Sports and heart disease. The special heart of an athlete: changes and recovery after stopping training

An athlete's heart is different from that of an ordinary person. Insufficient recovery of a champion often leads to overtraining, which causes disruption of long-term adaptations. A person may experience problems with sleep, appetite and performance, and apathy may occur. This condition is often caused by athlete's heart syndrome, which can be fatal.

The term "athletic heart" refers to the combination of functional and structural changes found in people who exercise for more than 1 hour each day. This phenomenon does not cause subjective complaints and does not require serious treatment. However, it is important to distinguish it from other dangerous diseases.

Signs of an athlete's heart

Increased physical activity increases the number of heart contractions. With constant exercise, the heart becomes more efficient and switches to economical energy consumption, while the heart rate (HR) does not increase significantly. This happens due to the fact that the organ increases in size, the pulse slows down and the force of contraction increases.

Often, athletes experience a breakdown of the adaptation mechanism, in which the heart cannot bear the heavy load. A person experiences the following symptoms:

Bradycardia. Characterized by sleep disturbances, poor appetite, and difficulty breathing. A person may experience pressing pain in the chest, concentration of attention decreases. He does not tolerate stress well and is periodically dizzy. Often such complaints are associated with infections present in the body. If the pulse drops to 40 beats, an examination of the organs should be performed.
Hypertrophy. A constant increase in intracardiac pressure causes an increase in the muscle layer. It manifests itself in the form of an increase in the size of the atria, disturbances in the conduction of impulses, and increased excitability of the heart muscle. The athlete experiences dizziness, chest pain, and shortness of breath.
Arrhythmia. With heavy loads, there is a physiological increase in the tone of the parasympathetic system. This condition causes various heart pathologies: ventricular extrasystole, atrial fibrillation, tachycardia. The athlete may experience chest pain, rapid heart rate, and shortness of breath. He appears to be in a pre-fainting state.
Hypotension. Athletes' blood pressure levels are lower than ordinary people. This occurs due to decreased peripheral arterial resistance and is often accompanied by bradycardia and low heart rate. Hypotension can cause loss of energy, headache and dizziness.

A person may not notice these changes, but soon complaints of dizziness and decreased performance appear. He begins to tire quickly and is bothered by fatigue. Over time, other pathologies develop and electrical instability of the tissue occurs, which leads to death.

Sudden cardiac arrest can occur against the background of improperly designed training, a sharp increase in workload, stress and depression, or exercise after an illness. Provoking factors are hereditary predisposition and use of doping agents.

The heart makes itself felt in former champions too. A person who has stopped training is subject to disturbances in autonomic influences on the heart. This condition manifests itself in the form of heart rhythm disturbances, shortness of breath, discomfort and congestion in the arms and legs.

Sometimes athlete's heart syndrome occurs in children. In young men, the vascular network is not as well developed as in men. Their body is not always ready for an ever-increasing load. The vessels cannot keep up with the increasing myocardial hypertrophy. This causes various heart pathologies in a child whose parents sent him to big-time sports.

Types of sports heart

There are two types of sports heart:

Physiological.
This type is characterized by the following indicators: pulse no more than 60 beats per minute, moderate sinus arrhythmia, bradycardia at rest. The physiological athletic heart is able to increase the amount of blood per minute by increasing stroke volume.
Pathological.
This type involves a change in the heart under the influence of physical stress. In this case, the organ is subjected to excessive load, which exceeds the reserve capabilities of the person. In this case, the athlete experiences a doubling of heart volume and severe tachycardia.

In order to promptly identify pathological changes in the functioning of the organ, it is important to undergo regular examinations using modern diagnostic methods.

Measures to identify pathology

In case of complaints about the functioning of the heart, it is necessary to undergo examinations and consult a doctor. Diagnosis includes echocardiography, ECG and stress testing. Additionally, 24-hour Holter ECG monitoring or stress echocardiography are used. It is impossible to diagnose athlete's heart syndrome on your own.

Often signs of pathology are detected during examination of other organs or during routine screening. It is important to be able to distinguish this syndrome from disorders caused by similar manifestations and posing a threat to life, for example, coronary artery disease.

Treatment

No specific therapy is required if there are no:

pain;
fainting;
ischemia;
arrhythmia;
increased fatigue;
conduction disturbance.

In this case, the changes are considered physiological. As a means of prevention, the following may be prescribed:

Beta blockers.
Adaptogens.
Vitamin and mineral complexes.
Nutritional supplements.

In case of serious cardiac dysfunction, complex treatment is carried out using cardiotonics, antihypertensive and antiarrhythmic drugs.

Proper nutrition plays an important role, especially for young athletes. The menu should contain a sufficient amount of protein, be rational and quite high in calories. You should eat foods rich in vitamins and minerals.

The diet must include the following products:

cottage cheese;
vegetables;
fruits;
fish;
meat;
juices

In advanced cases, surgical intervention and complete abstinence from sports activities are indicated, sometimes requiring the installation of a pacemaker.

