白质的mRNA升高。然而,BFR也可以引起DNA损伤,从狼疮Ku自身抗原蛋白p70的mRNA水平的增加来判断。
Blood flow restriction at resting periods of high-intensity load exercise increases Pax7 expression. miR-206 levels significantly decreased in the blood flow restriction leg compared to the control. Blood flow restriction can cause DNA damage, judging from the increase in messenger RNA levels of Ku70. Blood flow restriction (BFR) with low-intensity resistance training has been shown to result in hypertrophy of skeletal muscle. In this study, we tested the hypothesis that BFR during the rest periods between acute, high-intensity resistance exercise sessions (70% of 1 repetition maximum, 7 sets with 10 repetitions) enhances the effects of the resistance training. A total of 7 healthy young men performed squats, and between sets BFR was carried out on one leg while the other leg served as a control. Because BFR was applied during rest periods, even severe occlusion pressure (approximately 230 mmHg), which almost completely blocked blood flow, was well-tolerated by the participants. Five muscle-specific microRNAs were measured from the biopsy samples, which were taken 2 h after the acute training. Doppler data showed that the pattern of blood flow recovery changed significantly between the first and last BFR. microRNA-206 levels significantly decreased in the BFR leg compared to the control. The mRNA levels of RAC-β serine/threonine-protein kinase v22, nuclear respiratory factor 1, vascular endothelial growth factor, lupus Ku autoantigen protein p70 genes (p < 0.05), and paired box 7 (p < 0.01) increased in the BFR leg. The protein levels of paired box 7, nuclear respiratory factor 1, and peroxisome proliferator-activated receptor γ coactivator 1α did not differ between the BFR leg and the control leg. BFR, during the rest periods of high-load resistance training, could lead to mRNA elevation of those proteins that regulate angiogenesis, mitochondrial biogenesis, and muscle hypertrophy and repair. However, BFR also can cause DNA damage, judging from the increase in mRNA levels of lupus Ku autoantigen protein p70.
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