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1.
With the rising incidence of cardiovascular diseases, the concomitant mortality and morbidity impose huge burdens on quality of life and societal costs. It is generally accepted that physical inactivity is one of the major risk factors for cardiac disease and that exercise benefits the heart in both physiological and pathologic conditions. However, the molecular mechanisms governing the cardioprotective effects exerted by exercise remain incompletely understood. Most recently, an increasing number of studies indicate the involvement of epigenetic modifications in the promotion of cardiac health and prevention of cardiac disease. Exercise and other lifestyle factors extensively induce epigenetic modifications, including DNA/RNA methylation, histone post-translational modifications, and non-coding RNAs in multiple tissues, which may contribute to their positive effects in human health and diseases. In addition, several studies have shown that maternal or paternal exercise prevents age-associated or high-fat diet-induced metabolic dysfunction in the offspring, reinforcing the importance of epigenetics in mediating the beneficial effects of exercise. It has been shown that exercise can directly modify cardiac epigenetics to promote cardiac health and protect the heart against various pathological processes, or it can modify epigenetics in other tissues, which reduces the risk of cardiac disease and affords cardioprotection through exerkines. An in-depth understanding of the epigenetic landscape of cardioprotective response to exercise will provide new therapeutic targets for cardiac diseases. This review, therefore, aimed to acquaint the cardiac community with the rapidly advancing and evolving field of exercise and epigenetics.  相似文献   

2.
Heart failure represents the end point of a variety of cardiovascular diseases. It is a growing health burden and a leading cause of death worldwide. To date, limited treatment options exist for the treatment of heart failure, but exercise has been well-established as one of the few safe and effective interventions, leading to improved outcomes in patients. However, a lack of patient adherence remains a significant barrier in the implementation of exercise-based therapy for the treatment of heart failure. The insulin-like growth factor 1 (IGF1)–phosphoinositide 3-kinase (PI3K) pathway has been recognized as perhaps the most critical pathway for mediating exercised-induced heart growth and protection. Here, we discuss how modulating activity of the IGF1–PI3K pathway may be a valuable approach for the development of therapies that mimic the protective effects of exercise on the heart. We outline some of the promising approaches being investigated that utilize PI3K-based therapy for the treatment of heart failure. We discuss the implications for cardiac pathology and cardiotoxicity that arise in a setting of reduced PI3K activity. Finally, we discuss the use of animal models of cardiac health and disease, and genetic mice with increased or decreased cardiac PI3K activity for the discovery of novel drug targets and biomarkers of cardiovascular disease.  相似文献   

3.
目的探讨并评估运动康复锻炼对PCI术后患者心功能、运动耐力、不良心血管事件、生活质量的影响。方法检索运动康复锻炼对PCI术后患者心功能及生活质量的影响的相关研究文献。将运动干预后患者心功能相关指标、不良心血管事件发生情况、生活质量各维度评分与干预前、常规治疗对照组进行对比。结果较多研究显示,参加运动康复锻炼可改善患者心功能状态、降低不良心血管事件发生率、提高运动耐力及生活质量。也有部分研究表明,运动康复锻炼对术后患者部分心功能指标无明显改善,对部分不良心血管事件的发生无明显影响。结论长期规范化的运动康复训练,可显著提高PCI术后患者左心室射血分数、改善NYHA心功能分级、增大6 min步行距离、降低心源性死亡率、再发心绞痛率、血运重建率、冠状动脉造影、再住院风险、提高生活质量各维度评分而对再发心肌梗塞、冠状动脉搭桥术无明显影响。  相似文献   

4.
脂蛋白(a)[LP(a)] 在结构上类似低密度脂蛋白(LDL) 。血清中Lp(a) 浓度基本上受遗传决定,但有种族差异。Lp(a) 与心血管疾病之间联系有明显的独立性。冠心病是世界许多发达国家中引起死亡的主要因素,运动是预防冠心病的重要手段之一。因此近年来人们开始注意各种运动训练对Lp(a) 浓度的影响,以期探讨运动防治冠心病之机理。结果表明,长期耐力训练可轻度升高Lp(a) 浓度。初步推测,这种运动可能较有利于运动引起的血管微小创伤的修复,与其他血浆脂蛋白的变化一起对防治冠心病(CHD) 有积极作用。急性大强度运动后,可使受试者血Lp(a)浓度下降,表现出组织损伤之应激反应。  相似文献   