Contraindications for sports activities

There is a list of diseases that prevent access to sports. These include the following heart pathologies:

Defect (congenital and acquired).
Rheumatic diseases.
Hypertension.
Ischemic disease.

Children are contraindicated from playing sports in the following cases:

infections of teeth and ENT organs;
arrhythmia;
valve prolapse;
myocarditis;
heart disease;
chronic pathologies of internal organs;
cardiopsychoneurosis;
VSD with a crisis course;
age up to 6 years.

Doctors must monitor the health of athletes. Their work includes the following activities.

It's no secret that an athlete's heart is different from the heart of an ordinary person. Instead of 50-70 ml per contraction, it “pumps” up to 200 ml, and instead of pumping out about 5 liters per minute (normal for ordinary people in a calm state), the sports “pump” is capable of pumping up to 40 liters per minute (at a heart rate of 190-200) .

Who can know the athletic heart as well as one who specializes in this organ? Smolensky A.V., Doctor of Medical Sciences, Professor, Academician of the Russian Academy of Natural Sciences, Director of the Research Institute of Sports Medicine of the Russian State University of Physical Culture.

If these numbers don't give you a clear idea of what the athletic heart can do, try imagining four buckets that need to be emptied or refilled in just one minute! Estimate how long this will take if you use a regular water tap. Are you impressed now?

Adaptation is the main sports word.

As you know, the task of any training is to initiate adaptations in the body. The heart, like everything else, adapts to heavy loads. These adaptations can be of a different nature, but most often they are associated with hypertrophy (increase in size) of the left ventricle. Many people know about two types of hypertrophy, which for simplicity are called L-hypertrophy (increase in internal volume) and D-hypertrophy (increase in wall thickness). In fact, there are three possible types of changes in the heart associated with heavy loads: concentric hypertrophy, eccentric hypertrophy and concentric remodeling (see figure and table).

Each of these types of changes corresponds to its own set of signs that distinguish the changed heart from the organ of an ordinary healthy person (not an athlete). The first two types of changes, so to speak, are normal, but the third type is bad.

However, characterizing different types of changes in this way, it should be noted that any left ventricular hypertrophy of LVH is considered by modern medicine as an independent risk factor for the occurrence of pathologies that can manifest with age. Therefore, it is often said that once a person has formed a sports heart, he should continue playing sports in at least some form throughout his life.

As long as normal athletic form is maintained, the likelihood of problems occurring is low (on the contrary, an athletic person is healthier). However, with the transition to a sedentary lifestyle, the likelihood of problems increases, the most common of which is hypertension. And over the years it can give rise to a whole cluster of secondary diseases.

Why do athletes die?

Trying to justify that professional sport is harmful to health, examples of deaths among active athletes are often cited as evidence, without specifying their causes. It turns out that since a person played sports, that means he died from it. there are statistics that objectively indicate the causes of deaths in sports. So in the diagram we see, that the main cause of such deaths is a disease that has genetic causes: hypertrophic cardiomyopathy (abbreviated as HCM). It accounts for 36% of all known deaths in sports. This is one of the few diseases for which exercise is strictly contraindicated. To reliably detect HCM, it is necessary to take a sample of heart tissue for analysis. However, there are a number of signs revealed by simultaneous analysis of ECG and EchoCG, which make it possible to make a preliminary diagnosis and prescribe an unpleasant control procedure to confirm it. The prevalence of HCM in the population is approximately two cases per 1000 people. This means that every five hundredth person cannot seriously engage in sports, only physical education.

Another 17% of total sports deaths are caused by coronary artery abnormalities. It is also a hereditary disease, which is widespread, for example, in certain regions of Italy. This is very rare in Russia.

If you look further through this list, you will notice that most deaths are associated with one or another hereditary disease, and only a small number of them are associated with sports activities, and even then, first of all, not with heavy loads, but with various ways to increase performance. Translated from neat medical to colloquial: “There is no need to dope or manipulate blood”.

Separately, it is worth mentioning the mortality rate of children and adolescents during sports. The largest number of such deaths are associated (again) NOT with high load, but with thoracic concussion. It is a shake of the heart or a blow to the chest that is the most common cause child mortality in sports. This is the risk of any increased activity in which the described traumatic effects can be obtained: falling, colliding with obstacles, and so on.

Insufficient recovery and overtraining.

Let's continue talking about the heart. Insufficient recovery of athletes during the training process very often leads to overtraining. There are more than enough signs by which this condition can be identified - any doctor working with athletes will accurately determine them. And qualified athletes themselves know about existing control methods.

Overtraining causes disruption of long-term adaptations (for which the athlete trains). In the most severe cases, this further leads to neuroendocrine disorders and nervous overstrain, then to disturbances in organ function and primary stress damage to the myocardium. In a word, this is no joke!

The most common causes of overtraining are:
- weekly increase in loads by more than 10%,
- increasing the duration of the period of intense exercise to 3 weeks or more,
- inclusion of more than one type of intensive developmental work in one training session,
- insufficient recovery between developmental training sessions,
- early specialization in children's sports.

Primary signs of self-control: sleep and appetite disturbances, increased resting pulse, apathy, changes in normal blood pressure, decreased libido. Methods of medical control - based on blood tests with assessment of hormone levels.

