Effects of downhill treadmill running on uncoupling protein 3 mRNA expression

Eccentric biased exercise has been reported to elicit more muscle injury than concentric or isometric exercise and potentially generate increased oxidative stress one to two days post exercise. Increased oxidative stress has been shown to up-regulate the expression of UCP3 mRNA. The aim of this study was to investigate the effects of downhill running on skeletal muscle UCP3 mRNA expression. Twenty-four male Sprague Dawley rats were randomly assigned to run continuously for 30 minutes (30-C, n = 6), or run six 5-minute bouts separated by rest periods of 2 minutes (2-R, n = 6), 4 minutes (4-R, n = 6), and 6 minutes (6-R, n = 6) on a 16 degree declined treadmill at a speed of 16 m. min (-1). Sham control animals (n = 8) were placed in a treadmill chamber during the 30-minute run session. Semi-quantitative RT-PCR was conducted to evaluate UCP3 mRNA levels in the plantaris, a muscle used eccentrically during downhill running and tibialis anterior, a muscle which undergoes very little eccentric muscle contraction during this exercise. The level of gene expression was normalized to 18 S ribosomal mRNA expression from the same PCR product. Results are reported as mean +/- standard error. UCP3 of the plantaris muscles from 2-R animals (2.36 +/- 0.13) was significantly greater than UCP3 of the plantaris from control animals (1.72 +/- 0.13), p < 0.05. UCP3 of the tibialis anterior from the continuous group (1.51 +/- 0.17) was significantly less than the UCP3 of the tibialis anterior of the control group (2.09 +/- 1.4), p < 0.05. These data suggest that downhill treadmill running is associated with an increase in UCP3 mRNA expression in the plantaris muscle. These results indicate that exercise which is biased toward eccentric exercise may up-regulate UCP3 mRNA during the period post exercise when muscle damage and repair is elevated.     

中药对大鼠急性骨骼肌拉伤后骨骼肌α-actinmRNA表达的影响

本研究建立了急性骨骼肌拉伤的动物实验模型 ,观察了不同治疗措施对拉伤后动物骨骼肌α -actinmRNA表达的影响。结果表明 :(1)急性拉伤后即刻 ,动物骨骼肌α-actinmRNA表达量显著增高 ,伤后第 1天、第 2天保持显著性高水平 ,至第 5天恢复至正常水平 ,但第 14天又显著增高 ;(2 )舒筋活血类中药抑制骨骼肌拉伤后α -actinmRNA表达的第 2次升高。研究提示 ,舒筋活血类中药能更有效地促进急性骨骼肌拉伤后α -actinmRNA表达的恢复。     

Induction of mitochondrial stress proteins following treadmill running

PURPOSE: The purpose of this investigation was to examine the relationship between the expression of HSP60 and GRP75 and the oxidative potential of skeletal muscle as assessed by the citrate synthase activity following endurance training to sedentary controls. METHODS: Female Wistar rats were assigned to one of two groups: sedentary controls (N = 8) or endurance trained (N = 9). Endurance trained rats were run 60 min x d(-1) at 27 m x min(-1) up a 10% incline 6 d x wk(-1) for 8 wk on a motor-driven treadmill. RESULTS: Training produced a 47% increase in citrate synthase activity along with a 103% increase in the expression of HSP60 and a 105% increase in the expression of GRP75 in plantaris muscle. In addition, there was a significant correlation between the citrate synthase activity and expression of HSP60 found in plantaris muscle. CONCLUSIONS: These findings are consistent with the hypothesis that the adaptive response to treadmill running may require elevations in the expression of HSP60 and GRP75 to support protein import and folding.     

