Structural features of the athlete heart as defined by echocardiography.
The morphologic concepts of the "athlete heart" have been enhanced and clarified over the last 10 years by virtue of M-mode echocardiographic studies performed on more than 1,000 competitive athletes. Long-term athletic training produces relatively mild but predictable alterations in cardiac structure that result in an increase in calculated left ventricular mass. This increase in mass observed in highly trained athletes is due to a mild increase in either transverse end-diastolic dimension of the left ventricle or left ventricular wall thickness, or both. Cardiac dimensions in athletes compared with matched control subjects show increases of about 10% for left ventricular end-diastolic dimension, about 15 to 20% for wall thickness and about 45% for calculated left ventricular mass. Furthermore, there is evidence that the modest degree of "physiologic" left ventricular hypertrophy (both the cavity dilation and wall thickening) observed in athletes is dynamic in nature, that is, it may develop rapidly within weeks or months after the initiation of vigorous conditioning and may be reversed in a similar time period after the cessation of training. Several echocardiographic studies also suggest that the precise alterations in cardiac structure associated with training may differ depending on the type of athletic activity undertaken (that is, whether training is primarily dynamic [isotonic] or static [isometric]). Although the ventricular septal to free wall thickness ratio (on M-mode echocardiogram) is almost always within normal limits (less than 1.3), occasionally an athlete will show mild asymmetric thickening of the anterior basal septum (usually 13 to 15 mm). This circumstance may mimic certain pathologic conditions characterized by primary left ventricular hypertrophy such as nonobstructive hypertrophic cardiomyopathy. The long-term significance of increased left ventricular mass in trained athletes has not been conclusively defined. However, there is no evidence at this time suggesting that this form of hypertrophy is itself deleterious to the athlete or predisposes to (or prevents) the natural occurrence of cardiovascular disease later in life.
D000293:Adolescent; D000328:Adult; D000368:Aged; D016275:Atrial Function; D006332:Cardiomegaly / Q000473:pathology / Q000503:physiopathology; D002312:Cardiomyopathy, Hypertrophic / Q000473:pathology / Q000503:physiopathology; D002648:Child; D003163:Competitive Behavior / Q000502:physiology; D003645:Death, Sudden / Q000209:etiology; D004452:Echocardiography; D005260:Female; D006321:Heart / Q000033:anatomy & histology* / Q000502:physiology / Q000503:physiopathology; D006325:Heart Atria / Q000033:anatomy & histology; D006352:Heart Ventricles / Q000033:anatomy & histology / Q000503:physiopathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D010806:Physical Education and Training; D010807:Physical Endurance; D005082:Physical Exertion; D013177:Sports; D013997:Time Factors; D016276:Ventricular Function