5.
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.  相似文献   

6.
Individuals with schizophrenia have a greater risk for cardiometabolic risk factors (e.g. central obesity, insulin resistance, hypertension and dyslipidaemia), cardiovascular diseases and mortality. This risky profile may be explained by the adverse effects of antipsychotic medications and an unhealthy lifestyle (e.g. smoking, poor nutrition and low physical activity). In the general population, physical activity has been shown to be the optimal strategy to improve both cardiometabolic parameters and cardiorespiratory fitness levels. Accordingly, an emerging literature of non-pharmacological interventions (e.g. cognitive behavioural therapy, diet and physical activity) has been studied in individuals with schizophrenia. Therefore, the purpose of this review was 1) to conduct a critical literature review of non-pharmacological interventions that included some kind of physical activity (including supervised and unsupervised exercise training) and target cardiometabolic risk factors in individuals with schizophrenia. 2) To describe the contribution of physical activity alone by reviewing trials of supervised exercise training programmes only. A literature review via systematic keyword search for publications in Medline, PubMed, Embase and PsycINFO was performed. Many non-pharmacological interventions are efficient in reducing cardiovascular disease risk factors when combined with physical activity. Supervised physical activity has been successful in decreasing cardiovascular disease risk, and aerobic interval training appears to provide more benefits by specifically targeting cardiorespiratory fitness levels. In conclusion, physical activity is an effective strategy for addressing cardiovascular disease risk in individuals with schizophrenia. Long-term studies are needed to evaluate the feasibility and impact of exercise training programmes in individuals with schizophrenia.  相似文献   

7.
Cardiomyocytes comprise ∼70% to 85% of the total volume of the adult mammalian heart but only about 25% to 35% of its total number of cells. Advances in single cell and single nuclei RNA sequencing have greatly facilitated investigation into and increased appreciation of the potential functions of non-cardiomyocytes in the heart. While much of this work has focused on the relationship between non-cardiomyocytes, disease, and the heart's response to pathological stress, it will also be important to understand the roles that these cells play in the healthy heart, cardiac homeostasis, and the response to physiological stress such as exercise. The present review summarizes recent research highlighting dynamic changes in non-cardiomyocytes in response to the physiological stress of exercise. Of particular interest are changes in fibrotic pathways, the cardiac vasculature, and immune or inflammatory cells. In many instances, limited data are available about how specific lineages change in response to exercise or whether the changes observed are functionally important, underscoring the need for further research.  相似文献   

8.
常芸 《体育科研》2012,33(4):11-16
运动心脏作为运动员所特有的"高功能,高储备,大心脏"一直被认为是运动员良好体能状态的重要保障,但在运动训练监控中我们发现一些运动员或多或少存在某些心脏结构改变和心律失常现象,往往影响运动员的系统训练和竞技水平的提高,常常困扰着运动员和教练员。运动医学研究也显示,在大运动量训练与反复大强度运动后运动心脏细胞与亚细胞的形态结构与功能代谢发生了某些失代偿性改变,引起运动性心肌微损伤,而且,右心房、右心室及内膜下心肌组织是运动心脏对大运动量训练与反复大强度运动的敏感区域,又称易损部位。尽管目前运动性心肌微损伤现象已为人所知,且运动性心律失常发生也与运动性心肌微损伤有关,但其病因、病理及发病机制尚不十分明了,运动员心肌微损伤与运动性心脏意外的发生很难早期诊断、预测和防治。针对优秀运动员潜在心脏隐患的调研也证实优秀运动员存在较高的心律失常风险,且专项训练年限长的运动员更为常见,一些运动员因此而退赛,甚至退役。运动性心律失常已经成为影响运动员体能、健康以及正常训练比赛的重要原因之一,制约了部分优秀运动员竞技水平和比赛成绩的提高。部分退役运动员留下了永久性的心律失常。本文主要针对运动性心律失常的常见类型以及病理变化与发生机制进行了综述与探讨,并对未来研究前景进行了展望,希望开展运动性心律失常电生和分子病理的研究,规避运动场上心血管意外的发生,保障运动员健康、延长运动寿命。  相似文献   

9.
本文采用放射免疫方法测定血浆心钠素与采用超声心动法测定心功能相结合,对10名优秀的耐力运动员和10名普通大学生进行了逐级递增负荷运动试验,以探讨运动中心脏内分泌与心血管功能的变化及其相互关系。结果发现:心脏不仅是心钠素的产生和释放部位,也是心钠素作用的靶器官之一。  相似文献   