一氧化氮合酶抑制剂对7d尾部悬吊大鼠心血管脱锻炼的对抗效应

目的揭示模拟微重力大鼠心血管脱锻炼 (CVD)病理生理学变化 ;探索一氧化氮合酶抑制剂对抗模拟微重力大鼠CVD的效应。方法 - 30° 7d尾部悬吊 (TS 7d)模拟微重力生理效应。Wistar大鼠被随机分成 3组 :自由活动对照组 (CON)、7d尾部悬吊组 (TS 7d)和 7d尾部悬吊后用药组 (TS 7d +L NAME )。头向上倾斜 90°( + 90°HUT) 1 2 0min模拟立位应激时的生理效应 (simulatedorthostatism ,SO)。 1 0 - 6 MN 硝基 L 精氨酸甲酯 (N nitro L argininemethylester ,L NAME)经舌下静脉注射给药。PowerLab生理记录系统检测SO 1 2 0min颈动脉压和肢Ⅱ导心电 ,分析平均动脉压 (MAP)和心率(HR)。结果CON大鼠仅在SO 1 2 0min时出现一次低血压、心动过缓情节 ,TS 7d大鼠出现 7次低血压、心动过缓情节 ,TS 7d +L NAME大鼠仅MAP在SO 1 0min与CON大鼠比显著升高 ,其余参数在平卧位或SO期间与CON大鼠变化无差异。结论TS 7d大鼠出现的CVD与NO产生量增加有关 ,1 0 - 6 ML NAME能较好对抗CVD效应 ,可能与L NAME同NOS结合增加外周血管阻力和中枢交感输出增加有关 ,L NAME对血管周神经和肺循环动脉系统的作用在其中的贡献有待于进一步研究。     

Aging does not attenuate plantaris muscle hypertrophy in male Fischer 344 rats

PURPOSE: The present study examined the effect of extreme old age on the plasticity of the rat plantaris muscle in response to an increase in mechanical load. METHODS: Male Fischer 344 rats, aged 7 months (adult) and 25 months (old) underwent bilateral surgical ablation of the gastrocnemius muscle to functionally overload (OV) the fast-twitch plantaris muscle for 8 wk RESULTS: At 27 months of age, plantaris wet weight and cross-sectional area (CSA) were unaffected by age, but aging decreased peak isometric tension (Po) 27% (P < 0.05). Plantaris muscle myosin heavy chain composition indicated a loss of faster myosin heavy chains (MHC) isoforms with concomitant increases in slower MHC in old rats (P < 0.05). In adult rats, OV increased muscle CSA and Po 72% and 83%, respectively (P < 0.05). Similarly, OV increased CSA and Po 69% and 73%, respectively, in old rats (P < 0.05). Average fiber CSA increased 57% and 68% in adult-OV and old-OV rats, respectively (P < 0.05). CONCLUSION: Collectively, our data indicate that plantaris muscle mass and plasticity in response to increased mechanical load are well conserved in very aged male Fischer 344 rats.     

大豆异黄酮对围绝经期大鼠卵巢VEGF和NOS亚型mRNA表达的影响

目的 观察大豆异黄酮(SI)对围绝经期大鼠卵巢血管内皮生长因子(VEGF)及一氧化氮合酶亚型eNOS、iNOS mRNA表达的影响.方法 12月龄雌性Wistar大鼠42只,随机分为模型组,低(50mg/kg)、中(158 mg/kg)、高(500mg/kg)剂量SI组及尼尔雌醇(NI)组,另取3月龄大鼠10只作为青年组,灌胃给药8周.RT-PCR检测卵巢VEGF和NOS mRNA的表达;比色法检测血清和卵巢总NOS的活性.结果 围绝经期大鼠卵巢VEGF表达明显高于青年组(P＜0.01),eNOS、iNOS表达及血清、卵巢总NOS活性均较低(P＜0.01).经SI处理后,VEGF表达均明显下降,NOS表达及活性明显升高(P＜0.05或P＜0.01).结论 大豆异黄酮下调衰老卵巢VEGF mRNA表达,提高eNOS、iNOS表达及活性,可能是其改善围绝经期卵巢功能的机制之一.     

