运动、锌铜营养与自由基代谢—Ⅴ.锌缺乏对运动小鼠体内自由基生成与清除的影响

离乳Balb/c小鼠48只,按性别体重随机分成缺锌、对饲对照及自由进食对照三大组,每大组又分成运动和不运动两组。6周后进行锌、铜、丙二醛(MDA)、超氧化物歧化酶(SOD)、谷光甘肽过氧化物酶(GSH-Px)及过氧化氢酶(CAT) 的测定,并对肝组织直接进行低温ESR(电子自旋共振)波谱分析。实验结果提示:锌缺乏将导致运动及不运动小鼠体内的自由基生成增加和清除减少;运动训练虽可使正常小鼠体内的自由基防御能力加强,但却对锌缺乏小鼠体内的SOD、GSH-Px和CAT均无显著作用,相反,运动训练还可以使缺锌小鼠肝线粒体内的脂质过氧化产物进一步显著增加。     

补锌对缺锌大鼠烧伤后肠道细菌移位及毒血症的影响

目的:探讨补锌对大鼠烧伤后肠道细菌移位及毒血症的影响。方法:90只SD大鼠进食低锌饲料(含锌量:1.6ug·g-1)1周,造成缺锌模型,并随机分为正常对照组(A)、烧伤对照组(B)、烧伤治疗组(C)。B组和C组造成20%总体表面积Ⅲ度烧伤。B组伤后继续进食低锌饲料,C组伤后进食正常含锌饲料(含锌量:24.7ug·g-1)。采用甲基-3H胸腺嘧啶核苷([3H]-TdR)标记致病大肠杆菌,在烧伤前注人大鼠的胃肠道。在不同的时象点,检测血浆内毒素(LPS)含量、血和肝的3H放射活性。结果:(1)B、C组3H的放射活性和血浆LPS含量显著高于A组(P<0.05);同时,C组显著低于B组(P<0.05)。(2)B、C组肝的3H放射活性比A组显著增高(P<0.05),C组比B组低。结论:烧伤后补锌能减轻大鼠肠道细菌移位及毒血症。     

生酮饮食对小鼠骨骼肌力量及运动耐力的影响

目的:探讨生酮饮食对小鼠骨骼肌力量及运动耐力的影响.方法:20只小鼠随机分为标准饮食组(n=10)和生酮饮食组(n=10),按等能量喂养原则,分别给予两组小鼠标准饲料和生酮饲料4周,每天记录体重和进食量.4周后通过尾静脉采血测定血糖、血酮水平;采用负重游泳实验和在体腓肠肌收缩实验评价小鼠运动能力和骨骼肌力量,并测试腓肠...     

缺锌对大鼠力竭性游泳前后睾酮和锌水平变化的影响

本实验动态观察了缺锌和缺锌后补锌对大鼠力竭性游泳前后辜丸和血清睾酮、锌水平以及游泳能力的影响。结果显示：缺锌造成大鼠游泳能力大大降低，补锌后明显增加。不论安静时还是力竭性游泳后１２小时内，缺锌大鼠的血清和辜丸锌含量均显著低于对照和补锌大鼠。与对照和补锌大鼠相比，缺锌大鼠的血清和睾丸酮含量，安静时均较低，力竭性游泳后也呈现不同程度的降低。缺锌还造成大鼠辜丸重量的明显下降。结果表明，锌营养不良将损害运动能力。     

服食百臣奶昔与葡锌乳酸奶的生理效应及对运动能力的影响

当前,运动医学领域内出现了三个新的研究动向:一是运动与自由基生物学的基础理论;二是运动对锌铜代谢的影响;三是锌铜与自由基生物学的关系。其主要理论观点可综合为三点:(1)运动员普遍缺锌,而缺锌将直接影响运动成绩的提高;(2)补锌可加速自由基的消除,从而消除疲劳;(3)补锌可以直接提高肌肉力量与耐久力。这些理论是我     

半胱氨酸对训练小鼠力竭运动后不同组织自由基代谢和血清转氨酶活性的影响

选用雄性ICR小鼠 2 0只 ,随机分成 2组 ,即运动组和运动 +半胱氨酸组 ,训练 30天后进行 1次性力竭游泳运动 ,观察半胱氨酸对训练小鼠力竭运动后不同组织自由基代谢和血清转氨酶活性的影响。结果表明 :(1)运动 +半胱氨酸组小鼠力竭游泳时间明显长于运动组 (P <0 0 5 ) ;(2 )运动 +半胱氨酸组小鼠力竭游泳后即刻不同组织SOD活性显著高于运动组 (P <0 0 5 ) ;(3)运动半胱氨组小鼠力竭游泳后即刻不同组织MDA含量显著低于运动组 (P <0 0 5 ) ;(4)灌服半胱氨酸力竭游泳后即刻血清GPT、GOT活性显著低于运动组 (P <0 0 5 )。结论 :半胱氨酸具有提高力竭游泳后小鼠不同组织SOD活性 ,降低MDA含量 ,降低血清GPT、GOT活性和提高运动能力的作用。     

