低氧和低氧复合运动通过ERS-miR-208b-PGC-1α途径调控骨骼肌线粒体生物合成

目的:观察低氧及低氧复合运动对骨骼肌内质网应激(endoplasmic reticulum stress,ERS)及线粒体生物合成的影响,并探讨相关分子机制。方法:雄性Sprague-Dawley(SD)大鼠随机分为常氧对照组(NC组)、低氧对照组(HC组)和低氧复合运动组(HT组)。低氧干预为常压低氧帐篷,11.3%氧浓度持续暴露6周。运动干预为跑台训练(5°,15 m/min),60 min/d,6 d/周,共6周。低氧暴露结束后即刻处死大鼠,取双下肢股四头肌。紫外分光光度法检测股四头肌羰基化蛋白含量和谷胱甘肽巯基转移酶(GST)活性,荧光定量PCR法检测微小RNA-208b(miR-208b)表达,Western-blot法检测内质网应激相关蛋白葡萄糖调节蛋白78(GRP78)、蛋白激酶R样内质网激酶(PERK)总蛋白及磷酸化水平、真核起始因子2α(eIF2α)总蛋白及磷酸化水平、线粒体生物合成相关蛋白过氧化物酶体增殖物激活受体γ共激活因子-1α(PGC-1α)和细胞色素c氧化酶Ⅳ亚型(COXⅣ)蛋白表达。结果:与NC组比较,HC组骨骼肌羰基化蛋白含量、GRP78、p-PERK/...     

小檗碱对果糖诱导人肾小管细胞内质网应激PERK凋亡通路的影响

目的 探讨小檗碱对果糖诱导下肾小管上皮细胞凋亡的影响.方法 人肾小管上皮细胞株(HK-2细胞)于含10%胎牛血清的DMEM培养基中进行体外培养,然后随机分为正常组(C组)、果糖组(F组,含25mmol/L果糖培养液)、小檗碱组(B组,25mmol/L果糖+10μmol/L小檗碱)和TUDCA组(T组,25mmol/L果糖+2μmol/L TUDCA培养液).培养24h后收集细胞,Western blotting检测葡萄糖调节蛋白78(GRP78)、CHOP蛋白表达水平及蛋白激酶R样内质网激酶(PERK)、真核启始因子2α(eIF2α)的磷酸化水平,流式细胞仪检测各组细胞周期情况,TUNEL法检测各组细胞凋亡率.结果 与C组比较,F组GRP78、CHOP蛋白表达水平上调,同时p-PERK、p-eIF2α水平明显上升(P<0.05);与F组比较,B组、T组GRP78、CHOP、p-PERK、p-eIF2α表达水平均明显下降(P<0.05);T组与B组GRP78、CHOP、p-PERK、p-eIF2α表达水平比较无明显差异.与C组比较,F组HK-2细胞活力明显降低,细胞凋亡指数明显升高(P<0.05);与F组比较,B组和T组肾小管上皮细胞活力明显增加,细胞凋亡指数明显下降(P<0.05);T组B组细胞活力指数、细胞凋亡率比较无明显差异.结论 持续采用果糖培养HK-2细胞可激活细胞内PERK通路,引起内质网应激的发生,小檗碱能够抑制果糖诱导的PERK和eIF2α的磷酸化,下调GRP78、CHOP表达,从而调控PERK通路缓解细胞周期阻滞现象,降低细胞凋亡率.     

