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|Classification and external resources|
The human heart
|Classification and external resources|
The human heart
Athletic heart syndrome, (AHS) also known as athlete's heart, athletic bradycardia or exercise-induced cardiomegaly is a non-pathological condition commonly seen in sports medicine, in which the human heart is enlarged, and the resting heart rate is lower than normal.
Athlete's heart is common in athletes who routinely exercise more than an hour a day, and occurs primarily in endurance athletes, though it can occasionally arise in heavy weight trainers. The condition is generally believed to be a benign one, but may sometimes be hard to distinguish from other serious medical conditions. For example, on the results of an electrocardiogram (EKG) athletic heart syndrome may be mistakenly interpreted as evidence of serious heart disease.
Athlete's heart most often does not have any physical symptoms, although an indicator would be a consistently low resting heart rate. Athletes with AHS often do not realize they have the condition unless they undergo specific medical tests. This is because athlete's heart is a normal, physiological adaptation of the body to the stresses of physical conditioning and aerobic exercise. People diagnosed with athlete’s heart commonly display three signs that would usually indicate a heart condition if they were seen in a non-athlete: bradycardia, cardiomegaly, and cardiac hypertrophy. Bradycardia is a slower than normal heartbeat around 40–60 beats per minute. Cardiomegaly is the state of an enlarged heart. Cardiac hypertrophy is the thickening of the muscular wall of the heart, specifically the left ventricle, which pumps oxygenated blood to the aorta. In highly trained athletes' bodies, more blood and oxygen is required to the peripheral tissues of the arms and legs. A larger heart results in higher cardiac output, as more blood is pumped out with each beat. The raised cardiac output allows the heart to beat more slowly (hence the bradycardia).
Another sign of athlete's heart syndrome is an S3 gallop, which can be heard through a stethoscope. This sound can be heard as an irregularly shaped heart is filling with blood. The diastolic pressure creates a disordered flow of blood into the heart. However, if an S4 gallop is heard, the patient should be given immediate attention. An S4 gallop is a stronger and louder sound created by the heart if it is diseased in some way. It is typically a sign that there is a serious heart condition present in the athlete.
Athlete's heart is a result of dynamic physical activity such as (more than 5 hours a week) aerobic training, rather than static training such as weight lifting. During intensive prolonged endurance or strength training, the body signals the heart to pump more blood through the body to counteract the oxygen deficit building in the skeletal muscles. Enlargement of the heart is a natural physical adaptation of the body to deal with the high pressures and large amounts of blood that can affect the heart during these periods of time. Over time, the body will increase both the chamber size of the left ventricle, and the muscle mass and wall thickness of the heart.
Cardiac output, the amount of blood that leaves the heart in a given time period (i.e. liters per minute), is proportional to both the chamber sizes of the heart and the rate at which the heart beats. With a larger left ventricle, the heart rate can decrease and still maintain a level of cardiac output necessary for the body. Therefore, it is very common for athletes with AHS to have lower resting heart rates than nonathletes.
The heart becomes enlarged, or hypertrophic, due to intense cardiovascular workouts, creating an increase in stroke volume, an enlarged left ventricle (and right ventricle), and a decrease in resting pulse along with irregular rhythms. The wall of the left ventricle increases in size by about 15–20% of its normal capacity. There is no decrease of the diastolic function of the left ventricle. The patient may also experience an irregular heartbeat and a resting pulse rate between 40–60 beats per minute, also known as bradycardia.
The level of physical activity in a person determines what physiological changes the heart makes. There are two types of exercise: Static (strength-training) and dynamic (endurance-training). Static exercise consists of weight lifting and is mostly anaerobic, meaning the body does not rely on oxygen for performance. It also moderately increases heart rate and stroke volume (oxygen debt). Dynamic exercises are running, swimming, skiing, and cycling, which rely on oxygen from the body. This type of exercise also increases both heart rate and stroke volume of the heart. Both static and dynamic exercises involve the thickening of the left ventricular wall due to increased cardiac output, which leads to physiologic hypertrophy of the heart. It has been shown that once athletes stop training, the heart returns to its normal size.
Athlete's heart is usually an incidental finding during a routine screening or during tests for other medical issues. An enlarged heart can be seen at echocardiography or sometimes on a chest X-ray. Similarities at presentation between athlete's heart and clinically relevant cardiac problems may prompt electrocardiography (ECG) and exercise cardiac stress tests.
The ECG can detect sinus bradycardia, a resting heart rate of fewer than 60 beats per minute. This is often accompanied by sinus arrhythmia. The pulse of a person with athlete's heart can sometimes be irregular while at rest, but usually returns to normal after exercise begins.
