力竭运动诱导的氧化应激对大鼠红细胞Band 3蛋白的影响及其机制探讨

为了探讨力竭运动诱导的氧化应激反应对大鼠红细胞Band 3蛋白的影响,该文以大鼠跑步运动为模型,对三种不同运动条件下(静坐组、适度运动组和力竭运动组)大鼠红细胞抗氧化能力和氧化损伤程度进行了检测,并对氧化应激反应诱导的红细胞膜Band 3蛋白表达和分布情况及其调控的阴离子通道活性进行了分析。结果表明:力竭运动条件下大鼠红细胞受到严重的氧化应激损伤,红细胞内抗氧化能力下降;导致膜Band 3蛋白巯基交联为主的蛋白聚簇化反应及其阴离子转运能力的下降。Band 3蛋白的损伤将进一步诱导红细胞携氧和变形能力的下降,成为运动相关疾病的潜在致病因素。     

大鼠力竭运动诱导的氧化应激损伤对红细胞变形性的影响

目的:探讨一次性力竭运动诱导的氧化应激反应对大鼠红细胞的抗氧化能力和细胞变形性的影响。方法:大鼠分为3组(n=10):对照组(Control)、适度运动组(MRE)和力竭运动组(ERE)。力竭运动组大鼠运动的前20 min保持5%的坡度和20 m/min的速度,20 min后调整为15%的坡度和25 m/min的速度,直至运动力竭。适度运动组大鼠在5%的坡度和20 m/min的速度下跑40 min。检测各组大鼠红细胞的抗氧化能力,并对氧化应激反应诱导的红细胞膜蛋白巯基水平、膜脂质过氧化水平和膜蛋白SDS-Page电泳条带变化进行了分析。通过激光衍射法对不同运动组大鼠红细胞变形性进行了检测。结果:力竭运动条件下大鼠红细胞受到严重的氧化应激损伤,红细胞内抗氧化能力下降。导致膜脂质过氧化损伤和膜蛋白巯基交联为主的蛋白聚簇化,形成高分子聚合物(HMW)。力竭组大鼠红细胞变形性(0.314±0.013 at 3 Pa and 0.534±0.009 at 30 Pa)显著低于对照组(0.41±0.01 at 3 Pa and 0.571±0.008 at 30 Pa;P0.05 and P0.01,respectively)和适度运动组。结论:力竭运动诱导的氧化损伤导致了红细胞变形能力(EI)的显著下降,使红细胞在微循环的转运受到限制,导致组织缺血缺氧进而引起休克、死亡等运动性疾病。     

力竭运动诱导的大鼠红细胞氧化应激对谷胱甘肽合成的影响及其机制探讨

该文探讨了力竭运动诱导的大鼠红细胞氧化应激损伤对谷胱甘肽合成速率的影响及其机制。将50只雄性SD大鼠随机分为2组,分别是静坐对照组(sedentary control,C)和力竭运动组(exhaustive running exercise,E),力竭运动组又分为运动休息0(E0)h、1(E1)h、12(E12)h和24(E24)h组,每组10只。该研究对各组大鼠红细胞抗氧化物还原型谷胱甘肽(glutathione,GSH)、氧化型谷胱甘肽(oxidized glutathione,GSSG)、GSH/GSSG和TFG(total free glutathione)含量进行了检测与分析,评估了各组红细胞L-半胱氨酸转运能力及三价铁降低抗氧化能力差异,检测了各组大鼠红细胞TFG合成速率及其与L-半胱氨酸转运速率相关性。该研究构建黄了嘌呤/次黄嘌呤氧化酶体外氧化体系,观察了各组大鼠红细胞在体外氧化条件下L-半胱氨酸转运速率、TFG和FRAP(ferric-reducing antioxidant power)含量差异。结果显示,与静坐对照组相比,力竭运动组大鼠红细胞中GSSG含量增加,GSH、TFG含量下降,GSH/GSSG比值显著降低。力竭运动后大鼠红细胞L-半胱氨酸转运速率显著降低,FRAP水平下降。体外氧化导致大鼠红细胞L-半胱氨酸转运速率显著降低,FRAP水平下降。结果表明,力竭运动诱导大鼠红细胞严重的氧化应激损伤,导致红细胞L-半胱氨酸转运速率下降,使红细胞主要抗氧化物GSH合成效率下降。这些变化导致红细胞抗氧化能力进一步减弱,从而成为力竭运动损伤的潜在致病因素。     