10.
马拉松作为持续时间较长、强度较高的耐力运动,对心脏的影响是利大还是弊多,对马拉松参赛选手心脏产生哪些生理适应,又对心脏健康存在哪些潜在风险,经常困扰着运动医学研究者和马拉松参赛者。依据目前的国内外研究,全面综述分析了马拉松对心脏各腔室以及冠状动脉结构和功能的影响,深入探讨了马拉松与心肌损伤标志物、心律失常、心肌纤维化和心脏猝死之间的关系。研究结果:1)马拉松会引起心脏发生离心性肥大,心房和心室腔体积均会增大,提升心脏功能。一次马拉松运动后,心房和左右心室收缩与舒张功能均出现了短暂性的下降,舒张功能下降更明显,这是心脏的一种生理适应,数周内可恢复至正常水平;2)尽管马拉松与冠状动脉风险之间的关系仍存在争议,但与同龄和相同心血管风险因素的对照人群相比,马拉松运动员仍具有较低的冠状动脉斑块形成风险;3)马拉松诱导的循环心肌损伤标志物的升高是可逆的,是对剧烈运动的一种暂时生理性应激反应;4)马拉松运动猝死的风险较低,多数马拉松猝死的发生和参赛者遗传的显性或隐性心脏疾病有关。为预防赛场心血管意外,应该建立马拉松赛场心血管意外的预防体系,包括赛前心血管风险评估和筛查程序、增加并合理布置赛中救助力量。  相似文献   

11.
男排运动员无氧代谢能力与血流动力学指标的相关关系   总被引:2,自引:0,他引:2  
采用实验及对比方法,对男排运动员的心血管机能进行分析。结果显示,男排运动员安静时心脏具有较大的储备能力,交感神经的兴奋性、血压等均较高,运动后,心血管机能对运动负荷表现出较好的适应性;每搏血量和心脏指数可作为评判排球运动员无氧酵解能力的指标。  相似文献   

12.
有氧运动对大鼠心血管自主神经调节功能的影响   总被引:2,自引:0,他引:2  
首先对心率变异性(HRV)和动脉压力反射敏感性(BRS)的测试分析方法进行了选取和改进,然后以正常大鼠为实验对象,观察比较尾动脉血压、脉搏、左室内压、心肌收缩力、心率变异性、动脉压力反射敏感性等指标在8周中等强度游泳运动组大鼠和和安静对照组大鼠之间的差异,旨在分析长期参加有氧运动对心血管自主神经调节功能的影响,为心血管自主神经平衡状态发生改变提供实验证据。研究发现,与对照组大鼠相比,运动组大鼠心肌出现肥大、心脏泵血功能增强、心交感神经介导的动脉压力反射敏感性升高、心迷走神经介导的动脉压力反射敏感性未受影响、心交感神经紧张性变异和心迷走神经紧张性变异程度均增加。研究结果提示,长期有氧运动可增强心血管自主神经的调节功能,使交感神经和副交感神经的协调与对抗关系在一个更高的功能层面上建立新的平衡。  相似文献   

13.
运动康复是冠心病康复的核心内容,其中有氧运动是基础。冠心病常规运动康复程序是对患者开展康复评估及危险分层后,给予区分危险度后的个体化康复运动,运动处方的制定是关键。如何准确客观地确定有氧运动强度是冠心病康复运动处方的重要环节。本文综述了不同冠心病康复有氧运动强度设定方法的优势、局限性及其临床应用状况,以期为冠心病患者进行有氧运动提供安全有效的强度设定方法,促进心脏康复在国内的发展与推广。  相似文献   

14.
近百年来,诸学者对运动性心肌肥大的机制做了大量的研究工作,运动性心肌肥大是心肌细胞对运动诱发的各种刺激如神经体液、心脏内分泌、Ca^2 的调节及运动引起心肌细胞的基因表达的适应性变化,根据文献报道,本文拟对运动性心肌肥大的生物学机制做一综述。  相似文献   

15.
钙调神经磷酸酶信号转导途径与运动性心肌肥大研究进展   总被引:3,自引:0,他引:3  
任绮  邓树勋 《体育科学》2006,26(8):53-58
心脏通过重塑结构和体积应对生理和病理等刺激所造成的不同生理负荷的需求,长期运动训练能促进发生心肌生理性肥大反应但机制仍未阐明。钙离子/钙调素依赖的钙调神经磷酸酶信号转导途径参与心肌肥大反应过程。综述近年来关于钙调神经磷酸酶依赖的信号通路参与心肌肥大调节的分子信号机制,探讨阻止心肌病理生理性肥大的信号传递机制,以期预防运动性心血管疾病的发生。  相似文献   

