烟酸补充对单次非力竭离心运动大鼠骨骼肌SIRT1、p65及20S蛋白水解酶的影响

目的:观察补充烟酸对大鼠运动性骨骼肌损伤(EIMD)的影响。方法:成年大鼠90只随机等分为对照组(Cs)和烟酸组(Es),各组又分安静对照组、运动后即刻组、运动后24h、运动后48 h及运动后72 h组。运动方式:18 m/min,-16°,120 min。烟酸灌胃(10 mg/kg)每日1次至动物宰杀。腹主动脉血测肌酸激酶(CK)和乳酸脱氢酶(LDH)活性,比目鱼肌观察形态学变化及组蛋白去乙酰化酶1(SIRT1)、p65和20 S蛋白水解酶蛋白表达。结果:烟酸补充可减轻大鼠EIMD各时相点骨骼肌大量炎症灶的百分率,升高运动后即刻SIRT1水平及降低p65表达,对各时相点20 S蛋白水解酶及血清CK和LDH影响不明显。结论:烟酸通过上调骨骼肌SIRT1及降低p65表达,改善非力竭性EIMD炎症过程,但不影响20 S蛋白水解酶表达及血清CK和LDH水平。     

去乙酰化酶的功能及其在体育科学中的应用

Sirtuins(SIRTs)是依赖于烟酰胺腺嘌呤二核苷酸辅酶(nicotinamide adenine dinucleo-tide,NAD+)的去乙酰化酶。除了对染色质组蛋白赖氨酸残基去乙酰化实现对基因的表观遗传修饰外,SIRT1可以调节多种关键转录调节因子及辅因子活性。SIRTs所介导的生理过程包括控制氧化应激响应、能量内稳态控制和运动代谢适应等。体育活动对代谢性疾病的预防或对衰老的延缓可能与SIRTs活性密切相关。多种运动训练方式和补充SIRTs小分子活性物质都能提高骨骼肌、脂肪、心肌和脑等脏器的SIRTs活性,提升机体抗疲劳及能量代谢适应的能力。SIRTs可能是表征功能内稳态的潜在标志物。     

运动与衰老骨骼肌线粒体生物合成

线粒体生物合成依赖于细胞核与线粒体基因的协同表达.哺乳动物衰老过程中骨骼肌线粒体氧化磷酸化能力下降,其中线粒体数量和,或线粒体功能的缺失是其重要影响因素之一.运动可以诱导骨骼肌线粒体生物合成产生适应性变化,线粒体呼吸链产生的活性氧和自由基参与了?怂 线粒体到细胞核的信号传导.综述当前有关运动与线粒体生物合成的分子机理、运动对衰老状态下骨骼肌线粒体生物合成的影响以及在此过程中涉及的信号通路.     

运动对胰岛素抵抗骨骼肌AMPK/SlRTl/PGC-1α轴影响的研究述评

SIRTI(沉默信息调节因子2相关酶I)是依赖于辅酶NAD+的去乙酰化酶,不仅与衰老、凋亡、DNA修复有关,还与不同营养应激状态的细胞代谢转换相关.SIRT1和AMPK(腺苷酸活化蛋白激酶)是细胞内的能量感受器,通过磷酸化、去乙酰化调节着PGC-1a的活性.骨骼肌AMPK/SIRTl/PGC-lα轴的活性调控直接影响着其下游相关基因的表达,与胰岛素抵抗的发生与发展密切相关.     