Monitoring the condition of the heart.

Under particularly heavy loads typical of professional sports, almost all high-level athletes have certain changes in the myocardium. These changes can be both physiological (a normal result of adaptation) and pathological (diseases, including hereditary ones). It is worth recalling where we started: left ventricular hypertrophy is considered by modern medicine as an independent risk factor. However, this hypertrophy, as we remember, can be different: most often it is normal, but sometimes it is “bad”.

Taking into account such risks, it should be considered extremely important to periodically monitor the condition of the heart, and if there is the slightest suspicion of any serious abnormalities, conduct a more detailed examination. This is especially important after suffering “flu-like” illnesses (after which the likelihood of heart complications is very high) or when an unreasonable arrhythmia is detected.

Both smell like myocarditis (inflammation of the myocardium).

Athletes diagnosed with myocarditis should be suspended from training for up to six months, no matter how terrible a sentence this may seem. The conclusion that training can be continued is made only on the basis of a comprehensive examination of the heart, which will show that no clinically significant abnormalities have been detected.

Heart changes associated with professional sports, in some cases (especially in strength sports) lead to the fact that by middle age or older age (after the end of a sports career) people face the problem of high blood pressure. Quite often in such cases, one of the effective ways to combat the disease is to return to sports, but in a gentle manner. Therefore, many strength athletes (where these problems are most acute) continue to go to the gym at 50 and 60 years old. Of course, without the kind of stress that they allowed themselves during their professional sports activities.

The information below is primarily for specialists, however, do not forget that “Saving drowning people...” often becomes a problem for these same “... drowning people,” so it is useful to at least have this information just in case. So, signs of a normal athletic heart...

But, for comparison, signs of “bad” changes that can occur in athletes...

Source of information: www.1-fit.ru (2014).

Why might young athletes experience sudden cardiac arrest?

What physiological and pathological changes do sports activities lead to? Natalya Ivankina, a cardiologist of the highest category (Penza Regional Clinical Hospital named after N.N. Burdenko), talks about what happens to the heart during intense exercise.

Risk of sudden death

This is interesting! The US National Registry of Sudden Death in Young Athletes records up to 115 cases per year, i.e. every three days a young athlete dies in the United States. Football comes first statistically. In one season in 2004, three players died directly in football competitions: Cameroon national team midfielder Mark Vivien Foe, Slovenian goalkeeper Nejan Botonjic, Hungarian national team player Miklos Feher. In Russia, there are no statistics on cases of sudden death in athletes. But many remember the Olympic champion, figure skater Sergei Grinko, who died during training at the age of 28, and the hockey player Alexei Cherepanov, who died at the age of 19 during a match from cardiac arrest.

How the heart reacts to sports stress

The heart has a unique ability to adapt to constant and intense physical activity. Adaptive mechanisms are launched - and morphological and electrophysiological changes in the myocardium gradually occur. They allow you to develop energy that is inaccessible to an untrained heart, and produce high athletic results.

Changes in the condition of the heart that occur during sports are called “sports heart” in medicine. There are two options for this condition:

the heart is more efficient, adapted to high physical activity

heart pathologically altered as a result of excessive sports activities

Adaptive mechanisms in response to intense physical activity include:

Improving capillary blood circulation in the heart muscle, both due to the expansion of existing capillaries and due to the opening and development of new ones.

Physiological increase in heart mass. At the same time, the energy capabilities of myocardial cells and its contractility (strength and speed of heart contractions) increase.

Physiological enlargement of the cavities of the heart, leading to an increase in its capacity. During physical activity, this allows you to increase the amount of blood that the heart ejects in one contraction (stroke volume) - and therefore improve the blood supply to internal organs and skeletal muscles. And reduce the energy costs of the myocardium.

In a state of muscular rest and under moderate loads, the athletic heart functions more economically, which is manifested by a decrease in the number of heart contractions, up to 60-40 per minute, a slowdown in the speed of blood flow, and a tendency to lower blood pressure. At the same time, the duration of diastole, the phase during which the myocardium relaxes, increases. The heart rests most of the time, so energy costs and myocardial oxygen demand are reduced.

At maximum loads, the number of heart contractions can reach 200-230 beats, the amount of blood that the heart pumps per minute reaches 30-40 liters. Under such colossal loads, regulatory mechanisms are activated that facilitate the work of the heart due to the effective redistribution of blood, dilation of the blood vessels of working muscles, reducing resistance to blood flow, developing additional collateral blood circulation, and increasing the absorption of oxygen by tissues. All this is the result of a long-term adaptive reaction.

When does sport lead to pathological changes in the myocardium?

Failure of adaptation, with the gradual development of pathological changes in the heart, occurs if:

Sports activities do not have a system and are accompanied by exorbitant loads.
Physical activity is given against the background of infectious diseases.
There are genetic prerequisites for the development of maladjustment.
Various pharmacological drugs are used, including doping agents.

