Manual of Cardiovascular Medicine

I.INTRODUCTION. An athlete can be defined as one who participates in sport, either individually or with a team, which requires regular and often intense training. The competitive athlete, by definition, competes against others and places a high premium on excellence. The terms “athlete’s heart,” “athlete’s heart syndrome,” or “exercise-induced cardiac remodeling” refer to the structural, functional, and electrical adaptations that occur with prolonged and intense exercise training.

Morganroth initially put forward the concept of sport-specific cardiac remodeling in the 1970s. Divergent cardiac adaptation for dynamic and static sports became known as the Morganroth hypothesis.

A.Dynamic training. The metabolic requirement of working muscles increases during dynamic exercise (e.g., running). To meet demand, the cardiovascular system responds through two principal mechanisms: increased cardiac output (CO) and reduced peripheral vascular resistance (PVR). CO is determined by heart rate and stroke volume and, in athletes, can increase up to sixfold during vigorous exercise, compared to during resting conditions. The increase in preload and CO during endurance exercise creates a volume overload (isotonic) stress on the heart. In addition, exercise-induced reduction in PVR, through recruitment and dilation of peripheral vascular beds (mainly in working skeletal muscle), also contributes to increased CO.

The augmentation of CO during dynamic exercise is mainly driven by a rise in heart rate mediated by an autonomic nervous system (i.e., parasympathetic withdrawal and sympathetic augmentation). The maximal heart rate is largely determined by age and does not increase further with conditioning.

Stroke volume is mainly determined by the end-diastolic volume (i.e., chamber size) and, to a lesser degree, by the end-systolic volume (regulated by a sympathetically mediated augmentation of cardiac contractility). End-diastolic volume increases in trained athletes, which augments CO during exercise. Therefore, characteristic findings in the highly trained endurance athlete include resting bradycardia and a balanced increase in left ventricular (LV) dimensions and wall thickness (eccentric hypertrophy).

B.Static training. Conversely, the sustained contraction of peripheral muscle beds during static, or strength training (e.g., weight lifting) acts to compress peripheral blood vessels and causes a marked increase in PVR. This response is further augmented by an exercise-induced surge in sympathetic tone and catecholamine release. During intense strength exercise, the left ventricle may transiently have to work against a peripheral systolic blood pressure of up to 400 mm Hg. The increase in PVR is accompanied by only a limited increase in CO and, therefore, strength exercise mainly creates a pressure overload (isometric) stress on the heart. According to the Morganroth hypothesis, strength training will result in an increase in LV wall thickness that is not matched by an increase in LV chamber dimension (concentric hypertrophy). However, this theory was recently challenged by a meta-analysis performed by Utomi and coworkers, which failed to show a pattern of concentric hypertrophy in strength athletes, possibly because athletes participating in “pure” pressure overload sports (e.g., weight lifting) often have a training regimen that also includes volume overload exercise, as part of their conditioning. An increase in such “cross training” since the 1970s, when Morganroth first put forward the evidence of concentric hypertrophy in strength athletes, may explain why we see this phenomenon less frequently today.

Importantly, many sports (e.g., rowing and cycling) have overlapping physiology, exposing the heart to both volume and pressure overload stress. Nevertheless, sports are often classified according to the type(s) of stress placed on the cardiovascular system. For example, the 36th Bethesda Conference divide sports into nine categories based on these principles (Fig. 41.1). Knowledge of the expected cardiac changes according to the demands of their sports is important when evaluating the cardiovascular system of athletes. Furthermore, the degree of cardiac adaptation also varies according to age, gender, ethnicity, and genetic factors. Below, exercise-induced structural cardiac remodeling of the ventricles, atria, and aorta is described.

FIGURE 41.1 Classification of sports. This classification is based on peak static and dynamic components achieved during competition. It should be noted, however, that higher values might be reached during training. The increasing dynamic component is defined in terms of the estimated percent of maximal oxygen uptake (Max O₂) achieved. The increasing static component is related to the estimated percent of maximal voluntary contraction (MVC) reached. The lowest total cardiovascular demands (cardiac output and blood pressure) are IA, while the highest are IIIC. ^adanger of body collision; ^bincreased risk if syncope occurs. (Reprinted from Mitchell JH, Haskell W, Snell P, et al. Task Force 8: classification of sports. J Am Coll Cardiol. 2005;45(8):1364–1367. Copyright © 2005 American College of Cardiology Foundation. With permission.)