Unaltered aerobic power and endurance following glucocorticoid-induced muscle atrophy

The present study was undertaken to evaluate whether the muscle atrophy associated with glucocorticoid excess results in a reduction in maximal oxygen uptake (VO2max) and endurance during exercise. Female rats were administered single subcutaneous injections of cortisone acetate (CA) (100 mg X kg-1 b.w.) or the vehicle (1% carboxymethyl cellulose) for 14 consecutive days. The weights of plantaris muscles (which were used as a marker of the atrophy) of CA-treated rats were 27% less than those of plantaris muscles in the vehicle-treated rats. This condition also produced a 12-fold increase in free serum glucocorticoid concentrations (cortisol) but did not alter serum androgen (testosterone) levels. Peak VO2 (ml X kg-1 X min-1) and endurance were greater in CA-treated vs vehicle-treated animals; however, these effects were shown to be a function of body weight loss. Homogenate oxygen uptakes in the presence of pyruvate or palmitate were also similar in slow-twitch soleus, fast-twitch red vastus, and fast-twitch white vastus lateralis muscles between CA- and vehicle-treated groups. These data provide no evidence to demonstrate that the catabolic actions of glucocorticoids in skeletal muscle result in a decrement in work capacity through at least 14 d of treatment.     

Capillarization in skeletal muscle of rats with cardiac hypertrophy

PURPOSE: Exercise intolerance during chronic heart failure (CHF) is localized mainly in skeletal muscle. A decreased capillarization may impair exchange of oxygen between capillaries and muscle tissue and in this way contribute to exercise intolerance. We assessed changes in capillary supply in plantaris and diaphragm muscles of a rat aorta-caval fistula (ACF) preparation, a volume overload model for CHF. METHODS: An ACF was created under equithesin anesthesia. Plantaris and diaphragm muscles were removed 6 wk postsurgery and examined for myosin heavy chain (MyHC) content and capillary supply. RESULTS: Cardiac hypertrophy was 96% (P < 0.002) after ACF. The Type IIb MyHC content of the plantaris muscles increased (33.9 +/- 3.3 vs 49.8 +/- 3.8%; mean +/- SEM) at the expense of Type IIa MyHC (17.6 +/- 1.8 vs 11.2 +/- 1.7%) in ACF rats (P < 0.05). In the diaphragm, the number of Type I (32.1 +/- 2.3 vs 40.6 +/- 2.7%) and IIb fibers (40.6 +/- 1.9 vs 49.6 +/- 3.6%) increased at the expense of Type IIa fibers (26.8 +/- 2.5 vs 9.4 +/- 0.9%) (P < 0.05). The capillary number per fiber did not change, and this indicated that no capillary loss occurred with ACF. Also, the capillary density was maintained in the diaphragm and plantaris muscles of ACF rats. Furthermore, the coupling between fiber type, size, and metabolic type of surrounding fibers, with the capillary supply to a fiber, was maintained in rats with an ACF. CONCLUSION: The cardiac hypertrophy induced by volume overload seems adequate to prevent atrophy and changes in the microcirculation of limb and diaphragm muscles.     

EP2 receptor plays pivotal roles in generating mechanical hyperalgesia after lengthening contractions

We previously demonstrated that nerve growth factor (NGF ) and glial cell line‐derived neurotrophic factor (GDNF ) were upregulated after lengthening contractions (LC ) in exercised muscle through B2 bradykinin receptor activation and cyclooxygenase (COX )‐2 upregulation, respectively, and that these trophic factors sensitized nociceptors resulting in mechanical hyperalgesia (delayed‐onset muscle soreness, DOMS ). Here, we examined the prostaglandin receptor subtype involved in DOMS . The mechanical withdrawal threshold of the exercised muscle was measured before and after LC in rats administered prostaglandin E₂ receptor (EP ) antagonists before LC , or in wild‐type (WT ), EP 2 knockout (EP 2^−/−), and IP knockout (IP ^−/−) mice. The change in expression of NGF , GDNF , or COX ‐2 mRNA was examined using real‐time RT ‐PCR in the muscle in EP 2^−/− and WT mice. None of the antagonists to EP 1, EP 3, and EP 4 receptors (ONO ‐8713, ONO ‐AE 5‐599, and ONO ‐AE 3‐208, respectively) induced a significant difference in DOMS compared with controls in rats. WT and IP ^−/− mice developed mechanical hyperalgesia after LC , but EP 2^−/− mice did not. Upregulation of NGF , GDNF , and COX ‐2 mRNA was observed after LC in WT mice but not in EP 2^−/− mice. Injecting an EP 2 agonist (ONO ‐AE 1‐259‐01) into the mouse muscle increased expression of COX ‐2 mRNA . These results suggest that EP 2 contributes to generating mechanical hyperalgesia through positive feedback upregulation of COX ‐2 expression in muscle after LC.     