How pathological changes manifest themselves

It is quite obvious that the physiological dilatation of the athletic heart is limited to acceptable limits. Excessive cardiac volume (more than 1200 cm3), even in endurance athletes, may result from physiological dilatation becoming pathological. A significant increase in heart volume (sometimes up to 1700 cm3) indicates pathological processes in the heart muscle.

Under the influence of prolonged physical activity, contractile protein synthesis is activated, which leads to thickening of the walls of the heart. A progressive increase in myocardial mass has a number of unfavorable aspects.

Firstly, in hypertrophied myocardium, the growth of arteries and capillaries begins to lag behind the increase in the size of cardiomyocytes, which leads to a deterioration in the blood supply to the myocardium.

Secondly, with severe hypertrophy, the ability to completely relax the myocardium is lost, its elasticity decreases, and its contractility is impaired.

Thirdly, the volume of the atria increases, which is an unfavorable factor for development. The appearance of hypertrophic changes of a maladaptive nature should be considered as a risk factor for sudden death.

Despite the fact that a slower rhythm leads to more economical work of the heart, with severe bradycardia - less than 40 heart beats per minute - athletes experience a decrease in performance. In addition, at night, when all people experience a decrease in heart rate, in athletes it can be so pronounced that brain hypoxia occurs. Therefore, athletes with a contraction rate below 55 beats per minute should undergo additional medical evaluation, especially if they have experienced intermittent weakness, dizziness, or episodes.

A number of athletes experience a decrease in blood pressure of less than 100/60 mmHg, which can be either an adaptive reaction or a disorder of adaptation. The presence of low pressure may not manifest itself in any way and may be discovered by chance. If low blood pressure is detected, a medical examination is necessary.

It is important! The danger lies in the fact that the transition from a physiological sports heart to a pathological one occurs gradually and is almost imperceptible to the athlete himself. In addition, even with development, the disease can be asymptomatic for a long time.

Athletes may eventually develop cardiomyopathy. Doctors distinguish 4 clinical variants:

Asymptomatic, in which the athlete may not be bothered by anything other than decreased performance, fatigue after training, and mild . The main research method for the asymptomatic clinical variant is echocardiography, which reveals signs of myocardial hypertrophy and a decrease in its distensibility during diastole.
Arrhythmic variant, in which various rhythm and conduction disturbances are detected. Most often, athletes have arrhythmias such as extrasystoles and paroxysmal tachycardias. For a long time, these rhythm disturbances may not be of significant concern, but if intense training continues against their background, then severe electrical instability of the myocardium may develop, which will result in sudden death. Some athletes have “suppressed sinus node syndrome” with the development of bradycardia (sparse rhythm) - with a heart rate of less than 40 per minute. This condition is reversible, and for most athletes it disappears with the cessation of intense physical activity. To identify this variant of cardiomyopathy, Holter monitoring is used.

Cardiomyopathy with tension in the contractile function of the myocardium, manifested by delayed recovery after exercise. In such athletes, during exercise, despite an increase in heart rate, the amount of blood ejected by the heart per minute increases slightly or even falls. Some athletes may experience a drop in blood pressure during physical activity. The main method for identifying this variant is stress echocardiography.

A mixed option, combining various manifestations of the above options.

How to diagnose "athletic heart"

In order to promptly notice the occurrence of maladaptive changes, regular examination of athletes is necessary, which includes electrocardiography and echocardiography. If necessary, additional methods such as daily Holter electrocardiogram monitoring and stress echocardiography are used.

Recently, the issue of molecular genetic examination of elite athletes has been increasingly discussed, since it is believed that pathological myocardial hypertrophy more often develops in individuals with disorders at the gene level (DD genotype of the ACE gene).

Almost every sport involves sacrifice. Sacrifice your own health. Boxers suffer from the consequences of blows, powerlifters suffer from torn backs, torn muscle ligaments and tendons. Bodybuilders experience a large imbalance in hormones and very often end up on the operating table in the fight against gynecomastia. But there is one disease that is characteristic of all sports, and it does not depend at all on the specifics of training, but rather, it is associated with improperly organized training. No, this is not rhabdomyliosis, it is much worse - athlete's heart. Its consequences lead every 5th athlete astray from the path to Olympus.

What it is?

Let's look at what a sports heart is from a physiological point of view. Athletic heart is a traumatic-pathological change in cardiac contractile tissue, characterized by the presence of scar connective tissue. These are actually scars on the muscle that interfere with the normal and healthy contraction of the heart.

As a result, this leads to an increase in the load on the main channels, chronically increasing blood and intracranial pressure. Impairs the susceptibility of the main contractile structures to oxygen. Reduces life expectancy. Increases the risk of heart attack and stroke. And this is not a complete list of what sports heart syndrome can lead to.

Most often it manifests itself in athletes, however, for athletes with many years of experience, its consequences are not as catastrophic as for beginners. The thing is that over the years of training, the body adapts and increases the volume of contractile tissue in order to compensate for damage to the heart muscle and scar disconnected connections. However, if an athlete spends his entire life training at the limit of his capabilities, then, most likely, a heart attack as a result of athlete's heart syndrome will cause his death.

