IGF1–PI3K-induced physiological cardiac hypertrophy: Implications for new heart failure therapies,biomarkers, and predicting cardiotoxicity

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.     

IGF1–PI3K-induced physiological cardiac hypertrophy: Implications for new heart failure therapies,biomarkers, and predicting cardiotoxicity

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.     

穴位离子导入对皮艇运动员心肺功能的影响

采用RPE评分、运动成绩测试、心肺功能测试及心脏内分泌激素放射免疫法检测等方法对运动员心脏功能进行跟踪观察。结果表明：(1)穴位离子导入能明显改善运动员的主观感觉，提高专项成绩，改善心肺功能，降低无氧闲心率，提高有氧耐力，推迟心源性运动性疲劳的发生；(2)穴位离子导入可改善运动员心脏神经肽ET和CGRP的分泌，使之向更有利于适应运动负荷的方向发展。结论是：(1)心源性运动性疲劳的发生与多因素相关；(2)穴位离子导入能多环节、多层面地保护心肌和改善心脏功能，从而延缓疲劳产生和促进疲劳消除。     

运动对骨质影响的表观遗传机制研究进展

骨质变化除了与性别、年龄、激素水平、生活方式和机械受力等因素有关外,还与表观遗传调控途径有关。表观遗传调控的3大主要途径包括DNA甲基化、组蛋白修饰及非编码RNA。在遗传-环境范畴内,运动作为外源性力学刺激,可以通过调控DNA去甲基化促成骨生成,调控组蛋白修饰维持骨稳态和非编码RNA影响骨代谢通路,这些均是运动通过表观遗传途径改善骨质健康的可能机制。梳理近年来表观遗传调控在骨组织运动医学领域的研究进展,有助于为运动健骨和防治骨质疏松等代谢性疾病提供新思路。     

空气污染暴露与体育活动:如何保障健康

空气污染物是严重威胁人类健康的风险因子之一,长期空气污染暴露可导致心脑血管疾病、糖尿病、神经系统损伤和癌症等多种疾病。已有研究表明,在高浓度颗粒物污染下运动可导致呼吸系统和心血管组织炎症、功能下降,并影响运动机能。也有研究表明,长期规律性的运动健身产生的有益效应可抵抗颗粒物造成的机体损害,即“运动促进健康”和“空气污染危害健康”两者之间可能存在着一个平衡点。如何在空气污染环境中科学安全的运动健身,成为学者和大众共同关注的问题。从“空气污染对机体健康的危害”“空气污染对运动人群健康和运动能力的影响”“运动训练对空气污染所致健康损害的抵抗效应”“运动抵抗空气污染所致健康损害的相关机制”“空气污染环境下运动的保护措施”5个方面对国内外已发表的相关流行病学调查及实验研究进行总结与归纳。在此基础上,提出运动抵抗污染物所致机体损害的机制探索、空气污染环境下运动的安全阈值范围确定、运动健身环境污染预警机制的建立等,将是本研究领域具有重要科学与现实意义的研究选题和进一步的研究重点。     

Akute und chronische Effekte von Ausdauerbelastungen auf das Herz bei Sportlern, gesunden Normalpersonen und Patienten

Due to endurance exercise-induced increases of the cardiac biomarkers troponin and B-type natriuretic peptide (BNP), which are usually elevated in patients with acute myocardial infarction and heart failure and used in clinical practice as diagnostic tools in these diseases, the clinical and sportsmedical relevance of these exercise-induced increases was unclear. Therefore, the aim was to examine this topic systematically by consecutive studies. Considering the acute effects of endurance exercise, an intensity- and duration-dependent short-term elevation could be demonstrated in the majority of healthy athletes without pathological relevance. Considering the chronic effects of endurance exercise it could be shown that regular and competitive endurance exercise training induces an athlete??s heart with harmonic eccentric hypertrophy of the left and right ventricle, which also is not of pathological relevance. In conclusion it can be assumed from the results of these studies that acute and chronic endurance exercise is not harmful for the healthy heart.     

