Athletic heart syndrome

The human heart

Athletic heart syndrome, (AHS) also known as athlete's heart or athletic bradycardia, is a non-pathological condition commonly seen in sports medicine, in which the human heart is enlarged, and the resting pulse lowers, due to significant amounts of exercise, commonly aerobic exercise, and especially in endurance sports.

Athlete's Heart is common in athletes who routinely exercise more than an hour a day, and appears occasionally among heavy weight trainers. The condition is generally believed to be a benign, but may sometimes be hard to distinguish from other serious medical conditions. For example, the results of medical tests such as an electrocardiogram (ECG) can be mixed up with those of a serious heart disease by mistake.

Description

Athlete’s Heart is a result of dynamic physical activity such as (more than 5 hours a week) aerobic training or tennis, 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 40-70 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.

History

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.

Symptoms

Athlete's Heart most often does not have any physical symptoms, although an indicator would be a consistently low resting heart rate. In most cases, athletes do not realize they even have the syndrome until they go for their annual physical examination. The reason behind the "mystery" as to why there often are no symptoms when one’s heart is physically enlarged is because Athlete’s Heart is an adaptation of the body to the stresses of physical conditioning and aerobic exercise. When one is diagnosed with Athlete’s Heart, there are usually three characteristics that accompany the condition that would 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, or, in other words, more blood is being pumped out with each beat. With high cardiac output, the heart can allow itself to beat less, thus the bradycardia occurs. Another sign of Athlete’s Heart Syndrome is an S3 gallup, 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 gallup is heard, the patient should be given immediate attention. An S4 gallup 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.

According to recent research using imaging equipment capable of imaging the heart during exercise, the stroke volume of hearts of top athletes increases during exercise. This effect is absent in recreational athletes.

Diagnosis

AHS is usually diagnosed during a routine screening or during tests for other medical issues. An enlarged heart can be seen on an echocardiogram or sometimes a chest X-ray. Due to the similarities between AHS and more serious cardiac problems, an electrocardiogram (ECG) and exercise stress echo tests are sometimes performed. AHS and left ventricular hypertrophy are usually indistinguishable via EKG, however LVH is usually dismissed in the young and fit.

The EKG can detect sinus bradycardia, a resting heart rate of fewer than 60 beats per minute. This is often accompanied by sinus arrhythmia. The heartbeat of a person with AHS can sometimes be irregular while at rest, but usually returns to normal after exercise begins.

One common cardiovascular disease that has similar EKG reads is hypertrophic cardiomyopathy, which is characterized by the thickening of the heart's walls. This genetic disorder is found in 1 out of 500 Americans and is responsible for thousands of sudden death cases every year. Of all sudden death cases, only about 8% are exercise-related. The following table shows 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

Features Distinguishing Athletic Heart Syndrome From Cardiomyopathy

The medical history of the patient (endurances sports) and physical examination (bradycardia, and maybe a third or fourth heart sound) can give important hints.

• Electrocardiography (EKG) - typical findings in resting position are for example sinusbradycardia, atrioventricular block (I° and II°) and right bundle branch block - all those findings normalize during exercise
• X-ray examination of the chest shows an increased heart size
• Echo cardiogram - the differentiation between physiological and pathological increases of the heart's size is possible especially by estimating the mass of the wall (not over 130 g/m²) and its end diastolic diameter (not much less 60 mm) of the left ventricle.

Prognosis

Although the heart experiences structural changes (i.e. wall thickening) that are common with some cardiac disease, no unfavorable effects are evident. 80% of people affected by this syndrome show a decrease in such structural changes and in bradycardia with detraining. Unfortunately, the lack of long-term data limits the ability to determine whether or not the remaining 20% of people who do indeed have residual chamber enlargement have experienced any negative side effects.

Athlete’s Heart is not dangerous for athletes, but if a non-athlete has the symptoms of bradycardia, cardiomegaly, and cardiac hypertrophy, another possible illness is present. It is very important not to confuse Athlete’s Heart with the reason that some athletes have Sudden Unexpected Death (SUD) during or shortly after a workout. In many cases there are no signs that an athlete will experience SUD, but it is always due to an underlying heart disease and not Athlete’s Heart.

Treatment

No treatment is required for people with athletic heart syndrome. Athlete’s Heart does not pose any physical threats to the athlete, and there have been no negative long term effects tied to Athlete’s Heart.^{[citation needed]} 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 a differential diagnosis is difficult, typical treatment is deconditioning the athlete from exercise for a period of three months. During this time, the heart will return to its regular size. This deconditioning is usually met with resistance since it is changing the athlete’s lifestyle. The only risky aspect of Athlete’s Heart is if an athlete or non-athlete simply assumes that they have the condition, instead of making sure it is not 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 (Reggie White, Wes Leonard), 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 low-cost 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 practicioners, 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: immediate activation of the emergency response system, CPR (approximately 100 beats per minute; respirations may or may not be given, depending on the level of training), automatic (or manual, if trained) defibrillation in an effort at cardioversion and restoration of normal sinus rhythm, and if trained, administration of intravenous epinephrine or amiodarone (if not contraindicated, and only if initial defibrillation efforts fail; following the first shock and then the first injection, a second defibrillation, and then, another medication injection may be tried again; amiodarone was removed from the protocol for asystole treatment because of relative lack of effectiveness). 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 cardiac sinus rhythm. In any case, even if the cardiac event resolves quickly with few complications and emergency transport does not ensue, an urgent visit to the hospital or to one's physician or cardiologist is needed to narrow down the potential cause and ensure that, through testing, the heart and blood flow were not significantly and/or permanently impaired. Such incidents must never be downplayed or ignored, because the outcome of future episodes may not be so fortunate. Brugada syndrome

See also

• Left ventricular hypertrophy
• Cardiomyopathy
• Aerobic exercise
• Exercise intensity