游泳运动对D-半乳糖致衰老小鼠学习记忆和胆碱能神经系统功能的影响

目的:探讨游泳运动对D-半乳糖所致衰老小鼠学习记忆和胆碱能系统功能的影响。方法:50只昆明种小鼠随机分成5组:对照组、模型组、15 min/天游泳组、30 min/天游泳组、45 min/天游泳组。除对照组外,所有小鼠连续8周皮下注射D-半乳糖复制衰老模型。运动组小鼠从第5周开始运动,连续4周。Morris水迷宫实验评价小鼠空间学习记忆能力。行为测试结束后,检测小鼠脑组织丙二醛(MDA)含量和超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-PX)活性及皮层和海马组织中乙酰胆碱酯酶(ACh E)和胆碱乙酰化转移酶(Ch AT)的活性。结果:水迷宫实验结果显示:15 min/天和30 min/天游泳组逃避潜伏期显著短于模型组,目标象限搜索时间百分比、通过目标区域次数均显著多于模型组。酶活性检测结果显示:15min/天游泳组小鼠脑组织SOD显著高于模型组,GSH-Px活性高于模型组但无显著性,MDA含量显著低于模型组;30 min/天游泳组小鼠脑组织SOD和GSH-Px活性均显著高于模型组、MDA含量显著低于模型组;15 min/天和30 min/天游泳组皮层和海马组织中ACh E、Ch AT活性均显著高于模型组。结论:15 min/天游泳运动和30 min/天游泳运动均能提高衰老模型小鼠的空间学习记忆能力,其中以30 min/天游泳运动的效果最好,其机制可能与其提高脑组织抗氧化和清除自由基能力,增强中枢胆碱能神经系统功能有关。     

运动、锌铜营养与自由基代谢——Ⅲ.游泳训练对小鼠体内自由基生成与清除的影响

Balb-c小鼠20只,随机分成实验组和对照组,实验组小鼠进行游泳训练。6周后均处死取血、肝、心以测定丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)和过氧化氢酶(CAT)。结果显示,游泳训练并不会增加小鼠体内的MDA生成,且可显著提高小鼠体内CuZn-SOD、Mn-SOD以及肝线粒体GSH-Px等抗过氧化物酶的活力。     

补锌对耐力训练、力竭运动大鼠腓肠肌超氧化物岐化酶、谷胱甘肽过氧化物酶、总抗氧化能力以及Bax、Bcl-2 mRNA的影响

目的:探讨补锌对耐力训练、力竭运动大鼠腓肠肌超氧化物岐化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px,简称GPX)、总抗氧化能力(T-AOC)、细胞凋亡诱导和阻遏分子(Bax,Bcl-2)mRNA的影响。方法:将32只雄性SD大鼠随机分成对照组、耐力训练组、耐力训练补锌组和一次性力竭运动补锌组4组,每组8只。补锌方法为在饮用水中溶入ZnSO4.7H2O,[Zn]=227 mg/L。耐力训练组和耐力训练补锌组进行6周游泳耐力训练,每周6天。6周训练结束24小时后取材。一次性力竭运动组取材当日在同一泳池每隔15 min被放入2只大鼠,进行无负重游泳至力竭后取材。测定大鼠腓肠肌SOD、GPX、T-AOC活性,Bax、Bcl-2 mRNA表达。结果:耐力训练补锌组大鼠腓肠肌SOD活性显著高于对照组(P<0.05),GPX活性显著高于对照组和耐力训练组(P<0.05)。力竭运动补锌组大鼠腓肠肌GPX和T-AOC活性显著高于对照组(P<0.05)。耐力训练补锌组大鼠腓肠肌Bax mRNA表达显著低于对照组和耐力训练组(P<0.05),Bcl-2 mRNA表达显著高于对照组和耐力训练组(P<0.05)。力竭运动补锌组大鼠腓肠肌Bax,Bcl-2 mRNA表达均显著高于对照组(P<0.05)。结论:耐力训练提高大鼠腓肠肌GPX活性,增加Bcl-2 mRNA表达,降低大鼠腓肠肌Bax mRNA表达,补锌效果更明显。一次性力竭运动补锌提高大鼠腓肠肌GPX活性和T-AOC活性,增加腓肠肌Bcl-2 mRNA表达,但对Bax mRNA表达影响不明显。     

