运动员心脏 athlete's heart - PubMed 文献(第 4 页)
PubMed 共收录约 1,667 篇相关文献，本站只列出其中相关度最高的前 50 篇（共 5 页）；要看全部结果、按影响因子 / 分区 / 年份筛选，请前往完整搜索。
本页是「运动员心脏（athlete's heart）」PubMed 检索结果的第 4 页，列出第 31–40 篇相关文献；主题介绍见第 1 页。
运动员心脏 的 PubMed 搜索结果(第 4 页)
-
Improved Right Ventricular Performance with Increased Tricuspid Annular Excursion in Athlete's Heart. 运动员心脏中三尖瓣环位移增加改善右心室功能
Marathon runners (MTH) and patients with mitral regurgitation (MR) exhibit left ventricular (LV) overload, and LV geometric changes in these groups have been reported. In this study, right ventricular (RV) adaptation to chronic volume overload was evaluated in MTH and MR and normal controls together with interventricular septal remodeling and tricuspid annulus (TA) motion. A total of 60 age-matched subjects (including 19 MTH, 17 isolated chronic compensated MR patients, and 24 normal subjects) underwent conventional cine and tagged cardiac magnetic resonance imaging. Myocardial strain and curvature were computed on the interventricular septum and RV free wall. A dual-propagation technique was applied to construct RV volume-time curves for a single cardiac cycle. Similarly, the TA was tracked throughout the cardiac cycle to create displacement over time curve. Septal curvature was significantly lower in MTH and MR compared to controls. No significant differences in RV free-wall strain or RV ejection fraction were noted among the three groups. However, longitudinal TA excursion was significantly higher in MTH compared to controls (p = 0.0061). The peak late diastolic TA velocity in MR was significantly faster than MTH (p = 0.0031) and controls (p = 0.020). Increased TA kinetics allows for improved RV performance in MTH. Septal remodeling was observed in both MR and MTH, therefore a direct relationship of septal remodeling to TA kinetics in athlete's heart could not be elucidated in this study.
-
Sports-specific adaptations and differentiation of the athlete's heart. 运动特异性适应与运动员心脏的鉴别
Although the sports-specific adaptations and differentiation of an athlete's heart (AH) were first described 100 years ago, the condition is still an area of active debate. In clinical practice, there is often an obvious lack of basic knowledge concerning the prerequisites and well established extent of the structural and functional characteristics of an AH. Some misunderstandings arise from the somewhat misleading term 'athlete's heart' because not every athlete, even if he or she is training and competing at a very high level, develops an enlarged heart. Such a condition can only be expected after years of quantitative and qualitative demanding aerobic endurance training. Although the correlation with competitive performance of endurance events is rather low in trained athletes, the relationship between heart dimensions and ergometric performance represents an important criterion for differentiation between physiological and pathological cardiac enlargement. The assessment of measures exceeding the usual clinical limits, especially concerning volume-dependent echocardiographic parameters, also requires consideration of the strong influence of anthropometric data. The existence of a concentric left ventricular hypertrophy (LVH) in strength-trained athletes is still a topic of debate in the literature, but is rejected by most recent well-conducted trials. In our review. only bodybuilders using anabolic steroids exhibited a distinctly higher hypertrophic index compared with all other groups of endurance or strength athletes. Current unsolved issues in clinical sports medicine concern the early detection of myocardial complications in athletes exercising during infectious diseases, and the eligibility for competitive sport in cases of borderline LVH.
-
Myocardial contrast echocardiography for the distinction of hypertrophic cardiomyopathy from athlete's heart and hypertensive heart disease. 心肌对比超声心动图在鉴别肥厚型心肌病与运动员心脏及高血压性心脏病中的应用
Myocardial contrast echocardiography (MCE) is able to measure in vivo relative blood volume (rBV, i.e., capillary density), and its exchange frequency b, the constituents of myo-cardial blood flow (MBF, ml min-1 g-1). This study aimed to assess, by MCE, whether left ventricular hypertrophy (LVH) in hypertrophic cardiomyopathy (HCM) can be differentiated from LVH in triathletes (athlete's heart, AH) or from hypertensive heart disease patients (HHD). Sixty individuals, matched for age (33 +/- 10 years) and gender, and subdivided into four groups (n = 15) were examined: HCM, AH, HHD and a group of sedentary individuals without LVH (S). rBV (ml ml-1), b (min-1) and MBF, at rest and during adenosine-induced hyperaemia, were derived by MCE in mid septal, lateral and inferior regions. The ratio of MBF during hyperaemia and MBF at rest yielded myocardial blood flow reserve (MBFR). Septal wall rBV at rest was lower in HCM (0.084 +/- 0.023 ml ml-1) than in AH (0.151 +/- 0.024 ml ml-1, p <0.01) and in S (0.129 +/- 0.026 ml ml-1, p <0.01), but was similar to HHD (0.097 +/- 0.016 ml ml-1). Conversely, MBFR was lowest in HCM (1.67 +/- 0.93), followed by HHD (2.8 +/- 0.93, p <0.01), by S (3.36 +/- 1.03, p <0.001) and by AH (4.74 +/- 1.46, p <0.0001). At rest, rBV <0.11 ml ml-1 accurately distinguished between HCM and AH (sensitivity 99%, specificity 99%), similarly MBFR < or =1.8 helped to distinguish between HCM and HHD (sensitivity 100%, specificity 77%). rBV at rest, most accurately distinguishes between pathological LVH due to HCM and physiological, endurance-exercise induced LVH.
