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1.
支链氨基酸对运动力竭大鼠心肌损伤的保护作用   总被引:5,自引:0,他引:5  
以大鼠力竭运动为模型,研究了支链氨基酸(BCAA)对血清和心肌中乳酸脱氢酶(LDH),谷草转氨酶(GOT),肌酸激酶(CK),α-羟丁酸脱氢酶(α-HBDH)等酶的活性以及心肌中Ca2 ,Mg2 含量的影响。结果发现:力竭运动可造成大鼠血清和心肌中LDH,GOT,CK,α-HBDH 等酶的活性显著升高,心肌中Ca2 含量也显著升高,Mg2 含量显著下降。补充BCAA 可使大鼠力竭运动后血清和心肌中LDH,GOT,CK,α-HBDH 等酶的活性显著降低,心肌中Ca2 含量显著下降。提示,BCAA 可抑制大鼠力竭运动后血清和心肌中LDH,GOT,CK,α-HBDH 等酶的活力显著升高和心肌中钙超载。说明BCAA 有减少力竭运动后心肌损伤和维持心肌正常功能的作用。  相似文献   

2.
为了解耐力训练对大鼠心肌组织抗氧化防御系统SOD同工酶活性和mRNA表达的变化,运用分光光度法对6周耐力训练及一次性定量负荷运动后大鼠心肌组织主要抗氧化酶活性检测,并用RT-PCR法检测SOD同工酶mRNA表达。结果显示:耐力训练及一次性定量负荷运动大鼠心肌MDA水平显著下降(P<0.05),T-AOC显著升高(P<0.05),Cu Zn-SOD mRNA、Mn-SODmRNA表达增加,SOD活性和Cu Zn-SOD活性明显升高(P<0.05)。结论:耐力训练激活了心肌SOD同工酶mRNA表达,进而引起SOD活性和总抗氧化能力的提高,增强了机体清除自由基的能力,有效地起到氧化预适应的作用;耐力训练后再进行一次性定量负荷运动时,机体抗氧化能力明显提高,清除自由基的能力增强,减少了自由基对机体的损伤,提高机体抗运动疲劳能力。  相似文献   

3.
力竭运动造成心肌损伤的机制探讨   总被引:5,自引:0,他引:5  
目的探讨力竭运动造成心肌损伤的机制.方法以力竭运动为模型,观察了力竭运动后大鼠血清和心肌中四碘甲腺原氨酸(T4)、三碘甲腺原氨酸(T3)及心肌中T45′-脱单碘酶(T45′-DI)活性、环磷酸腺苷(cAMP)和环磷酸鸟苷(cGMP)含量的变化.结果力竭运动后血清和心肌中T3水平显著升高(P<0.01),T4水平无显著性改变,心肌中T45′-DI活力显著升高(P<0.01),心肌中cAMP和cGMP含量均显著升高(P<0.01).结论力竭运动引起甲状腺激素代谢的改变和心肌中第2信使含量的升高是造成心肌损伤的原因之一.  相似文献   

4.
目的:明确大负荷运动引起的心肌损伤基本特征,探讨运动预处理(EP)对其保护作用及作用机制。方法:成年雄性SD大鼠64只,随机分为安静对照组(AB组)、运动预处理对照组(AC组)、单纯大负荷运动组(B组)、运动预处理+大负荷运动组(C组);根据大负荷运动后即刻、6h、24h3个时相,又分别随机将B、C组依次分为B1、B2、B3与C1、C2、C3组。AC组与C组进行6周中等负荷跑台运动;C组于末次中等负荷运动后48h与B组进行一次性大负荷跑台运动。测定血清cTnI、CK-MB浓度;测定心肌SOD活性、MDA含量与Ca2+浓度、ATP含量(高效液相色谱仪法测定)及心肌细胞膜Na+-K+-ATPase、Ca2+-ATPase活性。结果:运动预处理可明显减轻大负荷运动引起的大鼠血清cTnI、CK-MB浓度升高程度。运动预处理可明显提高心肌SOD活性;明显减轻大负荷运动后心肌SOD指标下降程度及MDA、Ca2+指标的升高程度;明显减轻大负荷运动后心肌ATP含量及心肌细胞膜Na+-K+-ATPase、Ca2+-ATPase活性的下降程度。结论:EP对大负荷运动引起的心肌损伤具一定保护作用,这可能与EP提高的心肌SOD活性有关。  相似文献   

