共查询到19条相似文献，搜索用时 211 毫秒
1.
神经退行性疾病是一种以中枢神经系统或外周神经系统神经元结构和功能丧失为特征的神经系统疾病。线粒体功能障碍是阿尔茨海默病、帕金森病、亨廷顿病等多种常见神经退行性疾病的早期病理特征。大量研究表明运动可明显改善神经退行性病变症状,然而其调节机制目前还不清楚。鉴于运动是促进线粒体合成、活性与功能的重要调节因素,并且线粒体功能变化在神经退行性病变中发挥重要作用。主要从线粒体角度阐述运动对神经退行性疾病的影响及可能机制,包括线粒体生物合成、线粒体ROS和氧化应激、线粒体动力学、线粒体质量控制,为运动防治神经退行性疾病提供理论支持。 相似文献
2.
运动对线粒体的氧化损伤及线粒体营养的补充 总被引：3，自引：0，他引：3
剧烈的运动会增加机体的氧耗量,并且会破坏机体内部氧化系统和抗氧化系统之间的平衡.线粒体电子传递链以及黄嘌呤氧化酶是运动时细胞内产生自由基的主要来源.自由基的产生会对机体的抗氧化系统造成严重的损伤,它能够使蛋白质的构像发生改变,使底物或辅助因子的亲和力下降,导致酶的失活,但是这种结构改变引起的酶失活可能是可逆的,只要增加底物或辅酶的水平就可以使酶重新恢复活性.线粒体营养素要么参与线粒体的组成,要么其代谢对线粒体的结构和功能具有重大的影响,长期补充线粒体营养可以有效地保护线粒体功能的完整,推迟线粒体的衰退.主要针对烟酸、L-肉碱/L-乙酰肉碱(ALCAR)、α-硫辛酸-LA-二氢硫辛酸-DHLA-硫辛酰胺、辅酶Q10(CoQ)的功用进行讨论. 相似文献
3.
运动对鼠肝功能的影响(综述) 总被引：3，自引：0，他引：3
运动可导致鼠肝脏内的酶含量、酶活性及线粒体功能发生变化。不同的运动强度对肝功能产生不同的影响 ,因而要采取一定的策略和手段加强肝脏的代谢功能 ,防止运动对肝脏的损伤。这包括物理手段、服用中药和营养素补充。 相似文献
4.
自19世纪50年代被发现以来,有关线粒体的研究从未停歇.作为一种存在于大多数真核细胞中的双层膜细胞器,线粒体负责提供机体活动所需要的大部分ATP,同时参与多种细胞生理活动,为适应细胞不同条件下的需求,线粒体数目处于动态变化之中,同时线粒体也可以通过融合和分裂来实现形态和功能上的改变.运动作为一种有益健康的生活方式,其关键作用是能够激活肌肉细胞内过氧化物酶体增殖物激活受体γ辅助活化因子1α（PGC-1α）,从而诱导下游多种转录因子的表达,促进线粒体蛋白合成的增加,最终合成更多功能完善的线粒体,有效改善机体能量代谢.该综述将着重介绍线粒体营养素羟基酪醇、白藜芦醇及硫辛酸在运动状态下对线粒体代谢包括线粒体生成、线粒体融合和分裂的调控作用以及其潜在作用机制的研究进展. 相似文献
5.
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. 相似文献
6.
廖世雄 《哈尔滨体育学院学报》2008,26(3):134-136
亚高原情况下机体为了从低氧空气中争取更多的氧而增加呼吸量,影响了机体的正常酸碱平衡,使食欲减退,能量供应不足,线粒体功能受到影响,因此代谢降低。因此要制定科学的用餐计划,研制富含特定营养素的运动员专用食品或运动补剂,以使运动员获得足够的运动营养,从而取得理想的运动成绩。 相似文献
8.
主要阐述大运动量运动或训练后营养获得对免疫反应的机制.概述了营养和体液缺失对免疫功能的影响,探讨了运动与常量营养素(碳水化合物、脂肪和蛋白质)和氨基酸(尤其是谷氨酰胺)的利用对免疫功能的影响及运动诱导免疫抑制的病因学.常量营养素推荐摄入量将有助于降低大强度运动或训练对运动员免疫功能的负面影响. 相似文献
9.