低强度脉冲超声对磷酸三钙磨损颗粒诱导的假体周围骨细胞损伤的影响

目的:观察低强度脉冲超声(LIPUS)对磷酸三钙(tricalcium phosphate,TCP)磨损颗粒诱导的假体周围骨细胞(osteocyte)损伤的影响,并探讨其可能作用机理。方法:取6~8周龄ICR雄性小鼠30只,随机分为正常组、模型组和LIPUS治疗组,每组10只。模型组和LIPUS治疗组小鼠分别于第1、3、5、7、9和第11周向颅顶注射TCP磨损颗粒建立小鼠颅骨溶解模型。正常组小鼠颅顶皮肤仅接受阴性超声探头按压处理,治疗组小鼠颅顶皮肤接受LIPUS干预治疗3个月,实验结束后取颅骨。采用Micro-CT分析各组小鼠颅骨TCP磨损颗粒植入部位周围溶解情况;应用HE染色比较各组假体周围骨细胞活性;通过流式细胞术定量检测各组假体周围骨细胞凋亡情况;采用免疫印迹技术检测各组假体周围骨细胞牙本质基质蛋白(DMP-1)、骨硬化蛋白(SOST)、葡萄糖调节蛋白78(GRP78)、肌醇依赖酶1α(IRE1α)、X盒结合蛋白(XBP1s)、c-Jun氨基末端激酶(JNK)及磷酸化JNK(p-JNK)等蛋白表达水平。结果:与正常组比较,模型组小鼠假体周围骨细胞活性明显降低,细胞凋亡显著(P<0.05),其特征蛋白DMP-1显著下调,SOST明显上调,造成DMP-1/SOST增加(P<0.05),且内质网应激通路蛋白GRP78、IRE1α、XBP1s和p-JNK表达水平显著增加(P<0.05)。而LIPUS治疗组假体周围骨细胞损伤及内质网应激反应显著减弱,表现为假体周围骨细胞活性、数量和DMP-1/SOST明显增加(P<0.05),且IRE1α-XBP1-JNK通路的活化被显著抑制(P<0.05)。结论:LIPUS可阻止TCP磨损颗粒诱导的假体周围骨细胞损伤,其作用机制可能与抑制IRE1α-XBP1-JNK信号通路介导的内质网应激反应密切相关。     

急性有氧运动对糖尿病大鼠肝脏和胰腺内质网应激蛋白和血糖的影响

目的:探讨急性有氧运动对糖尿病大鼠肝脏和胰腺内质网应激蛋白和血糖的影响,为糖尿病的运动疗法提供参考。方法:SPF级雄性SD大鼠55只,高脂饲料喂养配合腹腔注射小剂量链脲佐菌素制备2型糖尿病大鼠动物模型后,随机分为安静组(DM)和大、中、小三个强度有氧运动组(HIE-1、MIE-1、LIE-1),三个有氧运动组进行急性跑台运动,其运动速度分别为20 m/min、15 m/min和10 m/min,相当于70%VO2max、50%VO2max和30%VO2max负荷强度,持续运动1 h。运动后即刻检测空腹血糖(FBG)、糖化血清蛋白(GSP)、空腹胰岛素(Ins)、肝脏和胰腺的GRP78和caspase-12含量,并计算胰岛素抵抗指数(IRI)、胰岛素敏感指数(ISI)和β细胞功能指数(HBCI)。结果:各运动组糖尿病大鼠急性运动后血清空腹胰岛素较安静组均显著下降(P<0.01,P<0.01,P<0.05),胰岛素抵抗指数显著降低,胰岛素敏感指数显著升高,其中,大、中强度运动组变化有统计学意义(P<0.01)。中、小强度运动组肝脏和胰腺内质网应激蛋白GRP78和caspase-12较安静组均显著降低。结论:急性有氧耐力运动可降低糖尿病大鼠血糖水平,增强胰岛素敏感性,降低内质网过度应激状态,其机制可能与内质网应激蛋白参与调节有关。     

葛根总黄酮对力竭运动大鼠肝脏部分抗氧化指标和超微结构的影响

目的:探讨补充葛根总黄酮对耐力训练大鼠力竭运动后肝脏部分抗氧化指标、肝糖原含量和超微结构的影响。方法:24只雄性SD大鼠随机分为安静对照组、运动训练组和训练服药组。运动训练组和训练服药组进行7周递增强度耐力训练。训练服药组每天灌服一次葛根总黄酮悬浮液,安静对照组和运动训练组灌服相同体积的蒸馏水。测定运动训练组和训练服药组力竭运动后即刻及安静对照组安静时肝脏超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)的活性与丙二醛(MDA)含量、糖原含量及运动至力竭的时间等指标,并在电镜下观察大鼠肝脏超微结构的变化。结果:(1)训练服药组大鼠力竭时间(116.32±6.20min)显著长于运动训练组(94.82±9.05min)(P<0.05)。(2)运动训练组肝脏组织T-SOD、GSH-Px和CAT活性显著低于安静对照组(P<0.05),CuZn-SOD活性和MDA含量显著高于安静对照组((P<0.05);训练服药组T-SOD、GSH-Px、CAT、铜锌超氧化物歧化酶(CuZn-SOD)活性显著高于运动训练组(P<0.05),而MDA显著低于运动训练组(P<0.05)。训练服药组肝糖原含量显著高于运动训练组(P<0.05)。训练服药组血清谷丙转氨酶(GPT)活性显著低于运动训练组(P<0.05)。(3)电镜观察发现,安静对照组线粒体结构完整;运动训练组线粒体形态变异明显,其膜、嵴均有溶解,断裂现象,甚至整个线粒体崩解,出现空泡化,基质电子密度降低,粗面内质网减少,出现不规则扩张、断裂、扭曲;训练服药组线粒体、粗面内质网发生了损伤,但程度较运动训练组轻。结论:葛根总黄酮可提高肝脏抗氧化酶的活性,促进机体自由基的消除,维护肝细织的正常结构,促进肝糖原合成,具有延缓运动疲劳发生的作用。     

