By Medifit Biologicals



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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.



Athletic heart syndrome is a heart condition that may occur in people who exercise or train for more than an hour a day, most days of the week. Athletic heart syndrome isn’t necessarily bad for you — if you’re an athlete. And it’s not what makes young athletes expire in mid-court. While it does lead to structural changes in the heart, a person with the condition usually doesn’t notice any symptoms. Athletic heart syndrome doesn’t require treatment and is important to diagnose only to rule out heart problems that are serious.

Like any other muscle, the heart gets stronger with exercise. Endurance exercises such as jogging, swimming, and cycling can make the organ bigger, allowing it to pump more blood with every beat. Short, intense workouts such as weight lifting further increase the pumping power by thickening the walls of the heart.

Just as body builders sculpt their abs and biceps into highly unusual shapes, many hard-core, competitive athletes develop extraordinary hearts. Not only is the heart extra large and thick, it also may produce some irregular rhythms (arrhythmia). A person with athletic heart syndrome may also have a markedly slow resting heart rate, in the range of 35 to 50 beats a minute. In addition, electrical impulses can take strange routes across the heart, causing abnormal readings on an electrocardiogram (ECG or EKG). Together, these changes produced by exercise are called athletic heart syndrome.



The concept that the cardiovascular system of trained athletes differs structurally and functionally from others in the normal general population remarkably extends over a century. During that time, there has also been periodic controversy about the true nature of athlete’s heart, ie, whether the findings are physiologically adapted, benign, and related only to training, or alternatively are potentially pathological and the harbinger of disease and disability.

running men on the background of the chart heartbeat. 3d

The clinical entity of athlete’s heart has been defined with increasing precision using a variety of techniques. Henschen is credited with the first description in 1899, using only a basic physical examination with careful percussion to recognize enlargement of the heart caused by athletic activity in cross-country skiers. Henschen concluded that both dilatation and hypertrophy were present, involving both the left and right sides of the heart, and that these changes were normal and favorable: “Skiing causes an enlargement of the heart which can perform more work than a normal heart.”

Subsequent investigators used quantitative chest radiography to show that heart size was increased in athletes, particularly those engaged in endurance sports with large aerobic requirements. Some early observers even regarded the heart of the trained athlete to be weakened owing to the “strain” created by continuous and excessively strenuous training and believed that athletes were subject to deteriorating cardiac function and heart failure.



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Cardiovascular adaptations to exercise have been systematically defined and differ with respect to the type of conditioning: endurance training (sometimes also described as dynamic, isotonic, or aerobic) such as long-distance running and swimming; and strength training (also referred to as static, isometric, power, or anaerobic) such as wrestling, weightlifting, or throwing heavy objects. Sports such as cycling and rowing are examples of combined endurance and strength exercise. Most athletic disciplines to some extent combine endurance and strength modes of physical conditioning, and training-related physiological alterations represent a complex set of central and peripheral mechanisms operating at structural, metabolic, and regulatory levels.

Acute responses to endurance exercise training include substantial increases in maximum oxygen consumption, cardiac output, stroke volume, and systolic blood pressure, associated with decreased peripheral vascular resistance. The immediate results of strength conditioning include only mildly increased oxygen consumption and cardiac output but substantial increases in blood pressure, peripheral vascular resistance, and heart rate.

Long-term cardiovascular adaptation to dynamic training produces increased maximal oxygen uptake due to increased cardiac output and arteriovenous oxygen difference. Strength exercise results in little or no increase in oxygen uptake. Thus, endurance exercise predominantly produces volume load on the left ventricle (LV), and strength exercise causes largely a pressure load.



The phenotypic overlap between exercise-induced cardiac remodeling and pathological structural heart disease is widely appreciated. Cardiac structural abnormality of unclear origin and significance may be detected during preparticipation cardiovascular disease screening, routine health examinations, or evaluation of the athlete with symptoms. Extreme cases of exercise-induced ventricular remodeling may be difficult to differentiate from mild forms of hypertrophic cardiomyopathy, familial or acquired dilated cardiomyopathy, and arrhythmogenic RV cardiomyopathy. The clinical task of differentiating marked exercise-induced remodeling from these important forms of disease remains important, with implications including sport restriction, pharmacological therapy, and placement of an implantable cardiac defibrillator.

The overlap between features of the athlete’s heart and characteristics of cardiomyopathy, specifically hypertrophic cardiomyopathy, that may affect young athletes has been coined the Maron gray zone. A valuable schema for approaching the athletic patient with LV hypertrophy of unclear origin has been presented, and remains useful in clinical practice. It is noteworthy that this diagnostic approach was developed at a time when noninvasive cardiovascular imaging was in its infancy and, for the most part, restricted to basic 2-dimensional echocardiography. Recent advances in cardiovascular diagnostics have proven to be useful additions to these original criteria.

Functional myocardial echocardiography, including tissue Doppler and speckle-tracking imaging, permits detailed and accurate assessment of myocardial function. Tissue Doppler imaging permits assessment of myocardial relaxation and contraction velocity. Across numerous studies, early diastolic relaxation velocity has been shown to be normal or increased in athletes with LV hypertrophy resulting from exercise-induced remodeling. In contrast, pathological forms of LV hypertrophy are typically associated with reduced early diastolic relaxation velocity and peak systolic tissue velocity. Tissue strain and strain rate may also provide useful insight into the origin of LV hypertrophy in athletes.