维生素C对衰老大鼠红细胞抗氧化能力的修复作用及其机制探讨

该文探讨了维生素C对衰老大鼠红细胞的抗氧化能力的修复作用及机制。将40只雄性SD大鼠按年龄分为4组:年轻对照组(Y)、年轻维生素C组(Yc)、年老对照组(A)和年老维生素C组(Ac)。对各组大鼠红细胞GSH、GSSG、GSH/GSSG和TFG含量进行检测。评估各组红细胞L-半胱氨酸转运能力及三价铁降低抗氧化能力差异。构建黄嘌呤/次黄嘌呤氧化酶体外氧化体系,观察各组大鼠红细胞在体外氧化条件下脂质过氧化、血红蛋白含量差异。研究发现,与年轻组大鼠相比,年老组大鼠红细胞中GSSG含量增加,GSH、TFG含量下降,GSH/GSSG比值显著降低。在年老组中,维生素C补充使TFG含量显著增加,L-半胱氨酸转运能力和三价铁降低抗氧化能力显著提升。体外氧化条件下,维生素C补充组大鼠红细胞所受氧化损伤程度显著减少,L-半胱氨酸转运能力增加。研究证明,衰老过程伴随着红细胞抗氧化能力的下降,腹腔注射维生素C可以通过提高红细胞L-半胱氨酸转运能力增加GSH抗氧化物含量,提高细胞抗氧化潜能,从而减少氧自由基诱导的损伤。     

低氧运动对Nrf2基因敲除大鼠运动能力和氧化应激的影响

Nrf2可调节多种抗氧化酶的表达,Nrf2的缺失可能影响机体的运动能力,而低氧可提高机体的抗氧化能力并改善运动能力。为了考察低氧运动对Nrf2基因敲除大鼠运动能力和氧化应激的影响,本研究分别在常氧和低氧环境(12%氧浓度)中对野生型大鼠和Nrf2敲除大鼠进行4周的跑台运动。研究显示,低氧运动可提高野生型大鼠的跑台运动力竭时间,Nrf2敲除可缩短大鼠的力竭时间;低氧运动可上调大鼠的Nrf2 m RNA表达量;Nrf2敲除明显抑制HIF-1α蛋白表达,而低氧运动可上调野生型和Nrf2敲除大鼠的HIF-1α蛋白表达;Nrf2敲除大鼠的骨骼肌ROS水平明显升高,并且低氧均可降低野生型和Nrf2敲除大鼠骨骼肌ROS水平。低氧运动可上调Nrf2敲除大鼠的CAT和GSH-PX蛋白表达。苏木精和伊红(HE)染色显示,Nrf2敲除大鼠在力竭跑台运动完成后出现更严重的骨骼肌病理改变,而低氧运动可减轻骨骼肌损伤。本研究认为,Nrf2敲除导致了大鼠骨骼肌中抗氧化酶的抑制及ROS的过量累积,从而造成了骨骼肌损伤并降低了运动能力。此外,低氧可通过上调Nrf2的表达,进而激活HIF-1α及抗氧化酶活性,从而提高运动能力,并防止骨骼肌损伤。     