NRG1基因修饰的骨髓基质干细胞移植对大鼠脊髓半横切损伤的修复作用及其机制

目的 探讨移植神经调节蛋白1(NRG1)基因修饰的骨髓基质干细胞(BMSCs)对大鼠脊髓半横切损伤(SCI)的修复作用及其可能机制。方法 分离培养大鼠BMSCs,转染NRG1基因,采用ELISA法测定BMSCs裂解液和培养液上清中NRG1蛋白含量,细胞计数法检测BMSCs增殖活性。43只健康8周龄SD大鼠,随机分为对照组(n=10)、SCI模型组(n=10)、BMSCs组(n=10)与NRG1-BMSCs组(n=13)。建立大鼠脊髓半横切损伤模型后,原位移植BMSCs和NRG1-BMSCs。移植第1、7、14、21、28天,采用BBB评分、斜板实验评估大鼠后肢运动功能;移植第7天,应用荧光显微镜观察移植细胞迁移及分布情况;移植第28天,采用HE染色和Nissl染色观察大鼠脊髓组织病理学变化,TUNEL染色检测脊髓组织细胞凋亡情况,Western blotting检测脊髓组织内质网应激相关蛋白[X-box结合蛋白1(XBP1)、C/EBP同源蛋白(CHOP)、转录激活因子4(ATF4)、ATF6和葡萄糖调节蛋白78(GRP78)]及凋亡相关蛋白[B淋巴细胞瘤-2蛋白(Bcl-2)、Bcl...     

缺氧诱导乳鼠心肌细胞内质网应激的时效性观察

目的 研究不同缺氧时间心肌细胞内质网应激蛋白的表达变化,探讨内质网应激在心肌细胞凋亡中所起的作用.方法 将体外培养的乳鼠心肌细胞随机分为0h(对照组)及缺氧6、l2、18、24、30h组,缺氧组通入95％N,及5％ CO2混合气体进行不同缺氧时间处理,对照组在常氧状态下培养,不给予缺氧刺激.采用Western blotting检测内质网应激蛋白GRP78、CHOP及Caspase-12的表达变化,采用流式细胞术检测心肌细胞凋亡情况.结果 对照组GRP78蛋白有一定量的基础性表达,缺氧6h后蛋白表达呈上升趋势,缺氧12h时表达显著增加(P＜0.05),缺氧18h时表达至高峰,但随着缺氧时间延长(＞18h)GRP78表达呈下降趋势.缺氧12h内质网应激蛋白CHOP、Caspase-12蛋白开始表达,缺氧18～30h呈持续升高(P＜0.05).流式细胞术检测显示,缺氧12h即出现典型的细胞凋亡特征,缺氧18、24、30h组心肌细胞凋亡数量明显增多,与对照组比较差异有统计学意义(P＜0.05).结论 内质网应激在心肌细胞缺氧不同时期发挥不同的作用.     

