Summary
There is overwhelming evidence that the heart of competitive athletes may differ from that of nonathletes, matched for age, gender and body size. Enlargement of the left ventricular internal diameter is most pronounced and reaches about 10% in athletes performing predominantly dynamic sports; mainly strength training athletes have a lesser increase of the internal dimension, which is limited to a mere 2.5%. Also the left ventricular wall appears to be thickened in all types of athletes compared with controls. In sports with high dynamic and low static demands, wall thickness is proportionate or slightly disproportionate to the size of the internal diameter so that relative wall thickness is not different from control or slightly increased (predominantly eccentric hypertrophy). In strength athletes the disproportionate increase of wall thickness averages about 12% (predominantly concentric hyper trophy). In sports with high dynamic and high static demands and requiring prolonged training, such as cycling, the increases of absolute and relative wall thickness reach 29% and 19%, respectively, and are more pronounced than in runners (mixed hypertrophy). A plausible interpretation of these results is that the development of so-called eccentric or concentric left ventricular hypertrophy according to the type of sports cannot be regarded as an absolute or dichotomous concept, because training regimens on the one hand and sports activities on the other are not exclusively dynamic or static and because the load on the heart is not purely of the volume or the pressure type. Most studies agree that left ventricular systolic and diastolic function is normal in the athlete at rest, whereas diastolic function seems to be enhanced in the exercising endurance athlete. The largest differences from control subjects have been observed in cyclists and rowers. Left ventricular wall thickness may increase up to 16 mm, and is usually associated with an increased LV internal diameter and normal systolic and diastolic LV function.
Introduction
There is no doubt that the heart can adapt to an increased hemodynamic load. In disease states, it is generally recognized that two types of chronic overload can effect the heart in different ways [1]. A volume load, as in aortic or mitral insufficiency, leads to an enlargement of the left ventricular internal diameter and a proportional increase of wall thickness. This type of adaptation is called eccentric left ventricular hypertrophy. A pressure load, as in aortic stenosis or hypertension, is associated with a thickening of the ventricular wall and an unchanged internal dimension, or concentric left ventricular hypertrophy. It was suggested that these cardiac adjustments serve to normalize systolic wall stress [1].
Physical activity is associated with hemodynamic changes and alters the loading conditions of the heart [2]. In dynamic exercise the emphasis is on movement with no or minimal development of force. The main hemodynamic features are increases in heart rate and stroke volume, the two components of cardiac output. Systemic vascular resistance drops but the net result is a slight to moderate rise in blood pressure. The load on the heart is predominantly of the volume type. In static exercise force is developed with no or minimal movement. The hemodynamic consequences involve a slight elevation of cardiac output, due to the increase of heart rate, and a more pronounced rise of blood pressure, resulting in a pressure load on the heart. From a theoretical point of view the hemodynamic alterations and the ventricular loading conditions during exercise could in the long run lead to left ventricular hypertrophy. However, whereas the load on the heart is continuous in pathological conditions, it is not in the athlete.
Several questions therefore arise: (1) Does the heart of athletes differ from that of nonathletes and are cardiac adaptations related to the type of physical exercise? (2) Are structural differences associated with alterations in cardiac function? (3) What is still “normal”?
Impact of different sports and training on cardiac structure
To test the hypothesis that exercise-related volume and pressure loads are associated with different cardiac adaptations, one should ideally dispose of athletes engaged in purely dynamic or static sports. In addition, the load on the heart should be of sufficient duration and intensity. Although athletic conditioning is rarely purely dynamic or static and the training programs of different athletes may overlap, long-distance running comes close to an ideal example of dynamic exercise. Other predominantly dynamic aerobic or endurance sports are swimming, rowing and cycling. Several sports are categorized as predominantly static or involve power training. This is the case for weight lifting, bodybuilding, wrestling and throwing events such as shot putting. The training regimens of these athletes are, however, not uniform. The power training can be static indeed but is sometimes described as dynamic involving only light-to-moderate weights. The actual duration of the static activity and therefore of the pressure load on the heart may be brief. Some of these athletes also engage in dynamic activities such as running. Numerous studies have applied echocardiography in athletes engaged in these sports and compared the results to those of nonathletes. An important question arises however: who should be in the control group? Ideally, these subjects should be normally active, and matched for age, gender and anthropometric characteristics.