美洲大蠊提取物对力竭运动大鼠心血管氧化损伤的保护作用

目的:通过美洲大蠊提取物(PAE)对力竭运动大鼠心肌自由基代谢的影响,探讨其对心肌氧化损伤的保护作用。方法:雄性SPF级健康SD大鼠40只,随机分为安静组、运动组、美洲大蠊提取物安静组、美洲大蠊提取物运动组(n=10)。服药组每天灌服2 ml美洲大蠊提取物(美洲大蠊提取物按50 mg/kg配制,溶于2 ml蒸馏水中灌胃给药),对照组每次灌蒸馏水2 ml。每天灌胃1次,连续灌胃14 d后,美洲大蠊提取物运动组与运动组大鼠进行一次性力竭游泳运动建立力竭模型,记录大鼠力竭运动时间。力竭运动结束时即刻取样,检测血清中丙二醛(MDA)含量、谷胱甘肽过氧化物酶(GSH-Px)和超氧化物歧化酶(SOD)活性,并检测观察心肌组织中一氧化氮合酶(NOS)基因的表达情况。结果:与安静组相比,一次力竭游泳后,运动组心肌SOD、GSH-Px的活性明显降低(P0.01),而MDA含量显著升高(P0.01);而美洲大蠊提取物能够显著提高力竭SD大鼠的心肌SOD、GSH-Px的活性(P0.01),降低MDA含量(P0.01),e Nos基因表达增高。结论:大鼠力竭运动后心肌会发生氧化损伤,美洲大蠊提取物干预后能够增加力竭运动后大鼠心肌的抗氧化能力,对力竭运动所致心肌损伤具有一定的保护作用,进而增强大鼠运动能力。     

连翘提取物可有效缓解力竭运动导致的骨骼肌组织氧化损伤

为了探讨补充连翘提取物后对力竭运动后大鼠体内抗氧化能力和肌肉损伤的影响,我们选择了60只雄性大鼠为研究对象,随机分成4组:控制组(C组)、力竭运动组(E组)、连翘组(F组)和连翘运动组(FE组),每组15只。连翘每天以每千克体重40 mg/kg剂量进行喂食,为期4周,力竭运动于最后1周进行跑步机适应,隔天以渐增式力竭运动跑至力竭。我们采用双因素方差分析来检验连翘补充与力竭运动对SD大鼠血液中肌酸激酶、乳酸脱氢酶、丙二醛、超氧歧化酶、谷胱甘肽过氧化物酶活性的影响。结果发现,力竭运动组的肌酸激酶、乳酸脱氢酶、丙二醛活性显著高于控制组,超氧歧化酶和谷胱甘肽过氧化物酶活性则显著低于控制组(p0.05)。连翘运动组乳酸脱氢酶、丙二醛活性皆显著低于力竭运动组(p0.05),超氧歧化酶活性则显著高于力竭运动组(p0.05),肌酸激酶和谷胱甘肽过氧化物酶则无显著差异(p0.05),说明补给连翘能有效防止力竭运动导致超氧歧化酶活性的降低和乳酸脱氢酶与丙二醛活性升高的情况,有助于增强大鼠体内的抗氧化能力,减缓因力竭运动导致氧化伤害和肌肉损伤的情况。我们的研究为连翘在力竭运动损伤保护中的应用提供了一定的帮助。     

一次性力竭运动致大鼠骨骼肌氧化应激的机制

目的:观察一次性力竭运动对大鼠骨骼肌氧化应激相关酶表达的影响。方法:雄性SD大鼠40只,分为4组(n=10),分别为对照组(C组)、力竭运动组(E组)、运动+PKC抑制剂组(EC组)、运动+NOX抑制剂组(EA组)。三组运动大鼠进行3 d的跑台适应性运动(5 m/min,1次/日,无坡度),然后休息1 d;EC组于运动前1 d和运动前1 h注射PKC抑制剂白屈菜红碱(5 mg/kg),EA组同期注射NADPH氧化酶抑制剂Apocynin(10 mg/kg),C组和E组注射同等剂量生理盐水;三组运动大鼠进行一次性跑台力竭运动,力竭后取大鼠的跖肌,DCF荧光探针检测活性氧(ROS),Western blot分析NOX2、NOX4、3-NT,免疫沉淀分析PKC、NOX2、NOX4。结果:与C组相比,E组的ROS水平、NOX2和NOX4蛋白表达、PKC-NOX2和PKC-NOX4复合物水平、3-NT生成均显著增加(P＜0.01,P＜ 0.05),EC组、EA组ROS无显著差异(P＞0.05),EC组NOX4蛋白表达显著增加(P＜0.05);与E组相比,EC组和EA组的ROS水平、NOX2和NOX4蛋白表达、PKC-NOX2和PKC-NOX4复合物水平、3-NT生成均显著降低(P＜ 0.01,P＜0.05)。结论:力竭运动诱导骨骼肌NOX2、NOX4蛋白表达增加,PKC通过调控NOX2介导ROS的生成。     

