Introduction

The initial report of cardiac enlargement in athletes is credited to the Swedish clinician Henschen who reported increased cardiac dimensions in elite Nordic skiers in 1899. Early chest radiography work demonstrated enlarged cardiac silhouettes among trained athletes thereby providing the first non-invasive confirmation of the physical examination findings of Henschen. Ultimately, the development and application of two-dimensional echocardiography facilitated characterization of numerous aspects of the athlete’s heart including ventricular chamber enlargement, myocardial hypertrophy, and atrial dilation. Most recently, advanced echocardiographic techniques and magnetic resonance imaging have begun to clarify important functional adaptations that accompany previously reported structural findings. This review will provide an overview of exercise physiology relevant to the athlete’s heart, highlight the common cardiac characteristics of the athlete, and delineate clinical imaging strategies for differentiating exercise-induced cardiac remodeling from pathologic cardiomyopathy.

Historical Overview of the Athlete’s Heart

Observations of cardiac enlargement in trained athletes date back to the late 1890s. In Europe, the Swedish clinician Henschen used the rudimentary yet elegant physical examination skills of percussion and auscultation to quantify cardiac dimensions in elite Nordic skiers [1]. Eugene Darling of Harvard University made similar observations during the same year in competitive university rowers [2]. Paul Dudley White, regarded by many as the father of modern cardiology, studied radial pulse characteristics among Boston Marathon competitors and was the first to document marked resting sinus bradycardia in long distance runners [3, 4]. The physical examination findings of Darling and Henschen were first confirmed by non-invasive imaging in the 1950s using chest radiography. Numerous case reports documented global cardiac enlargement in ostensibly healthy, exercise-trained athletes [5–7]. The subsequent introduction of 12-lead electrocardiography enabled widespread study of the electrical activity in the heart of the trained athlete [8–11]. In addition to careful characterization of brady-[12] and tachyarrhythmias,[13] electrocardiographic patterns of cardiac hypertrophy were observed in healthy exercise-trained individuals. The development and widespread application of two-dimensional echocardiography significantly enhanced our understanding of the athlete’s heart by providing precise quantification of ventricular chamber enlargement, myocardial hypertrophy, and atrial dilation. Most recently, advanced echocardiographic techniques and magnetic resonance imaging have begun to clarify important functional adaptations that accompany previously reported structural characteristics of the athlete’s heart.

Relevant Cardiovascular Exercise Physiology

Understanding the myocardial response to exercise requires a basic understanding of the explanatory physiology. There is a direct relationship between exercise intensity (external work) and the body’s demand for oxygen. The oxygen demand is met by increasing pulmonary oxygen uptake (VO2). The cardiovascular system, comprised of the heart and vasculature, is responsible for transporting oxygen rich blood from the lungs to the skeletal muscles. Numerous exercise-induced adaptations in the cardiovascular system enhance the efficiency of this process. The Fick equation (Cardiac Output = VO2 x Arterial-Venous O2 Δ) can be used to quantify the relationship between cardiovascular function and VO2 at rest and during exercise.

There is a direct relationship between VO2 and cardiac output in the healthy human. Cardiac output, the product of stroke volume and heart rate, may increase five to six-fold during a maximal exercise effort. Cardiac chamber enlargement is the principal cardiovascular adaptation conferred by exercise as it facilitates the generation of a large stroke volume. Stroke volume rises during exercise due to a combination of increased ventricular end diastolic volume and a sympathetically-mediated reduction in end systolic volume [14]. Left ventricular (LV) end-diastolic volume is determined by diastolic filling, a complex process that is dependent on heart rate/diastolic filling time, intrinsic myocardial relaxation, ventricular compliance, ventricular filling pressures, and additional factors.

Heart rate increases proportionally with exercise intensity and is responsible for the majority of cardiac output augmentation during exercise. Heart rate in the athlete may range from resting values of less than 40 beats per minute to greater than 200 beats per minute at peak exercise intensity. Heart rate augmentation during exercise requires a coordinated autonomic nervous system response characterized by rapid and sustained parasympathetic withdrawal coupled with sympathetic activation. Maximal heart rate varies among individuals, decreases with age [15], and is relatively unaffected by exercise training [16].