AMPK与Ⅱ型糖尿病的研究进展

糖代谢是一切物质代谢的基础,骨骼肌中的糖代谢在运动中起着重要的作用,直接影响机体的运动能力。近年来研究发现,腺苷酸活化蛋白激酶(AMPK)是一个调控能量稳态的重要激酶,也是一个参与许多信号传导通路的关键蛋白。作为能量代谢变化的感受器能够被运动中ATP/AMP的比值变化所激活,并作用于骨骼肌中,对骨骼肌中的糖代谢起着非常重要的调节作用,具体表现为可以增加骨骼肌中葡萄糖的转运,直接参与糖酵解调节,抑制糖原合成和糖异生,对运动能力具有重要影响,通过文献检索法AMPK在Ⅱ型糖尿病中的调节作用进行综述。     

间歇性低氧运动对大鼠骨骼肌线粒体解偶联蛋白3（UCP3）表达的影响

目的：探讨间歇性低氧运动对肥胖及正常SD大鼠骨骼肌线粒体解偶联蛋白-3表达的影响。方法：将100只雄性健康大鼠随机分为正常对照组（40只）和肥胖造模组（60只），从造模成功的SD大鼠中挑选40只，随机分为肥胖常氧安静组（A组）、肥胖常氧运动组（B组）、肥胖低氧安静组（C组）和肥胖低氧运动组（D组）。正常对照组随机分为正常常氧安静组（E组）、正常常氧运动组（F组）、正常低氧运动组（G组）和正常低氧安静组（H组），每组10只。第4周末次运动后24h左右进行采样，采样前所有大鼠禁食过夜，取后肢骨骼肌匀浆提取线粒体，用western blot的方法测定肥胖大鼠以及正常组大鼠的骨骼肌线粒体UCP3的蛋白表达水平。结果：正常组大鼠骨骼肌线粒体UCP3蛋白表达明显高于造模组大鼠（P〈0．05）；低氧安静及运动组大鼠骨骼肌线粒体UCP3蛋白的表达均明显高于常氧安静组（P〈0．05）；低氧或运动对大鼠骨骼肌线粒体UCP3蛋白的表达的影响与大鼠的体脂百分比有呈负相关的趋势。结论：肥胖大鼠骨骼肌线粒体UCP3蛋白的表达低于正常大鼠，4周的有氧运动以及间歇性低氧刺激使骨骼肌线粒体UCP3蛋白的表达增加，运动与间歇性低氧刺激相结合能使骨骼肌线粒体UCP3的表达水平高于单一的运动或间歇性低氧刺激。而且，低氧刺激以及低氧刺激与运动相结合使得大鼠的体重、体脂百分比降低幅度比单一的运动更加明显。     

离心运动对大鼠骨骼肌线粒体ATP酶活性及desmin表达影响的研究

目的:从细胞内线粒体Ca2+转运系统入手,探讨离心运动对大鼠骨骼肌细胞线粒体ATP酶活性及desmin表达影响,以期进一步揭示骨骼肌运动性损伤的发生机制.方法:雄性SD大鼠96只,体重304g±12g,随机分为安静对照组、运动后即刻组、运动后12h组、运动后24h组、运动后48h组、运动后72h组、运动后5d组、运动后7d组.采用一次性下坡跑训练建立运动损伤模型,取大鼠肱三头肌,部分肌肉做desmin免疫组化切片,并进行定量分析;余下肌肉差速离心提取线粒体,测定线粒体各ATP酶活性.结果:1)离心运动后大鼠骨骼肌desmin表达从运动后即刻到24h呈逐渐下降的趋势,以运动后24h下降最为明显,48h开始回升,第5d达到最高,第7d略有下降,但仍明显高于安静对照组.2)离心运动后即刻大鼠骨骼肌细胞线粒体Ca2+-ATPase、Ca2+-Mg2+-ATPase和Na+-K+-AT-Pase的活性显著下降,12h、24h酶活性有所恢复,仍然明显低于安静对照组;48h后各ATP酶结果与安静对照组均无显著差异.结论:大鼠离心运动后骨骼肌细胞线粒体ATP酶活性变化与desmin表达之间存在着某种密切相关的联系,线粒体钙调节失衡是导致骨骼肌运动损伤的一个重要原因;而离心运动后desmin表达的变化,对骨骼肌运动性损伤形态学变化的早期界定和损伤恢复程度的判断具有重要的参考价值.     