不同途径补锌对烫伤大鼠血清、组织中锌的影响

锌是体内最重要的微量元素之一 ,烧伤后锌经创面、尿液大量丢失 ,机体处于缺锌状态 ,引起许多病理变化[1] 。本实验主要观察了烫伤大鼠经不同途径补锌后血清及组织中锌含量的变化 ,为烧伤病人补锌提供实验依据。1　材料与方法1 1　动物分组　ＳＤ大鼠 80只 ,雄性 ,体重 ( 6 0± 3) ｇ ,随机分成 4组 ,Ｃ组 (对照组 ) 8只 ,Ｎ组 (正常组 )、Ｈ组 (口饲补锌组 )、Ｗ组 (创面补锌组 )各 2 4只。大鼠单独置于透明塑料笼内 ,乙醚麻醉Ｃ组大鼠 ,心外穿刺抽血活杀 ,留取全血、肝脏、股骨、烫伤皮肤。其他 3组乙醚麻醉后 ,10 %硫化钠背部脱毛 ,10 0…     

运动、锌缺乏对小鼠免疫细胞功能的影响

观察了运动、锌缺乏对小鼠免疫细胞功能的影响。结果表明锌缺乏和限制进食会损伤淋巴细胞对ＣｏｎＡ的增殖反应和ＩＬ－２分泌水平，运动会加重这种损伤作用；运动和饥饿诱导肝脏ＭＴ增加，但在锌缺乏和饥饿时运动对ＭＴ的诱导作用被掩盖；补锌能部分恢复受损的免疫细胞功能。     

Exercise and green tea extract stimulate fat oxidation and prevent obesity in mice

INTRODUCTION/PURPOSE: The purpose of the present study was to explore the combined effects of dietary supplementation with green tea extract (GTE) and regular exercise on the development of obesity in high fat-fed C57BL/6J mice. METHODS: Weight and age-matched male mice were divided into 5 groups of 10 mice each. Groups were treated as follows: a low-fat diet and not exercised (LF), a high-fat diet and not exercised (HF), a high-fat diet supplemented with GTE and not exercised (GTE-HF), a high-fat diet and exercised regularly (EX-HF), or a high-fat diet supplemented with GTE and exercised regularly (GTEEX-HF). The exercise modality was treadmill running. RESULTS: After 15 wk, GTE alone and regular exercise alone caused a 47 and 24% reduction in body weight gain induced by the high-fat diet, respectively, and when combined, resulted in an 89% reduction. In visceral fat accumulation, GTE alone, exercise alone, and their combination caused a 58, 37, and 87% reduction, respectively. Indirect calorimetry showed that the GTEEX-HF group had the highest energy expenditure and fat utilization in the sedentary condition after 4 wk. Furthermore, the GTEEX-HF group utilized more fat than the EX-HF group during exercise. GTE supplementation increased hepatic fatty acid oxidation both in the exercised and nonexercised groups. In addition, when combined with regular exercise, GTE supplementation also stimulated skeletal muscle fatty acid oxidation. CONCLUSION: In conclusion, dietary GTE and regular exercise, if combined, stimulate fat catabolism not only in the liver but also in skeletal muscle, and attenuate high-fat diet-induced obesity more effectively than each alone in C57BL/6J mice.     