The hemodynamic changes that occur during exercise constitute the primary stimulus for the numerous cardiac adaptations that are common among athletes. Hemodynamic conditions, specifically changes in cardiac output and peripheral vascular resistance, vary widely across sporting disciplines. Although considerable overlap exists, exercise activity can be segregated into two principal physiologic forms with defining hemodynamic characteristics [17]. Isotonic or endurance exercise, involves sustained elevations in cardiac output with normal or reduced peripheral vascular resistance. This form of exercise underlies activities including long distance running, cycling, rowing, and swimming. These activities result in a primary “volume” challenge for the heart that affects all four chambers. In contrast, isometric or strength exercise is characterized by short but intense bouts of increased peripheral vascular resistance and normal or only slightly elevated cardiac output. This increase in peripheral vascular resistance causes transient but potentially marked systolic hypertension and left ventricular “pressure” challenge. Strength training physiology is dominant during activities such as weightlifting, track and field throwing events, and American style football. Many sports, including popular team-based activities such as soccer, lacrosse, basketball, hockey, and field hockey involve significant elements of both endurance and strength exercise.

The Athlete in Clinical Cardiovascular Imaging Practice

Cardiovascular medicine practitioners typically become involved in the care of the athletic patient in two distinct contexts. First, athletic patients may present with symptoms including chest discomfort, inappropriate exertional dyspnea, palpitations, syncope, or decreased exercise tolerance. These patients require symptom-driven evaluation involving exercise testing, ambulatory rhythm monitoring, and non-invasive imaging to diagnose or exclude underlying cardiac pathology. Second, asymptomatic athletic patients may be referred when “abnormal” cardiovascular findings, most often abnormalities on 12-lead electrocardiogram, are detected during health maintenance/ medical insurance examinations, pre-operative testing, or pre-participation athletic screening. These patients may require one or more noninvasive imaging tests to differentiate physiologic cardiac adaptation from occult cardiomyopathy.

Clinicians responsible for the performance and/or interpretation of noninvasive cardiovascular imaging play an integral role in the assessment of the athletic patient. Imaging clinicians are commonly looked upon to determine whether an athlete has heart disease or benign adaptive cardiac remodeling. In practice, three specific findings are most commonly encountered during the imaging assessment of the athletic patient: 1.) Increased LV chamber dimension, 2.) Increased LV wall thickness and, 3.) Increased RV chamber dimension. These three principal findings account for the majority of clinical uncertainty as they each occur in the context of pathologic conditions that may affect athletic patients. As such, each of these entities will be discussed in detail in the following sections with a particular emphasis on differentiating adaptive from pathologic physiology.

The Dilated Left Ventricle

Enlargement of the LV is common among trained endurance athletes. This represents physiologic, eccentric LVH characterized by an increase in LV chamber size accompanied by proportionate increase in LV wall thickness. However, several cardiomyopathic states (idiopathic dilated cardiomyopathy [DCM], familial DCM, toxin-mediated DCM, etc.) can have similar degrees of LV chamber enlargement. It cannot be over emphasized that pathologic dilation, perhaps with the exception of that seen in early aortic insufficiency, is associated with normal or reduced LV wall thickness measurements (Fig. 1). Knowledge of the expected features of exercise-induced cardiac remodeling, coupled with a “tool-kit” for clinical evaluation, including history/physical examination, 12-lead electrocardiogram, and diagnostic imaging is necessary to distinguish physiologic from pathologic increase in LV chamber dilation. Echocardiography is the initial, primary imaging modality for assessment of LV size and function in athletes. Cardiac magnetic resonance imaging (MRI) can be used if needed for further characterization of the LV in athletes.