NADPH氧化酶抑制剂apocynin对力竭运动大鼠运动性蛋白尿的影响

目的：研究NADPH氧化酶抑制剂apocynin对力竭运动大鼠运动性蛋白尿产生的影响及其机制。方法：32只SD雄性大鼠随机分为安静对照组（C组）、对照+药物组（CA组）、力竭运动组（E组）、力竭运动+药物组（EA组）。药物注射按10 mg/kg体重,每天一次,连续3 d,并在末次药物注射1 h后进行一次性跑台力竭运动。测定运动后尿UP、血液BUN水平、肾脏ROS浓度、NOS活性、NOS与3-NT蛋白含量。结果：结果显示,E组UP、肾脏ROS、iNOS含量及活性、3-NT明显升高,而EA组的这些指标与C组相比无显著性差异。结论：力竭运动可明显增加肾组织NADPH氧化酶活性,从而产生大量的ROS,后者可迅速地与由肾脏iNOS催化生成的NO反应,产生过量的ONOO^-,诱发运动性蛋白尿的生成。     

麝香保心丸对一次性力竭运动大鼠心肌损伤标记物和C反应蛋白的影响

目的探讨麝香保心丸对一次性力竭运动大鼠心肌损伤标记物和C反应蛋白的影响。方法选择雄性Wistar大鼠52只,随机分成实验组和对照组,每组26只。两组大鼠每天自由进食饮水相同,实验组大鼠每天麝香保心丸2粒(每粒22.5 mg)分2次灌胃,共两周。两组均接受力竭游泳运动,制成力竭运动动物模型,分别测定和比较两组大鼠血清和心肌组织肌酸激酶(CK)、肌酸激酶同工酶(CK-MB)、肌钙蛋白T(Tn T)、B型脑钠肽(BNP)和C反应蛋白(CRP)水平。结果大鼠平均力竭运动游泳时间实验组较对照组明显延长(P0.01)。实验组血清和心肌组织CK、CK-MB、Tn T、BNP和CRP水平均明显低于对照组(P0.05)。结论麝香保心丸可显著降低力竭运动大鼠血清和心肌中CK、CK-MB、Tn T、BNP和CRP水平,能够减轻力竭运动后心肌损伤。     

Exercise-induced oxidative stress affects erythrocytes in sedentary rats but not exercise-trained rats.

Oxidant stress is one of the factors proposed to be responsible for damaged erythrocytes observed during and after exercise. The impact of exertional oxidant stress after acute exhaustive treadmill running on erythrocyte damage was investigated in sedentary (Sed) and exercise-trained (ET) rats treated with or without antioxidant vitamins C and E. Exhaustive exercise led to statistically significant increments in the levels of thiobarbituric acid-reactive substance (TBARS) and H2O2-induced TBARS in Sed rats and resulted in functional and structural alterations in erythrocytes (plasma hemoglobin concentrations, methemoglobin levels, and rise in osmotic fragility of erythrocytes with decrease in erythrocyte deformability). Administration of antioxidant vitamin for 1 mo before exhaustive exercises prevented lipid peroxidation (TBARS, H2O2-induced TBARS) in Sed rats without any functional or structural alterations in erythrocytes. Parameters indicating erythrocyte lipid peroxidation and deterioration after exhaustive exercise in rats trained regularly with treadmill running for 1 mo were not different from those in Sed controls. Erythrocyte lipid peroxidation (TBARS) increased in exhausted-ET rats compared with ET controls; however, the plasma hemoglobin, methemoglobin levels, and erythrocyte osmotic fragility and deformability did not differ. Exhaustive exercise-induced lipid peroxidation in ET rats on antioxidant vitamin treatment was prevented, whereas functional and structural parameters of erythrocytes were not different from those of the ET controls. We conclude that exertional oxidant stress contributed to erythrocyte deterioration due to exercise in Sed but not in ET rats.     

