Sports heart

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In sports medicine, an enlargement of the heart ( cardiomegaly ), which is caused by physical training in the context of competitive sports , in particular endurance sports , is referred to as the sports heart , athlete's heart or athlete's heart .

Intensive physical training leads to an increase in muscle mass ( muscle building ). This applies not only to the skeletal muscles , but also to the heart muscle . This hypertrophy of the heart muscle is considered to be an appropriate physiological response to increased stress. According to current scientific knowledge, the enlargement of the heart brought about by sport does not pose a health risk for the athlete.

In addition, there are typical pathological changes in the athlete, directly or indirectly caused by sport . These can be largely avoided through health monitoring appropriate to the increased exposure. Physiological and pathological changes can overlap.

History and title

In 1899, the Swedish doctor Salomon Eberhard Henschen diagnosed an enlarged heart in Finnish cross-country skiers before and after the competition by percussion of the chest . He concluded that an enlarged heart could do more than an untrained heart of normal size. This is called "athlete heart", "athlete heart", "sports heart" or "achievement heart". The English expression is athlete's heart. Medical scientists also observed that complete physical exhaustion was followed by additional enlargement of the heart, and assessed this as heart failure . This observation was considered incorrect for many years until, in 2000, echocardiographic examinations on triathletes after long-term physical exhaustion in the context of competitions were able to document a temporary enlargement of the left ventricle with reduced performance. The athlete's heart is only found in athletes with endurance training , and the more likely the more muscles they use.

training

The duration and type of exercise affect the extent to which the heart changes in size and structure. Short-term training is not yet able to influence the size of the heart, but it can improve the maximum oxygen consumption and the submaximal heart rate . Long-term training, on the other hand, creates an enlargement of the left ventricle, which disappears completely after the training has ended without any harmful effects. Although special types of training determine the structural changes in the heart muscle, the extent of the response to training varies considerably from person to person. In general, the heart rate at rest is significantly lower even in an average trained endurance athlete than in untrained people and can then be in the range of 30 to 50 beats per minute.

Eccentric and concentric hypertrophy

Isotonic , i.e. dynamic, athletes who train often develop eccentric heart muscle hypertrophy. The wall thickness increases slightly as does the end-diastolic volume, which means that the ratio of volume to wall thickness of the left ventricle remains normal.

In the pathological case, multiple heart valve insufficiencies are found more frequently in these athletes , and in the two leaflet valves, probably due to a stretching of their rings.

In contrast, athletes with isometric , i.e. static, training get concentric cardiac muscle hypertrophy, i.e. uniform wall thickening of all heart muscle sections in the left ventricle.

In concentric hypertrophy, there is no change in the flexibility ( compliance ) of the left ventricle, but this is different in athletes who take anabolic steroids . Studies have shown that these doping substances change normal physiological hypertrophy and lead to a pathological "stiffening" of the heart muscle. This reduction in the flexibility (compliance) of the left ventricle can represent a preliminary stage of diastolic heart failure.

Effects of exercise

There is no evidence that exercise can harm a healthy heart. On the contrary, training leads to an improved functional performance of the heart with a larger stroke volume and cardiac output . In addition, a decrease in sympathetic activity and, above all, an activation of the parasympathetic nervous system can be observed.

Physical examination

It is often difficult to distinguish physiological adaptation processes in athletes from changes with a disease value, which occur just as frequently in athletes as in the normal population. The simple physical examination and additional apparatus-based examination methods are used for this. The physical examination of competitive athletes reveals bradycardia at rest due to increased vagal tone and a particularly pronounced respiratory heart rate variation . As long as there are no symptoms associated with it, heart rates as low as 30 to 40 beats per minute can be tolerated. Also noticeable are a somewhat displaced heartbeat, a third and fourth heart sound (especially when lying down) and systolic heart murmurs - all normal for competitive athletes.

Apparative investigations

Electrocardiography (EKG)

For professional athletes are often found ECG -Changes. Corresponding to their increased vagal tone , these include sinus bradycardia with pauses and substitute rhythms as well as first and second degree atrioventricular block images of the Mobitz I type . These changes can easily be ended by physical exercise or the administration of atropine . Signs of left ventricular hypertrophy are the high amplitudes of the excitation curve. The pseudo-ischemic excitation regression disorder can simulate damage to the outer layer of the myocardium, such as that caused by a coronary circulatory disorder, or pericardial inflammation and should be further clarified by an exercise ECG.

roentgen

In the X-ray image of the chest is an enlargement of the heart showing a ratio of heart to the chest width of 0.5 to 0.6, which does not as in this case, pathologically is considered.

