Symmetric cardiac enlargement in highly trained endurance athletes: A two-dimensional echocardiographic study

Hauser, Andrew M.; Dressendorfer, Rudolph H.; Vos, Marc A.; Hashimoto, Takeji; Gordon, Seymour; Timmis, Gerald C.

doi:10.1016/0002-8703(85)90247-9

Cited by 81 publications

(36 citation statements)

References 29 publications

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“…Surprisingly, this physiological pattern of myocyte growth in the SHHFex did not translate into improved, or even maintained, cardiac function. The tendency for aerobic training to produce a concomitant increase in chamber diameter and wall thickness has been reported previously [17][18][19] and suggests both series and parallel addition of sarcomeres, consistent with eccentric hypertrophy. 1 The …”

Section: Discussionsupporting

confidence: 81%

Effects of Excessive Long-Term Exercise on Cardiac Function and Myocyte Remodeling in Hypertensive Heart Failure Rats

et al. 2007

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Abstract-The long-term effects of exercise on cardiac function and myocyte remodeling in hypertension/progression of heart failure are poorly understood. We investigated whether exercise can attenuate pathological remodeling under hypertensive conditions. Fifteen female Spontaneously Hypertensive Heart Failure rats and 10 control rats were housed with running wheels beginning at 6 months of age. At 22 months of age, heart function of the trained rats was compared with heart function of age-matched sedentary hypertensive and control rats. Heart function was measured using echocardiography and left ventricular catheterization. Cardiac myocytes were isolated to measure cellular dimensions. Fetal gene expression was determined using Western blots. Exercise did not significantly impact myocyte remodeling or ventricular function in control animals. Sedentary hypertensive rats had significant chamber dilatation and cardiac hypertrophy. In exercised hypertensive rats, however, exercise time was excessive and resulted in a 21% increase in left ventricular diastolic dimension (PϽ0.001), a 24% increase in heart to body weight ratio (PϽ0.05), a 27% increase in left ventricular myocyte volume (PϽ0.01), a 13% reduction in ejection fraction (PϽ0.001), and a 22% reduction in fractional shortening (PϽ0.01) compared with sedentary hypertensive rats. Exercise resulted in greater fibrosis and did not prevent activation of the fetal gene program in hypertensive rats. We conclude that excessive exercise, in the untreated hypertensive state can have deleterious effects on cardiac remodeling and may actually accelerate the progression to heart failure. Key Words: hypertension Ⅲ heart failure Ⅲ exercise Ⅲ hypertrophy Ⅲ myocytes Ⅲ voluntary wheel running Ⅲ SHHF R esearch has shown a predictable remodeling of cardiac myocyte shape underlying progression to heart failure (HF). 1 Initially, under hypertensive conditions, there is a marked increase in myocyte cross-sectional area (CSA) whereas cell length remains normal. Between the ages of 6 and 12 months in female spontaneously hypertensive heart failure (SHHF) rats, after a period of compensated hypertrophy, myocyte length begins to increase without further increase in CSA. This excessive addition of sarcomeres in series continues until the development of overt signs of HF at 24 months. 1 In the healthy heart, aerobic exercise training has been shown to increase myocardial mass, left ventricle (LV) chamber dimensions, and stroke volume. 2,3 In LV dysfunction and in HF patients, exercise has been shown to improve exercise tolerance and symptoms. This benefit has traditionally been attributed to peripheral adaptations. More recent studies, however, indicate that beneficial changes may be occurring centrally as well. As in the healthy heart, these adaptations include increased LV wall thickness and LV function 4,5 and enhanced myocardial ␤-adrenergic responsiveness. 6 Recent studies by Iemitsu et al 7 and Emter et al 8 showed that regular exercise training results in reversal of the fetal ge...

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Section: Discussionsupporting

confidence: 81%

Effects of Excessive Long-Term Exercise on Cardiac Function and Myocyte Remodeling in Hypertensive Heart Failure Rats

et al. 2007

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“…5,[9][10][11]24,26,27 Nonspecific ECG markers of pathology were also entered into analyses (left-and right-axis deviation, LV hypertrophy, RV hypertrophy, any TWI, and anterior TWI). Reproducibility of RV measurements was assessed with intraclass correlation coefficient analysis and reported as intraclass correlation coefficient (95% confidence interval [CI]).…”

Section: Discussionmentioning

confidence: 99%

“…24,25 Independent variables were selected on the basis of associations with LV or RV size in previous studies of athletes (age, sex, BSA, endurance sports, HD-HS sports, ethnicity, training intensity, LV end-diastolic diameter, LV mass index, pulmonary artery systolic pressure, and partial or complete right bundle-branch block). 5,[9][10][11]24,26,27 Nonspecific ECG markers of pathology were also entered into analyses (left-and right-axis deviation, LV hypertrophy, RV hypertrophy, any TWI, and anterior TWI). Reproducibility of RV measurements was assessed with intraclass correlation coefficient analysis and reported as intraclass correlation coefficient (95% confidence interval [CI]).…”

Section: Discussionmentioning

confidence: 99%

“…Limited data in white athletes indicate that the RV is subject to the same preload as the LV during exercise and exhibits structural and functional adaptation in synergy with the left side of the heart. 5,6 As such, physiological remodeling of the athlete's RV may mimic changes observed in arrhythmogenic right ventricular cardiomyopathy (ARVC), 7 which is responsible for as many as 22% of SCDs in young athletes in Europe. 3,8 The magnitude of athletic cardiac remodeling is dependent on a variety of demographic and sport-specific variables; large, adult male athletes engaging in endurance sports generally exhibit the greatest dimensions.…”