II.STRUCTURAL CARDIAC ADAPTATIONS WITH REPETITIVE EXERCISE. Structural cardiac remodeling (e.g., enlargement of cardiac chambers) can become evident as soon as 90 days after commencing on an intense exercise regimen. These adaptations improve both cardiac efficiency (e.g., lower heart rate for a given exercise intensity) and maximal exercise capacity (e.g., increase maximal CO).

A.The left ventricle. Volume overload stress, when applied repetitively, typically produces dilation of the left ventricle, accompanied by a balanced increase in wall thickness (eccentric hypertrophy). In a large series of young healthy athletes (n = 1,309), representing 38 different sporting disciplines, LV end-diastolic diameter (LVEDD) ranged from 38 to 66 mm (mean 48 mm) in women and 43 to 70 mm (mean 55 mm) in men. More than 40% of male athletes had LVEDD exceeding 54 mm, and 14% had very pronounced dilation exceeding 60 mm. Furthermore, a recent meta-analysis reported a mean LVEDD of 55 mm (95% CI: 54 to 56) and 52.4 mm (95% CI: 51.2 to 53.6) in endurance- and resistance-trained athletes, respectively. However, it is our experience that LVEDD can be significantly larger in highly trained endurance athletes. Indeed, one study evaluating 286 Tour de France cyclists reported that LVEDD exceeded 60 mm in more than 50% of the athletes.

Therefore, when considering that the upper normal limit of LV chamber size is usually defined as 58 mm for men, the diagnostic challenge in differentiating athlete’s heart from pathologic changes (i.e., dilated cardiomyopathy) becomes evident. This challenge is compounded by an occasionally observed low-normal or mildly reduced LV ejection fraction (EF) in highly trained endurance athletes. For example, in the study mentioned above, 6% of the Tour de France cyclists had an LVEF of ≤52%. In a study of National Basketball Association players (a sport with a greater static component than cycling), on the other hand, an EF <50% was observed only in <1%. A meta-analysis of studies comparing endurance- and resistance-trained athletes reported a normal EF in both groups, with no significant difference between the two. Mean EF was 63% (95% CI: 61 to 64) in the endurance-trained athletes and 66% (95% CI: 62 to 70) in the resistance-trained athletes. Therefore, although an EF that appears low can occasionally be seen in extreme endurance athletes, this finding is not as common as often supposed. When faced with a diagnostic dilemma in an apparently healthy athlete with LV dilation and reduced EF, it can be useful to perform an exercise test to demonstrate normal myocardial recruitment and supranormal exercise capacity. In addition, the healthy endurance athlete with LV dilation will invariably have four-chamber dilation, normal diastolic function, and eccentric hypertrophy. Abnormal diastolic function or findings isolated to the left ventricle, on the other hand, suggest pathology (Table 41.1).

TABLE 41.1 Summary of Cardiac Assessment to Differentiate Cardiac Pathology from Exercise-Induced Cardiac Remodeling
Exercise-Induced Cardiac Remodeling	HCM	DCM	ARVC
12-Lead ECG
Multiple training-induced features—see International Recommendations for ECG Interpretation in Athletes	LVH with TWI extending beyond V₂ (Caucasian) or V₄ (Black) athletes. ST-depression	Nonspecific ECG changes such as Q-waves, poor R-wave progression, ST-depression, and TWI	Delayed right precordial S-wave upstroke. TWI V₁–V₃. Epsilon waves
Echocardiogram
Balanced LV and RV dilation and symmetric hypertrophy. LVEDD >55 mm. Normal diastolic function and strain pattern	Asymmetric wall thickening. LVEDD <45 mm. Abnormal diastolic function and strain pattern. Dynamic outflow obstruction	Typically isolated LV dilation with reduced LVEF. Abnormal diastolic function and strain	Typically isolated RV dilation with reduced RVEF associated with regional akinesia, dyskinesia, or aneurysm formation
Magnetic Resonance Imaging
Balanced LV and RV dilation and symmetric hypertrophy. No LGE	Asymmetric hypertrophy. Patchy mid-wall or RV insertion point LGE. Abnormal papillary muscle morphology and attachment	Mid- or subepicardial LGE. Dilated LV with thinned myocardium	Dilated RV with regional akinesia, dyskinesia, or aneurysm formation. May see patchy LGE
Exercise Stress Testing
Normal/supranormal exercise capacity. LVEF normalizes with exercise in athletes with a borderline low resting LVEF	Exercise-induced LVOT gradient. Abnormal blood pressure response. Ventricular ectopy. Reduced functional capacity	Low-normal to abnormal exercise capacity. Reduced myocardial recruitment. LVEF typically does not completely normalize with exercise	Low-normal to abnormal exercise capacity. Poor myocardial recruitment. RVEF typically does not completely normalize with exercise
Additional Workup to Consider in Challenging Cases
–	Holter monitoring. Detraining and genetic testing	–	Signal-averaged ECG. Holter monitoring. Endomyocardial biopsy