复合微量营养素对营养缺乏小鼠游泳耐力的影响及其机制

目的 研究复合微量营养素的抗疲劳效果及可能机制.方法 取SPF级雄性昆明种小鼠125只,分别以下述不同的饲料喂养.全营养素饲料.即AIN-93M饲料,主要成分和比例为:玉米淀粉46.6％、酪蛋白14％、糊精15.5％6.蔗糖10％、豆油4％、纤维素5％、矿物盐粉3.5％、维生素粉1％、胱氨酸0.18％、叔丁基氢醌8ppm.营养素缺乏饲料,在AIN-93M饲料的基础上将维生素粉和矿物盐粉减少为原来的70％、50％或30％(后称70％、50％、30％微量营养素饲料),其余以淀粉补足.复合微量营养素粉添加饲料,在营养素缺乏30％饲料的基础上,将减少的维生素粉和无机盐粉以复合微量营养素粉补足,其主要成分及含量(g/kg)为:VitA 0.25、VitB10.3、Vit B2 0.3、Vit B6 0.35、烟酸1.5、VitD 0.05、VitC50、VitE 10以及碳酸钙180、甘氨酸铁1、乳酸锌1、玉米淀粉755.25.分别干喂养14d和28d后取不同饲料(AIN-93M饲料及70％、50％、30％微量营养素饲料)喂养的小鼠,于尾部系5％体重的铅丝进行负重游泳,记录小鼠游泳力竭时间.于喂养至28d时,取不同饲料(AIN-93M饲料及70％微量营养素饲料、复合微量营养素粉添加饲料)喂养的小鼠,使其负重游泳60min,游泳后立即取外周血测定生化指标,取肝组织测定肝糖原含量.结果 与AIN-93M饲料喂养小鼠相比,30％微量营养素饲料喂养小鼠的摄食量显著减少(P＜0.05),50％和70％微量营养素饲料喂养小鼠的摄食量变化并不显著,但70％、50％、30％饲料喂养小鼠的负重游泳时间均显著缩短(P＜0.05).与AIN-93M饲料喂养小鼠相比,营养素缺乏饲料喂养的小鼠负重游泳时间显著缩短(P＜0.05),复合微量营养素粉饲料喂养小鼠游泳时间与营养素缺乏饲料喂养小鼠比较差异无统计学意义(P＞0.05),但延长了13.2％.小鼠游泳后生化指标的变化趋势主要表现为血糖和肝糖原水平下降.乳酸、游离脂肪酸(NEFA)和尿素氮(NPN)水平升高.营养素缺乏饲料喂养小鼠的前述变化更为明显,而复合微量营养素粉饲料可有效缓解营养缺乏所致血糖和肝糖原水平下降,下调血乳酸、NEFA和NPN水平.结论 微量营养素摄入不足对小鼠游泳耐力有明显影响,复合微量营养素具有一定的抗疲劳作用,其机制可能与运动过程机体能量代谢的调控有关.     

Exercise Speeds Cutaneous Wound Healing in High-Fat Diet-Induced Obese Mice

PURPOSE: Obesity has been shown to impair cutaneous wound healing, which is associated with increased wound inflammation. Exercise is known to decrease obesity-associated inflammation and has been shown to speed cutaneous wound healing in aged mice. Therefore, we investigated whether treadmill exercise could speed cutaneous wound healing in obese, high-fat diet-fed mice. METHODS: We fed female C57Bl/6J mice a high-fat diet (45% calories from fat) for 16 wk to induce a state of obesity and insulin resistance. Mice then ran on a treadmill for 3 d before excisional wounding. On day 4, mice were wounded 1 h after exercise. Mice then exercised for 5 d after wounding, and healing was assessed by photoplanimetry for 10 d. RESULTS: As described previously, obesity impaired wound healing, with significantly larger wound sizes measured from days 3 to day 10 after wounding (P < 0.05). Exercise did not improve healing in lean mice fed a normal chow diet. However, wound size was significantly smaller in exercised obese mice compared with their lean counterparts (P < 0.05 at day 1, day 4, and day 5 after wound). Surprisingly, we were unable to detect any differences in gene or protein expression of proinflammatory cytokines interleukin-1β and tumor necrosis factor-α or the anti-inflammatory cytokine interleukin-10 in the wounds. Likewise, there were no differences in gene expression of chemokines monocyte chemoattractant protein-1 and keratinocyte chemoattractant or of growth factor platelet-derived growth factor in wounds of exercise and sedentary mice. CONCLUSION: This suggests an effect of exercise independent of alterations in inflammation. Future work should focus on early events after wounding, including exercise effects on hemostasis and myofibroblast function.     

Oral quercetin supplementation hampers skeletal muscle adaptations in response to exercise training

We aimed to test exercise‐induced adaptations on skeletal muscle when quercetin is supplemented. Four groups of rats were tested: quercetin sedentary, quercetin exercised, placebo sedentary, and placebo exercised. Treadmill exercise training took place 5 days a week for 6 weeks. Quercetin groups were supplemented with quercetin, via gavage, on alternate days throughout the experimental period. Sirtuin 1 (SIRT1), peroxisome proliferator‐activated receptor γ coactivator‐1α mRNA levels, mitochondrial DNA (mtDNA) content, and citrate synthase (CS) activity were measured on quadriceps muscle. Redox status was also quantified by measuring muscle antioxidant enzymatic activity and oxidative damage product, such as protein carbonyl content (PCC). Quercetin supplementation increased oxidative damage in both exercised and sedentary rats by inducing higher amounts of PCC (P < 0.001). Quercetin supplementation caused higher catalase (P < 0.001) and superoxide dismutase (P < 0.05) activity in the non‐exercised animals, but not when quercetin is supplemented during exercise. Quercetin supplementation increased SIRT1 expression, but when quercetin is supplemented during exercise, this effect is abolished (P < 0.001). The combination of exercise and quercetin supplementation caused lower (P < 0.05) mtDNA content and CS activity when compared with exercise alone. Quercetin supplementation during exercise provides a disadvantage to exercise‐induced muscle adaptations.     