-
Assessment of right heart function in the athlete's heart. 运动员心脏右心功能的评估
It is known that the heart of an athlete has been physiologically adapted by prolonged training. There are a large number of echocardiographic studies which have focused on left ventricular wall thickness and dilatation, but there are few studies concerning right heart function in the athlete's heart. The aim of this study was to assess right heart function in elite athletes by conventional and new echocardiographic methods. The study population consisted of 36 elite highly-trained male athletes and 16 age-matched healthy sedentary controls. Right atrial, right ventricular, and inferior vena cava dimensions, and pulsed Doppler measurements of tricuspid inflow and right ventricular outflow were obtained, and systolic (preejection period, ejection time, preejection time/ejection time, QV peak, isovolumic contraction time) and diastolic (E peak, A peak, E/A ratio, decelaration time, isovolumic relexation time) function parameters were measured. The myocardial performance index was calculated as (isovolumetric contraction time + isovolumetric relaxation time)/ejection time. In addition, right ventricular systolic and diastolic functions were determined by Pulsed wave tissue Doppler imaging (S, E, and A velocities) at the lateral corners of the tricuspid annulus. The left ventricular mass index (P < 0.005), and right atrial (P < 0.001), right ventricular (P < 0.001), and inferior vena cava dimensions (P < 0.001) were significantly greater in athletes than in controls. Tricuspid E peak, A peak, E/A ratio, deceleration time, isovolumic relaxation time, preejection period, right ventricular ejection time, preejection time/ejection time, isovolumic contraction time, QV peak, and myocardial performance index were found to be similar in athletes and in controls (P > 0.05). Systolic, early diastolic, and late diastolic tissue Doppler imaging velocities were not significantly different in athletes and controls (P > 0.05). Left ventricular hypertrophy (LV mass index >134 g/m2) was found in 15 of the athletes. Right atrial dimension was greater in the athletes with left ventricular hypertrophy than in those without hypertrophy (P < 0.05). All right ventricular systolic and diastolic echocardiographic parameters were similar in athletes with and without left ventricular hypertrophy (P > 0.05). The results of this study indicate that right ventricular systolic and diastolic functions do not deteriorate in the athlete's heart despite significant chamber dilatation. They suggest that these changes are a normal physiologic adaptation to prolonged training.
-
A Patient With Athlete's Heart Syndrome: When the Abnormal Is Normal. 一例运动员心脏综合征患者：当异常即为正常
Long-term athletic training can result in structural and conduction changes within the heart, leading to Athlete's heart syndrome (AHS). This syndrome is characterized by increased left ventricle (LV) dimensions, thickness, and mass. Dynamic exercise significantly contributes to these alterations, with sinus bradycardia being a common conduction abnormality, often accompanied by first-degree atrioventricular (AV) block. However, higher degrees of AV conduction abnormalities, such as second- and third-degree blocks, though rare, might occur due to parasympathetic hypertonia. Prompt evaluation is necessary to rule out underlying structural or infiltrative heart diseases. We present the case of a 66-year-old lifelong long-distance runner with marked sinus bradycardia, AV dissociation, and junctional escape rhythm, alongside left ventricular hypertrophy (LVH) and T-wave repolarization abnormalities. Subsequent studies ruled out possible pathologies, and the patient was diagnosed with AHS, characterized by cardiac remodeling and bradycardia due to prolonged cardiac loading. This case underscores the importance of clinical assessment, cardiac imaging, and exclusion of pathologic causes to distinguish normal physiological adaptations from potentially concerning conditions.
-
Sex differences in exercise-induced cardiac hypertrophy. 运动诱导性心脏肥厚的性别差异
Physiological cardiac hypertrophy (PCH), induced by intensive exercise or pregnancy, differs substantially from the pathological form of myocardial hypertrophy, accruing after aortic stenosis or chronic arterial hypertension. In contrast to pathological forms of cardiac hypertrophy, exercise-induced increase of left ventricular mass is related to cardiac myocytes enlargement, with no apparent sign of fibrosis or apoptosis, and does usually not result in cardiac failure. Recently published results obtained from various animal studies documented clear sex-specific regulation of exercise-induced cardiac hypertrophy in rodents, with a pronounced hypertrophic response to training load observed in female animals when compared to male littermate. In addition to increased cardiac hypertrophic response, females exhibited augmented lipolytic activity measured in adipose tissue in response to exercise, resulting in increased plasma free fatty acid levels, measured after training. Importantly, sex-specific differences in adipose tissue lipolysis and systemic fat metabolism induced by intensive training were also confirmed in human studies, performed on athletes and healthy volunteers. Since development of PCH during the physical training is accompanied by enhanced fatty acid oxidation and reduced glucose uptake, intensive lipolytic activity, measured in female adipose tissue could explain, at least in part, sex-specific differences observed in hypertrophic response to exercising. Given that sex hormones, such as estrogens and testosterone, in addition to their role in the regulation of adipose tissue metabolism, were also reported to modulate development of pathological myocardial hypertrophy, one may expect also a putative contribution of sex hormones in processes regulating the development and progression of PCH.
