Portal de Periódicos da CAPES

The Heart of Trained Athletes

2006; Lippincott Williams & Wilkins; Volume: 114; Issue: 15 Linguagem: Inglês

10.1161/circulationaha.106.613562

1524-4539

Barry J. Maron, Antonio Pelliccia,

Sport Psychology and Performance

HomeCirculationVol. 114, No. 15The Heart of Trained Athletes Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessReview ArticlePDF/EPUBThe Heart of Trained AthletesCardiac Remodeling and the Risks of Sports, Including Sudden Death Barry J. Maron and Antonio Pelliccia Barry J. MaronBarry J. Maron From the Hypertrophic Cardiomyopathy Center, Minneapolis Heart Institute Foundation, Minneapolis, Minn, and the Institute of Sports Medicine and Science, Rome, Italy. and Antonio PellicciaAntonio Pelliccia From the Hypertrophic Cardiomyopathy Center, Minneapolis Heart Institute Foundation, Minneapolis, Minn, and the Institute of Sports Medicine and Science, Rome, Italy. Originally published10 Oct 2006https://doi.org/10.1161/CIRCULATIONAHA.106.613562Circulation. 2006;114:1633–1644Young competitive athletes are widely regarded as a special subgroup of healthy individuals with a unique lifestyle who are seemingly invulnerable and often capable of extraordinary physical achievement.1–3 For more than 100 years, there has been considerable interest in the effects of intense athletic conditioning on the cardiovascular system.4–27 The advent of echocardiography more than 30 years ago provided a noninvasive quantitative assessment of cardiac remodeling associated with systematic training, and consequently, a vast body of literature has been assembled that is focused on the constellation of alterations known as "athlete's heart."4–27Athlete's heart is generally regarded as a benign increase in cardiac mass, with specific circulatory and cardiac morphological alterations, that represents a physiological adaptation to systematic training.1,6–27 However, the clinical profile of athlete's heart has expanded considerably over the last several years as a result of greater accessibility to large populations of trained athletes studied systematically with echocardiography, ECG, cardiac magnetic resonance, and ambulatory Holter ECG monitoring. As a consequence, there is increasing recognition of the impact that prolonged conditioning has on cardiac remodeling, which may eventually mimic certain pathological conditions with the potential for sudden death or disease progression.Over the last several years, sudden deaths of trained athletes, usually associated with exercise, have become highly visible events fueled by news media reports and with substantial impact on both the physician and lay communities.1,28–36 Interest in these tragic events has accelerated owing to their increased recognition; awareness that underlying, clinically identifiable cardiovascular diseases are often responsible; and the availability of treatments to prevent sudden death for high-risk athlete-patients. In the present review, we offer a comprehensive assessment of many issues that target the interrelation of intense physical exertion with cardiac structure and function, as well as the rare, potentially adverse consequences of sports.Athlete's HeartHistorical PerspectivesThe concept that the cardiovascular system of trained athletes differs structurally and functionally from others in the normal general population remarkably extends over a century.4 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.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.5 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."5Subsequent 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.4PhysiologyCardiovascular 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.37 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.Chamber MorphologyCardiac dimensional alterations associated with athletic training have been defined over the past 35 years in a number of cross-sectional echocardiographic (or cardiac magnetic resonance) studies, usually performed in highly trained individuals.1,6,9–26,38–42 The responses of individual athletes to systematic conditioning are not uniform. Training induces in ≈50% of trained athletes some evidence of cardiac remodeling, which consists of alterations in ventricular chamber dimensions, including increased left and right ventricular and left atrial cavity size (and volume), associated with normal systolic and diastolic function (Figure 1). For example, marked enlargement of the LV chamber (≥60 mm) occurs in ≈15% of highly trained athletes.10 This chamber enlargement may very occasionally be accompanied by a relatively mild increase in absolute LV wall thickness that exceeds upper normal limits (range 13 to 15 mm).9 LV remodeling with changes in mass is dynamic in nature and may appear to develop relatively rapidly, or more gradually, after the initiation of vigorous conditioning. Such changes, which are reversible with cessation of training, are most impressive in endurance athletes.18–20,27 However, there is considerable overlap in cardiac dimensions between a trained athlete population and age- and sex-matched sedentary controls.42 Athletes show relatively small (but statistically significant) increases of ≈10% to 20% for wall thickness or cavity size, and these values in most individual athletes remain within accepted normal limits.42Download figureDownload PowerPointFigure 1. Distribution of cardiac dimensions in large populations of highly trained male and female athletes. Top, LV end-diastolic cavity dimension; 14% of athletes have enlargement of 60 to 70 mm. Reproduced from Pelliccia et al10 with permission of the