安多霖对微波辐射致大鼠海马细胞色素C氧化酶变化的影响

目的探讨中药复方制剂（安多霖）对微波辐射后大鼠海马线粒体呼吸链细胞色素C氧化酶（cytochromec oxidase,COX）变化的影响。方法 100只Wistar雄性大鼠随机分为3个对照组,即正常对照组、辐射预防对照组、辐射治疗对照组和2个安多霖组,即3 g/（kg.d）安多霖预防组及3 g/（kg.d）安多霖治疗组,每组20只。安多霖预防组大鼠于给药后第15天进行微波辐射;安多霖治疗组大鼠于辐射后当天开始连续给药14 d,均1次/d。采用30 mW/cm2微波辐射15 min,于辐射后6 h和14 d活杀动物取海马,通过比色法检测大鼠海马COX活性的变化;采用实时定量PCR和Western印迹检测大鼠海马COXⅠ、ⅣmRNA以及COXⅠ蛋白表达变化。结果辐射预防和治疗两对照组于停药后6 h COX活性、COXⅠ、ⅣmRNA,COXⅠ蛋白均降低（P〈0.05或P〈0.01）;安多霖预防组较辐射预防对照组COX活性及基因表达有不同程度提高,与正常对照组无明显差异;安多霖治疗组与辐射治疗对照组相比明显提高（P〈0.05）,且基本恢复正常。结论给予3 g/（kg.d）安多霖对微波辐射致大鼠海马线粒体呼吸链COX表达降低有较明显改善作用,其治疗效果更为显著。     

肌球蛋白重链II_xmRNA表达可能为大鼠比目鱼肌废用的分子标志

目的建立大鼠跟腱切断模型 ,观测并比较跟腱切断与尾部悬吊大鼠比目鱼肌重量与肌球蛋白重链 (MHC)异构体mRNA表达的变化 ,为探讨骨骼肌废用性萎缩的机理提供实验线索。方法选取雄性SD大鼠 30只 ,随机分为 6组 ,每组 5只。直接切断跟腱 ,称量肌腱切断后第 1、3、7、1 4、2 1、2 8天比目鱼肌 (SOL)、腓肠肌内外侧头 (MG ,LG)与跖肌 (PL)的湿重。用RT PCR法观测SOLMHC异构体mR NA的表达。结果跟腱切断后第 3天 ,SOL出现明显萎缩 ,在第 7与 1 4天萎缩达最低点 ,从第 2 1天开始 ,萎缩的SOL重量有所恢复。MG、LG与PL重量的变化趋势与SOL基本一致。在正常SOL中 ,仅有MHCI与IIa mRNA表达。从跟腱切断的第 3天开始直至第 2 8天 ,SOL中出现MHCIIx mRNA的表达 ,但无MHCIIb 的表达。结论跟腱切断引起的SOL萎缩在出现时间与程度上 ,与尾部悬吊相似。两种模型均可引起SOL中MHCIIx mRNA表达 ,推测MHCIIx 可能为骨骼肌废用的分子标志     