5.
探讨力竭运动对大鼠心肌自由基生成的影响,将16只大鼠随机分为安静组和运动组,运动组采用跑台力竭运动模型,运动后即刻取样,测定血清中一氧化氮(NO)浓度、心肌中丙二醛(MDA)、超氧化物歧化酶(SOD)和过氧亚硝酸阴离子(ONOO-)含量。结果:力竭运动后,心肌中ONOO-和MDA显著升高(P<0.05),SOD活力显著下降(P<0.01),血清中NO含量有一定上升,但无统计学意义(P>0.05)。结论:力竭运动诱导心肌ONOO-的大量生成,其机制可能源于力竭运动导致心肌超氧阴离子的大量生成与NO的过量生成。  相似文献   

6.
姚俊  徐礼皙 《体育与科学》2005,26(6):65-67,59
本研究以SD大鼠为研究对象,将动物随机分为一次性运动服药及不服药组、耐力训练服药及不服药组、间歇训练服药及不服药组共六组.一次性运动组、耐力运动组和间歇运动组大鼠在最后一次运动完成后分别于运动后即刻、运动后24小时和运动后48小时处死取样,随后对心肌线粒体Mg^2+、Fe^2+、Mn^2+、Cu^2+等无机离子浓度的测定,研究不同运动方式和抗氧化剂对大鼠心肌无机离子代谢的影响,以期为运动训练提供参考.  相似文献   

7.
目的:探讨中药方剂炙甘草汤对反复力竭运动大鼠心肌的保护作用.方法:Wistar雄性大鼠60只,随机分成3组:对照组(20只),运动组(20只),运动+中药组(20只).运动组和运动+中药组进行每周6天、每天1次的力竭游泳,共2周.运动前1小时,对照组和运动组灌胃给予2.5毫升蒸馏水,运动+中药组灌胃给予炙甘草汤药液2.5毫升(生药含量为20%).最后一次给药后,测定大鼠力竭性游泳持续时间.腹主动脉取血,分离血清测定cTnI,取心脏,测定心肌SOD活性和MDA含量.结果:1)与运动组相比,运动+中药组的游泳持续时间显著增加;2)与对照组相比,其它两组cTnI均显著性升高;与运动组相比,运动+中药组cTnI显著性降低;3)与对照组相比,运动组SOD活性显著降低;与运动组相比,运动+中药组心肌的SOD活性显著升高;4)与对照组相比,运动组MDA含量显著升高;与运动组相比,运动+中药组大鼠心肌的MDA含量显著降低.结论:炙甘草汤能显著降低反复力竭运动大鼠心肌MDA水平,增加SOD活性,显著降低血清cTnI水平,延长大鼠力竭游泳持续时间,说明本中药方剂能降低反复力竭运动对心肌的损伤,从而提高运动耐力.  相似文献   

8.
郝喆  潘珊珊 《体育科学》2012,32(7):39-44
目的:探讨运动预适应(EP)对力竭所致心肌损伤的晚期保护效应中心肌εPKC表达变化。方法:SD大鼠分为对照组(C组)、力竭运动组(EE组)、晚期运动预适应组(LEP组)、晚期运动预适应+力竭运动组(LEP+EE组)。在EP模型基础上,用力竭跑台运动致大鼠心肌损伤。用免疫化学发光法检测血清cTnI的含量;用免疫印迹法与免疫组织化学法检测心肌εPKC定量与定位表达变化。结果:与C组比,EE组血清cTnI水平、εPKC蛋白水平显著升高,免疫反应阳性于心肌闰盘聚集;LEP组血清cTnI无明显变化,εPKC蛋白水平显著升高,免疫反应阳性于心肌闰盘聚集。与EE组比,LEP+EE组血清cTnI水平显著下降,蛋白水平无明显变化,免疫反应阳性未在心肌闰盘聚集。结论:εPKC参与了EP对力竭运动致心肌损伤的晚期保护效应。  相似文献   