重度低温诱导大鼠肾脏内质网应激通路活化研究

目的 观察轻度及重度低温条件下大鼠肾脏组织内质网应激 (endoplasmic reticulum stress ,ERS)通路相关分子表达及凋亡情况。方法 成年雄性SD大鼠,24只,随机分为3组,每组8只。分别为对照组（C组）,轻度低温组（MH组）和重度低温组（SH组）。利用低温水槽浸泡身体后将体温降低至目标体温后维持约60 min。术后复温12 h后,利用Western Blot实验观察各组的热休克蛋白70（heat?shock?protein 70,HSP70）,冷诱导RNA结合蛋白（Cold-inducible RNA-binding protein,CIRP）的表达变化及ERS通路相关分子蛋白激酶R样内质网激酶（PRKR-like endoplasmic reticulum kinase,PERK）、肌醇需求酶1α（serine/threonine-protein kinase/endoribonuclease inositol-requiring enzyme 1,IRE-1α）和免疫球蛋白重链结合蛋白（the immunoglobulin heavy chain binding protein,Bip）的活化情况,利用Western Blot和免疫组化方法观察ERS诱导凋亡分子C/EBP同源蛋白（the C/EBP Homologous Protein,CHOP）的表达以及分布。结果 和对照组比较,术后12 h,HSP70和CIRP均有不同程度上调。HSP70在MH组和SH组上调均较显著,CIRP蛋白在SH组上调更加显著。术后12 h,p-PERK和p-IRE-1均出现明显上调,Bip活化,提示ERS通路激活。重度低温组肾脏可观察到CHOP蛋白表达上调,进一步用免疫组化方法可以观察到CHOP主要表达在肾小管区域。结论 轻度及重度低温会诱导大鼠肾脏ERS通路活化,重度低温可诱导CHOP蛋白表达上调。     

运动和饮食调整对内质网应激介导非酒精性脂肪肝大鼠模型肝细胞凋亡的影响

目的:探讨运动和饮食调整对内质网应激介导非酒精性脂肪肝大鼠模型肝细胞凋亡的影响及其机制。方法:70只雄性SD大鼠中随机抽取20只为对照组,其余50只为模型组,对照组予普通饲料喂养,模型组予高脂饲料喂养。实验第8周,对照组和模型组各取10只做肝脏病理切片。确定NAFLD模型成功后,模型组随机分为4组:模型组(M组)、运动组(EM组)、饮食调整组(FM组)和运动结合饮食调整组(EFM组),每组各10只,对照组剩余10只大鼠编为C组。C组继续普通饲料喂养,M组和EM组继续高脂饲料喂养,FM组和EFM组由高脂饲料改为普通饲料喂养;EM组、EFM组给予有氧游泳运动干预,每周运动6 d,每天1次,每次60 min,连续8周,直至第16周实验结束。油红O染色观察肝脏病理形态变化,TUNEL法测肝细胞凋亡,western blot检测C/EBP同源蛋白(CHOP)、C-Jun氨基末端激酶(JNK)和Caspase12蛋白表达,免疫组化检测CHOP、JNK和Caspase12蛋白阳性表达。结果:(1)M组肝细胞脂滴数量显著高于C组,各干预组脂滴数量介于C组和M组之间;(2)M组肝细胞凋亡指数高于C组,CHOP、Caspase12、JNK蛋白表达及阳性表达较C组高;各干预组肝细胞凋亡指数低于M组,CHOP、Caspase12、JNK蛋白表达及阳性表达较M组低;(3)M组、EM组、FM组、EFM组4组双因素方差结果示:运动和饮食对CHOP、Caspase12、JNK蛋白表达具有主效应,且二者具有叠加交互效应。结论:内质网应激介导细胞凋亡参与NAFLD的发展,运动和饮食调整可延缓NAFLD的发展,且二者联合作用效果更佳,其机制与运动和饮食调整降低内质网应激介导细胞凋亡蛋白CHOP、JNK和Caspase12在肝细胞的表达,抑制肝细胞凋亡有关。     