American College of Physicians. Copyright 1999. Middle, Transverse left atrial dimension; 20% of athletes have transverse left atrial dimension ≥40 mm. Reproduced from Pelliccia et al22 with permission of the American College of Cardiology. Copyright 2005. Bottom, Maximum (Max.) LV wall thickness; 2% of men and 0% of women have wall thickness ≥13 mm. Reproduced from Pelliccia et al9 with permission of the Massachusetts Medical Society. Copyright 1991.The pattern and magnitude of physiologically increased LV mass may vary with respect to the nature of sports training13,27,41 (Figure 2). One metaanalysis15 and also the large database assembled at the Institute of Sports Medicine and Science (Rome, Italy)9–11,20–22,39,41 support in part an earlier hypothesis6 that specific morphological adaptations and changes in LV mass result from systematic training in different sports disciplines. The most extreme increases in cavity dimension or wall thickness have been observed in those elite athletes training in rowing, cross-country skiing, cycling, and swimming,9–11,20–22,26,39,41 whereas limited data in athletes participating in ultraendurance sports (such as triathlons) paradoxically show more modest alterations in cardiac dimensions.1,12 Of note, some misunderstanding persists as to whether strength training alone results in LV hypertrophy. Such sports are associated with only mildly increased wall thicknesses (often disproportionate relative to cavity size), whereas absolute values uncorrected for body surface area usually remain within the accepted normal range (≤12 mm; Figure 2).1,15,38,39,41,42Download figureDownload PowerPointFigure 2. Effect of specific sports training on LV cavity dimension or wall thickness in elite athletes, representing 27 different sporting disciplines. X-Country indicates cross-country; L.D. Running, long-distance running.Increases in LV cavity size and calculated mass associated with athletic training are determined in part by body surface area (or lean body mass).9–11,13 Larger athletes (particularly men) will generally demonstrate greater absolute LV cavity and wall thickness dimensions. However, the relative contributions of demographic and environmental or genetic determinants to LV remodeling in trained athletes has long been a subject of controversy.43 Data assembled in large athlete populations assessed with multivariate analysis show that 75% of variability in LV cavity size is attributable to nongenetic factors, such as body size, type of sport, gender, and age, with body surface area the largest of these components10 (Figure 3). The remaining 25% of cavity size variability is otherwise unexplained10,43 and possibly caused in small part by genetic factors. Indeed, recent investigations in trained athletes have demonstrated an association between LV remodeling (and increased LV mass in response to training) and the angiotensin-converting enzyme gene I/D (ACE I/D) and/or angiotensinogen (AGT M/T) polymorphisms.43,44 There is no compelling evidence linking the magnitude of training-related cardiac dimensional changes in athletes with the level of performance during competition. Download figureDownload PowerPointFigure 3. Impact of different clinical variables on LV end-diastolic cavity dimensions in a large population of male and female elite athletes. The relative impact of the examined variables (body size, gender, age, and type of sport) are shown here as a proportion of overall variability in LV cavity size.Left atrial remodeling is an additional physiological adaptation frequently present in highly trained athletes, most commonly those in combined static and dynamic sports (ie, cycling and rowing), and is largely explained by associated LV cavity enlargement and volume overload.22 Increased transverse left atrial dimensions (≥40 mm) are present in 20% of athletes and more substantially enlarged dimensions (≥45 mm) are evident in 2%. These latter dimensions overlap with those observed in patients with cardiac disease (Figure 1). Nevertheless, left atrial enlargement in athletes appears to be benign and largely confined to training in endurance sports, and is only rarely associated with atrial fibrillation ( 35 or 40 years) are caused predominantly by atherosclerotic coronary artery disease.1 Primary ventricular tachyarrhythmias are the mechanism of the vast majority of sudden deaths in athletes, with Marfan syndrome and aortic dissection the exceptions.An alternative demographic profile has emerged from the Veneto region of northeastern Italy in which ARVC61 is reported to be the most common cause of athletic field deaths.36 Such a predisposition to ARVC, which contrasts sharply with the US experience, could be based on a unique genetic substrate or the consequence of the long-standing Italian national preparticipation screening program,62 or both. Such systematic screening is less likely to identify and disqualify from competition athletes with ARVC than those with diseases more readily identified by screening, such as HCM.63DemographicsSudden cardiovascular death may occur in a wide variety of more than 30 competitive athletic disciplines, most commonly basketball and American football in the United States (and soccer in Europe), intense sports that also have high participation levels.1,32,33,35 These sudden death events also occur much more frequently in males (by 9:1); young women are probably less frequently affected because of their lower overall participation rates and absence from sports such as football.1,33,35Blacks account for a disproportionate number of sports-related sudden deaths owing to previously