9.
心肌肌钙蛋白的研究进展   总被引:1,自引:0,他引:1  
任绮  邓树勋 《体育学刊》2006,13(6):51-55
心肌肌钙蛋白是反映心肌损伤的一项生物标志物。与其它生化标志物相比,心肌肌钙蛋白对微小心肌损伤有更高的敏感性,升高即表明存在心肌损伤。研究表明在长时间大强度运动时人体内出现肌钙蛋白水平升高的现象。运用文献综述探讨心肌肌钙蛋白作为检测运动性心肌损伤标志物的应用意义。  相似文献   

10.
不同运动强度下大鼠血清cTnI、CK-MB和TNF-α的变化   总被引:2,自引:0,他引:2  
探讨过度训练大鼠心肌损伤、细胞因子的演变。方法:取健康雄性SD大鼠随机分为正常对照组、一般游泳训练组、过度训练组,分别于运动后即刻和24h检测血清CK-MB活性、cTnⅠ及TNF-α含量,电镜观察组织形态学变化。结果:过度训练组即刻和24h血清cTnⅠ、CK-MB及TNF-α均高于正常对照组和一般游泳训练组;过度训练组血清cTnⅠ、血清CK-MB与血清TNF-α均呈正相关;心肌病理组织学和超微结构改变在过度训练组即刻和24h均明显。结论:长期过度训练存在心肌损伤;肿瘤坏死因子参与了过度训练心肌损伤的发生、发展。  相似文献   

11.
马拉松作为持续时间较长、强度较高的耐力运动,对心脏的影响是利大还是弊多,对马拉松参赛选手心脏产生哪些生理适应,又对心脏健康存在哪些潜在风险,经常困扰着运动医学研究者和马拉松参赛者。依据目前的国内外研究,全面综述分析了马拉松对心脏各腔室以及冠状动脉结构和功能的影响,深入探讨了马拉松与心肌损伤标志物、心律失常、心肌纤维化和心脏猝死之间的关系。研究结果:1)马拉松会引起心脏发生离心性肥大,心房和心室腔体积均会增大,提升心脏功能。一次马拉松运动后,心房和左右心室收缩与舒张功能均出现了短暂性的下降,舒张功能下降更明显,这是心脏的一种生理适应,数周内可恢复至正常水平;2)尽管马拉松与冠状动脉风险之间的关系仍存在争议,但与同龄和相同心血管风险因素的对照人群相比,马拉松运动员仍具有较低的冠状动脉斑块形成风险;3)马拉松诱导的循环心肌损伤标志物的升高是可逆的,是对剧烈运动的一种暂时生理性应激反应;4)马拉松运动猝死的风险较低,多数马拉松猝死的发生和参赛者遗传的显性或隐性心脏疾病有关。为预防赛场心血管意外,应该建立马拉松赛场心血管意外的预防体系,包括赛前心血管风险评估和筛查程序、增加并合理布置赛中救助力量。  相似文献   