ARVC, arrhythmogenic right ventricular cardiomyopathy; DCM, dilated cardiomyopathy; ECG, electrocardiogram; HCM, hypertrophic cardiomyopathy; LGE, late gadolinium enhancement; LV, left ventricular; LVEDD, left ventricular end-diastolic diameter; LVEF, left ventricular ejection fraction; LVH, left ventricular hypertrophy; LVOT, left ventricular outflow tract; RV, right ventricular; RVEF, right ventricular ejection fraction; TWI, T-wave inversion.

Endurance training tends to augment diastolic filling, which can be demonstrated by high E-wave and mitral annular tissue velocities. The improved early LV relaxation and filling allows for preservation of stroke volume during exercise at high heart rates. In fact, it has been reported that endurance exercise training can attenuate, or even reverse, the decline in diastolic function typically seen with ageing.

The normal distribution of LV septal wall thickness has been investigated in several large series of athletes. In one study of Caucasian elite athletes (n = 947), wall thickness exceeded 12 mm in only 1.7%. Several other series corroborate that a thickness >13 mm is relatively rare in athletes. However, many of these studies were performed primarily in Caucasian male adult athletic cohorts. It has become clear that a number of factors have to be considered when assessing the athlete with increased wall thickness, including the sport type and training regimen, race, gender, and age of the athlete. For example, black athletes generally develop more hypertrophy in response to exercise compared to white athletes. In one large study (n = 300), 18% of black athletes had a septal wall thickness >12 mm, compared to only 4% of white athletes. Furthermore, in this study, 3% of black athletes, but none of the white athletes, developed significant LV hypertrophy (LVH) (>15 mm). The mechanism behind the augmented LVH response in black athletes, which is present across sporting disciplines, is not clear, but has been attributed to a combination of genetic, endocrine, and hemodynamic factors.

Because of phenotypic overlap with mild hypertrophic cardiomyopathy (HCM), athletes with a septal wall thickness of 13 to 15 mm are often considered to be in a diagnostic “gray zone.” In such cases, other echocardiographic parameters are often useful to differentiate physiologic LVH from HCM. For example, in athletes, septal wall thickness is typically accompanied by an increase in LV size (>55 mm). Importantly, LV chamber size appears to remain <50 mm even in HCM patients that participate in competitive sports against medical advice. An LV size >55 mm in HCM patients, on the other hand, is usually due to progressive myocardial fibrosis and thinning, accompanied by systolic dysfunction and heart failure symptoms. Such advanced HCM is typically not compatible with participation in competitive sports. Importantly, marked LVH is uncommon in very young athletes and should raise the suspicion for HCM, particularly if present before 16 years of age. Furthermore, physiologic LVH is usually accompanied by normal parameters of diastolic function and is not asymmetric. Myocardial deformation assessment using speckle tracking echocardiography is an emerging tool that may be a useful adjunct in differentiating HCM from athlete’s heart. Typically, strain is normal in the athlete, while there is a reduction in strain at the site of greatest hypertrophy and fibrosis in HCM. Of note, in <10% of cases, HCM may be limited to the apical segments of the left ventricle, which may be difficult to appreciate on echocardiography. Therefore, when the suspicion for HCM remains high, despite initial reassuring echocardiographic findings, contrast-enhanced echocardiography or magnetic resonance imaging (MRI) can be used. Cardiac MRI is also useful to identify asymmetric areas of hypertrophy and to identify scar using delayed gadolinium enhancement. Furthermore, MRI, in conjunction with echo, can be used to identify abnormalities of the mitral valve apparatus, which is seen in up to 75% of patients with HCM. If the diagnosis remains uncertain despite extensive imaging workup, detraining (i.e., exercise reduction or abstinence) may be used as a diagnostic tool. Detraining may induce regression of physiologic cardiac changes, whereas HCM-induced hypertrophy typically does not regress after stopping athletic activity. In a seminal study of six Olympic athletes, septal wall thickness was reduced from 13.8 ± 0.9 mm to 10.5 ± 0.5 mm following 6 to 34 weeks of voluntary training reduction. Currently, genetic testing for HCM is not a reliable method to rule out the presence of disease, but can be useful as a rule-in test, if positive (Table 41.1).

