Exercise and Heart Disease

From Athletes and Arrhythmias to Hypertrophic Cardiomyopathy and Congenital Heart Disease

Abbas Zaidi; Sanjay Sharma


Future Cardiol. 2013;9(1):119-136. 

In This Article

Cardiovascular Adaptation to Exercise: Defining the Limits of Normality

Regular physical exertion results in physiological electrical, functional and structural cardiac adaptations. Such changes have been most extensively documented in individuals participating in frequent, high-level exercise, such as professional athletes. High vagal tone in athletes results in bradycardia and repolarization anomalies on the resting ECG. Bradycardia permits enhanced diastolic filling, which in turn results in highly effective augmentation of stroke volume during exercise. Over a period of time, the increased preload and afterload associated with prolonged intensive exercise results in structural changes, characterized by modest left ventricular (LV) wall hypertrophy, as well as increased dimensions of the atria and ventricles (Figure 3). Although such changes are generally considered to be reversible and benign, they may result in a diagnostic overlap with pathological conditions, particularly the cardiomyopathies, in which vigorous exercise is associated with an increased risk of adverse events including sudden death. Thus, subtle indicators of pathology may be incorrectly interpreted as training-related, allowing a young individual to continue to engage in high-risk sporting activities. Conversely, an erroneous diagnosis of cardiomyopathy may result in disqualification from competition, with resultant loss of livelihood and emotional distress. Rigorous clinical algorithms are therefore required to assist in the differentiation between physiological and pathological remodeling. The most important pre-requisite for developing such an algorithm is the need for well-defined limits for physiological adaptation to exercise, with the most widely available tools being the ECG and echocardiogram.

Figure 3.

Physiological adaptation in the athlete's heart.
LV: Left ventricular.

Electrocardiographic Patterns in the Athlete

Electrocardiographic anomalies are common in athletes and usually reflect physiological, electrical and structural cardiac remodeling, as well as the effects of increased vagal tone. Frequently observed changes include rhythm and conduction alterations, increased voltages and repolarization anomalies. Sinus bradycardia is a common manifestation of training-induced vagotonia. A small number of athletes (~5%) also exhibit nodal rhythm or Mobitz type 1 (Wenkebach) second-degree atrioventricular block at rest. However, in the majority of athletes, this will revert to sinus rhythm with mild exertion, which should be taken as evidence of normal physiological conditioning.

Voltage criteria for LV hypertrophy (LVH) are frequently fulfilled, but correlate poorly with echocardiographic findings[16] and should not prompt further investigation in the absence of symptoms, positive family history, or associated anomalies, such as axis deviation and strain patterns. Common repolarization changes include J-point and ST-segment elevation, as well as high amplitude T-waves. The ST-segment usually exhibits a concave shape in the inferior and lateral leads and, in a minority of cases, a convex shape in the anterior precordial leads. Occasionally, specific repolarization anomalies overlap with incomplete expression of, or morphologically mild, cardiomyopathy. In particular, T-wave inversion in leads other than III, aVL, aVR or V1 should warrant further investigation in all Caucasian athletes over 16 years of age. However, T-wave inversion confined to leads V1–V4 in juvenile athletes and in adult athletes of African or Afro–Caribbean origin may be a normal variant (see below).

The ESC has produced consensus guidelines for interpretation of the 12-lead ECG in athletes.[29] Electrocardiographic anomalies are categorized into two groups (Box 2). Group 1 includes 'common and training-related' changes that should not cause alarm in the absence of a positive family history, symptoms or abnormal physical findings. Group 2 consists of 'uncommon and training-unrelated' changes that warrant additional diagnostic evaluation to exclude underlying heart disease.

It should be noted, however, that these guidelines are derived from adult Caucasian athletes and caution should be exercised when extrapolating to juvenile athletes (<16 years of age) and adult athletes of African or Afro–Caribbean descent. Magalski et al. reported that ECG abnormalities were twice as common in black compared with white athletes.[30] Basavarajaiah et al. documented the Sokolow–Lyon voltage criterion for LVH in 68% of black athletes compared with 40% of white athletes.[31] More striking were the differences in repolarization patterns between the two ethnic groups. ST-segment elevation was present in 85% of black and 62% of white athletes, whilst deep T-wave inversions (>0.2 mV) were seen in 12% of black athletes but none of the white athletes. Papadakis et al. reported deep T-wave inversions in 16% of a large cohort of black athletes, compared with only 2% in matched white athletes.[32] T-wave inversions in black athletes were largely confined to the anterior precordial leads, and extensive clinical evaluation did not reveal any underlying cardiac pathology associated with this pattern. Furthermore, a period of detraining in a subset of athletes led to resolution of these changes. In black athletes, therefore, deep T-wave inversions in leads V1–V4 are likely to represent a benign finding. By contrast, longitudinal follow-up revealed an association between inferior and/or lateral T-wave inversions and sudden death events or a subsequent diagnosis of HCM. Therefore, T-wave inversion extending to the inferior or lateral leads warrants detailed evaluation and prolonged longitudinal follow-up in athletes of any ethnicity. A typical ECG from a Caucasian athlete is shown in Figure 4A, with the ECG of a black African athlete shown for comparison in Figure 4B.