NO-cGMP参与大鼠骨骼肌线粒体生物合成:耐力训练和L-精氨酸补充的作用

目的:探讨6周耐力训练和补充一氧化氮(NO)前体L-精氨酸(L-Arg)是否可以促进骨骼肌中NO-cGMP的生成,研究NO在耐力训练诱导的骨骼肌线粒体生物合成中的信号作用。方法:24只雄性SD大鼠随机分为4组:正常对照组(NC)、6周跑台训练组(Ex)、6周L-Arg补充组(L-Arg)以及6周训练和L-Arg补充组(L-Arg+Ex)。训练组每天进行90分钟跑台训练,每周5天,共计6周。L-Arg补充组补充L-Arg,剂量为每天500mg/千克体重,为期6周。取小腿三头肌,采用硝酸还原酶法测定NO浓度;放射免疫法测定cGMP浓度;荧光定量PCR分析PGC-1α、NRF-1、Tfam和COX IV mRNA水平以及采用Western blotting测定PGC-1α与COX IV蛋白含量。结果:Ex组与NC组相比较,骨骼肌NO浓度轻微增加,cGMP浓度显著增加,NRF-1、Tfam和COX IV mRNA水平以及PGC-1α和COX IV蛋白水平均显著增加;L-Arg+Ex组与NC组相比,NO、cGMP浓度和NRF-1和Tfam mRNA水平显著提高,PGC-1α蛋白含量和COX IV mR-NA和蛋白含量显著增加。结论:NO-cGMP信号通路可能参与了耐力训练诱导的骨骼肌线粒体生物合成。     

Nitric oxide synthase expressions in mice skeletal muscle subjected to ischemia/reperfusion injury

Nitric oxide synthase (NOS) expressions in skeletal muscle subjected to ischemia/reperfusion (I/R) were studied using a hind limb tourniquet ischemia model in mice. A rubber band was applied to a hind limb for 3 h under isoflurane anesthesia followed by 1 or 4 h of reperfusion. Increased NADPH diaphorase activity and NOS immunoreactivity were histochemically detected in the cells of muscle that had been subjected to I/R. The results of RT-PCR of the muscle subjected to I/R showed that NOS mRNA expressions were not significantly increased until 4 h after the start of reperfusion. Since there was no significant difference between histochemical findings or between water contents of the hind limbs or organs in interleukin (IL)-6-deficient mice and the wild-type mice, IL-6 may not be involved in the early stage of I/R muscle injury such as that in this model. O(2)(-) production in the cells of muscle that had been subjected to I/R was observed using an in situ detection method with hydroethidine, and the O(2)(-) was inhibited by intravenous administration of L-NAME or L-NMMA, but not L-NIL, 30 min before tourniquet release. Further study is needed to evaluate the role of O(2)(-) produced by constitutive NOS in muscle subjected to I/R in the pathophysiology of tourniquet shock.     

有氧耐力训练对增龄大鼠骨骼肌线粒体生物合成的影响

目的:观察增龄大鼠骨骼肌线粒体生物合成的变化特点,探讨有氧耐力训练诱导增龄大鼠骨骼肌线粒体生物合成的分子机理。方法:中等强度跑台运动(64%VO2max,5°,15m/min,45min,每周5天)施加于2、12和17月龄雄性大鼠共12周,对照组正常饲养。12周后取大鼠比目鱼肌和股外侧深层肌进行分子生物学指标检测。结果:(1)增龄过程中,PGC-1α和NRF-1 mRNA表达、mtTFA蛋白表达随增龄显著增加,而mtTFA和COXIV mRNA表达、PGC-1α和COXIV蛋白表达随增龄无显著变化。(2)耐力训练后,5MT组PGC-1α mRNA和蛋白表达、15MT组PGC-1α mRNA表达显著高于各自对照组,5MT和15MT组NRF-1 mRNA表达分别显著高于各自对照组,20MT组PGC-1α mRNA和蛋白表达、NRF-1 mRNA表达相对于20MC组无显著变化,各月龄训练组mtTFA mRNA表达、COXIV mRNA和蛋白表达均显著高于各自对照组。结论:(1)增龄过程中PGC-1α、NRF-1、mtTFA和COXIV mRNA和蛋白水平的变化呈现非同步趋势,提示增龄过程中线粒体生物合成受复杂的多条途径调控;(2)耐力训练能够诱导PGC-1α、NRF-1、mtTFA和COXIV表达显著增加,促进骨骼肌线粒体生物合成;(3)耐力训练诱导骨骼肌线粒体生物合成的适应性积累效应随着大鼠年龄递增逐渐递减。     