A sad fact: one of the most famous athletes of our time, who died precisely from sports heart, due to a long-term violation of the training plan combined with the use of anabolic steroids, is Vladimir Turchinov, who passed away before reaching the age of 60.

How does it work?

A sports heart results from improper planning of the training process. It usually begins to develop in adolescence. The thing is that usually all the main sections associated with speed-strength sports have a group structure. This makes it easier for the trainer and more profitable commercially. And when a newcomer comes to an already established group, he is usually subjected to similar stress as those who have been studying for several years.

This causes:

Overtraining;
Chronic malaise;
Damage to the immune system;
Damage to liver cells.

But the most important thing that comes out is a sports heart. The thing is that every athlete who begins his training usually forms the intensity of the load depending on how he feels. Typically, health can be easily determined by two factors:

The amount of sugar in the blood. It determines the overall oxygen level. When sugar is low, the athlete begins to feel nausea, weakness and dizziness.
Pulse.

And it is the pulse that is responsible for the formation of a sports heart. The formation mechanism is extremely simple. Due to the beginner’s unpreparedness for serious loads, heart rate often rises above the fat burning zone. The heart is feverishly trying to cope with stress. At these moments, you can observe pumping, and sometimes even painful sensations in the chest area. However, the worst thing is that the heart, as a result of receiving microtraumas, begins to be overgrown not with ordinary muscle tissue, which helps improve the strength of contractions, and, therefore, in the future not experience overload, but with connective tissue.

What does this lead to?

The total volume of the heart muscle increases as the working surface decreases.
Connective tissue often partially blocks the coronary artery (which can later lead to a heart attack);
Connective tissue prevents the full amplitude of contraction.
With an increase in volume and a decrease in the force of contractions, the heart receives a consistently higher load.

As a result, once a mechanism is started, it is very difficult to stop.

Unfortunately, training is not always the factor in the development of a sports heart. Very often, hypoxia of the heart muscle and increased load occurs in the following cases:

Caffeine abuse;
Abuse of energy drinks;
Cocaine use (one-time or on an ongoing basis);
Using powerful fat burners based on clenbuterol and ephedrine (for example,).

As a rule, any of these factors combined with moderate-intensity training can lead to catastrophic results that will irreversibly affect the quality and duration of life.

Types of sports heart

A sports heart can be classified according to the following indicators:

How long ago the connective tissue was obtained;
Volume of affected areas;
Location of damaged areas.

On average, the classification is determined by the following table:

Disability category	Recency of obtaining connective tissue	Volume of affected area	Location of damaged areas	Possibility of surgical treatment
Normal person	Absent	Absent, or less than 1%	Far from major arteries	Not required
Minimal damage	Recent scarring can be stopped by reducing stress	From 3 to 10%	Far from major arteries	Not required
Experienced athlete	Long-standing scars to which the heart muscle has adapted by increasing the total volume of contractile tissue.	From 10 to 15%	Far from major arteries	Bypassing and cutting out sections is possible.
Disabled person of the first group		Over 15%
Disabled person of the second group	Not important. Extensive scars that interfere with the full contraction of the heart muscle	Over 20%	Partially blocks key arteries, interfering with normal blood flow at rest	Bypassing and cutting out sections is possible. High risk of death
Critical level of damage	Not important. Extensive scars that interfere with the full contraction of the heart muscle	Over 25%	Partially blocks key arteries, interfering with normal blood flow at rest	Impossible. It is recommended to install a pacemaker or use a heart muscle donor

How to diagnose?

Diagnosis of athlete's heart is possible only under the conditions of echocardiography. In addition, you will have to additionally pass a load test. It is not possible to independently determine athlete's heart syndrome.

However, if you notice one of the symptoms characteristic of sports heart, you should urgently consult a doctor:

Bradycardia;
Causeless tachycardia;
The appearance of pain during cardio;
Decreased strength endurance;
Chronic increase in blood pressure;
Frequent dizziness.

If any of them is detected, you need to find out the cause of its appearance in order to prevent the development of sports heart as a pathology in general.

Contraindications to sports

The only way to stop the development of athlete's heart syndrome is to temporarily stop physical activity for up to 5-6 years. What does this lead to? Everything is very simple. As a result of optimizing the body for modern needs, part of the connective tissue may be destroyed in the process of reducing muscle contractile fibers. This will not get rid of all the damage, but it can reduce its volume to 3%, which will allow it to function normally.

If you are a serious athlete and have discovered the first signs of athlete’s heart syndrome, you should first of all reconsider your training program.

The first step should be to purchase a heart rate monitor. During training, the pulse should not touch the fat-burning zone even at peak moments, which means that for a long time you will have to change the profile of your main training in order to increase endurance and the strength of heart contractions. Only after you carry out special cardio training (moderate cardio in the pulse zone of muscle tissue hypertrophy without pumping), and reduce your base heart rate by more than 20%, can you gradually return to the standard training regimen.

No, this does not mean that you need to completely eliminate barbell work. However, intensity, speed, number of sets, weight and recovery time should be reduced as much as possible. Only by rolling back your results for a long time can you gradually achieve them again without harm to the heart muscle. However, some sports (especially all-around strength) are simply contraindicated for athletes with this disease.