长期运动训练诱导SD大鼠骨骼肌糖原含量上调的分子机制

目的:探讨长期运动训练上调骨骼肌糖原含量的可能分子机理。方法:60只SD大鼠随机分为安静组和运动组,两组按照干预时间再分别分为1周组、4周组和8周组。各运动组进行5次/周、60 min/次的中等强度跑台运动,各安静组则在鼠笼内自由活动。末次实验后48 h处死动物,分别测定大鼠体重,血糖、血清胰岛素、肌糖原含量,葡萄糖摄取率,糖原磷酸化酶、糖原合酶、PP1活性,GLUT4、糖原合酶、磷酸化的糖原合酶、GSK-3α、GSK-3β、磷酸化的GSK-3α和GSK-3β、PP1c、RGL(GM)蛋白表达量。结果:(1)大鼠训练8周时体重显著低于安静组(P<0.05),而血糖和血清胰岛素在各时间点均无显著性变化(P>0.05);(2)肌糖原含量在训练1周时与安静组无显著性差异(P>0.05),训练4周和8周时显著升高(P<0.01);(3)运动组和安静组糖原磷酸化酶活性在各时间点均无显著性差异(P>0.05);(4)运动组GLUT4蛋白水平在各时间点均显著高于安静组(P<0.01),而胰岛素介导的葡萄糖摄取率则在训练4周和8周时显著高于安静组(P<0.01);(5)运动组糖原合酶的活性、总蛋白及磷酸化蛋白表达量在训练4周和8周时显著高于安静组(P<0.01);(6)4周和8周时,运动组PP1活性显著高于安静组(P<0.01),PP1c蛋白表达量无显著性变化(P>0.05),RGL(GM)蛋白水平显著低于安静组(P<0.01);(7)GSK-3α和GSK-3β总蛋白水平在训练1周时下降(P<0.01),而训练4周和8周时与安静组无显著性差异(P>0.05),GSK-3α磷酸化蛋白水平在训练1周、4周和8周时均显著性下降(P<0.01),GSK-3β磷酸化蛋白水平在各时间点均无显著性差异(P>0.05)。结论:(1)长期运动训练诱导的骨骼肌糖原含量增加是糖原合成增多而非糖原分解减少造成的;(2)长期运动诱导的糖原合成增加可能与肌细胞对葡萄糖转运增加、糖原合酶表达上调、PP1活性增加以及G-6-P对糖原合酶的变构激活等因素有关。     

运动性低血睾酮及补肾中药对大鼠能量代谢某些指标的影响

以SD雄性大鼠为研究对象 ,测定了安静对照 (C组 )、长期耐力运动 (T1组 )及运动性低血睾酮 (T2组 )状态下大鼠肝糖原、肌糖原浓度和骨骼肌磷酸肌酸激酶 (CK)、丙酮酸激酶 (PK)及苹果酸脱氢酶 (MDH)活性 ,并就补肾中药(T3组 )对上述指标变化的影响进行了探讨。结果发现 :经过 5周的大强度流动水游泳运动 ,T2组大鼠血清睾酮明显下降 (P <0 0 5 ) ,T1及T3组大鼠则无显著变化 ;运动各组大鼠肌糖原浓度虽有上升趋势 ,但无明显改变 ;T2及T3组大鼠肝糖原含量较C组明显增加 (P <0 0 5 ) ;各组大鼠股四头肌CK、PK活性均无明显差异 ;T2、T3组MDH活性有显著性提高 (P <0 0 5 )。我们认为 :运动性低血睾酮的内分泌变化 ,尚未影响到大鼠体内的糖储备和骨骼肌能量代谢其它指标的变化。补肾中药虽可对运动性低血睾酮的血睾酮浓度变化起纠正作用 ,但并未改变其它指标的变化。     

Exhaustive running: inappropriate as a stimulus of muscle glycogen super-compensation

Muscle glycogen super-compensation, as demonstrated after exhaustive cycling, may be affected by mode of exercise and state of training. Hence, we studied the effect of exhaustive running on post-exercise changes in muscle glycogen concentration in untrained subjects and compared the effect of tapered running with an exhaustive bout of running in well-trained runners. Six trained runners (T), 6 untrained subjects (UT), and 6 physically active subjects participated. Four hundred grams of carbohydrate were given for 2 d (PX2 and PX1) before exercise and 600 g for 3 d (R1, R2, and R3) with rest afterwards. Before exercise, T and UT were restricted in physical activity. Biopsies were obtained from the gastrocnemius muscle on PX2 and PX1 in T, and before (PX0), immediately after exercise (R0), and on R1, R2, and R3 in all groups. Muscle glycogen increased from 110 (+/-14) on PX2 to 180 (+/-11) mmol X kg-1 on PX0 in T (P less than 0.001). This PX0 value was higher than the PX0 value for UT, which was 102 (+/-8) mmol X kg-1 (P less than 0.005). R0 values were 57 (+/-14) and 26 (+/-4) mmol X kg-1, respectively. On R1, the glycogen concentration had increased to 127 (+/-10) and 87 (+/-3) mmol X kg-1 (P less than 0.001). No changes occurred during R2 and R3. In a supplementary study, physically active subjects rested (series I) or ran lightly for 40 min (series II) on PX2 and PX1, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of previous exhaustive exercise on metabolism and fatigue development during intense exercise in humans