冠心病康复中有氧运动强度设定方法的比较及展望

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。     

Potential adverse cardiac remodelling in highly trained athletes: still unknown clinical significance

Moderate endurance exercise has long been considered an essential element to maintain cardiovascular health, and sedentary behaviour in the general population has been related to a significant increase in all-causes of mortality, cardiovascular disease mortality and cardiovascular disease incidence. However, a growing group of people performs an intense exercise that leads to multiple heart adaptive changes that are collectively called “athlete’s heart”. In this review, we discussed the evidence of cardiac remodelling process secondary to repetitive and strenuous exercise in some predisposed athletes that produces intense and probably deleterious changes in cardiac morphology and function with no clear clinical significance in long-term follow-up. Moreover, we also discussed the individual biological response to exercise assessed by myocardial damage, inflammation, oxidative stress, fibrosis and ventricular hypertrophy biomarkers showing different intensities with equivalent exertion.     

运动干预调控肠道微生物介导认知功能的作用研究进展

认知功能障碍是神经系统疾病的重要特征表现,受诸多因素影响。肠道微生物在维持机体健康和多种疾病的发展中发挥作用,肠道微生物失衡与躯体运动能力和脑认知功能障碍,如阿尔茨海默病和帕金森病等神经退行性疾病关系密切。研究发现,运动干预可通过对肠道微生物的调节,建立肠-脑之间的联系,调控认知功能,改善神经退行性疾病,但不同方式的运动干预对肠道微生物的影响及其与认知功能的调节之间存在差异性。通过分析肠道微生物的生物学功能以及运动介导肠道微生物相关的改变与脑认知功能的关系,探讨肠道微生物在肠-脑神经联络以及运动调控肠道微生物改善认知功能的作用机理。     

马拉松运动对心脏的影响:生理适应和潜在风险

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。     

Running for your life: A review of physical activity and cardiovascular disease risk reduction in individuals with schizophrenia

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.     

心脏分子标志物NT-proBNP在运动预适应保护效应评价中的应用

目的:以运动预适应(EP)诱导心肌保护效应为研究基础,以心脏分子标志物NT-proBNP为研究核心,联合应用血清NT-proBNP与血清cTnI和心肌HBFP染色,综合评价EP对力竭运动心肌的保护效应;方法:SD大鼠100只,随机分为对照组(C组)、力竭组(EE组)、运动预适应组(EP组)和运动预适应+力竭组(EP+EE组)。采用一次间歇性大强度跑台运动建立EP模型,力竭跑台运动建立急性心肌损伤模型。用ELISA法检测血清NT-proBNP浓度,CLIA法检测血清cTnI浓度,HBFP染色法观察心肌缺血缺氧状况;结果:与C组比较,EE组血清NT-proBNP浓度显著升高(P<0.05),EP组变化不明显(P>0.05);与EP组比较,EP+EE组血清NT-proBNP浓度变化不明显(P>0.05);与EE组比较,EP+EE组血清NT-proBNP浓度显著下降(P<0.05)。各组大鼠血清NT-proBNP浓度与血清cTnI浓度、心肌HBFP染色结果的变化趋势一致;结论:EP是一种非损伤性预适应方式,能明显减轻力竭运动引起的急性心肌损伤和促进心脏功能恢复。血清NT-proBNP与血清cTnI和心肌HBFP染色联合应用具有互补性,有助于综合评价EP对力竭运动心肌的保护效应。     