Fig. 1
figure 1

Comparison of the echocardiographic features of left ventricle (LV) dilation secondary to eccentric hypertrophy from endurance exercise training (a–c) and secondary to idiopathic dilated cardiomyopathy (d–f). a Parasternal long-axis view demonstrating increased end-diastolic LV inner dimension (red line; 57 mm) and concomitant increased wall thickness (blue arrows; 13 mm interventricular septum [IVS] and 13 mm posterior wall thickness [PWT]). b Apical 4-chamber view demonstrating a dilated right ventricle (RV, yellow asterisk) adjacent to the dilated LV. c Tissue Doppler recording form the lateral mitral annulus demonstrating increased early diastolic peak tissue velocity (E’) of 24 cm/sec (gray arrow). d Parasternal long-axis view demonstrating increased end-diastolic LV inner dimension (red line; 63 mm) and normal to decreased wall thickness (blue arrows; IVS and PWT each 7 mm). e Apical 4-chamber view demonstrating normal RV size (yellow asterisk) adjacent to the dilated LV. f Tissue Doppler recording form the lateral mitral annulus demonstrating reduced E’ of 7 cm/sec (gray arrow)

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Pelliccia et al. reported echocardiographic LV end-diastolic cavity dimensions in a large group (n = 1309) of Italian elite athletes (73 % men) representing 38 different sports [18]. LV end-diastolic diameters varied widely from 38 to 66 mm in women (mean, 48 mm) and from 43 to 70 mm in men (mean, 55 mm). LV end-diastolic diameter was 54 mm or greater in 45 % and more than 60 mm in 14 % of the cohort. Markedly dilated LV chambers (defined as >60 mm) were associated with increased body mass and were most common among those participating in endurance sports (cycling, crosscountry skiing, and canoeing). In clinical practice, 53 to 55 mm is commonly used to define the upper limits of LV end-diastolic dimensions, thus rendering nearly one half of trained athletes in this study above the normal reference point. More recently, in a population of nearly 500 university athletes, we found that 25 % of the collegiate athletes exceeded the gender recommended limit for LV end-diastolic diameter [19].

The function of the dilated LV in athletes has also been the subject of investigation. Global function, measured as the LV ejection fraction, is generally normal among athletes [20]. However, it is noteworthy that a study of 147 cyclists participating in the Tour de France found that 11 % (n = 17) had an LV ejection fraction of 52 % or less [21], suggesting that healthy endurance athletes may demonstrate mildly reduced LV ejection fraction at rest. In our experience, this is encountered relatively often during the clinical assessment of experienced endurance athletes. Furthermore, eccentric LVH in endurance trained athletes is typically not isolated LV chamber enlargement. Frequently concomitant left atrial and RV dilation are present as discussed in detail below.

Novel echcocardiographic techniques, such as speckle-tracking imaging, have been used to study regional LV function in athletes with LV dilation secondary to eccentric hypertrophy. In a longitudinal study of endurance trained athletes, we observed increases in normal strains following a 90-day period of endurance exercise training in young competitive rowers [22]. Cross-sectional reports have identified differences in LV rotation and torsion when comparing cyclists and sedentary controls [23] and we observed changes in LV apical rotation and LV torsion after a period of endurance exercise training [24]. The importance of these regional LV function findings with respect to the understanding of exercise physiology and for differentiating athletic from pathologic remodeling is an important area of ongoing investigation.

Distinguishing pathologic states from eccentric hypertrophy observed in endurance athletes can be challenging since there is overlap in the magnitude of LV dilation that is observed. Specifically, idiopathic DCM, familial DCM, toxin-mediated (i.e., alcohol or chemotherapeutic agents) DCM, tachycardia-mediated DCM, and DCM secondary to valvular heart disease can produce degrees of LV dilation similar to that produced by exercise training. Differentiation of several of these etiologies will become clear with identification of triggers for pathology, such as associated valvular lesions or a history of tachyarrhythmia or exposure to a myocardial toxic agent. Additionally, the degree of reduction of LV ejection fraction may be greater in a number of causes of DCM, however early stage disease may have mild or minimal impairment of LV ejection fraction which may mimic changes seen in the athlete’s heart.

