Sports heart

Sports heart - a set of structural and functional changes that occur in the heart of people who exercise for more than 1 hour almost every day. The condition does not cause subjective complaints. Manifestations include bradycardia and / or systolic murmur. Often there are changes in ECG data. The diagnosis is established clinically or by echocardiography. There is no need for treatment. The sports heart matters because it must be distinguished from serious heart diseases.

[1], [2], [3], [4], [5], [6], [7]

Pathogenesis

Intensive long-term training of endurance and stability leads to physiological adaptation of the organism and the heart in particular. The volume of the left ventricle (LV) and the pressure in it increase, which over time leads to an increase in the muscle mass of the left ventricle, wall thickness and its size. Maximum stroke volume and cardiac output increase, contributing to a lower heart rate at rest and a longer diastolic filling time. Lower heart rate occurs primarily due to increased vagal nerve tone, but other factors that can reduce the activity of the sinus node may be important. Bradycardia reduces myocardial oxygen demand; at the same time, the total hemoglobin content and the ability of the blood to transport large amounts of oxygen increase. Despite these changes, systolic and diastolic functions remain normal. Structural changes in women are usually less pronounced than in men of the same age, body weight and fitness.

[8], [9], [10], [11], [12], [13], [14], [15], [16], [17], [18], [19], [20], [21]

Symptoms of the athletic heart

There are no subjective complaints. The manifestations are variable, but may include the following:

• bradycardia ;
• the push of the left ventricle, which is shifted to the left, increases and increases in amplitude;
• the noise of systolic ejection on the left at the lower border of the sternum;
• III heart tone (S ₃ ), arising from an early, rapid diastolic filling of the ventricles;
• IV heart tone (S ₄ ), which is best heard at rest against the background of bradycardia, since the diastolic time of filling the ventricles is increased;
• hyperdynamic pulse in the carotid arteries.

These symptoms reflect structural changes in the heart resulting from adaptation to intense physical exertion.

[22], [23]

Diagnostics of the athletic heart

Symptoms are usually found during routine screening or screening for other reasons. Most athletes do not need extensive diagnostics, although an ECG is necessary. If symptoms indicate heart disease, an ECG, echocardiography, and stress test are performed.

Athletic heart - the diagnosis of exclusion; it must be distinguished from disorders that cause similar manifestations, but are life-threatening (for example, hypertrophic or dilated cardiomyopathy, ischemic heart disease, arrhythmogenic dysplasia of the right ventricle).

An ECG reveals sinus bradycardia, sometimes a heart rate of less than 40 per minute. Sinus arrhythmia often accompanies a small heart rate. Bradycardia at rest can predispose to an increase in the frequency of atrial or ventricular arrhythmias, including atrial rhythm driver migration and (rarely) atrial fibrillation, but pauses after ectopic impulses do not exceed 4 s. Atrioventricular (AV) blockade of I degree is found in approximately one third of athletes. II degree of AV-blockade (mainly type 1), appearing at rest, but disappearing under load, is less common. Level III AV-blockade - pathological condition and indication for further examination. Changes in ECG data include a high voltage of the QRS complex with altered teeth or tooth relationships reflecting left ventricular hypertrophy, and early depolarization disorders with biphasic teeth in the anterior leads that reflect non-uniform repolarization with a decrease in sympathetic nervous system tone at rest. Both changes disappear under load. Deep inversion of the prong in the anterolateral leads and incomplete blockade of the right leg of the bundle of His are also possible. Changes in ECG data are weakly correlated with the level of fitness and work of the cardiovascular system.

Echocardiography helps distinguish the sports heart from cardiomyopathy, but there is no clear boundary between the physiological and pathological expansion of the heart. In general, the changes determined by echocardiography correlate poorly with the level of fitness and work of the cardiovascular system. Often reveal small mitral and tricuspid regurgitation.

During the load test, the heart rate remains below normal at a submaximal load, increases accordingly and is comparable to people who are not involved in sports, at maximum load. HR is quickly restored after the end of the load. The reaction of blood pressure is normal: systolic blood pressure increases, diastolic blood pressure drops, the average blood pressure remains relatively constant. Many changes in resting ECG data diminish or disappear during exercise; This finding is unique and pathognomonic for the sports heart syndrome, in contrast to pathological conditions. However, the pseudonormalization of the inverted T wave may reflect myocardial ischemia, so further examination of older athletes is necessary.

Features that distinguish sports heart syndrome from cardiomyopathy

Indicator	Sports heart	Cardiomyopathy
LV hypertrophy *	<13 mm	> 15mm
Final diastolic diameter of LV	<60mm	>70мм
Diastolic function	Normal (ratio E: A> 1)	Abnormal (ratio E: A <1)
Hypertrophy of the septum	Symmetrical	Asymmetric (with hypertrophic cardiomyopathy)
Family history	Not burdened	Can be burdened
BP response to stress	Normal	Normal or reduced systolic blood pressure response
Physical deterioration	Regression of LV hypertrophy	LV hypertrophy does not regress

* Range A from 13 to 15 mm indefinite. Range A from 60 to 70 mm indefinite. The ratio E: A is the ratio of the values of the early and late flow rates through the mitral valve.

[24], [25], [26], [27], [28], [29], [30], [31], [32]

Treatment of the athletic heart

It is not necessary to treat the sports heart, although it may take a 3-month interval of lack of training to detect regression of left ventricular hypertrophy in order to distinguish this syndrome from cardiomyopathy. Such an interval of lack of training can significantly contradict the life plans of an athlete and cause his resistance.

[33], [34], [35]

Forecast

Although structural changes in the heart are pronounced and resemble those of some heart diseases, no adverse effects develop. In most cases, structural changes and bradycardia regress after stopping training, although up to 20% of high-class athletes have a residual expansion of the heart chambers, which is a debatable issue, since there are no long-term data on whether the sports heart is in fact a benign condition.

[36], [37]