-
The hearts of competitive athletes: an up-to-date overview of exercise-induced cardiac adaptations. 竞技运动员的心脏：运动引起的心脏适应性的最新概述
Intense and regular physical exercise is responsible for various cardiac changes (electrical, structural and functional) that represent physiological adaptation to exercise training. This remodeling, commonly referred to as 'athlete's heart', can overlap with several pathological entities, in which sudden cardiac death may be the first clinical presentation. Although pre-competitive screening can identify athletes with life-threatening cardiovascular abnormalities, there are no widely used standardized pre-participation programs and those currently implemented are controversial. Data from personal and family history, features of physical examination and changes in the 12-lead electrocardiogram can raise the suspicion of cardiac disease and lead to early detection of entities such as hypertrophic cardiomyopathy. However, interpreting the electrocardiogram is often challenging, because some changes are considered physiological in athletes. Thus, clinical decision-making in such cases can prove difficult: missing a condition associated with an increased risk of life-threatening events, or conversely, mislabeling an athlete with a disease that leads to unnecessary disqualification, are both situations to avoid. This paper provides an up-to-date review of the physiological cardiac effects of exercise training and highlights key points that should be taken into consideration in the assessment of young competitive athletes.
-
[Morphological and functional features of circulatory system in retired and active elite athletes]. [退役和现役精英运动员循环系统的形态学和功能特征]
Regular physical activity over a long period of time increases the output of the cardiovascular system. That leads to development of a normal (physiological) athlete's heart. Bradycardia, cardiac hypertrophy, and arterial hypotension are three major characteristics of a normal athlete's heart. Changes in parameters of cardiovascular system and features of heart remodeling are determined by type, frequency, and duration of a physical activity. Excessive levels of physical activity could result in development of a pathologic athlete's heart, negatively affect hearts metabolism, and increase the risk of both atherosclerosis and myocardial infarction. Autopsy studies have shown that atherosclerosis, which leads to development of an ischemic heart disease, is often found in both young and elderly athletes. 56% of sudden deaths in all athletes were due to cardiovascular problems. Reports of ischemic heart disease in athletes of all ages have increased over the past few years. Echocardiographic features and clinical outcomes of stable angina and myocardial infarction in retired professional athletes are not well studied. Further studies are needed to improve diagnosis, prevention, treatment, and rehabilitation in elite athletes with ischemic heart disease.
-
A six-time Ultraman winner and a normal heart: A case report. 六届超级铁人赛冠军与正常心脏：一例病例报告
Number of subjects currently participating in high-endurance aerobic exercise training regimens and competitions has substantially increased in recent years. While there is no doubt that regular exercise practice is fundamental for the maintenance of a good health, there have been reports of cardiac structural changes of subjects exposed to strenuous endurance physical exercise. This article reports a case of a 47-year-old male very successful sportsman-including being a six-time Ultraman winner-who has accumulated more than 50,000 h of training and competition in his 35-year career, averaging 25-30 h/week. Despite this huge amount of aerobic exercise, about 25 times larger than typically recommended dose for health purposes (i.e. 75 min of vigorous exercise per week), no major abnormalities were detected in electrocardiograms (rest and maximal exercise), transthoracic echocardiogram, and magnetic resonance imaging. In fact, after this complete evaluation, his heart was found to be quite normal.
-
Cardiac effects of detraining in athletes: A narrative review. 运动员停止训练的心脏效应：一项叙述性综述
Routine physical activity stimulates numerous morphologic and functional adaptations of the cardiac system, which are commonly referred to as exercise-induced cardiac remodeling (EICR). EICR has been well documented in elite and recreational athletes, but comparatively little is known about the "reverse" cardiac adaptations during detraining in an athletic population. To assess the morphologic and functional cardiac effects of detraining in athletes. Eligible studies were identified in PubMed from inception to May 2020. Studies were included if they assessed the cardiac effects of detraining periods in athletes. A total of 16 studies from the literature search were identified and included in this review. These studies included athletes from multiple different sporting disciplines and detraining periods ranged from 3 weeks to 13 years. Detraining periods led to significantly decreased right ventricular and left (LV) ventricular dimensions, LV mass, and LV wall thickness, but only limited changes in systolic and diastolic functional parameters were observed. From the limited data available in this population, cardiac atrophy has been observed with short periods of detraining (1-8 weeks) but often spares systolic and diastolic heart function. Supplemental exercise training during times of rehabilitation to combat cardiac regression has not been vigorously studied in athletes, so the ideal frequency, intensity, and modality of exercise needed to maintain EICR remains unclear.