Recommendations to maintain immune health in athletes

Numerous studies over the last 35 years report an increase in upper respiratory infection (URI) symptoms in athletes during periods of heavy training and competition. Challenges athletes face such as heavy exercise and life stress influence immune function via activation of the hypothalamic–pituitary–adrenal axis and the sympathetic nervous system and the resulting immunoregulatory hormones. Both innate and acquired immunity are often reported to decrease transiently in the hours after heavy exertion, typically 15–70%: prolonged heavy training sessions in particular have been shown to decrease immune function; potentially providing an ‘open window’ for opportunistic infections. Whether the observed changes in immunity with acute strenuous exercise or periods of heavy training account for the increased susceptibility to URI symptoms remains contentious. Nevertheless, there is little doubt that URI symptoms hinder athletic training and competition; underpinning the need to identify the prominent risk factors and appropriate countermeasures. Recent studies have identified prominent risk factors, including: intensified training in the winter; long-haul travel; low energy availability; high levels of psychological stress and anxiety; and depression. Given the shared pathways and effector limbs for the body’s response to physical and psychological challenges, it is logical that psychological strain influences immunity and illness incidence in athletes under heavy training; indeed, stress and anxiety have recently been shown to modify the immune response to exercise. This mini-review provides new insights and evidence-based recommendations for coping with the various challenges that athletes encounter on immune health, including: heavy exercise; life stress; sleep disruption; environmental extremes and nutritional deficits.     

急性运动降低感染风险的免疫调节机制

由于新型冠状病毒(2019-nCoV)感染的肺炎疫情暴发,人们将居家运动作为提高免疫力与保持健康的重要手段,运动与免疫的关系再度受到关注。一般认为,在充分恢复的前提下进行规律的中高强度运动可提高免疫功能,而急性运动(acute exercise)可能抑制免疫功能并增加感染风险。急性运动后外周血淋巴细胞计数及功能降低、免疫球蛋白A水平分泌减少被认为是运动抑制免疫的理论基础。但目前这种独立于非运动因素影响免疫功能增加感染风险的认识受到了现有研究的挑战。急性运动可通过应激反应将淋巴细胞亚群迅速动员至循环中,运动结束后,淋巴细胞亚群又会迅速迁移至外周组织。淋巴细胞的重新分布(lymphocyte redeployment)可能是一种进化保守的免疫机制,这一过程强化了外周组织的免疫监视与调节功能,有助于提升机体抵抗感染能力。因此,从这一视角就急性运动对机会性感染风险及免疫功能影响的现状进行综述。     

运动康复锻炼对PCI术后患者心功能及生活质量影响的系统综述

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...     

运动促进线粒体功能在改善神经退行性疾病中的分子机制

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。     

运动性心律失常研究现状与前景

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。     

特殊人群的运动、感染风险和免疫机能

有关运动与免疫的研究,大都集中在研究运动对普通人群和运动员上呼吸道感染的影响以及免疫机能的影响,这些研究的大部分案例都是针对年轻人和健康人群的。那么,运动免疫学领域还很大,尤其是对那些疾病、亚健康和特殊年龄段的人群的研究仍是相对薄弱的地方。对特殊人群(HIV感染人群、老年人、儿童、肥胖和糖尿病)的运动、感染风险和免疫机能进行综述。     

Acute effects of walking on inflammatory and cardiovascular risk in sedentary post-menopausal women

Biochemical markers of inflammation are emerging as new predictors of risk of cardiovascular disease (CVD) and may alter acutely with exercise. Few studies have been conducted on the effects of walking on these markers or whether different walking intensities elicit varied effects. As there is growing interest in modifiable lifestyle factors such as walking to reduce CVD risk, these inflammatory responses warrant investigation. The aim of this study was to compare the effects of walking at 50% versus 70% of predicted maximal heart rate on C-reactive protein (CRP), plasma fibrinogen, and triglycerides in sedentary post-menopausal women. Twelve post-menopausal women (mean age 58 years, s +/-6; stature 1.62 m, s+/-0.06; body mass 66.8 kg, s +/-6.2) completed two 30-min treadmill walks in a randomized cross-over design. Fasted blood samples were taken (for the determination of plasma fibrinogen, CRP, and lipids) before, immediately after, and 1 and 24 h after exercise. Triglyceride concentrations decreased from pre-exercise to 24 h post exercise at both walking intensities (time x group interaction, P < 0.05). No significant effects were observed for plasma fibrinogen, CRP, total cholesterol, low-density or high-density lipoprotein cholesterol (time x group interaction, P > 0.05). The results of this study suggest that fasting plasma triglycerides are decreased on the morning after 30 min of brisk walking at either 50% or 70% of maximal heart rate (moderate and vigorous intensity).