undiagnosed HCM.1,33,35 This observation contrasts sharply with the striking underrepresentation of blacks in clinically identified HCM populations, suggesting that socioeconomic status and ethnicity may play an important role in determining access to echocardiography and consequently the clinical diagnosis of HCM.Other Risks of SportsA substantial number of other sudden deaths in athletes occur in the absence of cardiac disease and under diverse circumstances.1,54,56 These deaths are caused by severe blunt head, spine, and other bodily trauma (eg, during football or pole vaulting), heat stroke, uncontrolled bronchial asthma, ruptured cerebral artery aneurysm, and possibly sickle cell trait. Stroke, myocardial infarction, and sudden death have been linked to substance abuse with cocaine, anabolic steroids, or nutritional supplements (including ephedrine).64Two other circumstances in which trauma-related sudden death occurs during sports involve blunt, nonpenetrating, and often innocent-appearing blows to the precordium or neck54,56 (Figures 8 and 9). Virtually instantaneous death has been reported during ice hockey in which high-velocity blows to the neck by the puck trigger arterial rupture and subarachnoid hemorrhage54 (Figure 9). The likely mechanism is reflex hyperextension of the head that causes vertebral artery dissection at its fixed anchor point within the foramina transversarium. Download figureDownload PowerPointFigure 8. Blow to an unprotected area of the upper neck by a hockey puck (accompanied by abrupt reflex hyperextension) can result in sudden death (upper panel). Mechanism involves arterial dissection and rupture at the anatomic point where the vertebral artery courses through the boney canal of the foramina transversarium and penetrates the posterior atlanto-occipital membrane or dura mater (lower panel). Vertebral artery is rigidly anchored at this point (as it enters the transverse process of the first cervical vertebra) and becomes the point of rupture leading to massive hemorrhage into the subarachnoid space and instantaneous death. Lt. indicates left; Rt., right.Download figureDownload PowerPointFigure 9. Stop-frame images of an aborted commotio cordis event during a televised professional hockey game. A, Flight of the puck from a slap shot (arrowheads and arrow) toward the victim (*). B through F, After precordial blow, victim (*) is seen progressively falling toward the surface of the ice. E and F, Enlarged stop frames showing final collapse.More commonly, precordial blows may trigger ventricular fibrillation without structural injury to ribs, sternum, or the heart itself (commotio cordis56,65; Figure 10). These events are more common causes of athletic field deaths than most of the aforementioned cardiovascular diseases (Figure 6). Commotio cordis is most frequently caused by projectiles that are implements of the game and strike the chest at a broad range of velocities (eg, hockey pucks or lacrosse balls [up to 90 mph]), but more frequently result from blows with only modest force (eg, a pitched Little League baseball striking a batter at 30 to 40 mph) or by virtue of bodily contact (eg, a karate blow or when 2 outfielders tracking a baseball collide).56Download figureDownload PowerPointFigure 10. Differential diagnosis between athlete's heart and cardiac disease. Gray zone of overlap between physiological hypertrophy and pathological cardiomyopathies (including myocarditis, HCM, and ARVC). Adapted from Maron1 with permission of the Massachusetts Medical Society. Copyright 2003.On the basis of clinical observations and an experimental animal model (which replicates commotio cordis), the mechanism by which ventricular fibrillation and sudden death occur requires a blow directly over the heart, exquisitely timed to within a narrow 10- to 30-ms window just before the T-wave peak during the vulnerable phase of repolarization.65 Basic electrophysiological mechanisms of commotio cordis are largely unresolved, although selective K+ATP channel activation appears to play a role.1Only ≈15% of commotio cordis victims survive, usually in association with timely cardiopulmonary resuscitation and defibrillation.56 However, there are reports of both successful66 and unsuccessful resuscitation with automated external defibrillators.67 Strategies for primary prevention of commotio cordis include innovations in sports equipment design. However, although softer-than-normal ("safety") baseballs reduce the frequency of ventricular fibrillation under experimental conditions,65 they do not provide absolute protection in the field.56 At present, chest barriers with proven efficacy in preventing commotio cordis are not yet available. In fact, under laboratory conditions, commercial chest protectors are uniformly ineffective in preventing chest blow–induced ventricular fibrillation.68Several sudden cardiac deaths have been reported in Belgian cyclists, with the suggestion that athletic participation produced ventricular tachyarrhythmias.69 Mechanisms responsible for this disproportionate rate of cardiac events are largely undefined. An infectious cause, with vector-borne pathogens (and myocarditis), has been implicated in a cluster of sudden deaths among Swedish orienteers.70Athlete's Heart and Cardiovascular DiseaseBecause of the potentially adverse consequences of underlying cardiovascular disease in young athletes, considerable attention has been focused on clinically distinguishing physiologically based athlete's heart from a variety of structural heart diseases (Figure 10).1,7,19,20,22,24,71,72 This differential diagnosis has critical implications