Biventricular myocardial adaptation to different training protocols in competitive master athletes

D’Andrea, Antonello; Caso, Pio; Scarafile, Raffaella; Salerno, Gemma; Corato, Giuseppe De; Mita, Claudia; Salvo, Giovanni Di; Allocca, F.; Colonna, D; Caprile, Mario; Ascione, Luigi; Cuomo, Sergio; Calabrò, Raffaele

doi:10.1016/j.ijcard.2006.03.041

Cited by 59 publications

(40 citation statements)

References 32 publications

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“…The endurance athletes, due to the increased blood flow, have larger LV and RV chamber sizes in diastole. The strength‐trained athletes, on the other hand, are seen to have more often normal cavity sizes although they have increased LV wall thickness . The RV function plays an important role in exercise performance.…”

Section: Morphological and Functional Changes In Right Ventricle In Amentioning

confidence: 99%

Changes in right ventricular morphology and function in athletes

Koshy

George

2018

Echocardiography

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Section: Morphological and Functional Changes In Right Ventricle In Amentioning

confidence: 99%

Changes in right ventricular morphology and function in athletes

Koshy

George

2018

Echocardiography

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“…Pathological conditions, including diabetes, hypertension, and myocardial infarction, can increase the width or length of individual cardiomyocytes, leading to gross changes in ventricular structure. Interestingly, certain hypertrophic changes observed in diseased states are mimicked by exercise training, however, these are physiologic in nature (D'Andrea et al, 2007). Hypertrophy, regardless of mechanism, may lead to hypertension, infarction, or arrhythmia, ultimately predisposing individuals to heart failure (Gaasch and Zile, 2004).…”

Section: Introductionmentioning

confidence: 99%

“…Hypertrophy, regardless of mechanism, may lead to hypertension, infarction, or arrhythmia, ultimately predisposing individuals to heart failure (Gaasch and Zile, 2004). This fact underlies the importance of understanding and differentiating the mechanisms of physiologic- and pathologic-induced hypertrophy (D'Andrea, Caso, 2007, Gielen et al, 2010). Figure 1 provides a visual representation of the gross similarities and differences in these mechanisms.…”

Section: Introductionmentioning

confidence: 99%

“…Volume overload causes cardiomyocytes to grow eccentrically through serial sarcomere addition, increasing myocardial mass and chamber volume. Concentric hypertrophy, a result of parallel addition of sarcomeres in the cardiomyocyte, increases heart wall thickness without increasing chamber volume, creating greater pressure output (D'Andrea, Caso, 2007, Fernandes, Soci, 2011). Endurance-based aerobic exercise training requires consistent blood flow to skeletal muscle, thus favoring an eccentric building mechanism to meet the increased volume demands.…”

Section: Introductionmentioning

confidence: 99%

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In vitro effects of exercise on the heart

et al. 2014

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Pathologic and physiologic factors acting on the heart can produce consistent pressure changes, volume overload, or increased cardiac output. These changes may then lead to cardiac remodeling, ultimately resulting in cardiac hypertrophy. Exercise can also induce hypertrophy, primarily physiologic in nature. To determine the mechanisms responsible for each type of remodeling, it is important to examine the heart at the functional unit, the cardiomyocyte. Tests of individual cardiomyocyte function in vitro provide deeper understanding of the changes occurring within the heart during hypertrophy. Examination of cardiomyocyte function during exercise primarily follows one of two pathways: the addition of hypertrophic inducing agents in vitro to normal cardiomyocytes, or the use of trained animal models and isolating cells following the development of hypertrophy in vivo. Due to the short lifespan of adult cardiomyocytes, a proportionately scant amount of research exists involving the direct stimulation of cells in vitro to induce hypertrophy. These attempts provide the only current evidence, as it is difficult to gather extensive data demonstrating cell growth as a result of in vitro physical stimulation. Researchers have created ways to combine skeletal myocytes with cardiomyocytes to produce functional muscle cells used to repair pathologic heart tissue, but continue to struggle with the short lifespan of these cells. While there have been promising findings regarding the mechanisms that surround cardiac hypertrophy in vitro, the translation of in vitro findings to in vivo function is not consistent. Therefore, the focus of this review is to highlight recent studies that have investigated the effect of exercise on the heart, both in vitro and in vivo.

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“…However, athletic hypertrophy is thought to be a benign, physiological response without the prognostic significance of hypertensive hypertrophy. Although standard Doppler echocardiography has been widely used to distinguish athlete’s heart syndrome from pathological LVH, conflicting data have been reported about the nature (physiological versus pathological) of LVH in elite athletes and veterans 8 9. …”

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confidence: 99%