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高强度力量训练对青年男性淋巴细胞凋亡的影响及其机制研究

时间:2022-04-14 08:21:30 浏览次数:


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摘 要: 目的:观察高强度力量训练(HST)或中等强度力量训练(MST)对淋巴细胞凋亡的影响并探讨其可能机制。方法:20名青年男性分别进行一次急性HST和MST,分别于训练前、训练后即刻、训练后3 h以及训练后24 h取静脉血测定淋巴细胞凋亡率、线粒体膜电位(MMP)、CD95受体、Bcl-2蛋白表达以及血清肿瘤坏死因子α(TNF-α)、白细胞介素6(IL-6)、C-反应蛋白(CRP)和皮质醇含量。将新鲜淋巴细胞与HST前的血清、HST后3 h的血清、米非司酮(MIF,糖皮质激素受体阻断剂)預处理的HST后3 h血清以及单独加入介质(分别为L-乳酸、rIL-6、rCRP和皮质醇)的培养基共培养24 h,用流式细胞仪检测淋巴细胞凋亡率。结果:HST后3 h 淋巴细胞凋亡率、CD95受体、血清IL-6、CRP和皮质醇升高(P<0.05),MMP和Bcl-2蛋白表达降低(P<0.05),24 h时除Bcl-2蛋白仍低于训练前(P<0.05)外,上述其他各指标均恢复至训练前水平(P>0.05)。HST后3 h血清皮质醇含量与淋巴细胞凋亡率显著正相关(r=0.69,P<0.05)。MST后所有指标均无显著性变化(P>0.05)。HST后3 h血清与淋巴细胞共培养后细胞凋亡率明显高于训练前血清(P<0.05)。将淋巴细胞与单一血清介质进行共培养,其中L-乳酸、rIL-6和rCRP对淋巴细胞凋亡率均无显著性影响(P>0.05),皮质醇则明显提高淋巴细胞凋亡率(P<0.05),在训练后3 h血清中加入MIF则显著降低淋巴细胞凋亡率(P<0.05)。结论:力量训练诱导淋巴细胞凋亡存在运动强度依赖性,皮质醇经由糖皮质激素受体介导的信号转导通路可能参与了高强度力量训练诱导淋巴细胞凋亡的过程。

关键词: 力量训练;淋巴细胞;凋亡;机制

中图分类号:G804.2   文献标识码:A  文章编号:1006-2076(2018)06-0091-08

Abstract: Objective: To observe effects of high-intensity strength training (HST) and moderate-intensity strength training (MST) on lymphocyte apoptosis in jnvenile males and investigate the possible mechanism. Methods: 20 jnvenile males performed a bout of acute HST and MST, apoptotic rate of lymphocytes, mitochondrial membrane potential (MMP), CD95 receptor, Bcl-2 protein as well as serum tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), C-reaction protein (CRP) [JP+1]and cortisol content were measured in venous blood before training, immediate after training, 3 h and 24 h after training respectively. Freshly isolated lymphocytes and serum of pre-HST, serum of 3 h after HST, mifepristone (MIF, glucocorticoid receptor blocking pharmacon) preconditioning of 3 h after HST, medium of selected serum parameters (L-lactic acid, rIL-6, rCRP and cortisol) incubated for 24 h and apoptotic rate of lymphocytes was determined by flow cytometer. Results:Apoptotic rate of lymphocytes, CD95 receptor, serum IL-6, CRP and cortisol increased (P<0.05), MMP and Bcl-2 protein expression decreased (P<0.05) 3 h after HST, all indexes above except lowered Bcl-2 protein recovered to pre-training level (P>0.05) 24 h after HST. A significant positive correlation was observed between the increase of apoptosis and cortisol levels (r=0.69, P<0.05) 3 h after HST. There was no significant change of all indicators after MST (P>0.05). Incubation of in serum 3 h after HST indicated an increase apoptotic rate of lymphocytes than serum of pre-training (P<0.05). Selective incubation of lymphocytes in concentrations of selected serum parameters corresponding to levels found post in HST serum demonstrated that L-lactic acid, rIL-6 and rCRP had no effects on apoptotic rate of lymphocytes (P>0.05), while cortisol raised apoptosis (P<0.05). This result was confirmed by attenutation of apoptosis after addition of MIF before incubation in serum 3 h after HST (P<0.05). Conclusion:Strength exercise induced lymphocyte apoptosis in an intensity-dependent way. Cortisol signaling via glucocorticoid receptors might be an important mechanism for lymphocyte apoptosis after strength exercise.

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