Effects of endurance training and acute exhaustive exercise on antioxidant defense mechanisms in rat heart

We investigated whether 8-week treadmill training strengthens antioxidant enzymes and decreases lipid peroxidation in rat heart. The effects of acute exhaustive exercise were also investigated. Male rats (Rattus norvegicus, Sprague-Dawley strain) were divided into trained and untrained groups. Both groups were further divided equally into two groups where the rats were studied at rest and immediately after exhaustive exercise. Endurance training consisted of treadmill running 1.5 h day(-1), 5 days week(-1) for 8 weeks. For acute exhaustive exercise, graded treadmill running was conducted. Malondialdehyde level in heart tissue was not affected by acute exhaustive exercise in untrained and trained rats. The activities of glutathione peroxidase and glutathione reductase enzymes decreased by both acute exercise and training. Glutathione S-transferase and catalase activities were not affected. Total and non-enzymatic superoxide scavenger activities were not affected either. Superoxide dismutase activity decreased by acute exercise in untrained rats; however, this decrease was not observed in trained rats. Our results suggested that rat heart has sufficient antioxidant enzyme capacity to cope with exercise-induced oxidative stress, and adaptive changes in antioxidant enzymes due to endurance training are limited.     

Carnitine supplementation effects on nonenzymatic antioxidants in young rats submitted to exhaustive exercise stress

Previous studies have demonstrated that exercise stress increases oxidative stress in rats. However, antioxidant supplement therapy effects on reactive oxygen substances are conflicting. We evaluated the effects of carnitine on renal nonenzymatic antioxidants in young rats submitted to exhaustive exercise stress. Wistar rats were divided into 3 groups: (a) control group (not submitted to exercise stress), (b) exercise stress group, and (c) exercise stress and carnitine group. The rats from group 3 were treated with gavage administration of 1 ml of carnitine (5 mg·kg?1) for 7 consecutive days. The animals from groups 2 and 3 were submitted to a bout of swimming exhaustive exercise stress. Kidney samples were analyzed for reactive substances to thiobarbituric acid by malondialdehyde (MDA), reduced glutathione (GSH), and vitamin-E levels. Carnitine treatment attenuated MDA increase caused by exercise stress (1: 0.16 ± 0.02 vs. 2: 0.34 ± 0.07 vs. 3: 0.1 ± 0.01 mmmol per milligram of protein; p < 0.0001). It also increased the renal levels of GSH (1: 23 ± 4 vs. 2: 23 ± 2 vs. 3: 58 ± 9 μmol per gram of protein; p < 0.0001); however, it did not change renal vitamin E (1: 24 ± 5 vs. 2: 27 ± 1 vs. 3: 28 ± 5 μM per gram of tissue; p < 0.001). In conclusion, carnitine improved oxidative stress and partially improved the nonenzymatic antioxidant activity in young rats submitted to exhaustive exercise stress.     