12.
The objective of this study was to determine the effect of a marathon run on serum lipid and lipoprotein concentrations and serum muscle enzyme activities and follow their recovery after the run. These blood concentrations were measured before, immediately after, and serially after a marathon run in 15 male recreational runners. The triglyceride level was significantly elevated postrace, then fell 30% below baseline 1 day after the run, and returned to baseline after 1 week. Total cholesterol responded less dramatically but with a similar pattern. High-density lipoprotein cholesterol remained significantly elevated and low-density lipoprotein cholesterol was transiently reduced for 3 days after the run. The total cholesterol/high-density cholesterol ratio was significantly lowered for 3 days. Serum lactate dehydrogenase activity significantly doubled postrace and then declined but remained elevated for 2 weeks. Serum creatine kinase activity peaked 24 hr after the run, with a 15-fold rise, and returned to baseline after 1 week. The rise of these enzymes reflects mechanically damaged muscle cells leaking contents into the interstitial fluid. It is concluded that a prolonged strenuous exercise bout in recreational runners, such as a marathon, produces beneficial changes in lipid blood profiles that are significant for only 3 days. However, muscle damage is also evident for 1 week or more from the dramatic and long-lasting effect on enzyme levels. Laboratory values for these runners were outside normal ranges for some days after the race.  相似文献   

13.
Abstract

The objective of this study was to determine the effect of a marathon run on serum lipid and lipoprotein concentrations and serum muscle enzyme activities and follow their recovery after the run. These blood concentrations were measured before, immediately after, and serially after a marathon run in 15 male recreational runners. The triglyceride level was significantly elevated postrace, then fell 30% below baseline 1 day after the run, and returned to baseline after 1 week. Total cholesterol responded less dramatically but with a similar pattern. High-density lipoprotein cholesterol remained significantly elevated and low-density lipoprotein cholesterol was transiently reduced for 3 days after the run. The total cholesterol/high-density cholesterol ratio was significantly lowered for 3 days. Serum lactate dehydrogenase activity significantly doubled postrace and then declined but remained elevated for 2 weeks. Serum creatine kinase activity peaked 24 hr after the run, with a 15-fold rise, and returned to baseline after 1 week. The rise of these enzymes reflects mechanically damaged muscle cells leaking contents into the interstitial fluid. It is concluded that a prolonged strenuous exercise bout in recreational runners, such as a marathon, produces beneficial changes in lipid blood profiles that are significant for only 3 days. However, muscle damage is also evident for 1 week or more from the dramatic and longlasting effect on enzyme levels. Laboratory values for these runners were outside normal ranges for some days after the race.  相似文献   

14.
Carnitine is an essential co‐factor in the catabolism of fats as an energy source. The primary purpose of this study was to investigate the effect of running a marathon on the metabolism of carnitine by endurance‐trained athletes, and to evaluate the effect of carnitine administration on the performance of such exercise. The effects of marathon running on mitochondrial enzymes and cellular anti‐oxidants were also examined to assess whether the expression of these activities is altered by exercise. Subjects were 10 experienced male marathon runners aged between 19 and 25 years. Running a marathon caused a fall in the plasma content of unesterified carnitine (37%) and an increase in the level of acetylcarnitine present (288%). Loading of the athletes with L‐carnitine for 10 days before running a marathon abolished the exercise‐induced fall in plasma‐free carnitine (P<0.05) whilst amplifying the production of acetylcarnitine (P<0.05). Carnitine loading of the athletes studied made no detectable improvement in performance of the marathon (P > 0.05). Cytochrome oxidase, succinate cytochrome C reductase and Superoxide dismutase activities present in skeletal muscle were unaltered by marathon running. However, such exercise caused a large increase in the tissue content of oxidized glutathione (189%) at the expense of reduced glutathione (–18%).  相似文献   

15.
耗竭运动对大鼠心肌线粒体功能的影响   总被引:4,自引:0,他引:4  
采用耗竭运动方式,观察了大鼠运动后心肌线粒体脂质过氧化水平、超氧化物岐化酶活性和还原型谷胱甘肽含量的变化。发现运动后即刻心肌线粒体脂质过氧化水平显著升高,超氧化物岐化酶活性和还原型谷胱甘肽含量显著下降。结果提示耗竭运动时,心肌线粒体内源性自由基的产生是耐力性运动疲劳和运动损伤的原因之一。  相似文献   