螺旋藻对大鼠运动性骨骼肌损伤保护作用的研究

观察螺旋藻对大鼠力竭运动后自由基代谢及肌肉损伤标志酶的影响,发现螺旋藻能使力竭运动后骨骼肌线粒体自由基生成减少,抗氧化酶活性增强;使血清中肌肉损伤标志酶水平降低。显示螺旋藻对运动性骨骼肌损伤有显著的保护作用,是较为理想的运动营养补剂。     

过度训练对大鼠骨骼肌糖代谢的影响

目的:观察大鼠在过度训练状态下骨骼肌糖代谢的变化,探讨过度训练对糖代谢的影响。方法:将SD大鼠随机分为对照组(7只,Con)、运动组(8只,Mtr)和过度训练组(9只,Otr),进行9周跑台训练,其中Otr组后3周为力竭性运动。运动后分别测定骨骼肌糖原含量,LDH、PK、SDH、SOD酶的活性及MDA浓度,电镜观察肌组织的变化。结果:Otr组肌糖原含量较Mtr组降低,各种酶活性受到不同程度的抑制,MDA浓度升高,线粒体水肿,呈空泡状。结论:大鼠连续力竭性运动所致过度训练存在骨骼肌糖代谢功能紊乱,其可能与力竭性运动引起的自由基损害有关。     

运动对骨骼肌线粒体影响的研究进展

本文通过文献资料法,对近年来运动对骨骼肌线粒体形态结构分布、能量代谢、动力学、凋亡、自噬及生物合成方面的影响进行综述.结果发现运动后线粒体发生了再分布并且形态结构和能量代谢相关酶活性出现改变,动力学变化是线粒体对运动的早期适应反应.运动可以影响线粒体自噬、凋亡和生物合成过程,有助于维持线粒体的质量.通过研究,有助于深入认识运动对骨骼肌线粒体影响的分子机制.     

Aerobic training but no resistance training increases SIRT3 in skeletal muscle of sedentary obese male adolescents

In recent years, prevalence of obesity in children and adolescents has increased. A strategy for prevention and management of obesity is aerobic training (AT) due to its effectiveness to decrease fat mass. AT increases the content of SIRT3, a mitochondrial protein that increases the expression of PGC-1α and NFR1, thereby enhances mitochondrial function and metabolic health. Resistance training (RT) provides metabolic benefits but its effect on SIRT3 content is unknown. To compare the effect of AT and RT on SIRT3, PGC-1α and NRF-1 protein levels in skeletal muscle of sedentary obese adolescents. Twenty-seven sedentary obese male adolescents (age: 16.7?±?0.9 years; BMI: 33.7?±?4.3?kg/m²) completed a 1-month control period prior to randomization to one of two supervised exercise protocols: AT (3 days/week, 40 min/day, 70–80% peak heart rate) or RT (3 days/week, 11 exercises, 2 sets/exercise, 12 repetitions/set) for 12 weeks. Biopsies were obtained from the vastus lateralis muscle before and after 12 weeks to analyse SIRT3, PGC-1α and NRF-1 proteins content. Peak oxygen consumption (VO_2peak) and anthropometric variables were evaluated before and after training. AT increased SIRT3 content, which was associated with improvements in PGC-1α content and body fat percentage. RT did not affect SIRT3 or PGC-1α. VO_2peak increased only in AT. The increase in muscle mitochondrial SIRT3 was observed only following AT. In contrast, RT increased muscle mass without improving SIRT3 in obese male adolescents.     

运动与解偶联蛋白3(UCP3)介导的线粒体活性氧代谢调控研究进展

解偶联蛋白3是线粒体内膜上的一种转运蛋白,研究证实解偶联蛋白3与线粒体能量代谢、线粒体活性氧生成及脂肪代谢等有关。就解偶联蛋白3的结构、分布、表达调控及其介导的线粒体活性氧生成等相关问题作一综述。     