Evaluation of LV diastolic function may also aid in the differentiation of physiologic and pathologic LV chamber dilation. Most studies of diastolic function in athletes have used 2-dimensional pulsed-Doppler (trans-mitral) and tissue Doppler echocardiography. Endurance exercise training leads to enhanced early diastolic LV filling as assessed by E-wave velocity and mitral annular/LV tissue velocities [25, 26, 27•]. These changes are due to a combination of enhanced intrinsic lusitropy and training-induced increases in LV preload. It is likely that the observed improvements in resting LV diastolic function, particularly the ability of the LV to relax briskly during early diastole, are retained during exercise and contribute to stroke volume preservation during exercise at high heart rates. In contrast, DCM due to pathologic causes mentioned above is typically associated with impairment in echocardiographically-derived measures of LV diastolic function [28].

In summary, LV chamber dilation in athletes is an expected response to sustained endurance training. In a patient with this background, LV enlargement with preserved or mildly reduced systolic function accompanied by RV dilation of similar magnitude and left atrial dilation can be considered a benign adaptive process. Enhanced diastolic function in the setting of LV dilation is characteristic of the eccentric LVH observed in endurance athletes. Additionally, ongoing investigations defining normative values for LV strain, rotation and torsion in endurance athletes may make these measures of regional myocardial function a useful adjunctive method for distinguishing physiologic and pathologic LV chamber enlargement. In general, “cut-off” values for LV end-diastolic diameter are not helpful given the overlap between exercise-induced cardiac remodeling and cardiomyopathic states. When resting evaluation of the LV results in considerable doubt in regard to the etiology of LV dilation, exercise testing is very useful to confirm LV augmentation and to document above normal exercise capacity in the hearts of trained athletes.

The Thick Left Ventricle

Thickening of the LV, without concomitant LV chamber dilation, occurs less frequently then LV chamber dilation in trained athletes. LV wall thickening (i.e., physiologic LVH) is most likely to occur in strength (isometric) trained athletes and poses a great diagnostic challenge given the potential for overlap with mild forms of hypertrophic cardiomyopathy (HCM). The differential diagnosis of physiologic LVH versus HCM has critical implications for athletes and their physicians because the diagnosis of HCM necessitates disqualification from most competitive sports. Additionally, athletes with HCM and associated high risk features may require implantable cardioverter defibrillators as a prophylactic measure to prevent sudden cardiac death. Cardiac imaging, in the form of echocardiography and MRI, are crucial tools in the proposed diagnostic algorithm to distinguish exercise-induced LVH from HCM [29•].

Pelliccia et al. reported echocardiographic measurements of LV wall thicknesses among 947 elite Italian athletes. Within this exclusively white cohort, a small but significant percentage of athletes (1.7 %) had LV wall thicknesses of 13 mm or greater, and all of these individuals had concomitant LV cavity dilation [30]. Sharma et al. similarly reported a low incidence (0.4 %) of an LV wall thickness greater than 12 mm among 720 elite junior athletes and confirmed that increased LV wall thickness is associated with increased chamber size in young athletes [31]. In our study of nearly 500 university athletes, not a single healthy college athlete had LV wall thickness > 14 mm [19]. Clinical assessment of LVH in athletes, particularly with respect to differentiating adaptive from pathologic hypertrophy, requires consideration of training status, body size, and ethnicity.

Unlike LV chamber dilation in athletes, LV wall thickness “cut-off” values can be helpful. Maximum LV wall thickness of 15 mm in young trained athletes likely represents the upper limit of physiologic LVH [30]. In patients with HCM, including those who are asymptomatic and regularly involved in lifestyles, maximum LV wall thickness averages 21 – 22 mm and 30 mm or more in about 10 % of patients [32]. However, an important minority of patients with HCM show no or only mild wall thickening in a gray zone of 13 to 15 mm, which overlaps with that found in elite athletes. This “gray zone” hypertrophy poses the greatest diagnostic dilemma and is where cardiac imaging can be utilized to help clarify the diagnosis.

