Effects of exercise on neurogenesis in the dentate gyrus and ability of learning and memory after hippocampus lesion in adult rats

Objective To explore the effects of exercise on dentate gyrus (DG) neurogenesis and the ability of learning and memory in hippocampus-lesioned adult rats. Methods Hippocampus lesion was produced by intrahippocampal microinjection of kainic acid (KA). Bromodeoxyuridine (BrdU) was used to label dividing cells. Y maze test was used to evaluate the ability of learning and memory. Exercise was conducted in the form of forced running in a motor-driven running wheel. The speed of wheel revolution was regulated at 3 kinds of intensity: lightly running, moderately running, or heavily running. Results Hippocampus lesion could increase the number of BrdU-labeled DG cells, moderately running after lesion could further enhance the number of BrdU-labeled cells and decrease the error number (EN) in Y maze test, while neither lightly running, nor heavily running had such effects. There was a negative correlation between the number of DG BrdU-labeled cells and the EN in the Y maze test after running. Conclusion Moderate exercise could enhance the DG neurogenesis and ameliorate the ability of learning and memory in hippocampus-lesioned rats.     

高能合剂对低氧鼠运动耐力和某些生化指标的影响

为提高高原劳动能力,我们研制了含有多种糖、维生素、氨基酸和无机盐的高能合剂。在小白鼠减压缺氧(模拟海拔高度10000m)游泳实验中,高能合剂组和对照组的存活时间分别为:72.3±1.3min和58.8±1.2min(P相似文献   

Protein carbonyls are acutely elevated following single set anaerobic exercise in resistance trained men

The purpose of this investigation was to determine if a single set of strenuous squat exercise would result in an acute oxidative stress, as demonstrated previously by a single sprint. Thirteen resistance trained men performed one set of 15 repetitions of barbell squats using 70% of one repetition maximum and a 30 s maximal cycle sprint on two different occasions. The total work performed was calculated for each exercise bout. Heart rate, perceived exertion, blood lactate, protein carbonyls, 8-hydroxydeoxyguanosine, and malondialdehyde were measured before and within 1 min following exercise. No differences were noted between the squat and sprint tests for total work, heart rate or perceived exertion. An exercise test by time interaction was evident for blood lactate with values greater following sprinting compared to squatting (P = 0.0005). Postexercise protein carbonyls were not different between exercise tests but were elevated above rest (P = 0.04) by 111% and 74% following sprinting and squatting, respectively, while 8-hydroxydeoxyguanosine and malondialdehyde were relatively unaffected by either exercise test. These data indicate that a single bout of strenuous squatting and sprinting performed by resistance trained men results in elevated protein carbonyls, while having little impact on 8-hydroxydeoxyguanosine or malondialdehyde during the immediate postexercise period.     

正常人在静态和运动状态下"死腔/潮气"估测值和实测值的比较

目的研究正常人静态及运动状态下死腔/潮气(VD/VT)估测值和实测值的关系.方法23名受试者行心肺运动试验,同步实时测定摄氧量和二氧化碳排出量,分别在运动前及运动高峰时抽取动脉血,根据Bohr的公式,得出VD/VT实测值,同时再用呼气末CO2分压(PetCO2)代替PaCO2,计算VD/VT,得出VD/VT估测值.结果根据病史、体检、肺功能和运动前后的心电图判断23名受试者均为正常受试者.静态时的VD/VT估测值和VD/VT实测值分别为0.359±0.109和0.354±O.106,两者无显著性差异(P=0.710),相关分析显示两者高度相关(r=0.911,P＜0.001).运动高峰时的VD/VT估测值和VD/VT实测值分别为0.234±0.070和0.248±0.094,两者无显著性差异(P=0.748),相关分析表明两者显著相关(r=0.783,P＜0.001).与静态时比较,运动时估测和实测VD/VT均明显下降.结论对于正常成人,无论是在静态或最大运动状态下,可用无创方法计算VD/VT代替VD/VT实测值.     