Echocardiography - heart echo

However, echocardiography is best suited to assess the dimensions of the heart . It is important to distinguish between physiological myocardial hypertrophy caused by exercise and congenital pathological hypertrophic cardiomyopathy (HCM), because HCM leads to a high rate of sudden cardiac death in younger people, especially during physical exertion . Asymmetrical hypertrophy of the left ventricle and a wall thickness over 13 mm, as it can be exceeded in endurance athletes such as racing cyclists or rowers, are suspect. In these cases, an examination of relatives and / or a temporary stop of exercise is recommended to see if the wall thickening regresses. If this does not occur or if there are unexplained sudden deaths in the family, HCM and thus a serious risk for the athlete are more likely. Echocardiography also reveals an enlargement of the heart cavities and helps to differentiate it from dilated cardiomyopathy . The end-diastolic diameter of the left ventricle usually remains below 55 mm, and rarely exceeds 65 mm in individual endurance athletes.

Exercise and heart disease

Pre-existing heart diseases occur in athletes, as in the average population. Serious incidents can also occur in competitive conditions with minor cardiac diseases.

In very rare cases with pronounced risk factors such as heavy nicotine abuse and severe lipid metabolism disorders and, above all, with a corresponding history of family members, coronary heart disease also occurs in younger athletes. Angina pectoris , heart attack, and sudden cardiac death are possible consequences.

Sudden cardiac death in hypertrophic cardiomyopathy occurs without warning symptoms . It is a congenital disease. In the case of abnormal ECG results, premature, unexpected and unclear deaths in the family and syncope, research must be carried out into this disease. By this disease affected people may not competitive sports exercise more.

Much more dangerous, but less common in Central Europe, is arrhythmogenic right ventricular cardiomyopathy , a congenital disease in the course of which it leads to fatty transformation. a. the right ventricle, and which can cause fatal cardiac arrhythmias during exercise. Competitive athletes with near-cardiac death have to train off and have a rhythm monitor implanted.

After feverish, banal infections, myocarditis can occur. Life-threatening cardiac arrhythmias can occur during physical exertion. A secondary disease is dilated cardiomyopathy , which can lead to fatal cardiac arrhythmias when exercised. Therefore, a longer break from training should be observed in the case of cardiac arrhythmias under stress and heart problems after infectious diseases.

Congenital heart diseases, such as anomalies in the coronary arteries, can trigger critical circulatory disorders in athletes. The aortic stenosis is a risk of disease for athletes.

Tall adolescent athletes, often basketball players and ballet dancers, can have latent Marfan syndrome and aortic rupture while exercising. In the case of sudden and severe heart pain, no time should be lost until this suspected diagnosis can be ruled out or confirmed in an emergency.

Ion channel defects , which today are counted among the primary cardiomyopathies, can lead to cardiac arrhythmias and sudden cardiac death during physical exertion.

swell

  1. ^ V. Fuster, W. Alexander, RA O'Rourke (Ed.): Hurst's The Heart. 11th edition. McGraw-Hill, New York 2004, ISBN 0-07-142264-1 , p. 2249.
  2. ^ R. Rost: The athlete's heart. Historical perspectives - solved and unsolved problems. In: Cardiol Clin. 15, 1997, pp. 493-512.
  3. ^ W. Kindermann : The sport heart. In: German magazine for sports medicine. 51, 2000, pp. 307-308.
  4. ^ LR Thomas, PS Douglas: Echocardiographic findings in athletes. In: PD Thompson (Ed.): Exercise and Sports Cardiology . McGraw-Hill, New York 2000, pp. 43-70.
  5. ^ AC Pearson et al.: Left ventricular diastolic function in weight lifters. In: Am J Cardiol. 58, 1986, pp. 1254-1259. PMID 2947454
  6. ↑ A. Urhausen et al .: One- and two-dimensional echocardiography in bodybuilders using anabolic steroids. In: Eur J Appl Physiol. 58, 1989, pp. 633-640. PMID 2731533
  7. ^ R. Engberding: Dilatative Kardiomyopathie. In: FA Flachskampf: Practice of echocardiography. The reference work for echocardiographic diagnostics. Georg Thieme Verlag, Stuttgart / New York 2002, p. 221.

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