B.The right ventricle. Pressure overload–induced cardiac remodeling, seen in strength training, is usually limited to the left ventricle by virtue of mitral valve shielding. Endurance exercise–induced cardiac remodeling, on the other hand, affects all cardiac chambers including the right ventricle. The thin-walled right ventricle typically responds to volume overload stress by dilation, without concomitant hypertrophy. However, right ventricular (RV) response to exercise stress has been less well characterized than in the left ventricle, and “cutoff” values to define normal ranges are less well defined. In a recent study of 102 endurance athletes, RV chamber dilation exceeded the upper limit of normal in >50%. Importantly, the RV enlargement was accompanied by LV dilation in almost all cases. Isolated RV dilation, on the other hand, is rare in athletes and should raise the suspicion for a pathologic process (e.g., arrhythmogenic right ventricular cardiomyopathy [ARVC]). Furthermore, because exercise-induced RV dilation tends to be a global process, any significant regional changes (aneurysmal or saccular dilation, or regional akinesia) warrant further investigation (Table 41.1).

C.The atria. Left atrial (LA) enlargement (>40 mm anterior–posterior dimension by echocardiography) is common in athletes as a result of increased preload. One study of 1,777 athletes demonstrated that it was present in >20%, with a much higher prevalence in endurance-trained athletes. An upper limit of 45 mm in women and 50 mm in men has been suggested to differentiate athlete’s heart from pathologic conditions. Recent studies have also shown a high prevalence of right atrial (RA) enlargement. Assessment of atrial function plays an important role in differentiating athlete’s heart from pathology. The atria initially act as a “reservoir” during ventricular systole as the left atrium fills with blood, then a “conduit” as blood passively flows into the ventricle during early diastole, and finally as a “booster” during atrial contraction. These functions can be measured on echocardiography. The left atrium responds to exercise-induced increases in preload by augmenting reservoir and conduit functions although LA active emptying is lower in athletes. Similarly, speckle tracking echocardiography exhibits normal reservoir function and reduced active contribution of the atrium to ventricular filling at rest. Reduced reservoir function and unbalanced enlargement of the atria are features more consistent with pathology.

D.The aorta. Volume and pressure overloads during endurance and strength exercise, respectively, place a significant hemodynamic stress on the aorta. A recent meta-analysis showed that the aortic root diameter measured at the sinus of Valsalva and the aortic valve annulus was 3.2 and 1.6 mm greater in athletes (n = 5,580) compared to matched nonathletic controls (n = 727). However, there are conflicting data whether endurance- or strength-type exercise produces more aortic root dilation. Regardless, this small increase in aortic dimensions is considered clinically insignificant. Marked aortic root dilation (>4 cm) is unusual in athletes and should raise the suspicion for an underlying pathologic process.

III.ELECTROPHYSIOLOGIC CARDIAC ADAPTATIONS TO REPETITIVE EXERCISE. Exercise-induced cardiac remodeling not only affects cardiac structure and mechanical function but can also induce profound cardiac electrophysiologic changes. As a result, an athlete’s electrocardiogram (ECG) has the potential to raise alarm for an underlying cardiomyopathy, and false-positive findings have remained one of the major arguments against including the 12-lead ECG as part of the initial pre-participation screening of athletes in the United States. To better identify athletes who need further evaluation and to avoid false-positive test results, several ECG criteria have been proposed. The Seattle Criteria, published in 2012, reduced the false-positive rate from as high as 40% in criteria used in the early 2000s, to ~10%. The recently published International Criteria for ECG Interpretation in Athletes, further reduces the false-positive rate without affecting sensitivity, mainly by no longer categorizing isolated LA and RA enlargement, RV hypertrophy (RVH), and left and right axis deviation as abnormal. This is based on data showing that such ECG findings have a very low diagnostic yield in athletes. Normal and abnormal ECG findings in athletes according to the international criteria are shown in Figure 41.2. An additional category of “borderline” changes is now used; features seen in isolation are considered benign but if there is more than one borderline feature, further evaluation is recommended.