Treatment methods

There are several main ways to treat athlete's heart. However, none of them will completely eliminate this syndrome forever. The thing is that damaged areas, like the lungs of a smoker, even with complete recovery, will never function as before.

Surgical intervention.
Complete loss of motor abilities.
Drug strengthening of the heart muscle.
Increasing the useful volume to compensate for non-working areas.
Installation of a pacemaker.

The most effective early treatment for athlete's heart syndrome is an integrated approach, which affects the reduction of physical activity with general strengthening due to drug intervention. In second place is an increase in the useful volume of the heart. It is with this factor that experienced athletes compensate for the mistakes of youth and damage associated with overtraining of the body.

However, if changes in cardio-contractile tissues are pathological, or scar-connective tissue partially blocks important arteries, then the classical method of treatment will no longer help. Only forced catabolism is possible (an extremely dangerous undertaking that can end in unpleasant consequences), or surgical intervention.

Today, the practice of surgical laser removal of damaged tissue is more common than even 10 years ago. However, the chances of successful surgery for injuries in key areas of the contractile muscle are still much less than 80%.

Installation of a pacemaker may only be suitable for those people who suffer from sports heart, coupled with age-related degenerative changes in the soft tissues of the ventricles.

The only effective method that can completely eliminate sports heart syndrome is a donor heart transplant.

Therefore, it is easier to prevent it than to then, 10 years after the end of your sports career, go under the surgeon’s knife and risk your own life due to improperly planned training complexes.

To summarize

A sports heart is not a death sentence. As a rule, the majority of young men who began to engage in strength athletics early have total injuries of up to 10%, which absolutely do not interfere with them in everyday life due to adaptation. However, if the duration of your injuries is short, this is a reason to identify errors in the training method, and most importantly, to remove them for the purpose of prevention. It is quite possible that for this it will be enough to add creatine phosphate on an ongoing basis, or take a course of preventative medications for the heart muscle. Sometimes reducing the intensity of your training is enough.

In any case, if you begin to control your heart rate and not reach high engine speeds, you will be able to avoid sports heart disease, which means that your life expectancy, as well as the prevention of other pathologies of heart disease, will increase significantly.

Remember - physical education helps improve your own health, but sports always make its followers disabled. Therefore, even if you are intensively preparing for a new Crossfit challenge, you should not overwork yourself. After all, no sporting achievements or awards are worth your life.

When treating dystrophic changes, it is necessary to take into account their genesis.

In case of excessive exposure to catecholamines on the myocardium, the use of beta-blockers is recommended, and in case of insufficient catecholamine exposure, levodopa (a precursor of catecholamines).

The use of drugs that improve myocardial metabolism is also indicated: Rhythmocor, Cardioton, ATP-LONG, ATP-forte, Potassium orotate, Folic acid, Calcium pangamate, anabolic steroids, Cocarboxylase, multivitamins, pyridoxal phosphate, vitamin B12, Riboxin, carnitine preparations.

Preventive pharmacotherapy of the early stages of chronic physical overstrain of the heart involves the use of drugs that, in their action, can be regarded as activating the synthesis of nucleic acids and proteins, normalizing electrolyte balance, and having an adrenolytic effect. However, their purpose should be differentiated depending on the presence of the predominant factor - dilatation and/or hypertrophy, since this involves influencing the main pathogenetic mechanism of manifestations of the “sports” heart - systolic and/or diastolic function of the myocardium.

In the case of predominance of myocardial hypertrophy, assessed by the mass of the left ventricular myocardium and the myocardial mass index, over dilatation, the use of metabolic drugs that enhance plastic processes in the myocardium should be limited, since at the stage of a pathological “athletic” heart the development of hypertrophy may increase. In this case, drugs with an energizing effect are indicated that enhance the formation of ATP and creatine phosphate, which are necessary to enhance both systole and diastole. For this purpose, preparations of adenosine triphosphoric acid and its coordination compounds that provide a more stable effect are recommended - ATP-LONG, ATP-forte, Egon. The mechanism of action of these drugs is based on the effect on the purinergic receptors of the heart, which leads to the limitation of calcium “overload” of myocytes, vasodilation of the coronary arteries, reduction of afterload and economization of cardiac activity. In addition, coordination complexes are less susceptible to deamination by adenosine deaminase, which provides a prolonged effect, in contrast to adenosine triphosphoric acid. Metabolic products ATP-LONG and ATP-forte are capable of activating intracellular de novo ATP synthesis through the stage of formation of purine bases.

The action of creatine phosphate (Neoton) is based on the suppression of 5-nucleotidase activity, which leads to a decrease in the breakdown of ATP in cells, especially in red blood cells. Creatine phosphate preparations, through de novo synthesis, increase the pool of intracellular creatine phosphate, helping to enhance myocardial contractile activity. More attractive from this point of view are chelated compounds of creatine phosphate with magnesium ions (Reaton), which ensures higher effectiveness of the drug, since in the form of a chelate complex it is less susceptible to destruction and can be used in the form of tablets containing 0.5 g of the active substance. Reaton is the first tableted chelate complex of creatine phosphate.

