The athlete's heart

Prior, David; Gerche, André La

doi:10.1136/heartjnl-2011-301329

Cited by 148 publications

(152 citation statements)

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“…17,19,28 Five athletes had a RVEF <45% which is considered as the lower reference limit of normal for the left and right ventricular systolic ejection fraction in athletes, as measured by MRI. 27 However, lower values may also be physiological, at least in some endurance athletes with athlete's heart. 27 In general, RVEF in athletes (52±8%) was within the range reported by other studies, 19,[23][24][25]29 whereas some studies showed even higher RVEFs for athletes.…”

Section: Functional Parametersmentioning

confidence: 99%

“…27 However, lower values may also be physiological, at least in some endurance athletes with athlete's heart. 27 In general, RVEF in athletes (52±8%) was within the range reported by other studies, 19,[23][24][25]29 whereas some studies showed even higher RVEFs for athletes. [17][18][19]24,28 These discrepancies may be attributable to the use of different methods of image analysis, thus affecting volume parameters and consecutively EF.…”

Section: Functional Parametersmentioning

confidence: 99%

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Right and Left Ventricular Function and Mass in Male Elite Master Athletes

et al. 2016

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Background— It is under debate whether the cumulative effects of intensive endurance exercise induce chronic cardiac damage, mainly involving the right heart. The aim of this study was to examine the cardiac structure and function in long-term elite master endurance athletes with special focus on the right ventricle by contrast-enhanced cardiovascular magnetic resonance. Methods and Results— Thirty-three healthy white competitive elite male master endurance athletes (age range, 30–60 years) with a training history of 29±8 years, and 33 white control subjects pair-matched for age, height, and weight underwent cardiopulmonary exercise testing, echocardiography including tissue-Doppler imaging and speckle tracking, and cardiovascular magnetic resonance. Indexed left ventricular mass and right ventricular mass (left ventricular mass/body surface area, 96±13 and 62±10 g/m 2 ; P <0.001; right ventricular mass/body surface area, 36±7 and 24±5 g/m 2 ; P <0.001) and indexed left ventricular end-diastolic volume and right ventricular end-diastolic volume (left ventricular end-diastolic volume/body surface area, 104±13 and 69±18 mL/m 2 ; P <0.001; right ventricular end-diastolic volume/body surface area, 110±22 and 66±16 mL/m 2 ; P <0.001) were significantly increased in athletes in comparison with control subjects. Right ventricular ejection fraction did not differ between athletes and control subjects (52±8 and 54±6%; P =0.26). Pathological late enhancement was detected in 1 athlete. No correlations were found for left ventricular and right ventricular volumes and ejection fraction with N-terminal pro-brain natriuretic peptide, and high-sensitive troponin was negative in all subjects. Conclusions— Based on our results, chronic right ventricular damage in elite endurance master athletes with lifelong high training volumes seems to be unlikely. Thus, the hypothesis of an exercise-induced arrhythmogenic right ventricular cardiomyopathy has to be questioned.

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Section: Functional Parametersmentioning

confidence: 99%

Section: Functional Parametersmentioning

confidence: 99%

Right and Left Ventricular Function and Mass in Male Elite Master Athletes

et al. 2016

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“…Numerous studies concerning the cellular and molecular remodeling (10) as well as structural and morphological changes (22,37,40) have been published in recent years; however, we still have limited data about the functional aspects of exercise-induced cardiac hypertrophy.…”

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confidence: 99%

“…Cardiac enlargement in athletes has been reported since the late 1890s (6), and several aspects of athlete's heart have been intensively investigated in humans (28,40) as well as in experimental animals (48). A number of animal models of exercise-induced cardiac hypertrophy have been developed, and several types of endurance exercise training have been recognized to effectively induce physiological cardiac hypertrophy in experimental animals, such as treadmill running, voluntary wheel running, and swim training (11,15,30,48).…”

mentioning

confidence: 99%

“…ATHLETE'S HEART HAS BEEN DESCRIBED as the complex structural, functional, and electrical cardiac remodeling induced by longterm exercise training (40). Exercise training-induced cardiac hypertrophy is an important physiological adaption, which includes balanced increase of left ventricular (LV) and left atrial diameters, cardiac mass, and LV wall thicknesses effected by myocyte hypertrophy and neoangiogenesis (10,12,25,36,37).…”

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Rat model of exercise-induced cardiac hypertrophy: hemodynamic characterization using left ventricular pressure-volume analysis