FIGURE 41.2 The international criteria for ECG interpretation in athletes. AV, atrioventricular; ECG, electrocardiogram; LBBB, left bundle branch block; LVH, left ventricular hypertrophy; PVC, premature ventricular complex; RBBB, right bundle branch block; RVH, right ventricular hypertrophy; SCD, sudden cardiac death. (Reprinted from permission from Sharma S, Drezner JA, Baggish A, et al. International recommendations for electrocardiographic interpretation in athletes. J Am Coll Cardiol. 2017;69(8):1057–1075. Copyright © 2017 Elsevier. With permission.)

A.Cardiac rate, rhythm, and conduction changes in athletes. Extensive exercise may result in profound resting sinus bradycardia (occasionally as low as 30 beats/min), sinus arrhythmia, ectopic atrial and junctional rhythm, first-degree atrioventricular (AV) block, and second-degree Mobitz type I AV block. These changes are attributed mainly to a shift in autonomic balance with repetitive exercise resulting in a heightened parasympathetic (vagal) tone and concomitant sympathetic withdrawal. Importantly, when physiologic, these changes disappear with exercise (a state of heightened sympathetic tone and vagal withdrawal). In the absence of symptoms, such changes are considered normal in athletes. In contrast, second-degree Mobitz type II AV block and third-degree AV block are extremely rare in athletes and are more suggestive of cardiac conduction disease.

Incomplete right bundle branch block (iRBBB) is seen in up to one-third of athletes and has been attributed to RV remodeling and dilation, which results in an increase in cardiac conduction time and is considered a normal variant. Complete RBBB, although seen in only 1% of athletes, is now considered to be a borderline ECG finding according to the new international recommendations. Complete left bundle branch block is not an athletic adaptation and should trigger further evaluation.

Ventricular arrhythmias are not uncommon in athletes. In one study, 355 competitive athletes with frequent premature ventricular complexes (PVCs) on screening ECG and/or a history of palpitations were further evaluated using 24-hour Holter monitoring. Athletes were subsequently divided into three groups based on the total number of PVCs and/or presence of non-sustained ventricular tachycardia (NSVT): group A (n = 71; >2,000 PVCs /24 hour and/or ≥1 episode of NSVT/24 hour), group B (n = 153, ≥100 to <2,000 PVCs and no NSVT), and group C (<100 PVCs and no NSVT). Overall, 93% of athletes had no significant cardiac abnormalities after extensive further cardiac testing including echocardiogram, MRI, and exercise ECG. In 7% (n = 26) of athletes, a cardiac abnormality was identified (mitral valve prolapse with mild mitral regurgitation in 11, ARVC in 7, myocarditis in 4, and dilated cardiomyopathy in 4). The prevalence of cardiac abnormalities was 30%, 3%, and 0% in groups A through C, respectively, suggesting that the presence of >2,000 PVCs/24 hour and/or NSVT in an athlete should trigger further evaluation, keeping in mind that pathology will be identified less than a third of the time.

B.Voltage criteria for ventricular hypertrophy and atrial enlargement. Voltage criteria for LVH are common in athletes and present in up to 70% of male athletes. It is particularly common in adolescent athletes (attributed to the thinner chest wall) and black athletes (attributed to more pronounced underlying ventricular hypertrophy). Increased QRS voltage criteria, when present in isolation, do not warrant further investigation. However, in the presence of pathologic Q-waves, ST-depression, T-wave inversion (TWI), or symptoms, LVH on ECG warrants further investigation with an echocardiogram or other testing modalities as clinically indicated, primarily to rule out HCM (Fig. 41.3).

FIGURE 41.3 Summary of the changes associated with athlete’s heart and the overlap between cardiomyopathy. ARVC, arrhythmogenic right ventricular cardiomyopathy; HCM, hypertrophic cardiomyopathy; LBBB, left bundle branch block; LVH, left ventricular hypertrophy; PVC, premature ventricular complex; TWI, T-wave inversion. (Adapted from permission from Prakash K, Sharma S. The electrocardiogram in highly trained athletes. Clin Sports Med. 2015;34(3):419–431. Copyright © 2015 Elsevier. With permission.)