牛磺酸对力竭运动大鼠心肌线粒体损伤的保护作用 总被引：7，自引：0，他引：7
以大鼠力竭性运动为模型,观察了牛磺酸对大鼠力竭运动时心肌线粒体脂质过氧化、超氧化物歧化酶、总Ca++浓度的影响。结果显示,牛磺酸可降低大鼠力竭运动后心肌线粒体脂质过氧化水平,提高大鼠力竭运动后心肌线粒体超氧化物歧化酶(SOD)的活性,保持大鼠力竭运动后心肌线粒体总Ca++浓度。结果提示,牛磺酸可减少力竭运动后因脂质过氧化而产生的自由基,降低自由基对心肌线粒体的攻击,维持线粒体膜的功能,说明牛磺酸有保护心肌线粒体的功能和防止心肌线粒体损伤的作用。 相似文献
10.
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. 相似文献
11.
《运动与健康科学(英文)》2020,9(5):394-404
Dementia is one of the greatest global challenges for health and social care in the 21st century. Alzheimer's disease (AD), the most common type of dementia, is by no means an inevitable consequence of growing old. Several lifestyle factors may increase, or reduce, an individual's risk of developing AD. Much has been written over the ages about the benefits of exercise and physical activity. Among the risk factors associated with AD is a low level of physical activity. The relationship between physical and mental health was established several years ago. In this review, we discuss the role of exercise (aerobic and resistance) training as a therapeutic strategy for the treatment and prevention of AD. Older adults who exercise are more likely to maintain cognition. We address the main protective mechanism on brain function modulated by physical exercise by examining both human and animal studies. We will pay especial attention to the potential role of exercise in the modulation of amyloid β turnover, inflammation, synthesis and release of neurotrophins, and improvements in cerebral blood flow. Promoting changes in lifestyle in presymptomatic and predementia disease stages may have the potential for delaying one-third of dementias worldwide. Multimodal interventions that include the adoption of an active lifestyle should be recommended for older populations. 相似文献
12.
阿尔茨海默病（Mzheimer disease,AD）是一种常见的老年性痴呆症,由于神经元丧失以及神经递质的缺少导致各种认识和认知功能障碍。神经保护肽慢病毒（rLent／NT4-NAP）感染AD大鼠鼻黏膜后能够分泌表达神经保护肽（NAP）,NAP能抑制细胞凋亡,对AD产生保护作用。运动可以对AD大鼠产生有利影响,从而延缓AD大鼠病情。本文采用综述的办法,详细介绍了rLent／NT4-NAP和运动对AD模型大鼠的影响。通过以上论述。为预防、减缓和治疗AD提供相关理论依据。 相似文献
13.
对近些年来关于ROS在AD发生发展中的机理进行分析,探讨运动预防及延缓AD发生的机制;活性氧（reac-tive oxygen species,ROS）在阿尔茨海默病（Alzheimer s disease,AD）中的作用机理以及运动对活性氧诱导的阿尔茨海默病的影响。结果表明：AD的发生发展与活性氧密切相关,活性氧参与AD病理性特征的老年斑和神经纤维缠结形成,并且促进神经元死亡。运动作为干预条件可以有效地预防和延缓活性氧诱导的AD症。活性氧对AD的发生起重要作用,运动可预防和延缓AD的发生。 相似文献
14.
Background:Despite the strong evidence of aerobic exercise as a disease-modifying treatment for Alzheimer’s disease(AD)in animal models,its effects on cognition are inconsistent in human studies.A major contributor to these findings is inter-individual differences in the responses to aerobic exercise,which was well documented in the general population but not in those with AD.The purpose of this study was to examine inter-individual differences in aerobic fitness and cognitive responses to a 6-month aerobic exercise intervention in community-dwelling older adults with mild-to-moderate dementia due to AD.Methods:This study was a secondary analysis of the Effects of Aerobic Exercise for Treating Alzheimer’s Disease(FIT-AD)trial data.Aerobic fitness was measured by the shuttle walk test(SWT),the 6-min walk test(6MWT),and the maximal oxygen consumption(VO2max)test,and cognition by the AD Assessment Scale-Cognition(ADAS-Cog).Inter-individual differences were calculated as the differences in the standard deviation of 6-month change(SDR)in the SWT,6MWT,VO2max,and ADAS-Cog between the intervention and control groups.Results:Seventy-eight participants were included in this study(77.4±6.3 years old,mean±SD;15.7±2.8 years of education;41%were female).VO2max was available for 26 participants(77.7±7.1 years old;14.8±2.6 years of education;35%were female).The SDR was 37.0,121.1,1.7,and 2.3 for SWT,6MWT,VO2max,and ADAS-Cog,respectively.Conclusion:There are true inter-individual differences in aerobic fitness and cognitive responses to aerobic exercise in older adults with mild-tomoderate dementia due to AD.These inter-individual differences likely underline the inconsistent cognitive benefits in human studies. 相似文献
15.