To enhance energy processes in the myocardium, the use of lipoic acid is indicated, which takes part in the synthesis of acetyl-coenzyme A, which reduces the amount of lactate produced and increases the formation of pyruvic acid, which is an active energy substrate. An increase in energy production and a decrease in the accumulation of lactate in myocardiocytes is inherent in cocarboxylate and especially in its chelate form with magnesium ions - Alactone. The drugs affect the alternative pathway for energy production in myocytes, activating the transketolase reaction of the pentose phosphate shunt for glucose oxidation.

Another drug that directly affects the reactions of the pentose phosphate shunt is Rhythmocor. Rhythmocor contains gluconic acid in the form of magnesium and potassium salts. The bioavailability of the drug is about 95%, which avoids the side effects of magnesium on the gastrointestinal tract, since the absorption of other magnesium drugs from the gastrointestinal tract does not exceed 40%. Gluconic acid stimulates the pentose phosphate pathway of glucose oxidation in the myocardium, increasing energy production in the myocardium and skeletal muscles and helps reduce the severity of clinical and ECG manifestations of the “athletic” heart syndrome, and also significantly improves physical performance. Rhythmocor also has an antiarrhythmic effect, which allows us to consider it as a means of pathogenetic therapy for mitral valve prolapse.

It should be noted that magnesium in the form of a salt of gluconic acid is found in the preparation Cardioton, which also contains folic acid and hawthorn extract (vitexin glycoside). The latter has moderate cardiotonic activity, which differs in its mechanism of action from cardiac glycosides, which makes it possible to use Cardioton for mitral valve prolapse, including with a “sports” heart. Vitexin, which is included in cardioton, realizes its effect through strengthening the adaptive Frank-Starling mechanism, and not through an increase in calcium ions in myocardiocytes, which distinguishes it favorably from cardiac glycosides, which are contraindicated in the case of diastolic dysfunction in a “sports” heart.

To enhance energy processes, the use of L-carnitine preparations is indicated. By improving the utilization of fatty acids, carnitine reduces energy deficiency by stimulating the formation of ATP in mitochondria. In addition, carnitine preparations can increase the ejection fraction without affecting the development of myocardial hypertrophy. Carnitine can also reduce acidosis.

In case of a “sports” heart, the prescription of drugs containing respiratory enzymes - cytochrome C (Cytomac) and Coenzyme Q10 Compositum is also justified. The drugs improve tissue respiration by influencing electron transport in the mitochondrial respiratory chain and enhance oxidative phosphorylation.

In case of severe hypertrophy and development of systolic dysfunction of the myocardium and concomitant cardiac arrhythmias, as well as in persons with sympathicotonia, the administration of beta-blockers is indicated. Their use is contraindicated in case of bradycardia (heart rate less than 55 beats/min); if necessary, dose selection should be titrated and take into account the fact that beta-blockers are included in the list of drugs prohibited by WADA.

In case of a dilated form of an “athletic” heart, in addition to energy-acting drugs, the prescription of drugs that affect the plastic metabolism of the myocardium may be justified.

It is generally accepted to prescribe Methyluracil in combination with folic acid and vitamin B12. Another regimen includes Potassium orotate, cocarboxylase and vitamin B15. If there is a heart rhythm disorder, Rhythmocor or Panangin is added to the above-described regimens. It is also possible to prescribe anabolic steroids. By enhancing protein biosynthesis, they are able to increase the mass of the myocardium, normalizing the ratio of the mass of the ventricular myocardium to the size of the cavities. The drugs have different androgenic-anabolic indexes, which should be taken into account when using them. The drugs are contraindicated in adolescence. It should be remembered that anabolic steroids are classified as doping drugs, so their prescription must be strictly justified and only for therapeutic purposes!

To prevent chronic overexertion syndrome in athletes, the use of various multivitamin regimens is also proposed (Seifulla, 1999). There are also known attempts to develop methods for the prevention of chronic overexertion syndrome in young athletes using adaptogens of plant origin (Polysol-2, Antihypoxin), methods of physical rehabilitation, as well as the use of antioxidants (Ascorbic acid, Tocopherol acetate, Methionine) (Polyakov, 1994; Azizov, 1997; Aidaeva, 1998).

The effectiveness of therapy with magnesium preparations has been shown for manifestations of disadaptation to physical activity, while the use of Magnesium orotate helps to increase physical performance in athletes (Dzhalalov, 2000; Bogoslav, 2001).

Preparations containing magnesium (Magne-forte, Ritmokor, Magne-B6, Magnerot) are most justified in the presence of tonogenic dilatation. Natural antagonists of calcium ions, they help reduce the “calcium” overload of myocytes, thereby improving the diastolic function (relaxation) of the myocardium, which leads to activation of the Frank-Starling mechanism and increased contractile function. In case of severe diastolic dysfunction, it is possible to use dihydropyridine calcium channel blockers (Amlodipine, Lacidipine). However, their pronounced hemodynamic (BP-lowering) effect should be taken into account. Therefore, it is better to give preference to magnesium-containing drugs. In addition, some drugs have a pronounced antiarrhythmic effect (Ritmokor, Magnerot), which allows their administration to prevent cardiac arrhythmias. These drugs do not affect the heart rate, so they can be prescribed for bradycardia.

