The History of the Athlete’s Heart

In 1974, Prof. Dr. Josef Schmidt of Münster wrote in this journal – called  “Sportarzt + Sportmedizin“ at the time – a noteworthy eulogy to the Swedish Doctor Henschen (22). The Internist Prof. Salomon Eberhard Henschen, Director of the Medical University Hospital in Uppsala who later worked at the famous Karolinska-Institute in Stockholm, via percussion (!) observed cardiac enlargement in cross-country skiers. He termed this observation athlete’s heart. His conclusions as well as his diagnostic sovereignty were impressive.

Henschen interpreted the large heart, which had generally been stigmatized as pathological to that time, as a physiological adaptation process when associated with increased performance capacity, primarily due to extensive endurance training.

Nonetheless, discussion of cardiac enlargement in athletes was controversially discussed in the decades that followed. Especially clinicians presumed myocardial damage, latent heart failure or recruitment of cardiac reserves. On the other hand, the pathologist Linzbach introduced the concept of physiological cardiac hypertrophy and defined a critical cardiac weight (14). He postulated that hearts enlarged by sports do not exceed a weight of 500g. The cardiologist and sports physician Reindell in Freiburg published his signpost monograph which presented the state-of-the art at the time and was expanded by numerous of his own, especially radiological and electrocardiographic , studies (17). He is considered the Father of Athlete’s Heart in Germany.

In the decades that followed, athlete’s heart was confirmed as a physiological adaptation process using echocardiography and other imaging procedures  (7, 18, 21, 23). Briefly stated, a marked increase in sports-related volume stress leads to physiological cardiac remodeling. The cardiac muscle mass increases, all cardiac cavities become enlarged, an excentric hypertrophy results (5, 9, 11, 20). In African/Afro-Caribbean  athletes, left ventricular hypertrophy is more pronounced (3). Athlete’s heart is a harmoniously enlarged heart (Fig. 1). In extreme cases, athlete’s hearts may become nearly double the size of normal hearts. On the other hand, not every type of high-performance sports leads to athlete’s heart, as long as the scope of the endurance training is limited, as it is in strength and speed sports. Athlete’s hearts are less common than is generally assumed.

While left ventricular muscle mass is predominantly determined in clinical cardiology, cardiac volume is customary in sports medicine to evaluate training-related adaptation. Since the 1980s, echocardiography has replaced radiological determination of cardiac size and can be repeated as required thanks to the lack of radiation exposure. In healthy hearts, there is high correlation between the two methods (6). Cardiac volume correlates with competition performance in endurance sports, but in individual cases, even athletes with only slightly enlarged hearts can achieve peak performance while athletes with very large hearts are not always the best in competition (8). Henschen’s claim that “the big heart wins” must thus be relativized.

Is there a special type of the athlete‘s heart in strength athletes? Morganroth et al. observed a concentric left-ventricular hypertrophy among shot-putters and wrestlers in 1975, and hypothesized that endurance and strength sports lead to different cardiac adaptations (15). The increased afterload due to elevated blood pressure at maximum strength stress is assumed to be the cause. Nowadays, there is some doubt about the dichotomous pattern of structural cardiac adaptations (25, 26). The chamber walls in strength athletes are not thicker than those of endurance athletes. The relative wall thickness, that is the relation between wall thickness and enddiastolic diameter of the left ventricle, shows no significant difference between untrained persons, endurance athletes and strength athletes (25). A frequently ignored confounder is possible anabolic abuse. The relevant studies provide either no or only rudimentary information. Anabolic-androgenic steroids can induce left-ventricular hypertrophy, often accompanied by impaired diastolic function (24, 25). Thickened chamber walls with normal-sized or even small left ventricle are suspicious for anabolic abuse, provided there is no pathological pressure stress or hypertrophic cardiomyopathy.

Athlete’s heart is often accompanied by electrocardiographic changes. Most of these were already described by Reindell in 1960 (17): sinus bradycardia, sinus arrhythmia, ectopic atrial rhythm, first-degree AV-block, second-degree AV-block (Mobitz Type I), incomplete right bundle branch block, elevated QRS voltages. They are also included in the latest international interpretation recommendations of athlete ECGs as physiological changes and required, if they are
asymptomatic, no further clarification. Early repolarization and convex ST segment elevation with subsequent negative T-waves in V1-V4 are rated physiological in Black athletes. Isolated negative T-waves may occur in 2-4% with athlete’s heart, but they must be clarified in order to rule out structural heart disease.

Since the millennium, possible cardiac damage due to extensive and extreme endurance sports has been discussed, that is typical stress for the development of athlete’s heart.  Extensive endurance training over many years may promote atrial fibrillation in male athletes in middle and advanced age (1, 13). Younger athletes, on the other hand, are not at increased risk for atrial fibrillation (16). Among other things, elevated parasympathic tone and atrial enlargement are discussed as causal mechanisms.

The function and structure of the right ventricle in endurance athletes is under controversial discussion (4, 12). Some studies have reported a reversible right-ventricular dysfunction following exhaustive endurance stress like marathon runs and triathlons. A possible development of arrhythmogenic right-ventricular cardiomyopathy due to years of extensive endurance training is speculated (12). A high increase of non-invasively-measured pulmonary arterial pressures with resultant high right-ventricular wall stress under exercise is assumed as an essential cause (12). However, the pulmonary arterial pressures measured with Swan-Ganz catheters in high-performance athletes at maximum exercise  are considerably lower (10). Moreover, it is assumed that extensive endurance sports may cause myocardial fibroses, since late enhancement has been found in individual endurance athletes (27). Finally, the findings of single observational studies do not prove sports-related damage, since other factors like interim illness, especially myocarditis, or abuse of performance-enhancing substances must be taken into account.

The transient increases in the cardiac markers Troponin I and T, along with BNP resp. NT-proBNP, observed especially after exhausting endurance exercise have also led to speculations about myocardial damage (19). At rest, the cardiac markers in athletes with and without athlete’s heart are not elevated. The exercise-induced increase in Troponin is probably attributable to that portion located in the zytosol of the cardiomyocytes, that is, not bound to the contractile proteins, making cell necroses unlikely. Otherwise it would be hard to imagine that an athlete’s heart could remain healthy over time. The exercise-induced increase of BNP resp. NT-proBNP is probably attributable to an increase in myocardial wall stress in addition to the increase in catecholamines.

In recent years, some studies have reported an increase in coronary calcification in endurance athletes in middle-age. On the other hand, most of the athletes in these studies performed with cardio-CT had normal calcification scores (2). Atherosclerotic plaques were most frequent in athletes with a high training level and several years of endurance training. These athletes had particularly stable plaques, so that a low risk of ruptures can be assumed. Shear forces in increased coronary blood flow during exercise, inflammation reactions and free radicals are discussed as mechanisms. The mortality in not elevated in athletes with a high training level and coronary calcification.
In conclusion it can be stated that athlete’s heart is a physiological adaptation with with increased performance. The heart is harmonically enlarged and excentrically hypertrophied. Prerequisite is extensive endurance training at a high level. Concentric hypertrophy, which is often interpreted as a special heart in strength-trained athletes must be eludicated. Possible damages have been discussed since the first description of athlete’s heart in 1899. More recent studies report possible right-ventricular damage, myocardial fibroses and increased coronary calcification. Prospective longitudinal studies are needed for a final evaluation. Epidemiological studies speak against cardiac damage, since they show that the life expectancy of successful national and international endurance athletes is not reduced, but rather increased.