阿尔茨海默病(AD)是目前最为常见的痴呆类型,其发病机制复杂,尚未完全阐明。研究发现,胰岛素信号通路在AD发病机制中发挥重要作用。运动可以通过激活胰岛素信号通路,调控下游分子表达,改善AD病理表现。从磷脂酰肌醇-3-激酶/丝苏氨酸激酶(PI3K/AKT)、丝裂原活化蛋白酶(MAPK)和Wnt 3条胰岛素信号通路视角切入,探讨运动改善AD的可能分子机制,为AD治疗提供理论依据。 相似文献
16.
Ramadan fasting, involving abstinence from fluid and food from sunrise to sundown, results in prolonged periods without nutrient intake and inflexibility with the timing of eating and drinking over the day. Dietary choices may also change due to special eating rituals. Although nutrition guidelines are specific to the sport, to the periodized training and competition calendar, and to the individual, many promote the consumption of carbohydrate and fluid before and during exercise, and consumption of protein, carbohydrate, and fluids soon after the session is completed. Failing to meet overall nutritional needs, or to provide specific nutritional support to a session of exercise, is likely to impair acute performance and reduce the effectiveness of training or recovery. Muslim athletes who fast during Ramadan should use overnight opportunities to consume foods and drinks that can supply the nutrients needed to promote performance, adaptation, and recovery in their sports. Because of the benefits of being able to consume at least some of these nutrients before, during or after an exercise session, the schedule of exercise should be shifted where possible to the beginning or end of the day, or during the evening when some nutritional support can be provided. 相似文献
17.
神经营养因子(neurotrophic factors,NFs)缺失是导致脑功能衰退及神经退行性疾病的重要因素。帕金森病(Parkinson’s disease,PD)属于神经退行性疾病的一种,患者常表现出静息性肌肉震颤、运动性肌力缺失、运动迟缓、姿势僵硬不稳、步态异常等病症,其病理基础是中脑黑质致密部基底神经节多巴胺(dopamine,DA)能神经元丢失和DA减少。研究认为,运动可通过促进NFs的表达,促进DA能神经元的存活和DA的增多,改善PD的病理和病症。其机制可能与运动诱导NFs增多,进而调节PD病理相关分子酪氨酸羟化酶、N-甲基-D-天冬氨酸受体、突触素、α-突触核蛋白表达以及改善氧化应激、线粒体功能障碍和神经炎症反应等有关,但其中的确切调节机制尚未得以完全揭示。同时,运动模式、运动强度和运动时间等因素,也在运动调节NFs表达中影响干预的差异。运动产生的机械刺激,引发血液循环通过血脑屏障与脑内信号分子的变化,激活脑内NFs相关信号通路,从而促进NFs调节PD脑内的相关信号分子,改善或缓解PD。通过分析运动干预调控NFs的表达,进而作用于脑内PD病理相关分子,探讨NFs在运动调控PD病理中的作用及机制。 相似文献
18.
19.
Cardiovascular disease is the leading cause of human death worldwide. Autophagy is an evolutionarily conserved degradation pathway,which is a highly conserved cellular degradation process in which lysosomes decompose their own organelles and recycle the resulting macromolecules.Autophagy is critical in maintaining cardiovascular homeostasis and function, and excessive or insufficient autophagy or autophagic flux can lead to cardiovascular disease. Enormous evidence indicates that exercise training plays a beneficial role in the prevention and treatment of cardiovascular diseases. The regulation of autophagy during exercise is a bidirectional process. For cardiovascular disease caused by either insufficient or excessive autophagy, exercise training restores normal autophagy function and delays the progression of cardiovascular disease.An in-depth exploration and discussion of exercise-mediated regulation of autophagy in the cardiovascular system can broaden our view about the prevention of various autophagy-related diseases through exercise training. In this article, we review autophagy and its related signaling pathways,as well as autophagy-dependent beneficial effects of exercise in cardiovascular system. 相似文献