It is important to distinguish between athlete's heart and hypertrophic cardiomyopathy, a serious cardiovascular disease characterized by thickening of the heart's walls, which produces a similar ECG pattern at rest. This genetic disorder is found in 1 out of 500 Americans and is a leading cause of sudden cardiac death in young athletes (although only about 8% of all cases of sudden death are actually exercise-related). The following table shows some key distinguishing characteristics of the two conditions.
|Feature||Athletic Heart Syndrome||Cardiomyopathy|
|Left ventricular hypertrophy||< 13 mm||> 15 mm|
|Left ventricular end-diastolic diameter||< 60 mm||> 70 mm|
|Diastolic function||Normal (E:A ratio > 1)||Abnormal (E:A ratio < 1)|
|Septal hypertrophy||Symmetric||Asymmetric (in hypertrophic cardiomyopathy)|
|Family history||None||May be present|
|BP response to exercise||Normal||Normal or reduced systolic BP response|
|Deconditioning||Left ventricular hypertrophy regression||No left ventricular hypertrophy regression|
Athlete's heart is not dangerous for athletes (though if a non-athlete has symptoms of bradycardia, cardiomegaly, and cardiac hypertrophy, another illness may be present). Athlete's heart is not the cause of sudden cardiac death during or shortly after a workout, which mainly occurs due to hypertrophic cardiomyopathy, a genetic disorder.
No treatment is required for people with athletic heart syndrome. Athlete's heart does not pose any physical threats to the athlete and, despite some theoretical concerns that the ventricular remodeling might conceivably predispose for serious arrhythmias, there is no evidence of any increased risk of long-term events. It is recommended that the athlete see a physician and receive a clearance to be sure that the symptoms are due to athlete’s heart and not another heart disease, such as cardiomyopathy. If the athlete is uncomfortable with having athlete's heart or if a differential diagnosis is difficult, deconditioning from exercise for a period of three months will allow the heart to return to its regular size. However, one long-term study of elite trained athletes found that dilation of the left ventricle was only partially reversible after a long period of deconditioning. This deconditioning is often met with resistance to the accompanying lifestyle changes. The real risk attached to athlete's heart is if an athlete or non-athlete simply assumes that they have the condition, instead of making sure they do not have a life-threatening heart illness.
Due to the fact that several well-known and high profile cases of athletes experiencing sudden unexpected death due to cardiac arrest, such as Reggie White and Marc-Vivien Foé, there is a growing movement to make an effort to have both professional and school-based athletes screened for cardiac and other related conditions, usually through a careful medical and health history, a good family history, a comprehensive physical examination including auscultation of heart and lung sounds and recording of vital signs such as heart rate and blood pressure, and increasingly, for better efforts at detection, such as an electrocardiogram.
An electrocardiogram (ECG) is a relatively straightforward procedure to administer and interpret, compared to more invasive or sophisticated tests; it can reveal or hint at many circulatory disorders and arrhythmias. Part of the cost of an ECG may be covered by some insurance companies, though routine use of ECGs or other similar procedures such as echocardiography (ECHO) are still not considered routine in these contexts. Widespread routine ECGs for all potential athletes during initial screening and then during the yearly physical assessment could well be too expensive to implement on a wide scale, especially in the face of the potentially very large demand. In some places, there is a shortage of funds, portable ECG machines, or qualified personnel to administer and interpret them (medical technicians, paramedics, nurses trained in cardiac monitoring, advanced practice nurses or nurse practitioners, physician assistants, and physicians in internal or family medicine or in some area of cardiopulmonary medicine).
If sudden cardiac death occurs, it is usually because of pathological hypertrophic enlargement of the heart that went undetected or was incorrectly attributed to the benign "athletic" cases. Among the many alternative causes are: episodes of isolated arrhythmias which degenerated into lethal VF and asystole, and various unnoticed, possibly asymptomatic cardiac congenital defects of the vessels, chambers, or valves of the heart. Other causes include carditis, endocarditis, myocarditis, and pericarditis whose symptoms were slight or ignored, or were asymptomatic.
The normal treatments for episodes due to the pathological look-alikes are the same mainstays for any other episode of cardiac arrest: Cardiopulmonary resuscitation, defibrillation to restore normal sinus rhythm, and if initial defibrillation fails, administration of intravenous epinephrine or amiodarone. The goal is avoidance of infarction, heart failure, and/or lethal arrhythmias (ventricular tachycardia, ventricular fibrillation, asystole, or pulseless electrical activity), and so ultimately to restore normal sinus rhythm.
The athlete's heart was first described in 1899 by S. Henschen. He compared the heart size of cross-country skiers to those who lived sedentary lives. He noticed that those who participated in competitive sports displayed symptoms of athlete’s heart syndrome. Henschen believed the symptoms were a normal adjustment to exercise, and felt there was no need for concern. Henschen believed that the entire heart became enlarged, when in fact it is only the left side that becomes hypertrophic. He also believed athletes with AHS lived shorter lives than those who did not acquire the syndrome. Because his research occurred throughout the 19th century, technology was limited, and it became difficult to come up with appropriate ways to measure the hearts of athletes. Few believed in Henschen’s theory about athletes having larger hearts than those who did not participate in sports. Today, Henschen’s original theory has proved to be correct.