Influence of biological sex and exercise on murine cardiac metabolism

Although the structural and functional effects of exercise on the heart are well established, the metabolic changes that occur in the heart during and after exercise remain unclear. In this study, we used metabolomics to assess time-dependent changes in the murine cardiac metabolome following 1 session of treadmill exercise. After the exercise bout, we also recorded blood lactate, glucose, and ketone body levels and measured cardiac mitochondrial respiration. In both male and female mice, moderate- and high-intensity exercise acutely increased blood lactate levels. In both sexes, low- and moderate-intensity exercise augmented circulating 3-hydroxybutryrate levels immediately after the exercise bout; however, only in female mice did high-intensity exercise increase 3-hydroxybutyrate levels, with significant increases occurring 1 h after the exercise session. Untargeted metabolomics analyses of sedentary female and male hearts suggest considerable sex-dependent differences in basal cardiac metabolite levels, with female hearts characterized by higher levels of pantothenate, pyridoxamine, homoarginine, tryptophan, and several glycerophospholipid and sphingomyelin species and lower levels of numerous metabolites, including acetyl coenzyme A, glucuronate, gulonate, hydroxyproline, prolyl-hydroxyproline, carnosine, anserine, and carnitinylated and glycinated species, as compared with male hearts. Immediately after a bout of treadmill exercise, both male and female hearts had higher levels of corticosterone; however, female mice showed more extensive exercise-induced changes in the cardiac metabolome, characterized by significant, time-dependent changes in amino acids (e.g., serine, alanine, tyrosine, tryptophan, branched-chain amino acids) and the ketone body 3-hydroxybutyrate. Results from experiments using isolated cardiac mitochondria suggest that high-intensity treadmill exercise does not acutely affect respiration or mitochondrial coupling; however, female cardiac mitochondria demonstrate generally higher adenosine diphosphate sensitivity compared with male cardiac mitochondria. Collectively, these findings in mice reveal key sex-dependent differences in cardiac metabolism and suggest that the metabolic network in the female heart is more responsive to physiological stress caused by exercise.     

Metabolic cost of level,uphill, and downhill running in highly cushioned shoes with carbon-fiber plates

BackgroundCompared to conventional racing shoes, Nike Vaporfly 4% running shoes reduce the metabolic cost of level treadmill running by 4%. The reduction is attributed to their lightweight, highly compliant, and resilient midsole foam and a midsole-embedded curved carbon-fiber plate. We investigated whether these shoes also could reduce the metabolic cost of moderate uphill (+3°) and downhill (–3°) grades. We tested the null hypothesis that, compared to conventional racing shoes, highly cushioned shoes with carbon-fiber plates would impart the same ～4% metabolic power (W/kg) savings during uphill and downhill running as they do during level running.MethodsAfter familiarization, 16 competitive male runners performed six 5-min trials (2 shoes × 3 grades) in 2 Nike marathon racing-shoe models (Streak 6 and Vaporfly 4%) on a level, uphill (+3°), and downhill (–3°) treadmill at 13 km/h (3.61 m/s). We measured submaximal oxygen uptake and carbon dioxide production during Minutes 4–5 and calculated metabolic power (W/kg) for each shoe model and grade combination.ResultsCompared to the conventional shoes (Streak 6), the metabolic power in the Vaporfly 4% shoes was 3.83% (level), 2.82% (uphill), and 2.70% (downhill) less (all p < 0.001). The percent of change in metabolic power for uphill running was less compared to level running (p = 0.04; effect size (ES) = 0.561) but was not statistically different between downhill and level running (p = 0.17; ES = 0.356).ConclusionOn a running course with uphill and downhill sections, the metabolic savings and hence performance enhancement provided by Vaporfly 4% shoes would likely be slightly less overall, compared to the savings on a perfectly level race course.     

