摘要
目的:探讨有氧训练对机体运动热应激下免疫机能与自由基代谢的影响及其可能机制。方法:健康雄性SD大鼠51只,随机选取45只分为对照组(A组)、热应激组(B组)、6周有氧训练组(C组)1、次有氧运动加热应激组(D组)与6周有氧训练末次加热应激组(E组),其余6只用于乳酸阈强度的测定。各组实验后取血清测定IL-2、SOD、MDA水平。结果:(1)B、D、E组经高温暴露后,大鼠肛温迅速升至39.65±0.25℃、41.02±0.14℃与39.97±0.29℃,均表现出呼吸急促、流汗、烦躁不安等,为典型的热应激症候。(2)B组血清IL-2、SOD、SOD/MDA均显著低于A组,MDA高于A组;D组血清IL-2、SOD、SOD/MDA均显著低于A组(P<0.01)与B组(P<0.05),MDA显著高于A组(P<0.01)与B组(P<0.05)。(3)C组血清IL-2、SOD(P<0.05)、SOD/MDA(P<0.05)高于A组,MDA显著低于A组;E组血清IL-2、SOD(P<0.05)、SOD/MDA(P<0.05)均高于D组,MDA显著低于D组。结论:运动热应激可导致自由基生成增多,加重组织细胞膜结构与功能的损害,导致温度调节的信号通路中断,体温失衡,可能通过调节神经—内分泌—免疫系统,抑制IL-2的分泌。IL-2可作为评价机体运动热应激下免疫机能变化的重要指标。有氧训练可拮抗运动热应激对免疫系统的损害。
Objective： To investigate influences of aerobic exercise training on body immune function and free radical metabolism under heat stress and its pos- sible mechanism. Mcthods： 45 of 51 healthy male SD rats were randomly selected and divided into control group （group A）,heat stress group （group B）,6 weeks of aerobic training group （group C） ,a bout of aerobic exercise and heat stress group （group D） and 6 weeks of aerobic training and heat stress group （ group E）, and the remaining six for the determination of lactate threshold intensity. IL - 2, SOD, MDA levels of each group were measured in serum obtained after experiment. Results： （ 1 ） after high temperature exposure, in group B, D, E rat rectal temperature rapidly to 39.65 ± 0.25 ℃,41.02 ± 0.14℃ and 39. 97± 0.29℃ respectively ,with rapid breathing, sweating, irritability, etc., which are typical symptoms of heat stress. （2） levels of serum IL- 2, SOD, SOD/MDA in group B were significantly lower than that in group A,MDA was higher than that in group A; D senan levels of IL- 2,SOD,SOD/MDA were significantly lower than that in group A （ P 〈 0.01 ） and gronp B （ P 〈 0.05）, MDA was significantly higher than that in group A （ P 〈 0.01 ） and group B （ P 〈 0.05 ）. （3） In group C, serum levds of IL - 2, SOD （ P 〈 0.05）, SOD/MDA （ P 〈 0.05 ） were higher than that in group A, MDA was significantly lower than that in group A; In group E, serum levels of IL - 2, SOD （ P 〈0. 05 ）, SOD/MDA （ P 〈 0.05） were higher than that in group D, MDA was sig- nificantly Lower than that in group D. Conclusion： Exercise heat stress may cause mare free radicals, and increase damage of cell membrane structure and function of tisme, leading to interruption of the signaling pathways re4gulating the temperature, and imbalance of temperature, Possibly through regulation of nerve - endocrine - immune function and inhibition of IL - 2 secretion. IL - 2 can be used as an inmportant indicator of immune
出处
《吉林体育学院学报》
2011年第6期1-4,共4页
Journal of Jilin Sport University
基金
江苏省高校自然科学基础研究项目(08KJB340001)