Perivascular fat alters reactivity of coronary artery: effects of diet and exercise

ABSTRACT: Perivascular adipose tissue (PAT) has been reported to blunt agonist-induced arterial tone via a relaxing factor acting in a paracrine manner.The purpose of this study was to test the hypothesis that PAT of porcine coronary artery blunts constriction similarly and that this anticontractile effect of PAT is altered by diet and/or exercise training. METHODS: Fourteen adult male pigs were fed a normal-fat (NF) diet, and 10 adult male pigs were fed a high-fat/cholesterol (HF) diet. Four weeks after the initiation of diet, pigs were exercised (EX) or remained sedentary (SED) for 16 wk, yielding four groups: 1) NF-SED, 2) NF-EX, 3) HF-SED, and 4) HF-EX. Left circumflex coronary artery (LCX) rings were prepared with PAT left intact or removed. LCX reactivity to acetylcholine (ACh), endothelin (ET-1), bradykinin (BK), and sodium nitroprusside (SNP) was assessed in vitro using standard techniques. RESULTS: The results demonstrate that both ACh and ET-1 elicited dose-dependent increases in tension from LCX rings from all groups. Removal of PAT had no significant effect on ACh-induced contractions in any group. In contrast, removal of PAT increased ET-1-induced tension in LCX from NF-SED, HF-SED, and HF-EX but not NF-EX. PAT had no significant effect on relaxation responses to BK except in HF-EX animals, where removal of PAT increased BK-induced relaxation. PAT removal decreased SNP-induced relaxation in HF-LCX, but not LCX from NF pigs, suggesting basal release of a relaxing factor LCX from HF pigs. CONCLUSION: PAT blunts contractions induced by ET-1 in LCX from NF and HF pigs. Whereas EX abolished this effect of PAT in NF pigs, exercise did not alter the anticontractile effect in HF pigs.     

Meal-induced thermogenesis following exercise training in the rat

The effects of treadmill exercise on the thermic effect of a meal were studied in male Sprague-Dawley rats (370 to 400 g, 4 to 5 months of age). Rats were exercised for 60 min, 5 d.wk-1 for 8 to 10 wk, at a speed of 27 m.min-1 and with a grade of 8%. Sedentary (N = 9) and exercised (N = 8) rats were given food and water ad libitum. Oxygen consumption was measured at rest and following the ingestion of a meal consisting of 81% carbohydrate, 9% protein, and 10% fat (by calories). In those animals that were exercised, oxygen consumption measurements were performed 24 h after the completion of an exercise bout. Although all animals gained weight during the experimental period, the exercised group gained significantly less than did the sedentary rats. Resting oxygen consumption [ml/(min X g body mass.67)] was not significantly different between the exercised and sedentary rats. The ingestion of the high carbohydrate meal significantly increased mass-independent oxygen consumption above resting values in both groups; the values for the exercised rats were greater than those for the sedentary rats. However, there were no differences between the exercised and sedentary rats in meal-induced oxygen consumption when the data were expressed as a function of lean body mass [ml/(min X g lean body mass)] or as mass-independent lean body mass [ml/(min X g lean body mass.67)]. These data suggest that exercise-trained rats have increased diet-induced thermogenesis and may be one factor in the loss of weight sometimes found in response to exercise.     

苯那普利对动脉粥样硬化形成及循环内皮细胞与假血管血友病因子的影响作用

观察苯那普利对高胆固醇饲喂的家兔动脉粥样硬化形成及其对循环内皮细胞 (CEC)、假血管血友病因子(vWF)的影响。 2 4只新西兰雄性大白兔随机分成 3组 ,对照组饲喂普通饲料 ,动脉粥样硬化组饲喂 1 %胆固醇饲料 ,苯那普利组饲喂 1 %胆固醇及苯那普利5mg/d。实验前、实验后 5周、实验后 1 0周分别抽血测血脂、vWF、CEC计数。第 1 0周末处死大白兔 ,计算主动脉斑块面积。结果显示 ,苯那普利治疗组与动脉粥样硬化组血脂水平无明显变化 ,但动脉粥样硬化斑块面积却明显减少(P <0 0 1 ) ,其血浆vWF浓度亦明显降低(P <0 0 1 )。提示苯那普利具有抗动脉粥样硬化作用 ,其机制可能与保护内皮功能有关