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Exercise and LV Remodeling

Endurance athletes engage in prolonged daily exercise thereby eliciting repeated

increases in heart rate, blood pressure, stroke volume and cardiac output that consequently lead to increases cardiac mass and dimensions [97]. Endurance training places increased

hemodynamic demand on the heart, that when repeated chronically throughout life acts as a physiological stimulus for cardiac adaptations [98]. The frequent increased blood flow generated by endurance training places a volume load on the ventricles which contributes to significant cardiac remodeling [82]. There are established upper limits of normal cardiac remodeling

associated with “athlete’s heart” that are necessary to distinguish physiological from pathological adaptations. The magnitude of cardiac structural changes detected in athletes is large and if detected in the general population would indicate clinical cardiac abnormalities.

Previous studies utilizing echocardiography have clearly established a link between training and LV enlargement (9, 22). Conventionally, 2DE M-mode echocardiography was used to determine LV hypertrophy and dilation (23). Numerous cross sectional studies have examined

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LV remodeling in endurance and strength trained athletes [99-106]. Overwhelmingly these studies found that LVM is significantly higher in athletes compared to controls [99-106]. Moreover, the data show that the highest degree of LV hypertrophy occurs in athletes with the largest body size and in those athletes participating in endurance sports. Hence, more recent studies control for body surface area, body fat percentage and/or lean body mass.

Endurance and resistance exercise are associated with distinctly different LV structural adaptations. Cardiac adaptations to endurance exercise training and strength training are largely defined based on volume and pressure overload, respectively. Morganroth et al. first used echocardiography to image and define the athlete’s heart and stated that cardiac remodeling is specific to each training modality [99]. According to the “Morganroth Hypothesis” typically, endurance athletes engaging in continuous dynamic exercise (i.e. running), experience prolonged elevations in cardiac output (increases from 6 L/min to 40 L/min during intense exercise) [107], presenting the heart with a volume load. This stimulates eccentric cardiac hypertrophy,

manifesting as an increase in LV internal dimension and mass with minor changes in LV wall thickness [8, 99]. Contrastingly, strength athletes (i.e. weight lifters) engaging in predominately static or isometric exercise, experience increases in blood pressure as high as approximately 320/250 mmHg [108, 109], presenting the heart with a pressure load. This stimulates concentric LV hypertrophy, whereby LV wall thickness and mass increase, with little to no change in LV wall dimensions [12]. Athletes that incorporate both dynamic and static components (i.e. rowers and cyclists) exhibit a significant increase in LV wall thickness and even larger increase in LV internal dimensions. These athletes experience extreme pressure and volume loads on the myocardium.

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Additional aspects of myocardial remodeling in athletes include right ventricular chamber enlargement [110], atrial dilation [10] and mild aortic remodeling. Remodeling, specifically enlargement of the athlete’s LV, is beneficial in providing the ability for the heart to pump more blood with greater contractile force. However, a larger myocardium requires more oxygen consumption and energy and thus has greater metabolic requirements compared to a smaller myocardium. If increases in myocardial oxygen demand are not met, myocardial ischemia occurs and fibrosis can develop. Thus, LV hypertrophy is associated with myocardial fibrosis or

scarring, which is a pathological substrate for arrhythmias and increased risk for SCD. Indeed, LV hypertrophy in endurance athletes may be of pathological concern. Recent studies have examined LV function in athletes at rest using cross-sectional designs [111]. Conventionally, ejection fraction has been used to measure LV function and this has been determined to be relatively normal in athletes except for a few studies [111]. Recent advances in functional

cardiac imaging including LV strain measured by STE has also suggested that endurance training may lead to beneficial changes in LV function [112, 113] or in some cases diminished LV

function at rest, that cannot be detected using LV ejection fraction. This paradox in the literature regarding LV function in athletes needs to be explored further.

The athlete’s heart provokes controversial discussions with respect to its cardiovascular health implications and predispositions to disease. Traditionally, LV remodeling and hypertrophy in endurance athletes have been primarily attributed to volume overload placed on the heart chambers. Cardiac functional parameters may give better insight into LV structural adaptations and future risk for pathological adaptations in endurance-trained athletes. Additionally, evidence suggests increased chronic hemodynamic (arterial) load (i.e blood pressure, arterial stiffness and

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wave reflections) may help to partially explain LV remodeling in response to long-term endurance training.

Imaging of the Endurance Athlete’s Heart

Echocardiographic and MRI studies demonstrate that athletes have larger hearts [7, 12]. Recent developments in imaging technology enable researchers to assess in depth myocardial morphology and function. Conventional echocardiography techniques to measure structure and function include, M-mode, Tissue Doppler imaging (TDI) and 2-dimensional echocardiography (2DE), however these technique have limitations (Table 1). Recent developments in 3-

dimensional echocardiography (3DE) have helped provide more detailed morphological and functional myocardial measurements. [114]. 3DE offers more comprehensive details of LV remodeling as it can distinguish differences in length, shape of LV chamber, geometry, function and synchronicity of contraction between different populations, including athletes [49, 114]. 3DE evaluation of cardiac chamber volumes and mass avoids geometric assumptions made by 2DE acquisition and has the capability to assess regional LV wall motion and strain. As a novel imaging technique, 3DE is able to detect cardiac structure and function in a similar way to cardiac magnetic resonance imaging (CMRI). 3DE is as accurate as cardiac magnetic resonance imaging (considered the gold standard for assessing cardiac structure/function) for quantifying myocardial structure and function. 3DE has ideal image spatial resolution and quality that is not influenced by body size allowing for precise cardiac chamber size, mass and function

measurements. Moreover, when 3DE is compared to CMRI in the assessment of ventricular morphology optimal intra-observer and inter-observer reliability is observed compared with other standard imaging techniques [49, 114, 115]. Therefore, 3DE is a reliable, accurate, novel

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imaging technique that may provide novel insight into pathological versus physiological cardiac structural and functional adaptations in athletes.