The present study examined how metabolic response and work capacity are affected by previous exhaustive exercise. Seven subjects performed an exhaustive cycle exercise (～130%‐max; EX2) after warm‐up (CON) and 2 min after an exhaustive bout at a very high (VH; ～30 s), high (HI; ～3 min) or low (LO; ～2 h) intensity. Compared with CON, performance during EX2 was reduced (P<0.05) more in HI and LO than in VH (61±4% and 68±3% vs 35±4%). The muscle glycogen before EX2 was lower (P<0.05) in LO than in HI and VH, but the muscle glycogen utilization rates during EX2 were not different. Muscle glycogen concentration before EX2 was related (P<0.05) to the mean rate of muscle glycogen utilization during EX2 in HI and VH, and the mean rate of muscle lactate accumulation in LO. In HI, muscle pH before EX2 was lower (P<0.05) compared with VH and LO, but the same in HI and VH at the end of EX2. In HI, muscle pH before and after EX2 was inversely related (P<0.05) to the decrease in EX2 performance. Thus, muscle glycogen availability and low muscle pH do not per se control but appear to affect the rate of glycogenolysis/glycolysis and fatigue development during a repeated high‐intensity exercise lasting 1/2–2 min.     

人参皂甙Rg_1促进小鼠力竭游泳后体能恢复的作用

目的 :研究人参皂甙Rg1对力竭运动后小鼠体能恢复的作用 ,并从糖代谢角度探讨其机理。方法 :以小鼠为实验动物 ,测定力竭游泳时间和不同恢复时间点的血糖浓度、肌糖原含量、肝糖原含量及血乳酸浓度。结果 :(1 )人参皂甙Rg1给药组小鼠第二次力竭游泳时间较对照组明显延长。 (2 )力竭游泳后恢复期 ,糖原含量的增加、血乳酸浓度降低比对照组明显加快。结果表明 ,人参皂甙Rg1能促进力竭游泳后体能的恢复 ,其机制可能与其能促进糖原合成及加速乳酸清除有关。     

Carbohydrates do not accelerate force recovery after glycogen-depleting followed by high-intensity exercise in humans

Prolonged low-frequency force depression (PLFFD) induced by fatiguing exercise is characterized by a persistent depression in submaximal contractile force during the recovery period. Muscle glycogen depletion is known to limit physical performance during prolonged low- and moderate-intensity exercise, and accelerating glycogen resynthesis with post-exercise carbohydrate intake can facilitate recovery and improve repeated bout exercise performance. Short-term, high-intensity exercise, however, can cause PLFFD without any marked decrease in glycogen. Here, we studied whether recovery from PLFFD was accelerated by carbohydrate ingestion after 60 minutes of moderate-intensity glycogen-depleting cycling exercise followed by six 30-seconds all-out cycling sprints. We used a randomized crossover study design where nine recreationally active males drank a beverage containing either carbohydrate or placebo after exercise. Blood glucose and muscle glycogen concentrations were determined at baseline, immediately post-exercise, and during the 3-hours recovery period. Transcutaneous electrical stimulation of the quadriceps muscle was performed to determine the extent of PLFFD by eliciting low-frequency (20 Hz) and high-frequency (100 Hz) stimulations. Muscle glycogen was severely depleted after exercise, with a significantly higher rate of muscle glycogen resynthesis during the 3-hours recovery period in the carbohydrate than in the placebo trials (13.7 and 5.4 mmol glucosyl units/kg wet weight/h, respectively). Torque at 20 Hz was significantly more depressed than 100 Hz torque during the recovery period in both conditions, and the extent of PLFFD (20/100 Hz ratio) was not different between the two trials. In conclusion, carbohydrate supplementation enhances glycogen resynthesis after glycogen-depleting exercise but does not improve force recovery when the exercise also involves all-out cycling sprints.     

La récupération après l'exercice. Analyse de la réplétion des réserves énergétiques