Hypoxic exercise training causes erythrocyte senescence and rheological dysfunction by depressed Gardos channel activity

Despite enhancing cardiopulmonary and muscular fitness, the effect of hypoxic exercise training (HE) on hemorheological regulation remains unclear. This study investigates how HE modulates erythrocyte rheological properties and further explores the underlying mechanisms in the hemorheological alterations. Twenty-four sedentary males were randomly divided into hypoxic (HE; n = 12) and normoxic (NE; n = 12) exercise training groups. The subjects were trained on 60% of maximum work rate under 15% (HE) or 21% (NE) O(2) condition for 30 min daily, 5 days weekly for 5 wk. The results demonstrated that HE 1) downregulated CD47 and CD147 expressions on erythrocytes, 2) decreased actin and spectrin contents in erythrocytes, 3) reduced erythrocyte deformability under shear flow, and 4) diminished erythrocyte volume changed by hypotonic stress. Treatment of erythrocytes with H(2)O(2) that mimicked in vivo prooxidative status resulted in the cell shrinkage, rigidity, and phosphatidylserine exposure, whereas HE enhanced the eryptotic responses to H(2)O(2). However, HE decreased the degrees of clotrimazole to blunt ionomycin-induced shrinkage, rigidity, and cytoskeleton breakdown of erythrocytes, referred to as Gardos effects. Reduced erythrocyte deformability by H(2)O(2) was inversely related to the erythrocyte Gardos effect on the rheological function. Conversely, NE intervention did not significantly change resting and exercise erythrocyte rheological properties. Therefore, we conclude that HE rather than NE reduces erythrocyte deformability and volume regulation, accompanied by an increase in the eryptotic response to oxidative stress. Simultaneously, this intervention depresses Gardos channel-modulated erythrocyte rheological functions. Results of this study provide further insight into erythrocyte senescence induced by HE.     

Ganoderma lucidum polysaccharides supplementation attenuates exercise-induced oxidative stress in skeletal muscle of mice

The present study was designed to determine the effects of Ganoderma lucidum polysaccharides (GL-PS) on exhaustive exercise-induced oxidative stress in skeletal muscle tissues of mice. The mice were divided into four groups (three GL-PS administered groups and the control group). The control group was administered with distilled water and GL-PS administered groups were administered with GL-PS (50, 100 and 200 mg/kg body weight per day). After 28 days, the mice performed an exhaustive swimming exercise, along with the determination of superoxide dismutase (SOD), glutathione peroxidase (GPX), catalase (CAT) activities and malondialdehyde (MDA) levels in the skeletal muscle of mice. The results showed that GL-PS could increase antioxidant enzymes activities and decrease the MDA levels in the skeletal muscle of mice. This study provides strong evidence that GL-PS supplementation possessed protective effects against exhaustive exercise-induced oxidative stress.     

Participation of caspase-3-like protease in oxidation-induced impairment of erythrocyte membrane properties

Erythrocytes are very susceptible to oxidative stress, having a high content of intracellular oxygen and hemoglobin. In the present study, exposure to oxidative stress resulted in a significant impairment of erythrocyte membrane functions, such as deformability and anion exchange. Band 3 protein, also known as anion exchanger-1, plays an important role in these two functions. We show that oxidative stress activated caspase-3 inside the erythrocytes, which resulted in band 3 protein cleavage. Interestingly, inhibition of the caspase-3 with its specific inhibitor not only suppressed the digestion of band 3 protein, but also blunted the functional damage to erythrocytes, such as deformability and anion exchange, without changing the level of peroxidation of membrane lipids. These results provide experimental evidence that activation of caspase-3 plays an important role in the oxidative stress-induced impairment of membrane functions of erythrocytes.     

Evidence for a role of taurine in the in vitro oxidative toxicity of neutrophils toward erythrocytes