Radovits

Oláh

Lux

et al. 2013

American Journal of Physiology-Heart and Circulatory Physiology

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Radovits T, Oláh A, Lux Á, Németh BT, Hidi L, Birtalan E, Kellermayer D, Mátyás C, Szabó G, Merkely B. Rat model of exercise-induced cardiac hypertrophy: hemodynamic characterization using left ventricular pressure-volume analysis. Am J Physiol Heart Circ Physiol 305: H124 -H134, 2013. First published May 3, 2013 doi:10.1152/ajpheart.00108.2013.-Long-term exercise training is associated with characteristic structural and functional changes of the myocardium, termed athlete's heart. Several research groups investigated exercise training-induced left ventricular (LV) hypertrophy in animal models; however, only sporadic data exist about detailed hemodynamics. We aimed to provide functional characterization of exercise-induced cardiac hypertrophy in a rat model using the in vivo method of LV pressure-volume (P-V) analysis. After inducing LV hypertrophy by swim training, we assessed LV morphometry by echocardiography and performed LV P-V analysis using a pressureconductance microcatheter to investigate in vivo cardiac function. Echocardiography showed LV hypertrophy (LV mass index: 2.41 Ϯ 0.09 vs. 2.03 Ϯ 0.08 g/kg, P Ͻ 0.01), which was confirmed by heart weight data and histomorphometry. Invasive hemodynamic measurements showed unaltered heart rate, arterial pressure, and LV enddiastolic volume along with decreased LV end-systolic volume, thus increased stroke volume and ejection fraction (73.7 Ϯ 0.8 vs. 64.1 Ϯ 1.5%, P Ͻ 0.01) in trained versus untrained control rats. The P-V loop-derived sensitive, load-independent contractility indexes, such as slope of end-systolic P-V relationship or preload recruitable stroke work (77.0 Ϯ 6.8 vs. 54.3 Ϯ 4.8 mmHg, P ϭ 0.01) were found to be significantly increased. The observed improvement of ventriculoarterial coupling (0.37 Ϯ 0.02 vs. 0.65 Ϯ 0.08, P Ͻ 0.01), along with increased LV stroke work and mechanical efficiency, reflects improved mechanoenergetics of exercise-induced cardiac hypertrophy. Despite the significant hypertrophy, we observed unaltered LV stiffness (slope of end-diastolic P-V relationship: 0.043 Ϯ 0.007 vs. 0.040 Ϯ 0.006 mmHg/l) and improved LV active relaxation (: 10.1 Ϯ 0.6 vs. 11.9 Ϯ 0.2 ms, P Ͻ 0.01). According to our knowledge, this is the first study that provides characterization of functional changes and hemodynamic relations in exercise-induced cardiac hypertrophy.exercise-induced cardiac hypertrophy; pressure-volume analysis; systolic function; diastolic function; cardiac mechanoenergetics ATHLETE'S HEART HAS BEEN DESCRIBED as the complex structural, functional, and electrical cardiac remodeling induced by longterm exercise training (40). Exercise training-induced cardiac hypertrophy is an important physiological adaption, which includes balanced increase of left ventricular (LV) and left atrial diameters, cardiac mass, and LV wall thicknesses effected by myocyte hypertrophy and neoangiogenesis (10,12,25,36,37).Cardiac enlargement in athletes has been reported since the late 1890s (6), and several aspects of athlete's heart have been intensively inv...

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Testing Athletes for Risk of Cardiac Disease

Brosnan

Prior

2012

Encyclopedia of Life Sciences

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Although regular exercise offers a degree of protection from cardiovascular disease, there is a transient increase in the risk of sudden cardiac death (SCD) during athletic activity for both young competitive athletes (YCAs) and older leisure athletes. SCD in YCAs usually occurs as a result of inherited diseases of the heart's structure. These diseases usually cause no symptoms prior to SCD, so many sporting bodies are now recommending preparticipation screening (PPS) for all YCAs to identify and enforce restriction of sports participation in those most at risk of SCD. There is ongoing debate about the effectiveness and cost‐effectiveness of such a strategy. Premature coronary artery disease (CAD) is responsible for most cases of SCD in athletes over 35 years of age, but is not yet clear whether PPS programs in this population could also prevent SCD by detecting those most at risk. Key Concepts: Causes of sports related sudden cardiac death differ depending on the age of the athlete; CAD is most common in those over 35 years of age, and structural, usually genetic cardiac abnormalities more common in those under 35. In older leisure athletes, the cardiovascular benefits of exercise outweigh the risks of sports related SCD. Most of the diseases responsible for SCD in YCAs are detectable on ECG. Athletic training causes alterations to the ECG and echocardiogram, which can lead to diagnostic dilemmas, particularly in black, adolescent or endurance athletes. Imaging modalities such as cardiac MRI (CMR) can help differentiate physiological cardiac adaptations from pathological changes in athletes. There is evidence that PPS with an ECG may reduce the incidence of SCD in YCAs. SCD in older leisure athletes most often occurs as a result of plaque rupture in coronary arteries that were not previously critically narrowed. Most tests for coronary artery ischaemia depend on the presence of flow limiting coronary lesions, thus are of limited use in the athletic population with silent CAD. There is a paucity of evidence for the efficacy of PPS in older leisure athletes.

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The athlete's heart

Cited by 148 publications

References 36 publications

Right and Left Ventricular Function and Mass in Male Elite Master Athletes

Right and Left Ventricular Function and Mass in Male Elite Master Athletes

Rat model of exercise-induced cardiac hypertrophy: hemodynamic characterization using left ventricular pressure-volume analysis

Testing Athletes for Risk of Cardiac Disease

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