Section: Editorial See P 1757 Clinical Perspective On P 1792mentioning

confidence: 99%

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Physiological Right Ventricular Adaptation in Elite Athletes of African and Afro-Caribbean Origin

et al. 2013

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Background-Regular, intensive exercise results in physiological biventricular cardiac adaptation. Ethnicity is an established determinant of left ventricular remodeling; black athletes (BAs) exhibit more profound LV hypertrophy than white athletes (WAs). Right ventricular (RV) remodeling has not been characterized in BAs, although the issue is pertinent because BAs commonly exhibit ECG anomalies that resemble arrhythmogenic RV cardiomyopathy. Methods and Results-Between 2006 and 2012, 300 consecutive BAs (n=243 males) from 25 sporting disciplines were evaluated by use of ECG and echocardiography. Results were compared with 375 WAs and 153 sedentary control subjects (n=69 blacks). There were no ethnic differences between RV parameters in control subjects. Both BAs and WAs exhibited greater RV dimensions than control subjects. RV dimensions were marginally smaller in BAs than in WAs (proximal outflow tract, 30.9±5.5 versus 32.8±5.3 mm, P<0.001; longitudinal dimension, 86.6±9.5 versus 89.8±9.6 mm, P<0.001), although only 2.3% of variation was attributable to ethnicity. RV enlargement compatible with diagnostic criteria for arrhythmogenic RV cardiomyopathy was frequently observed (proximal outflow tract ≥32 mm; 45.0% of BAs, 58.5% of WAs). Anterior T-wave inversion was present in 14.3% of BAs versus 3.7% of WAs (P<0.001). Marked RV enlargement with concomitant anterior T-wave inversion was observed in 3.0% of BAs versus 0.3% of WAs (P=0.005). Further investigation did not diagnose arrhythmogenic RV cardiomyopathy in any athlete. Conclusions-Physiological RV enlargement is commonly observed in both black and white athletes. The impact of ethnicity is minimal, which obviates the need for race-specific RV reference values. However, in the context of frequent ECG repolarization anomalies in BAs, the potential for erroneous diagnosis of arrhythmogenic RV cardiomyopathy is considerably greater in this ethnic group. (Circulation. 2013;127:1783-1792.)Key Words: cardiomyopathy ◼ echocardiography ◼ electrocardiographic screening ◼ ethnicity ◼ exercise © 2013 American Heart Association, Inc.Circulation is available at http://circ.ahajournals.org DOI: 10.1161/CIRCULATIONAHA.112.000270Continuing medical education (CME) credit is available for this article. Go to http://cme.ahajournals.org to take the quiz. Received December 6, 2012; accepted March 4, 2013. From St. George's University of London, London, United Kingdom (A.Z., S. Ghani, R.S., N.S., S. Gati, M.P., S.S.); University Hospital Lewisham, London, United Kingdom (A.Z., S. Ghani, N.S., S. Gati, S.S.); Liverpool John Moores University, Liverpool, United Kingdom (D.O.); and Imperial College Healthcare NHS Trust, London, United Kingdom (V.F.P. [WAs]). 10,11 The influence of ethnicity on athletic RV remodeling has never been characterized, even though healthy BAs frequently reveal ECG repolarization anomalies that resemble those observed in ARVC.12 Furthermore, BAs comprise a growing number of elite sports participants worldwide, and for reasons that remain incompletely under...

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“…30 Larger left atria were first noted in 1985 in a small study of endurance athletes. 31 Another study revealed left atrial enlargement in older individuals with a significant history of exercise training. Pelliccia et al showed increased transverse left atrial dimensions (≥ 40 mm) in 20% of athletes and more substantially enlarged dimensions (≥ 45 mm) in approximately 2%.…”

Section: Atriamentioning

confidence: 99%

Cardiac Imaging in Athletes

Khan

Safi

Wood

2016

Methodist DeBakey Cardiovascular Journal

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Athletic heart syndrome refers to the physiological and morphological changes that occur in a human heart after repetitive strenuous physical exercise. Examples of exercise-induced changes in the heart include increases in heart cavity dimensions, augmentation of cardiac output, and increases in heart muscle mass. These cardiac adaptations vary based on the type of exercise performed and are often referred to as sport-specific cardiac remodeling. The hemodynamic effects of endurance and strength training exercise lead to these adaptations. Any abnormalities in chamber dilatation and left ventricular function usually normalize with cessation of exercise. Athletic heart syndrome is rare and should be differentiated from pathologic conditions such as hypertrophic cardiomyopathy, left ventricular noncompaction, and arrhythmogenic right ventricular dysplasia when assessing a patient for athletic heart syndrome. This paper describes specific adaptations that occur in athletic heart syndrome and tools to distinguish between healthy alterations versus underlying pathology.

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Symmetric cardiac enlargement in highly trained endurance athletes: A two-dimensional echocardiographic study

Cited by 81 publications

References 29 publications

Effects of Excessive Long-Term Exercise on Cardiac Function and Myocyte Remodeling in Hypertensive Heart Failure Rats

Effects of Excessive Long-Term Exercise on Cardiac Function and Myocyte Remodeling in Hypertensive Heart Failure Rats

Physiological Right Ventricular Adaptation in Elite Athletes of African and Afro-Caribbean Origin

Cardiac Imaging in Athletes

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