16.
Respiratory muscle fatigue has been reported following short bouts of high-intensity exercise, and prolonged, moderate-intensity exercise, as evidenced by decrements in inspiratory and expiratory mouth pressures. However, links to functionally relevant outcomes such as breathing effort have been lacking. The present study examined dyspnoea and leg fatigue during a treadmill marathon in nine experienced runners. Maximal inspiratory and expiratory pressure, peak inspiratory and expiratory flow, forced vital capacity, and forced expiratory volume in one second were assessed before, immediately after, and four and 24 hours after a marathon. During the run, leg effort was rated higher than respiratory effort from 18 through 42 km (P < 0.05). Immediately after the marathon, there were significant decreases in maximal inspiratory pressure and peak inspiratory flow (from 118 +/- 20 cm H(2)O and 6.3 +/- 1.4 litres x s(-1) to 100 +/- 22 cm H(2)O and 4.9 +/- 1.5 litres x s(-1) respectively; P < 0.01), while expiratory function remained unchanged. Leg maximum voluntary contraction force was significantly lower post-marathon. Breathing effort correlated significantly with leg fatigue (r = 0.69), but not inspiratory muscle fatigue. Our results confirm that prolonged moderate-intensity exercise induces inspiratory muscle fatigue. Furthermore, they suggest that the relative intensity of inspiratory muscle work during exercise makes some contribution to leg fatigue.  相似文献   

17.
运用文献资料、专家访谈等方法对马拉松项目竞技能力特点进行分析与重构。(1)马拉松项目整体特点是:马拉松是以有氧代谢为主的体能主导类长距离竞速项目,体能是核心、技战术是重点、心智是辅助。(2)马拉松项目的体能特点为:力量耐力、专项耐力、速度耐力和基础耐力是马拉松项目的主导体能运动素质。各耐力素质训练适宜区域为:5-15 km;30-35 km;20-30 km;40-50km。(3)马拉松项目技术特点:身体重心起伏小,前脚掌外侧着地过渡到全脚掌,没有扒地动作,前摆大腿不能抬起太高;上坡步长缩短、步频加快;下坡步长适当加大。(4)马拉松战术特点:熟悉路线与对手是首要;依5 km公里分段、按"时间储备"定目标是关键;半程保、大半程加、后6km冲刺是关键;一定阶段摆脱对手、拉开距离、独立控制与把握节奏是核心。  相似文献   

18.
运用文献资料、专家访谈等方法对马拉松项目竞技能力特点进行分析与重构。(1)马拉松项目整体特点是:马拉松是以有氧代谢为主的体能主导类长距离竞速项目,体能是核心、技战术是重点、心智是辅助。(2)马拉松项目的体能特点为:力量耐力、专项耐力、速度耐力和基础耐力是马拉松项目的主导体能运动素质。各耐力素质训练适宜区域为:5-15 km;30-35 km;20-30 km;40-50km。(3)马拉松项目技术特点:身体重心起伏小,前脚掌外侧着地过渡到全脚掌,没有扒地动作,前摆大腿不能抬起太高;上坡步长缩短、步频加快;下坡步长适当加大。(4)马拉松战术特点:熟悉路线与对手是首要;依5 km公里分段、按"时间储备"定目标是关键;半程保、大半程加、后6km冲刺是关键;一定阶段摆脱对手、拉开距离、独立控制与把握节奏是核心。  相似文献   

19.
Moderate endurance exercise has long been considered an essential element to maintain cardiovascular health, and sedentary behaviour in the general population has been related to a significant increase in all-causes of mortality, cardiovascular disease mortality and cardiovascular disease incidence. However, a growing group of people performs an intense exercise that leads to multiple heart adaptive changes that are collectively called “athlete’s heart”. In this review, we discussed the evidence of cardiac remodelling process secondary to repetitive and strenuous exercise in some predisposed athletes that produces intense and probably deleterious changes in cardiac morphology and function with no clear clinical significance in long-term follow-up. Moreover, we also discussed the individual biological response to exercise assessed by myocardial damage, inflammation, oxidative stress, fibrosis and ventricular hypertrophy biomarkers showing different intensities with equivalent exertion.  相似文献   

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