The pattern of LVH as visualized on cardiac imaging is an important factor in gray-zone cases. In exercise-induced physiologic LVH, although the anterior ventricular septum may be the segment of the LV that is maximally thickened, the overall pattern is symmetric, usually with a difference of ≤ 2 mm between all segments of the LV [30]. Thus, physiologic LVH is typically concentric LVH. In contrast, in HCM, the distribution of LVH is usually asymmetric [32] (Fig. 2). Although the anterior ventricular septum is generally the most thickened, other areas (such as posterior ventricular septum, anterior free wall, or apex) may show the most marked degree of thickening. Asymmetric LVH must therefore be considered pathologic until proven otherwise.

Fig. 2
figure 2

Comparison of increased left ventricle (LV) wall thickness in concentric hypertrophy secondary to strength training (a) and in hypertrophic cardiomyopathy (HCM), (b). a Parasternal long-axis echocardiogram of an athlete with “gray zone” hypertrophy, with relative symmetry between the interventricular septum (IVS; yellow asterisk, 13 mm) and the posterior wall thickness (PWT; red asterisk, 12 mm). b Parasternal long-axis echocardiogram demonstrating HCM with marked asymmetric increase in LV wall thickness. IVS (yellow asterisk) measures 27 mm and PWT (red asterisk) 13 mm. Prominence of a papillary muscle is also noted. The LV cavity size is small in HCM

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Evaluation of diastolic function with echocardiography has been used to aid in the differentiation of HCM from athlete’s heart. Most patients with HCM show abnormal Doppler diastolic indexes of LV filling, independent of whether symptoms or outflow obstruction is present [33]. In contrast, athletes with LVH have shown normal LV filling patterns [34]. However, use of trans-mitral filling pattern can be limited given that it is load-dependent. More recent studies have focused on tissue Doppler echocardiography assessment of diastolic function, which is less-load dependent [35, 36], although these studies have not focused exclusively on strength-trained athletes. A recent longitudinal study including male American football players with concentric LVH showed relative impairment of LV relaxation by tissue Doppler echocardiography. This suggests that the study of diastolic function in strength-trained athletes requires further study before conclusions can be drawn about using these diastolic parameters to distinguish physiologic LVH from HCM. Study of myocardial mechanics, including strain, torsion and untwisting [37] in patients with HCM are emerging, although more work is needed before these parameters may be used to distinguish physiologic and pathologic LVH.

Cardiac MRI has a growing role in the differential diagnosis of concentric LVH of the athlete’s heart and HCM. Cardiac MRI can be superior to echocardiography for identifying the presence of LVH, particularly when increased wall thickness is limited to focal areas of the anterior free wall, posterior septum, and apex [38••]. Furthermore, contrast-enhanced cardiac MRI with late gadolinium enhancement (LGE) can detect areas of myocardial fibrosis after injection of intravenous gadolinium. A significant percentage of patients with HCM demonstrate LGE, often in a patchy, multifocal mid–myocardial distribution, particularly in regions of LVH or at the RV / LV hinge points within the interventricular septum. LGE on cardiac MRI has been associated with ventricular tachyarrhythmias on ambulatory monitoring, suggesting a link between myocardial fibrosis and arrhythmia [39]. As such, we routinely utilize MRI in the evaluation of patients with suspect or diagnosed HCM to accurately quantify maximum wall thickness and to determine the extent of associated fibrosis.

In situations of gray-zone LVH that remain ambiguous despite clinical and imaging evaluation, prescribed detraining and subsequent echocardiography (and/or cardiac MRI) to assess for LVH regression may be useful. Maron et al. documented regression of eccentric LVH among Olympic athletes over 6–34 weeks (mean 13 weeks) [40]. The largest detraining report included 40 elite Italian male athletes with eccentric LVH (LV dimension = 61.2 ± 2.9 mm, LV wall thickness = 12.0 ± 1.3 mm) [41]. These athletes demonstrated complete normalization of wall thickness and significant but incomplete reduction in cavity dilation after 5.8 ± 3.6 years of detraining. The response of concentric LVH in strength athletes, the true mimicker of HCM, to prescribed detraining has not been as well studied. We recently completed an analysis in five strength-trained athletes with concentric LVH, and showed significant regression of LV mass, LV wall thickness, and left atrial size occurred during detraining [42•]. Although regression was observed at 3 months, 6 months was required for complete normalization of all cardiac parameters.