Cardiac magnetic resonance imaging has similarly emerged as an invaluable tool for the evaluation of the athlete with indeterminate cardiac enlargement. Cardiac magnetic resonance allows highly accurate assessment of myocardial thickness, chamber volumes, tissue composition, extracardiac anatomy, and cardiac magnetic resonance–derived reference values in athletes have been published. Importantly, the use of gadolinium contrast with delayed imaging provides information about the presence and location of myocardial fibrosis. Recent data document myocardial fibrosis patterns that are relatively specific to certain cardiomyopathies and highlight the utility of cardiac magnetic resonance for the assessment of indeterminate cardiac enlargement in the athlete. At the present time, we use cardiac magnetic resonance in athletes with either indeterminate echocardiographic imaging or clinical features that suggest a diagnosis that may not be definitively assessed by echocardiography (ie, myocarditis). The interested reader is referred to a recently published comprehensive review on this topic.

At the present time, there is no single diagnostic test with adequate accuracy for differentiating adaptive from pathological cardiomyopathy. Consequently, we encourage clinicians faced with this diagnostic dilemma to begin the assessment with an integrated consideration of personal and family medical history, 12-lead ECG, and echocardiography. In many cases, this relatively basic but informative triad will provide sufficient information for informed diagnostic decision making. In cases that remain unclear after this initial evaluation, further measures, including tissue Doppler echocardiography, speckle-tracking echocardiography, magnetic resonance imaging, cardiopulmonary exercise testing, prescribed detraining, and disease-specific genetic testing, may be considered.



Cardiological findings in athletes are often similar to those observed in clinical cases. Electrocardiographic and cardiac imaging abnormalities as well as physical findings may be the same in both of these groups. Bradycardia and rhythm disturbances are the most common abnormalities in athletes. Most athletes with abnormal electrocardiograms are asymptomatic and numerous investigators have failed to detect heart disease in association with such electrocardiograms. In contrast to cardiac dysfunction observed in clinical cases, enhanced or normal ventricular systolic and diastolic function have been reported in athletes. In endurance athletes, this is associated with very high values for maximal aerobic power (VO2max). Absolute and body size-normalised cardiac dimensions in most athletes do not approach values from chronic disease states, and may not exceed echocardiographic normal limits. In addition, pathological and physiological enlargement appear to be biochemically and functionally different. Myosin ATPase enzyme expression and calcium metabolism are different in rats with pathologically or physiologically induced enlargement. The reported biochemical differences underlie systolic and diastolic dysfunction in pathological enlargement. Conversely, trained rodents and humans have demonstrated enhanced systolic and diastolic function. It is important to note that cardiac enlargement observed in athletes is the result of normal adaptation to physical conditioning and/or hereditary influences. Conversely, pathological changes result from disease processes which can lead in turn to reduced function, morbidity and mortality. Since the mid 1970s echocardiography has been used to compare cardiac dimensions in male endurance- and resistance-trained athletes. A sport-specific profile of eccentric and concentric enlargement has been documented in endurance and resistance athletes, respectively. Subsequent studies of athletes have examined factors such as age, sex and degree of competitive success to determine their contribution to these sport-specific cardiac profiles. Unique athletic subgroups have also been analysed and have included ballet dancers, rowers, basketball players and triathletes. However, there is a paucity of data on cardiac dimensions in female athletes. Finally, physical conditioning studies have also examined echocardiographic dimensions before and after endurance and resistance training. Significant enlargement of internal dimensions, wall thickness or left ventricular mass have been reported but such increases are relatively small and by no means universal. Several conflicting explanations for enlarged cardiac dimensions appear in the literature. Chronic volume and pressure haemodynamic overloading during physical conditioning has been proposed to explain eccentric and concentric cardiac enlargement in endurance- and resistance-trained athletes respectively. However, twin studies suggest that hereditary factors may be important determinants of cardiac dimensions and/or the degree of cardiac adaptability to physical conditioning.

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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 exercisecardiac 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.

Regarding differential diagnosis, left ventricular hypertrophy is usually indistinguishable from athlete’s heart and at ECG, but can usually be discounted in the young and fit.

It is important to distinguish between athlete’s heart and hypertrophic cardiomyopathy, a serious cardiovascular disease characterised 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).



An enlarged heart, arrhythmia, and unusual ECG readings would all be signs of serious trouble for the average person. In fact, the rhythms and ECG readings associated with athletic heart syndrome often mimic life-threatening disorders. But athletic heart syndrome itself is harmless. The “abnormal” changes in the athlete’s heart are actually a testament to the body’s ability to adapt.

If an athlete has symptoms of chest pain, reports irregular beats, or has passed out, he or she should get a medical exam to pinpoint the problem. Your doctor may want to run extra tests to determine whether the symptoms are a normal sign of your body’s ability to adapt to training, or whether there’s some abnormality in your heart. These tests may include an electrocardiogram, sonogram (a picture of the heart using sound waves), or another type of test.

Of course, some athletes really do have heart trouble. Occasionally, seemingly healthy young basketball or football players drop dead in the middle of a game or a practice. In almost every case, doctors trace the death to an unsuspected condition, such as congenital heart disease, but one that has nothing to do with athletic heart syndrome.



Since athletic heart syndrome is harmless, there’s no reason to treat it unless you experience regular light-headedness, chest pains, or you lose consciousness. If you really want a “normal” heart again, all you have to do is stop exercising. Soon, your heart, along with the rest of your body, will sag back into its former shape. But why not keep everything extra strong and healthy for a while? You should be proud of your athletic body, heart included.

By Medifit Biologicals