Production of hydrogen peroxide and secretion of myeloperoxidase by stimulated neutrophils resulted in myeloperoxidase-catalyzed oxidation of chloride to hypochlorous acid (HOCl), the reaction of HOCl with taurine to yield taurine monochloramine (TauNHCl), and accumulation of TauNHCl in the extracellular medium. When erythrocytes were present, the yield of TauNHCl was lower as the result of uptake of TauNHCl into erythrocytes. The zwitterion taurine was not taken up, but the anion TauNHCl and other anionic oxidants including taurine dichloramine (TauNCl2) and L-alanine chloramines were transported into erythrocytes by the anion-transport system. Oxidation of intracellular components such as glutathione (GSH) by taurine chloramines resulted in reduction of the chloramines and trapping of taurine within erythrocytes. At high oxidant:erythrocyte ratios, TauNHCl also oxidized hemoglobin (Hb) and depleted ATP, but caused little lysis. TauNCl2 was much more effective as a lytic agent. At low oxidant:erythrocyte ratios, the chloramines caused net loss of GSH when no glucose was provided, but Hb was not oxidized and GSH content returned to normal when glucose was added. Therefore, anionic chloramines may mediate oxidative toxicity when the neutrophil:erythrocyte ratio is high. Under more physiologic conditions, chlorination of taurine by neutrophils and the uptake and reduction of TauNHCl by erythrocytes prevents accumulation of oxidants and may protect blood cells, plasma components, and tissues against oxidative toxicity.     

Myocardial proteome changes in aortic stenosis rats subjected to long-term aerobic exercise

The effects of exercise training (ET) on the heart of aortic stenosis (AS) rats are controversial and the mechanisms involved in alterations induced by ET have been poorly clarified. In this study, we analyzed the myocardial proteome to identify proteins modulated by moderate-intensity aerobic ET in rats with chronic supravalvular AS. Wistar rats were divided into four groups: sedentary control (C-Sed), exercised control (C-Ex), sedentary aortic stenosis (AS-Sed), and exercised AS (AS-Ex). ET consisted of five treadmill running sessions per week for 16 weeks. Statistical analysis was performed by ANOVA or Kruskal–Wallis and Goodman tests. Results were discussed at a significance level of 5%. At the end of the experiment, AS-Ex rats had higher functional capacity, lower blood lactate concentration, and better cardiac structural and left ventricular (LV) functional parameters than the AS-Sed. Myocardial proteome analysis showed that AS-Sed had higher relative protein abundance related to the glycolytic pathway, oxidative stress, and inflammation, and lower relative protein abundance related to beta-oxidation than C-Sed. AS-Ex had higher abundance of one protein related to mitochondrial biogenesis and lower relative protein abundance associated with oxidative stress and inflammation than AS-Sed. Proteomic data were validated for proteins related to lipid and glycolytic metabolism. Chronic pressure overload changes the abundance of myocardial proteins that are mainly involved in lipid and glycolytic energy metabolism in rats. Moderate-intensity aerobic training attenuates changes in proteins related to oxidative stress and inflammation and increases the COX4I1 protein, related to mitochondrial biogenesis. Protein changes are combined with improved functional capacity, cardiac remodeling, and LV function in AS rats.     

Stress biomarkers in rats submitted to swimming and treadmill running exercises

The objective of the present work was to compare stress biomarkers (serum ACTH and corticosterone hormones) during known intensity swimming and treadmill running exercises performed by rats. Adult Wistar rats (n=41) weighing 320-400 g at the beginning and 420-500 g at the end of the experiment, previously adapted to exercise and with Maximal Lactate Steady State (MLSS) already determined were used. The animals were divided into the following subgroups: (1) sacrificed shortly after session of 25 min of exercise (swimming or treadmill) at the MLSS intensity or (2) sacrificed after exhaustive exercise (swimming or treadmill) at intensity 25% higher than MLSS. For comparison, a control group C was sacrificed at rest. Two-way ANOVA was used to identify differences in the stress parameters (P<0.05). At both exercise intensities serum ACTH concentrations were significantly higher for the swimming group compared to running and control groups, while serum corticosterone concentrations in swimming and running groups were significantly higher than in the control group. The differences were more pronounced at the higher intensity (25% higher than MLSS). The swimming group showed higher concentrations for both hormones in relation to the running group. Only acute swimming exercise induced activity of the hypothalamic-pituitary-adrenal axis responses expected to stress: elevations in the serum ACTH and corticosterone concentrations.