With tonogenic dilatation, it is possible to use drugs that inhibit the carnitine-dependent mechanism of fatty acid oxidation - Trimetazidine, Ranolazine. However, their use should be of a course nature. It should be remembered that with the hypertrophic form of the “athletic” heart, their use is inappropriate.

In recent years, the homeopathic method has been increasingly used to prevent and eliminate the consequences of the negative effects of intense sports on the body. This method has no scientific basis. Homeopathic remedies have been shown to be completely ineffective in clinical trials. And the people who use them, as a rule, are victims of charlatans.

It should be noted that cardiac pathology can also appear in teenage athletes. Young athletes with a pathological “sports” heart should be under constant supervision of a cardio-rheumatologist.

In addition, Quercetin, Lipin, Glycine, Tanakan, etc. are used.

The correct training regimen is of great importance in preventing the development of pathological “sports” heart.

The scientific substantiation of sports training regimes in childhood, adolescence and youth is important (Khrushchev, 1991).

This also applies to the physical health program. The threshold value of exercise intensity that provides a minimal health effect is considered to be work at the level of 50% of VO2max or 65% of the maximum age-related heart rate (corresponds to a heart rate of about 120 beats/min for beginners and 130 beats/min for trained runners). Training at a heart rate below these values is ineffective for developing endurance, since the stroke volume of blood in this case does not reach its maximum value and the heart does not fully use its reserve capabilities.

Metabolic drugs in pediatric practice (S.S. Kazak, 2006)

Name	Doses and routes of administration
Actovegin (Solcoseryl)	Orally 1 tablet three times a day or 2-5 ml intravenously in a stream or drip in 100 ml of isotonic sodium chloride solution every 24 hours - 10 days
ATF-LONG	60-80 mg per day
Inosine (Riboxin)	Inside 1-2 tablets. (200-400 mg) three times a day for 4-6 weeks or 5-10 ml of a 2% solution IV in a stream or drip once a day, 10-14 days
Potassium orotate	20 mg/kg per day orally in three divided doses
Lipoic acid	Inside, 1-2 tablets. Two to three times a day
Magnesium orotate	Inside, 1 tablet. (500 mg) twice daily for 6 weeks
Magne-B 6	Inside 1 tablet. or 1/2 ampoules (5 ml) twice a day
Mega-L-carnitine	Orally 1 ml (0.5 g of carnitine) once or twice a day
Mildronate	1 drop inside. (250 mg) once or twice a day for 2-3 weeks or 1.0-2.5-5.0 ml parenterally (50 mg/kg) 10% solution per day, course 5-10 days
Neotone (phosphocreatinine)	1-2 g intravenously in 200 ml of 5% glucose solution once or twice a day. Course dose 5-8 g
	Orally 10-20 mg/kg three times a day for 2-3 weeks or 2-5 ml IV slowly or drip in a 5-10% glucose solution
Preducgal (Trimetazidine)	Inside 1/2 table (20 mg) three times a day
Cytochrome C	0.5 mg/kg per day (4-8 ml of 0.25% solution) intravenously in 200 ml of 5% glucose solution once a day
Carnitine chloride	20% solution up to 6 years - 14 drops, after 6 years - from 25 to 40 drops two to three times a day for 3-4 weeks
Phosphaden	1 mg/kg up to 6 years twice a day, after 6 years three times a day or 2% solution 25 mg/kg per day intramuscularly two to three times a day for 10-14 days
Rhythmocore	Capsules 0.36 g, children over 6 years old By 1 drop. Twice a day, over 12 years - 1 drop, three times a day

Consequently, the range of safe loads that have a training effect in health-improving physical education, depending on age and level of preparedness, can range from 120 to 150 beats/min. Training with a higher heart rate in recreational running cannot be considered advisable, since it has a clear sports focus. This is confirmed by the recommendations of the American Institute of Sports Medicine (AISM).

When choosing training loads for young athletes, the characteristics of their hemodynamics should be taken into account. So, according to I.T. Korneeva et al. (2003), at rest in young athletes with a normokinetic type of blood circulation, the chronoinotropic mechanism is practically not involved in ensuring cardiac output, and athletes with this type of blood circulation should be considered as insufficiently adapted to perform endurance work. For young athletes with a hyperkinetic type of blood circulation, volumetric, low-intensity loads should be recommended, and for young athletes with a normokinetic type of blood circulation, an increase in the volume of loads in a gentle increasing mode.

The problem of the physiological and pathological “sports” heart remains relevant and in modern conditions is caused by increasing physical and psycho-emotional stress in sports, intense struggle during competitions, and a high level of sports achievements. A properly developed training process under medical supervision with adequate pharmacological support makes it possible to prevent the development of a pathological “sports” heart and maintain the health of athletes.