We tested the hypothesis of divergent cardiac adaptations in different sports by applying meta-analytical techniques to published echocardiographic data on competitive long-distance runners, cyclists and strength athletes [3,4]. For inclusion in the meta-analysis, studies had to meet the following criteria: (a) Study populations consisting of homogeneous groups of male competitive long-distance runners or cyclists, or of athletes engaged in strength training, such as weight or power lifters, bodybuilders, throwers, wrestlers and bobsledders. (b) Inclusion of a nonathletic control group for each group of athletes, matched for gender, age (average difference ≤5%) and body surface area (difference ≤5%). (c) Assessment of left ventricular internal diameter and wall thickness by use of echocardiography.
Long distance runners
Table 1 summarizes the results of the meta-analysis of echocardiographic data of young male long-distance runners, which involved 135 athletes and 173 control subjects from 10 reports [3]. The runners were competitive athletes, who had trained for several years and ran on average about 100 km/week; aerobic power was approximately 40% higher than in controls. Whereas athletes and nonathletic controls did not differ in age, body surface area was slightly but significantly lower in the runners, despite the strict selection criteria for inclusion in this analysis. Heart rate was 14 beats/min lower in athletes than in controls, left ventricular internal diameter 4.8 mm higher and the septum and the posterior wall were thicker by 1.5 and 1.6 mm, respectively. Calculated left ventricular mass was larger by 67 g or 48% (p <0.001).
Table 1.
Results of the meta-analysis of long-distance runners and matched controls.
It is noteworthy that the meta-analysis on runners reveals that relative wall thickness, that is the ratio between wall thickness and internal diameter, was slightly but significantly higher in the runners than in the controls; the percent difference averaged 7.8% (p ≤ 0.05). Therefore, the increase in wall thickness was somewhat more pronounced than expected in the long-distance runners, who have generally been considered to develop pure eccentric left ventricular hypertrophy. These findings can most likely be explained by the fact that training regimens on the one hand and sports activities on the other are not exclusively dynamic and that the load on the heart is not purely of the volume type. The data thus indicate that male long-distance runners have a larger left ventricular mass than nonathletic control subjects, due to a larger left ventricular internal dimension and a slightly disproportionate thickening of the left ventricular wall, compatible with predominantly eccentric left ventricular hypertrophy. However, the term hypertrophy should be used with caution because the results of most athletes fall within normal limits.
Few data are available in female long-distance runners and matched controls. The results confirm a higher left ventricular mass and internal dimension in athletes than in controls. However, Spirito et al. [5] noted that female athletes have smaller left ventricular cavity dimension and smaller wall thickness than males of the same age and body size who were training in the same sport.
Cyclists
Table 2 summarizes the results of the metaanalysis of male cyclists and matched controls [3]. There were 69 athletes and 65 controls from 4 studies. Age and body surface area were similar in athletes and controls. Heart rate was lower by 16 beats/min in the cyclists. Left ventricular internal diameter, septal and posterior wall thickness were larger by 4.5, 2.6 and 2.7 mm, respectively. The difference in left ventricular mass averaged 102 g or 64% (p <0.01). The higher left ventricular mass seems to be restricted to competitive cyclists and was not observed in recreational cycle tourists [6].
Table 2.
Results of the meta-analysis of cyclists and matched controls.
In the meta-analysis of male cyclists, the athletes' relative wall thickness exceeded that of the control subjects by 19% (Table 2), indicating that cycling is not only associated with an increase of the internal diameter but also with a disproportionate thickening of the wall. This could be explained by the fact that cycling involves static activity of the upper part of the body and by the increase of blood pressure associated with intensive cycling. In an analysis of 947 elite athletes, Pelliccia et al. [7] observed that absolute wall thickness was independently associated with body surface area, age and male sex, but also with certain sports such as rowing and cycling. They did, however, not analyse relative wall thickness as the dependent variable in multiple regression analysis.
The various studies on cyclists agree that left ventricular mass is larger than in matched nonathletes due to a larger left ventricular internal diameter and wall thickness. A large training quantity may lead to a disproportionate increase in wall thickness which could be related to the static component involved in cycling.