大强度运动对大鼠心肌线粒体膜通透性转换孔状态的影响

目的观察大鼠一次性大强度游泳运动后不同时相心肌线粒体膜通透性转换孔(PTP孔)的性状和心肌超微结构等指标的变化情况,探讨线粒体损伤与PTP孔变化之间的关系.方法将32只成年雄性SD大鼠随机分为A组(空白对照组,n=8)和B组(大强度运动组,n=24).B组又随机分为运动后即刻组(B1组,n=8),运动后12 h组(B2组,n=8)和运动后24 h组(B3组,n=8).检测各组大鼠线粒体前向角散射(FSC)、线粒体90°侧向角散射(SSC)和线粒体内Rhodamine123的荧光强度值(FL1);电镜观察各组大鼠左室前壁心肌纤维超微结构变化情况.结果B2组FSC值显著高于其他3组(P＜0.05),B2组SSC值和FL1值显著低于其他3组(P＜0.05).电镜结果表明,大强度运动可造成大鼠心肌线粒体损伤,以运动后12 h损伤最为严重.结论大强度游泳运动可能诱发大鼠心肌线粒体膜通透性转换孔的开放,促使线粒体外的物质内流并影响线粒体内结构的改变;大面积的线粒体损伤可能与心肌线粒体膜通透性转换孔的开放有重要的关联性.     

疲劳性运动后骨骼肌线粒体钙,镁代谢和立体计量学的研究

结果提示:急性运动过程中线粒体离子代谢紊乱抑制线粒体氧化磷酸化过程,减少 ATP 生成,进而造成线粒体肿胀、嵴破坏,进一步抑制氧化磷酸化,加剧离子代谢紊乱的“恶性循环”可能是运动性骨骼肌疲劳的重要原因。耐力训练通过提高线粒体的代谢机能,改善运动中线粒体离子代谢,以维持其正常形态可能是耐力训练增强机体抗疲劳能力,提高运动机能的重要机制。     

线粒体可塑性与运动健康适应的关系

长期的耐力训练或运动不仅能够提高运动能力,还能促进身体健康,减少慢性疾病的发病几率,但具体机制还不清楚.骨骼肌对耐力运动的健康适应表现为增加肌糖原含量和胰岛素敏感性、氧化型肌纤维的转化以及提高线粒体的数量与功能.线粒体的形态结构、数量和质量,具有高度的可塑性,各种生理应激都能充分的调节线粒体的可塑性.运动训练不仅刺激肌细胞线粒体的生物合成,还通过线粒体分裂和融合对线粒体网状结构进行重塑,并且通过线粒体质量控制清除旧的、受损的或功能失调的线粒体.研究线粒体可塑性与运动适应动态变化中的作用,从线粒体形态、结构和动力重构角度出发,了解线粒体和能量代谢的关系,为代谢疾病、退行性疾病寻找明确的靶标提供一定的理论基础.     

磷脂酶A2 对线粒体膜渗透性转运的影响

力竭运动后,大鼠心肌线粒体钙离子发生明显变化,这种钙离子转运发生的紊乱是由于线粒体膜的渗透性发生改变而引发的。巯基基团的氧化作用在增加膜渗透性转运是必需的,但不是唯一的条件,磷脂酶Ａ２（ＰＬＡ２）也是膜渗透性转运的诱导因素,线粒体释放钙离子需要依赖ＰＬＡ２增加内膜渗透性的反应物（如溶血磷脂）。因此,力竭运动导致的ＰＬＡ２活性增加及由此引发的线粒体钙运输变化可能是运动疲劳发生的分子机制之一。     

力竭性运动中肝脏线粒体电子漏对电子传递与质子转移偶联的影响

以SD大鼠递增负荷急性力竭跑台运动为疲劳模型,分别测定了运动后即刻肝脏线粒体:(1)超氧阴离子(O_2)生成及膜脂质过氧化水平;(2)呼吸链复合体Ⅰ Ⅲ和Ⅱ Ⅲ0电子传递与质子泵出比值(H~ /2e)。结果表明:线粒体电子漏(O_2)和膜脂质过氧化水平(MDA含量)显著增加(P<0.05);苹果酸及谷氨酸和琥珀酸两种呼吸底物启动的呼吸链复合体Ⅰ Ⅲ和Ⅱ Ⅲ的总H~ /2e分别降低18.63和15.89％(均 P<0.001)。研究提示,线粒体电子漏是运动性内源自由基的重要来源,而且线粒体电子传递—质子转移之间的偶联破坏与运动诱导线粒体电子漏生成增多有关。