In summary, although less common than LV chamber dilation, increased LV wall thickness in athletes is more problematic as it may mimic HCM, the leading cause of sudden cardiac death in athletes. Wall thickness “cut-off” values can be helpful, as LV wall thickness > 15 mm should be considered pathologic until proven otherwise. Additionally, the pattern of LVH is useful, as LVH in strength-trained athletes is typically symmetric, and the presence of asymmetry is indicative of HCM. Cardiac MRI for the evaluation of the magnitude and pattern of LVH, as well as for the presence of LGE, is increasingly utilized in distinguishing physiologic and pathologic LVH. In gray-zone cases (13–15 mm wall thickness), prescribed detraining to evaluate for regression of LVH in athletes may be diagnostic, although more data describing the expected extent and time course of LVH regression in strength athletes is needed. Cardiopulmonary exercise testing may also be a useful discriminator, as even asymptomatic HCM patients typically attain lower peak oxygen consumption [43].

The Dilated Right Ventricle

Enlargement of the RV is common among trained endurance athletes. However, RV enlargement may alternatively be a marker of an occult cardiomyopathic disease process. This overlap often leads to significant diagnostic uncertainty in the athletic patient with this finding. Thorough understanding of the expected features of physiologic RV remodeling and how they differ from findings associated with diseases of the RV is of paramount importance to the imaging clinician. Echocardiography remains the most widely used tool for cardiac imaging in athletes and should be regarded as the first line test for assessment of the RV. However, limitations of RV imaging by echocardiography are well recognized thereby ensuring an important role for cardiac MRI.

Endurance exercise requires both the LV and RV to accept and eject relatively large quantities of blood. Consequently, the cardiovascular response to repetitive endurance exercise includes biventricular remodeling. For the thin-walled RV, this remodeling typically takes the form of mild RV dilation without significant concomitant hypertrophy. It cannot be over emphasized that RV dilation in the endurance-trained athlete is associated with concomitant LV remodeling and that isolated RV enlargement should raise suspicion of a pathologic process. Biventricular remodeling was documented in an early M-mode echocardiographic study which demonstrated symmetric RV and LV enlargement in a small (n = 12) cohort of highly trained endurance athletes [44]. Henriksen et al. subsequently examined RV and LV measurements using M-mode and two-dimensional echocardiography in elite male endurance athletes (n = 127) [45]. Endurance athletes, when compared to sedentary controls, demonstrated significantly larger RV cavities and a trend toward thicker RV free walls. Scharhag et al. performed a more recent MRI study which confirmed that RV enlargement is common among endurance athletes [46], and data from other recent studies are consistent with this finding [47].

The finding of RV enlargement may be concerning given the fact that RV dilation also occurs in the context of several diseases that occur among athletes. Disease considerations in the athletic patient with RV dilation include: arrhythmogenic right ventricular cardiomyopathy (ARVC), primary or secondary pulmonary hypertension, sarcoidosis, myocarditis, coronary artery disease with prior RV infarction, and the recently described entity exercise-induced RV cardiomyopathy. ARVC, a condition characterized by fibro-fatty replacement of the right ventricle and a corollary predisposition to malignant ventricular arrhythmia, is the most common diagnostic consideration as this disease has been associated with sudden death in the context of exercise. Diagnostic criteria for ARVC that integrate family history, electrocardiography, tissue histology, and cardiac imaging (echocardiographic and MRI parameters) have been proposed [48••].