耐力训练与补充不同剂量L-Arg对大鼠股外肌NOS基因表达的影响

目的:本研究旨在探讨耐力训练和补充不同剂量外源性L-Arg对耐力训练后和力竭运动恢复期大鼠股外肌NOS基因表达的影响.方法:采用定量反转录聚合酶链式反应(QRT-PCR)检测股外肌NOS三种亚型(eNOS、nNOS、iNOS)的基因表达.结果:耐力训练显著上调eNOS、nNOS表达(P< 0.01),有上调iNOS表达的趋势;补充小剂量L-Arg可下调nNOS的表达(P < 0.05),有上调iNOS表达的趋势;补充大剂量上调nNOS表达(P < 0.05),有下调iNOS表达的趋势.结论:耐力训练上调eNOS、nNOS、iNOS的表达;补充外源性L-Arg对nNOS、iNOS基因表达的影响可能存在一定的剂效关系.     

Effects of suspension hypokinesia/hypodynamia on rat skeletal muscle

We studied the effects of suspension hypokinesia/hypodynamia (H/H) on properties of soleus and plantaris muscles of rats. Our objective was to compare the effects of this model to those of disuse atrophy. After 12 d of H/H, there were significant decreases in soleus and plantaris muscle wet weight and citrate synthase activity. Soleus muscle was affected to a greater extent than plantaris muscle. There was a significant decrease in non-collagen protein content of H/H soleus muscle. Triceps brachii muscles did not display significant changes in any parameters measured, suggesting that observed changes were not due to systemic factors. There was no significant change in the water content of H/H soleus or plantaris muscles. Suspension H/H causes muscle changes different from those secondary to limb immobilization, in which soleus and plantaris muscles are equally affected.     

肌球蛋白重链Ⅱx mRNA表达可能为大鼠比目鱼肌废用的分子标志

目的：建立大鼠跟腱切断模型，观测并比较跟腱切断与尾部悬吊大鼠比目鱼肌重量与肌球蛋白重链（MHC）异构体mRNA表达的变化，为探讨骨骼肌废用性萎缩的机理提供实验线索。方法：选取雄性SD大鼠30只，随机分为6组，每组5只，直接切断跟腱，称量肌腱切断后第1，3，7，14，21，28天比目鱼肌（SOL），腓肠肌内外侧头（MG，LG）与跖肌（PL）的湿重，用RT－PCR法观测SOL MHC异构体mRNA的表达，结果：跟腱切断后第3天，SOL出现明显萎缩，在第7与14天萎缩达最低点，从第21天开始，萎缩的SOL重量有所恢复，MG，LG与PL重量的变化趋势与SOL基本一致。在正常SOL中，仅有MHC1 MHC Ⅱb的表达。结论：跟腱切断引起的SOL萎缩在出现时间与程度上，与尾部悬吊相似，两种模型均可引起SOL中MHC，Ⅱx mRNA表达，推测MHCⅡx可能为骨骼肌废用的分子标志。     