Voltage criteria for RVH are present in up to 12% of athletes. Most experts do not recommend further evaluation of this ECG finding in the absence of symptoms or other abnormalities, which is recognized in the new International Criteria for ECG Interpretation in Athletes (Fig. 41.2). Similarly, voltage criteria for RA and LA enlargement are also common in athletes. Any of these findings in isolation are considered normal adaptations to training; however, if there are more than one of these features or they are associated with other abnormalities, further testing is warranted.

C.Repolarization changes. Exercise-induced changes in autonomic tone and/or electrical remodeling may also produce repolarization changes in athletes, including the early repolarization pattern (ERP) and TWI. ERP is present in up to 90% of athletes and is considered a normal variant in asymptomatic athletes. Interestingly, ERP may develop before, and independent of, LVH.

TWI is one of the more challenging ECG changes to interpret in athletes, as they are also the hallmark of many cardiomyopathies, including ARVC and HCM. Importantly, the prevalence and morphology of TWI vary across demographic factors such as age, gender, and race. For example, TWI is present in approximately 5% of white athletes and in up to 25% of black athletes. Furthermore, in black athletes, TWI commonly extends to leads V₂ to V₄, without any evidence of underlying pathology (Fig. 41.4).

FIGURE 41.4 The 12-lead electrocardiogram demonstrates convex ST-segment elevation in anterior leads (V₁ to V₄) followed by T-wave inversion. Note that the repolarization pattern has normalized in lead V₅.

The international criteria only consider TWI to be abnormal if T-waves are >1 mm in depth in more than two leads, excluding V₁, III, and aVR (except in black athletes where V₂ to V_{₄ are also excluded). TWI should be considered abnormal if extending beyond V₂ in white athletes, beyond V₄ in black athletes, or if it is accompanied by Q-waves or ST-depression. In ambiguous cases, the ST-segment preceding TWI may offer important diagnostic clues. In patients with ARVC, precordial TWI is usually preceded by an isoelectric ST-segment, whereas the ST-segment in athletes with TWI is usually convex. In one study, T-waves normalized with submaximal exercise in healthy athletes, which may offer another diagnostic tool beyond echocardiography and MRI. As a last resort, detraining can be used because TWI typically normalizes in athletes after 6 weeks of exercise restriction. In one study, pathologic TWI was associated with cardiac disease in 44.5% of athletes when extensive investigation was performed using echocardiography, cardiac MRI, exercise testing, and 24-hour Holter monitoring. Echocardiography only identified about half of these abnormal cases, which has led many experts, including the authors of the International Recommendations for ECG Interpretation in Athletes, to advocate more extensive investigations in these athletes. However, it is unclear how broadly applicable these data are, and further race-, body habitus-, and sport-specific studies are needed.}

Athletes have slightly longer QT-intervals compared to nonathletes, which has been primarily attributed to LVH. It has been reported that 6% of athletes have a corrected QTc exceeding the upper limit of normal (470 in men and 480 in women). However, it should be kept in mind that a prolonged QTc in isolation (i.e., in the absence of other long QT syndrome criteria) only has a positive predictive value of 7%. Further evaluation is therefore essential, and the diagnosis should not be made solely based on the ECG. Of note, QT-intervals are notoriously difficult to measure in athletes because of the common presence of sinus arrhythmia and U-waves. In sinus arrhythmia, an average QTc based on several beats should be used and care must be taken to exclude the U-wave. The shape of the T-wave should also be carefully investigated for notched or bifid morphologies, as they may be suggestive of a true ion-channel disorder.

IV.RISK OF EXCESSIVE EXERCISE. It is undisputed that habitual moderate and vigorous exercise promotes health. Paradoxically, for individuals with unrecognized cardiac disease there is an increased risk of an adverse cardiac event during strenuous exercise. Recognizing this causal relationship, pre-participation screening and eligibility/disqualification guidelines have been implemented in many parts of the world to reduce this risk. A more recent concern is whether, at the extremes of exercise, the cardiovascular benefits of exercise are offset by adverse effects on the cardiac structure and function of otherwise normal hearts. Some have suggested that the benefits of exercise exhibit an inverted J-shaped relationship to overall health, even in individuals without underlying cardiac disease. Proposed mechanisms are that repeated high-intensity exercise, without sufficient recovery time, results in inflammation, myocardial injury, and accelerated atherosclerosis, ultimately leading to fibrosis and adverse cardiac remodeling. Several studies have shown that sinoatrial node disease, advanced heart block, and atrial fibrillation are more common in veteran athletes compared to sedentary peers. It has been suggested that extreme endurance exercise may even accelerate coronary atherosclerosis. One study showed that veteran marathon runners have higher coronary artery calcium scores compared to age-matched sedentary controls. The study drew criticism over potential recruitment bias, because of a higher proportion of former smokers in the athlete group. However, more recent studies, including a study with master athletes having no coronary artery disease risk factors, also found a higher proportion of athletes with high coronary artery calcium scores, compared to age-matched sedentary controls. When taken together, the data appear to suggest that longstanding exercise promotes formation of calcified coronary artery plaques. The clinical significance of this, however, remains uncertain.