16.
Aerobic exercise and resistance training have been proven to be beneficial for patients with heart failure. Current reimbursement guidelines exclude these patients from our traditional cardiac rehabilitation program, so at Newton Wellesley Hospital a clinic model was developed for the disease management and exercise of heart failure patients.Key Words: heart failure, physical therapy, exercise  相似文献   

17.
Abstract

With an ageing population there is an increased prevalence of individuals living with cardiovascular disease (CVD). Characteristics of older aerobically fit individuals with previously diagnosed CVD have not been studied. Therefore, our knowledge is limited as to how, or if, aerobically fit individuals with CVD attempt to adapt their physical activity and the intensity of their training programmes. The objective of this paper is to characterise the physical activity habits and behaviours of older aerobically fit individuals with CVD. We identified 28 aerobically fit patients with CVD from those who completed a minimum of 15 and 12 min of the Bruce treadmill protocol for men and women, respectively. Consenting participants responded to questionnaires regarding physical activity levels, competitive event participation and self-monitoring since diagnosis of heart disease. Average age and treadmill time of participants were 56 and 49 years and 15.6 and 13.0 min for males and females, respectively. Data were obtained regarding recent medical history (medical diagnoses, surgeries/procedures). Despite the majority of individuals participating in the same or more activity since their diagnosis, 25% indicated that their condition limited their activity and 39% reported having symptoms during activity. Nearly all participants (93%) indicated that they monitored their heart rate during exercise. However, only 14% of participants stated that their physician advised them on how to exercise safely. It is necessary for physicians and cardiac rehabilitation programmes to be involved in safe and effective exercise programming to allow individuals to return to sport after CVD.  相似文献   

18.
周勇  赵霞 《福建体育科技》2007,26(2):19-20,26
通过对58名中年女性实施6个月的有氧健身操锻炼,探讨有氧健身操对中年女性身体成分和心肺功能的影响。结果显示,长期参加有氧健身操锻炼,可以降低体脂、静态心率及血压,提高台阶指数和肺容量,对预防中年女性心血管疾病具有重要作用。  相似文献   

19.
High-altitude exposure challenges the cardiovascular system to maintain oxygen delivery to the mitochondria under conditions of hypoxic stress. Following acclimatisation (3–5 days), stroke volume (SV) falls to below sea-level values but heart rate remains elevated, such that cardiac output is maintained compared to sea level. The decrease in SV has been a topic of research for over 40 years, but the underlying mechanisms are incompletely understood. Impaired systolic contractile function secondary to reduced coronary arterial oxygen tension has been investigated as a potential cause for the decrease in SV. However, despite in vitro evidence of impaired cardiac contractile force in severe hypoxia, the majority of studies to date have reported enhanced in vivo ventricular systolic function at rest and during exercise in humans up to and above 5000?m. However, the elevated function observed at rest has recently been suggested to reduce the functional reserve available during exercise. While in vivo systolic function appears enhanced at high altitude, a decrease in left ventricular end-diastolic volume (EDV) and altered filling patterns of both ventricles has been observed. The reduction in ventricular filling will undoubtedly affect SV, and four potential mechanisms have been proposed to explain the reduction in left ventricular filling. In this article, both historical and recent reports of systolic function at high altitude will be reviewed, and evidence supporting and refuting each of the four mechanisms underpinning reduced left ventricular filling will be discussed.  相似文献   

20.
Growing evidence has demonstrated exercise as an effective way to promote cardiovascular health and protect against cardiovascular diseases However, the underlying mechanisms of the beneficial effects of exercise have yet to be elucidated. Animal exercise studies are widely used to investigate the key mechanisms of exercise-induced cardiovascular protection. However, standardized procedures and well-established evaluation indicators for animal exercise models are needed to guide researchers in carrying out effective, high-quality animal studies using exercise to prevent and treat cardiovascular diseases. In our review, we present the commonly used animal exercise models in cardiovascular research and propose a set of standard procedures for exercise training, emphasizing the appropriate measurements and analysis in these chronic exercise models. We also provide recommendations for optimal design of animal exercise studies in cardiovascular research, including the choice of exercise models, control of exercise protocols, exercise at different stages of disease, and other considerations, such as age, sex, and genetic background. We hope that this position paper will promote basic research on exercise-induced cardiovascular protection and pave the way for successful translation of exercise studies from bench to bedside in the prevention and treatment of cardiovascular diseases.  相似文献   

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