According to the intensity and the duration of exercise, depletion of substrates may be important. After exhaustive exercise the muscular store of creatine phosphate (CP) could be almost entirely depleted while the ATP store is half depleted. The resynthesis of both substrates occurs rapidly (5 min) during recovery. However, the repletion of CP is totally inhibited if the local circulation to the muscle is occluded. It is suggested that the initial fast phase of CP resynthesis is limited by the availability of oxygen whereas the subsequent slow phase is limited by the hydrogen ion transport out of the muscle.After liver glycogen is depleted by prolonged exercise, gluconeogenesis becomes necessary through lactate, pyruvate, glycerol and amino acids. As estimated from splanchnic uptake of gluconeogenic precursors, 60–65% of newborn glucose leave the liver and are taken up by the muscles which have been active. Total repletion of liver glycogen is completed 48 h after cessation of exercise with adequate glucose supply.Rapid muscle glycogen occurs in response to carbohydrate feeding following prolonged exercise, leading sometimes to supercompensation. Usually the repletion of glycogen is completed after 24 h if a normal diet (55% carbohydrate) is taken up by the subject. The synthesis of glycogen depends on several factors namely, (1) a persistent increase in glucose uptake by the muscle following exercise, up to 4–6 h, (2) an increase in insulin sensitivity which persists for 4 h following the exercise, (3) an inverse relation between the active form of glycogen synthase and glycogen content, (4) lactate which is rapidly incorporated into glycogen in fast-twitch fibres. It seems probable that glucose is the major substrate for glycogen synthesis in muscle following prolonged exercise of moderate intensity. In contrast, short bouts of heavy exercise result in glycogen repletion from lactate which could play an extended role in this context. Eventually, the regulation of glycogen resynthesis in muscles and liver following exercise depends on several ligands which operate on different key-enzymes.After prolonged physical exercise, lipoprotein lipase activity in skeletal muscle remains increased for several hours or days according to the type of exercise. Post-exercise ketosis occurs in untrained subjects and may be due to a lower carbohydrate intake than that of athletes. Hepatic malonyl-CoA, in subjects who have sufficient liver glycogen, is likely to be the responsible factor for the degree of post-exercise ketosis between trained and untrained subjects.Increased sensitivity to insulin after exercise also stimulates amino acid transport in red fibre muscles. After short bouts of exercise, protein synthesis rates in muscles appear to decrease in the first hour after exercise, but in the second hour after work increase to levels greater than normal.‘Substrate cycles’ appear to be involved in the ‘ultra slow’ component of post-exercise oxygen consumption. It has been calculated that substrate cycles and the repletion of glycogen and protein could account for an extra oxygen uptake of 50 l for a period of 12 h following prolonged and intensive exercise.     

开心散对缺氧和力竭运动小鼠的抗氧化及抗疲劳作用研究

目的 研究中药复方开心散的耐缺氧及抗疲劳作用.方法 通过小鼠常压耐缺氧实验观察开心散的耐缺氧作用及对脑组织中SOD活力和MDA含量的影响.观察开心散在小鼠转轮疲劳模型上运动力竭小鼠被电击的次数和对肝糖原、肌糖原、肌乳酸含量和血清中SOD活力和MDA含量的影响.结果 中、高剂量(250、500 mg/kg)组的开心散能明...     

急性离心运动后骨骼肌超微结构、钙依赖性蛋白酶和泛素的动态变化

目的:探讨1次离心运动后大鼠骨骼肌超微结构、Calpains和Ubiquitin的动态变化。方法:30只雄性SD大鼠随机分为对照组和1次离心运动后即刻组、24 h组和7天组。各运动组大鼠进行1次下坡跑运动,速度16 m/min,坡度?16°,运动100 min后休息10 min,再运动100 min,总时间200 min。分别在急性运动后即刻、24 h和第7天取材,测定血清LDH、CK活性和股四头肌超微结构及Calpain-1、Calpain-2和Ubiquitin含量。结果:①1次离心运动后即刻组大鼠股四头肌肌丝排列混杂、卷曲;运动后24 h出现轻度溶解、断裂,Z线不规则,局部Z线消失;运动后7天超微结构与对照组相比无显著变化。血清CK和LDH活性变化与股四头肌超微结构变化一致。②与对照组相比,运动后即刻组大鼠股四头肌Calpain-1、Calpain-2和Ubiquitin含量均有所降低,但均无显著性差异;运动后24 h组股四头肌Calpain-1、Calpain-2和Ubiquitin含量均显著高于对照组和运动后即刻组;运动后7天组与运动后24 h组相比均显著下降,而与对照组相比均无显著性差异。结论:①1次离心运动所致的骨骼肌损伤有一定的延迟性,骨骼肌损伤在运动后即刻从整体看并不严重,但在运动后24 h出现明显损伤,运动后7天基本恢复。②急性离心运动后骨骼肌Calpain和Ubiquitin含量变化与骨骼肌损伤的动态变化基本一致。