老化皮肤的胶原与弹性组织变化研究

目的：探讨光曝露情况及年龄因素对皮肤中弹性组织、Ⅰ/Ⅲ型胶原及基底膜Ⅳ型胶原的影响,进而探索皱纹形成的组织学原因。方法：对80例取自不同年龄志愿者的曝光部位（眶周/前额、面颊）及非曝光部位（腹部/臀部）的皮肤组织进行HE染色、Weigert染色、苦味酸天狼猩红染色及免疫组化处理,采用显微形态观察和半定量分析。结果：各部位皮肤基底膜内Ⅳ型胶原的含量无差异;随着曝光时间增加,前额/眶周皮肤中Ⅰ型胶原减少率最大,弹性变性物质增加率最大。结论：前额/眶周皮肤的胶原显著减少和弹性变性物质明显增生,是该部位皮肤皱纹早发的重要原因。     

运动对大鼠腓肠肌一氧化氮含量和铁转运蛋白表达的影响

目的观察游泳运动后大鼠腓肠肌一氧化氮(NO)含量及铁转运相关蛋白表达的变化,探讨运动对骨骼肌铁代谢的调节机制。方法20只雌性SD大鼠随机分为对照组和运动组(每天游泳1.5小时,6次/周),每组10只。实验10周后分别采用试剂盒测定两组大鼠腓肠肌和血清一氧化氮合酶(NOS)活性及NO含量,免疫组织化学方法测定腓肠肌二价金属离子转运体1(DMT1)、膜铁转运蛋白1(FP1)和转铁蛋白受体1(TfR1)的表达,分析其平均光密度变化。结果(1)运动组大鼠血清和腓肠肌NO含量和NOS活性均显著高于对照组(P<0.05);(2)运动组大鼠腓肠肌DMT1(IRE)和TfR1表达较对照组显著增加,FP1表达显著减少(P<0.05),而DMT1(non-IRE)表达无明显变化。结果提示运动可能通过增加NOS活性刺激NO合成增加,进而调节腓肠肌铁转运蛋白的表达,提高腓肠肌摄铁能力,以满足运动中机体对铁的需求。     

运动对骨质疏松的影响

本研究对运动影响骨质疏松的机制,运动对骨代谢、骨生物力学、骨密度的影响的研究现状与进展进行综述,可为骨质疏松症的预防和治疗提供理论参考资料。     

Effect of low glycogen on glycogen synthase in human muscle during and after exercise

Subjects cycled at a work load calculated to elicit 75% of maximal oxygen uptake on two occasions: the first to fatigue (34.5 ± 5.3 min; mean ± SE), and the second at the same workload and for the same duration as the first. Biopsies were obtained from the quadriceps femoris muscle before and immediately after exercise, and 5 min post-exercise. Before the first experiment, muscle glycogen was lowered by a combination of exercise and diet, and before the second, experiment muscle glycogen was elevated. In the low glycogen condition (LG), muscle glycogen decreased from 169 ± 15 mmol glucosyl units kg^-1dry wt at to rest to 13 ± 6 after exercise. In the high glycogen condition (HG) glycogen decreased from 706 ± 52 at rest to 405 ± 68 after exercise. Glycogen synthase fractional activity (GSF) was always higher during the LG treatment. During exercise in the HG condition, those subjects who cycled for < 35 min (n= 3) had GSF values in muscle which were lower than at rest, whereas those subjects who cycled for > 35 min (n= 4) had values which were similar to or higher than at rest. Thus the change in GSF in muscle during HG was positively related to the exercise duration (r= 0.94; y = 254–17x + 0.3x²; P < 0.001) and negatively related to the glycogen content at the end of exercise (r=–0.82; y= 516–2x + 0.001x²; P < 0.05). During LG exercise GSF remained constant. GSF increased markedly after 5 min post-exercise in both HG and LG conditions. cAMP dependent protein kinase activity increased similarly during both LG and HG exercise and reverted to the preexercise values 5 min post-exercise. It is concluded that muscle contraction decreases GSF, but low glycogen levels can attenuate or abolish the decrease in GSF. The rapid increase of GSF during recovery from exercise does not require glycogen depletion during the exercise.