Imaging criteria for ARVC include the presence of abnormal morphologic features, regional RV dysfunction, and diagnostic cut-offs for RV enlargement (Table 1). The findings of structural abnormalities including focal RV free wall sacculation/aneurysms or regional functional impairment cannot be explained by athletic training and should prompt careful consideration of underlying ARVC. Resting global RV function as assessed by echocardiography (fractional area change, tricuspid annular plane systolic excursion, etc.) or MRI (RV ejection fraction) may be mildly reduced at rest in trained athletes. Strain and strain rate imaging have recently been used to confirm normal RV contractile reserve in trained athletes during exercise [49•]. Although further study is necessary, this technique may prove useful in differentiating ARVC from athletic RV dilation.

Table 1 Imaging criteria for establishing the diagnosis of arrhythmogenic right ventricular cardiomyopathy [48••]
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The use of RV size criteria for ARVC should be applied to athletes with great caution. A recent study carefully examined echocardiographic RV dimensions in athletes and demonstrated that RV size often exceeds values proposed for ARVC diagnosis [50••]. As such, we do not routinely consider the finding of RV dilation in the endurance athlete to be pathologic unless accompanied by additional clinical or image-based findings suggestive of ARVC. An imaging specific comparative assessment of exercise-induced RV dilation and ARVC is presented in Table 2.

Table 2 Comparison of cardiac imaging findings in exercise-induced RV remodeling and arrhythmogenic RV cardiomyopathy
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Although exercise-induced cardiac remodeling is typically regarded as a beneficial adaptation to exercise, recent data suggest that extremely high levels of endurance exercise may lead to pathologic changes. In competitive rowers, we previously reported physiologic RV dilation with focal deterioration of interventricular septal function after a period of intense exercise training [22]. Specifically, we found significant reductions in systolic circumferential strain within the interventricular septum among collegiate rowers after 90-days of team-based training. In this setting, the magnitude of circumferential strain impairment was tightly correlated with the degree of concomitant RV dilation. More recently, La Gerche et al. used cardiac MRI to document septal fibrosis in the locations of RV fiber insertion among a small group of long-distance runners, cyclists, and triathletes. This septal fibrosis was encountered among individuals with the most marked RV dilation and was associated with an increased incidence of ventricular arrhythmias [51]. Thus, it appears possible that select individuals may experience some adverse forms of cardiac remodeling (i.e., fibrosis with arrhythmogenic substrate) following high volumes of long-term training. Further work will be necessary to define the scope, imaging hallmarks, and clinical implications of this evolving issue.

In summary, RV dilation in athletes is an expected response to sustained endurance training. In a patient with this background, mild to moderate RV enlargement with preserved or mildly reduced systolic function accompanied by LV remodeling (eccentric LV hypertrophy) of similar magnitude can be considered a benign adaptive process. In contrast, isolated RV enlargement, RV enlargement in the setting of focal RV dysfunction or structural abnormality, or RV enlargement in the setting of symptoms or abnormal family history should prompt consideration of an explanatory disease process. Exercise-induced RV cardiomyopathy, a seemingly rare condition characterized by diffuse RV enlargement, mild hypokinesis, myocardial septal fibrosis, and ventricular arrhythmia is a recently described entity that appears to affect only athletes who subject themselves to high levels of training over extended periods of time. Future work will be required to determine the importance of this condition in the evaluation of the athlete with RV enlargement.

Conclusion

The initial report of the athlete’s heart dates back to over 100 years ago. Since that time, advances in cardiac imaging, particularly echocardiography and cardiac MRI, have allowed for characterization of the structural cardiac changes that can develop in athletic individuals. The sporting discipline, specifically whether training is primarily endurance (isotonic) or strength (isometric), affects the magnitude and type of cardiac adaptation. Despite our improved understanding of exercise-induced cardiac remodeling, three common findings among athletes remain challenging in clinical practice. These include increased LV chamber dimension, increased LV wall thickness, and increased RV chamber dimension. Distinguishing these entities from a cardiomyopathy requires the integration of a number of diagnostic techniques, including cardiac imaging. Further studies investigating novel imaging techniques, including assessment of regional LV and RV function, as well as examining the myocardial response to exercise, hold promise to make the distinction between physiologic adaptation and pathology more clear in the future.