低氧运动对SD大鼠骨骼肌超微结构与LPO水平的影响
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摘要
目的:探讨低氧运动对SD大鼠骨骼肌肌纤维结构与脂质过氧化(LPO)水平的影响。方法:对三组SD大鼠分别采取常氧训练、急性低氧运动和间歇低氧训练,采用透射电镜观察大鼠骨骼肌肌纤维超微结构的变化,并采用荧光法分析骨骼肌中细胞液和线粒体的脂质过氧化水平。结果:急性低氧环境无论安静、运动或训练均可造成骨骼肌超微结构的损伤,运动时较安静时明显;经过4wk的慢性间歇低氧训练后观察未见明显损伤,在4wk的慢性间歇性低氧训练后再进行安静状态急性低氧应激,骨骼肌的损伤减轻。急性低氧组LPO水平增高,而持续低氧训练可降低LPO水平。结论:急性低氧环境可导致应激反应和直接损伤骨骼肌,4wk的慢性间歇低氧训练可减轻低氧环境对骨骼肌的损伤。
objective:To investigate the effect of hypoxia exercise on the peroxidation of SD rat skeletal muscle fiber structure and lipid(LPO)level influence.Method:Normoxic training are adopted,acute hypoxia and intermittent hypoxia training on three groups of SD rats,to observe the ultrastructural changes of skeletal muscle fiber in rats by transmission electron microscopy,and analysis of liquid lipid cells and mitochondria in skeletal muscle peroxidation level by fluorescence method.Results:Acute hypoxia environment can cause the damage of ultrastructure of skeletal muscle injury regardless of quiet,exercise or training,movement is more obvious than quiet;there is no significant injury after 4wk of chronic intermittent hypoxia training;the injury of skeletal muscle relieves with the 4WK of chronic intermittent hypoxia training after the quiet state of acute hypoxia stress.While LPO level of acute hypoxia group increases,continuous hypoxia training can reduce the level of LPO.Conclusion:Acute hypoxia environment can result in stress reaction and direct muscle injury,4wk chronic intermittent hypoxia training can alleviate the injury of skeletal muscle caused by the hypoxia environment.
objective:To investigate the effect of hypoxia exercise on the peroxidation of SD rat skeletal muscle fiber structure and lipid(LPO)level influence.Method:Normoxic training are adopted,acute hypoxia and intermittent hypoxia training on three groups of SD rats,to observe the ultrastructural changes of skeletal muscle fiber in rats by transmission electron microscopy,and analysis of liquid lipid cells and mitochondria in skeletal muscle peroxidation level by fluorescence method.Results:Acute hypoxia environment can cause the damage of ultrastructure of skeletal muscle injury regardless of quiet,exercise or training,movement is more obvious than quiet;there is no significant injury after 4wk of chronic intermittent hypoxia training;the injury of skeletal muscle relieves with the 4WK of chronic intermittent hypoxia training after the quiet state of acute hypoxia stress.While LPO level of acute hypoxia group increases,continuous hypoxia training can reduce the level of LPO.Conclusion:Acute hypoxia environment can result in stress reaction and direct muscle injury,4wk chronic intermittent hypoxia training can alleviate the injury of skeletal muscle caused by the hypoxia environment.
引文
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[12]魏优秀,雷晓妮,刘平,等.间歇运动对老龄小鼠骨骼肌组织自由基代谢的影响[J].中国老年学杂志,2009,29(22):2895—2896.
[13]Marjolein V,Bret H G,Stephen B K,et al.Muscle mass,muscle strength,and muscle fat infiltration as predictors of incident mobility limitations in Well-functioning older persons[J].Journal of Gerontology,2005,60A(3):324—333.
[14]Wim Derave,Bert O E,Monique R,et al.Soleus muscles of SAMP-8mice provide an accelerated model of skeletal muscle senescence[J].Experimental Gerontology,2005,40(1):562—572.
[15]Kim Jeong-Su,Jacob M W,Lee Sang-Rok.Dietary implications on mechanisms of sarcopenia:roles of protein,amino acids and antioxidants[J].The Journal of Nutritional Biochemistry,2010,21(1):1—13.
[2]YJPeng,NRP rabhakar.Effect of twoparad i gms of chronic intermittent hypoxia on carotid body sensorya ctivity[J].J App Physiol,2004,96(3):1236—1242.
[3]Costa LE,Boveris A,Koch OR,at al.Liver and heart mitochondria in rats submitted to chronic hypobaric hypoxia.Am J Physiol[J].1988,255(1Pt 1):C123—129.
[4]Lochner A,Kotze JC,Gevers W.Mitochondrial oxidative phosphorylation in myocardial anoxia:effects of albumin[J].J Mol Cell Cardiol,1976,8(6):465—480.
[5]N Terrados,E Jansson,C Sylvén,et al.Is hypoxia a stimulus for synthesis of oxidative enzyme and myoglobin[J].J Appl Physiol,1990,68(6):2369—2372.
[6]蒋明朗.间歇性低氧训练对小鼠自由基代谢的影响[D].西安体育学院,2000.
[7]Usher-Smith J A,X u W,Fraser JA,et.al.Alterations in calcium homeostasis reduce member ane excitability in amphibian skeletal muscle[J].European Journal of Physiology,2006,453(2):211—221.
[8]赵鹏,路瑛丽,冯连世,等.低氧训练对葡萄糖转运与利用能力的影响[J].体育科学,2008,28(7):51—60.
[9]黄丽英,林文,翁锡全.高住低练对大鼠心肌线粒体活性氧的影响[J].中国运动医学杂志,2005,24(6):665—667.
[10]冯连世.高原训练与低氧训练[J].体育科学,2005,25(11):2.
[11]刘晓莉,侯莉娟,刘斌贝,等.间歇性无氧运动对小鼠脑、心肌、骨骼肌抗氧化能力及脂质过氧化损伤的影响[J].中国运动医学杂志,2004,23(4):390—394.
[12]魏优秀,雷晓妮,刘平,等.间歇运动对老龄小鼠骨骼肌组织自由基代谢的影响[J].中国老年学杂志,2009,29(22):2895—2896.
[13]Marjolein V,Bret H G,Stephen B K,et al.Muscle mass,muscle strength,and muscle fat infiltration as predictors of incident mobility limitations in Well-functioning older persons[J].Journal of Gerontology,2005,60A(3):324—333.
[14]Wim Derave,Bert O E,Monique R,et al.Soleus muscles of SAMP-8mice provide an accelerated model of skeletal muscle senescence[J].Experimental Gerontology,2005,40(1):562—572.
[15]Kim Jeong-Su,Jacob M W,Lee Sang-Rok.Dietary implications on mechanisms of sarcopenia:roles of protein,amino acids and antioxidants[J].The Journal of Nutritional Biochemistry,2010,21(1):1—13.