Figure 4.

Electrocardiographic patterns in athletes.
(A) The ECG of a healthy Caucasian athlete, demonstrating sinus bradycardia and left ventricular hypertrophy by voltage criteria. (B) The ECG of a healthy black African long-distance runner. Convex ST-segment elevation with deep T-wave inversion is evident in leads V1–V4. By contrast, the ECG of a black athlete with hypertrophic cardiomyopathy is shown in (C). Note the deep T-wave inversion in the lateral leads (V4–V6), as well as left ventricular hypertrophy and bi-atrial enlargement by voltage criteria.

Morphology of the Athlete's Heart

It is well established that athletes exhibit on average a 10–20% increase in LV wall thickness (LVWT) and LV end-diastolic diameter (LVEDD). More recent studies demonstrate a symmetrical training-related increase in right ventricular (RV) dimensions.[33] However, these biventricular changes are highly variable and there is considerable overlap with non-athletic controls matched for age and gender.

Upper Reference Limits & Determinants of Cardiac Dimensions

Physiological adaptation to exercise is influenced by a number of demographic factors including age, sex, size and ethnicity, as well as sporting discipline. In general, large, male athletes participating in endurance sports have the greatest cardiac dimensions. In addition, black athletes exhibit a greater magnitude of LVH than their Caucasian counterparts. The key determinants of cardiac dimensions in the athlete's heart are summarized in Figure 5. Echocardiographic upper reference limits for LVEDD, LVWT and RV dimensions in athletes are summarized in Table 1, according to gender, race and age, with reference limits for non-athletes[34] given for comparison.

Figure 5.

Determinants of cardiac dimensions in the athlete's heart.

In a seminal study, Pelliccia et al. demonstrated values for LVWT exceeding reference limits for non-athletes in more than a quarter of a cohort of predominantly Caucasian male and female athletes.[35] However, values in the range compatible with HCM (>12 mm) were extremely uncommon (2%), with none exhibiting a LVWT greater than 16 mm. Pelliccia et al. also reported a large range of LV cavity dimensions in elite athletes, with greater values seen in males.[36] Marked cavity dilatation in the range compatible with dilated cardiomyopathy (DCM; LVEDD ≥60 mm) was evident in 14% of athletes, although none exceeded 70 mm. The distribution of cardiac dimensions in these studies is depicted in Figure 6.

Figure 6.

Range of left ventricular dimensions in athletes. (A) LVWT values from male and female athletes together. (B) LVEDD values for male and female athletes separately. In both studies, participants were predominantly Caucasian.
DCM: Dilated cardiomyopathy; HCM: Hypertrophic cardiomyopathy; LVEDD: Left ventricular end-diastolic diameter; LVWT: Left ventricular wall thickness.
Adapted with permission from [35, 36].

Male athletes exhibit greater increases in cardiac dimensions than female athletes. Pelliccia et al. compared 600 female athletes with matched female sedentary controls and male athletes.[37] Although LVWT and LVEDD were greater in female athletes than female controls, both dimensions were greatest in male athletes. LVWT greater than 12 mm was seen in 2% of male athletes compared with none of the female athletes, whilst LVEDD greater than 60 mm was exhibited by 24% of male athletes but by less than 1% of female athletes.

Adult athletes demonstrate a greater degree of cardiac remodeling than adolescent athletes of similar sex and sporting discipline, who are physically less mature and have been exposed to shorter periods of intense training. Therefore, in adolescent athletes, values for LV cavity dimensions and wall thickness exceed those of age- and sex-matched sedentary controls, but are lower than those seen in adult athletes. In a study by Makan et al.[38] no adolescent athletes exhibited LVEDD greater than 60 mm, whilst in a study by Sharma et al.,[39] LVWT exceeding 11 mm was evident in only 0.4% of cases.

Spirito et al. documented that the extent of LV remodeling is influenced by the type of sporting discipline, with the most marked increases in cavity dimensions and wall thickness seen in elite rowers, cross-country skiers, cyclists and swimmers, followed by long-distance runners, soccer and tennis players.[40] Similar findings were recently reported in the right ventricle in a large echocardiographic study by D'Andrea et al.,[41] as well as in a cardiac magnetic resonance (CMR) study by Luijkx et al.,[33] with male athletes engaging in endurance sports exhibiting the greatest degree of physiological RV cavity enlargement.

In a study of cardiac dimensions in black athletes, Basavarajaiah et al. demonstrated LVWT ≥13 mm in 18% of black athletes, compared with 4% of white athletes matched for age, size and sporting discipline.[31] LVWT ≥15 mm was seen in 3% of black athletes but in none of the white athletes. Similarly, Rawlins et al. documented LVWT ≥12 mm in 3% of black female athletes but in no matched white female athletes.[42] The upper limits for physiological LVH in black male and female athletes are therefore considered to be 15 and 12 mm, respectively.