An evolving concept in sports cardiology is exercise-induced adverse remodeling of the right ventricle, that is, “exercise-induced ARVC.” During endurance exercise, the right ventricle is subjected to the same preload as the left ventricle. However, because the pulmonary vascular resistance (in contrast to the systemic vascular resistance) decreases only minimally with exertion, pulmonary artery pressures may exceed 80 mm Hg during vigorous exercise in some athletes, exerting a disproportionately large afterload stress on the thin-walled right ventricle. The concept of exercise-induced RV insult is supported by studies showing a correlation between post-exertional right (but not left) ventricular dysfunction and cardiac biomarker (e.g., Troponin and B-type natriuretic peptide) release. Furthermore, malignant ventricular arrhythmias in veteran endurance athletes originate from the right ventricle in the majority of cases and have been associated with significantly reduced right ventricular EF. Finally, mice and rat models have demonstrated that excessive exercise can induce RV fibrosis and accelerate development of the ARVC phenotype in genetically predisposed animals. The concept of chronic exercise–induced cardiac damage is depicted in Figure 41.5.

FIGURE 41.5 Theoretical model of chronic exercise-induced cardiac arrhythmogenic remodeling. RV, right ventricular. (From Sharma S, Zaidi A. Exercise-induced arrhythmogenic right ventricular cardiomyopathy: fact or fallacy? Eur Heart J. 2012;33(8): 938–940. Reproduced by permission of Oxford University Press.)

However, it should be emphasized that these studies are generally small cross-sectional studies evaluating small subsets of lifelong extreme endurance athletes. Despite these concerns it should be emphasized that the risk of adverse cardiovascular events is significantly higher in those who lead a sedentary lifestyle compared to individuals who regularly participate in any level of exertion. Further, longitudinal studies of elite athletes including Olympians, Tour De France cyclists, and cross-country skiers have reported an increase in their life expectancy compared to the general population. Overall, the remarkable benefits of regular exercise are well defined and should be promoted for most individuals to improve cardiovascular health.

V.ELIGIBILITY AND DISQUALIFICATION FOR ATHLETES WITH CARDIAC DISEASE. Eligibility and disqualification recommendations for athletes with cardiac abnormalities have been published by the American College of Cardiology/American Heart Association and the European Society of Cardiology. These guidelines are extensive and a complete overview of this topic is beyond the scope of this chapter; however, it is important to recognize that many of the recommendations are based on the assumption that exercise is a modifiable risk factor for sudden cardiac death (SCD). For most cardiac conditions, this assumption is largely unproven and based on expert opinion. As newer data have emerged, such recommendations have been modified. For example, athletes with ICDs were previously restricted from all competitive sports with the exception of IA (low static, low dynamic) sports; current guidelines suggest they may now participate in higher static and dynamic component sports after appropriate counseling if free from appropriate device therapies for a period of 3 months. This modification was based on the results of a registry of such athletes who continued to compete against medical advice and demonstrated no increased risk of SCD. Similarly, athletes with long QT syndrome were previously disqualified from most competitive sporting activities until objective data demonstrated a low risk of cardiac events in those who are asymptomatic and are taking appropriate treatment. Conversely, continued participation in competitive sports has been shown to accelerate progression of certain diseases, such as ARVC, along with increasing the risk of ventricular arrhythmias. Therefore, significant exercise restrictions should be recommended in athletes with ARVC. It is clear that these decisions are nuanced. Many sports cardiologists advocate transitioning away from a strict paternalistic framework for decision making regarding eligibility to compete for athletes with cardiac disorders in favor of a shared decision-making model. This model incorporates appropriate counseling of the patient and other relevant stakeholders (such as family and team) regarding the risks and benefits and uncertainties of continued exercise in the context of the underlying cardiac disorder and encourages participation of all parties in reconciling this information with their personal preferences and beliefs.