FDP对微波辐射后大鼠海马COX表达的影响

目的探讨1, 6-二磷酸果糖(FDP)对微波辐射后大鼠海马线粒体呼吸链相关基因细胞色素c氧化酶(cytochrome c oxidase,COX)表达的影响。方法Wistar雄性大鼠随机分为假辐射组(5只),辐射组(10只)和辐射+药物组(10只)。采用30mW/cm²微波辐射,辐射+药物组于辐射前3d 腹腔注射350mg/kg FDP,连续给药3或10d,1次/d。于辐射后6h和7d活杀取海马,采用反转录-聚合酶链反应(RT-PCR)和图像分析检测大鼠海马组织COX亚基Ⅰ、Ⅱ和Ⅳ mRNA表达,通过Western blot和图像分析检测大鼠海马组织COX Ⅰ蛋白表达变化。结果辐射后6h和7d大鼠海马COX Ⅰ、Ⅱ和Ⅳ mRNA表达均较假辐射组降低,药物组大鼠海马COX Ⅰ、Ⅱ和Ⅳ mRNA与相应辐射组相比均见表达增加,以给药后3d(辐射后6h)组增加最为显著(t_{COX Ⅰ}=3.2205,t_{COX Ⅱ}=3.5762,t_{COX Ⅳ}=3.0408,P<0.05)。辐射后6h和7d大鼠海马COX Ⅰ蛋白表达均较假辐射组减少,给药后3d(辐射后6h)与辐射后6h相比COX Ⅰ蛋白表达升高(t=2.9614,P<0.05),给药后10d(辐射后7d)与辐射后7d相比改变不显著。结论FDP对微波辐射后大鼠海马线粒体呼吸链相关基因COX表达降低有一定的促恢复作用。     

A weight-lifting exercise model for inducing hypertrophy in the hindlimb muscles of rats.

A new method for strength-training of rat hindlimb muscles, comparable to human weight lifting, is compared with sprint training by a treadmill. The new training apparatus that can induce rats to perform human squats was designed. Squat training was composed of isotonic high-intensity, short-duration, and graded overload exercises. After 60 min of one bout of all-out squat and sprint training, serum creatine kinase activities were markedly increased in the squat group (P less than 0.001), but no significant changes were observed in the sprint group. These responses were reflected in the histological sections of the muscles. Some splitting and small fibers were observed only in the squat group, suggesting that different stimulations were applied to the muscles of both the squat and sprint groups. At the end of 12 wk of both types of training, performed 4-5 d.wk-1, the number of fibers in the plantaris muscles of the squat group was greater by 14% than that in the control and sprint groups (P less than 0.001), suggesting hyperplasia following hypertrophy. These results indicated that the muscle strength-training model presented here may provide a new insight into the muscle hypertrophy associated with hyperplasia induced by heavy resistance training.     

尾部悬吊大鼠肺动脉和胸主动脉血管反应性及一氧化氮合酶抑制剂的影响

目的进一步明确大小循环动脉对模拟微重力(simulated microgravity,SM)适应机理,阐明SM后立位耐力降低机理,为SM后立位耐力降低寻找新的对抗措施。方法一30。尾部悬吊(TS)大鼠模拟微重力的生理效应。尾部悬吊7d(TS7d)和14d(TSl4d)后的肺动脉(PA)和胸主动脉(TA)环对68mmol／LKCl、累加浓度的苯肾上腺素(PE)和乙酰胆碱(ACh)的反应性作了观察。加入10^-5mol／LNOS抑制剂N-硝基-L-精氨酸甲酯(N-nitro-L-arginine methylester,L-NAME)孵育20min后重复检测对PE的收缩反应和ACh的舒张反应。结果TS7d、TSl4d大鼠PA和TA对KCl及PE的收缩反应非常显著降低;TS7d大鼠PA和TA对ACh的舒张反应显著或非常显著增强,TS14d大鼠PA无变化,TS14dTA仅有增强趋势。加入10^-5mol／L L-NAME后TS7d、TS14d大鼠PA对PE的收缩反应3组无差异,TS7d、TS14d大鼠TA对PE的收缩反应仍有降低;TS7dPA对ACh的舒张反应显著或非常显著降低,其余无变化。结论TS大鼠PA和TA收缩反应的降低可能归因于内皮舒张功能的增强。10^-5mol／LL-NAME可逆转TS后大鼠PA和部分逆转TA的收缩反应降低的实事表明其对内皮细胞的舒张功能有抑制作用．可用于抑制立位耐力降低。