Athletes engaged in predominantly static sports
The training regimens of a number of sports involve predominantly static exercise. A drawback of several studies or of subgroups is the mismatch of athletes and control subjects, probably due to difficulties arising from the unusual body size of athletes. Table 3 summarizes the results of the meta-analysis, which comprises data of athletes, who were predominantly engaged in strength training and whose body surface area was comparable to that of the control subjects [3]. The 6 selected studies involved 42 weight or power lifters, 40 bodybuilders, 50 wrestlers, 25 throwers and 21 bobsledders, that is a total of 178 athletes, and 105 control subjects of similar age and body size. Heart rate was not significantly different between the groups. The left ventricular internal diameter, septal thickness and posterior wall thickness were larger by 1.3, 1.4 and 1.2 mm, and left ventricular mass by 39 g or 25% (p <0.05) in the athletes. Their relative wall thickness was 12% (p <0.05) higher than in controls. In general there is no convincing evidence of an increased septal to posterior wall ratio in strength athletes, as has been claimed in older studies with inadequate matching of weight lifters and controls.
Table 3.
Results of the meta-analysis of strength athletes and matched controls.
The data on athletes in whom strength training is an important component of the training regimen, suggest that predominantly concentric left ventricular hypertrophy may be observed, but it should be noted that the increase in left ventricular mass is small. Both absolute and relative wall thickness are higher than in controls, but the combined analysis also reveals a slightly higher left ventricular internal diameter. These results can be explained by the fact that training regimens and sports activities are not purely static and that the duration of the actual load on the heart is usually limited.
Cardiac function in athletes
Left ventricular systolic function
Left ventricular systolic function has most often been studied by use of echocardiography or radionuclide ventriculography, and expressed as fractional shortening of the left ventricular internal dimension or ejection fraction. The meta-analysis on long-distance runners, cyclists and strength athletes, and the results from a number of other sports, revealed that these indices of systolic function were usually not different between athletes at rest and matched control subjects [3,4]. In addition, the increase of fractional shortening or ejection fraction on dynamic exercise was not different from control in long-distance runners [8,9]. In some studies, however, fractional shortening or ejection fraction at rest was significantly higher or depressed in athletes, but these values were still within normal limits [4]. Other indices of systolic function, such as the peak posterior wall velocity, the peak velocity of the internal diameter change or peak ejection rate were similar in athletes and controls [4]. The data therefore suggest a normal left ventricular systolic function in athletes.
The evaluation of contractility in man is complicated, however, by the fact that contractile indices are influenced by afterload, preload and/or heart rate. In cyclists the relationship between the fractional shortening index and systolic wall stress was similar to that obtained in matched sedentary subjects [10]. Further appreciation of subtle changes is difficult, however, from non-invasive studies alone.
Left ventricular diastolic function
Left ventricular diastolic function has been studied by use of mechanocardiography, radionuclide techniques, imaging echocardiography and Doppler velocimetry. At rest, the atrial wave on the left ventricular apex cardiogram of cyclists and the left ventricular filling rate by radionuclide measurements in runners and aerobically trained subjects were similar to control values. Imaging echocardiography revealed that peak rates of chamber enlargement or filling, posterior wall movement or wall thinning were not different from control in runners, swimmers, cyclists, triathletes, throwers, power lifters and basketball players [4]. The ratio of the transmitral Doppler peak-flow velocity during atrial contraction (A) to the peak-flow velocity during rapid left ventricular filling (E) (or vice versa) was normal in runners, swimmers, cyclists, triathletes, weight lifters, throwers and basketball players [4]. In some studies, however, the A-wave was proportionately lower than the E-wave. This can probably be ascribed to the lower heart rate which prolongs the diastolic filling period and reduces the atrial component. The overall evidence obtained with various techniques therefore suggests that left ventricular diastolic function at rest is similar in athletes and nonathletes. However, evidence is accumulating that left ventricular diastolic function, assessed by radionuclide ventriculography, imaging or Doppler echocardiography, is enhanced in the exercising endurance-trained athlete [4,9], as compared with untrained control subjects, which favours adequate filling of the ventricle when the diastolic period gets shorter at higher heart rates.
Limits of athlete’s heart
Pelliccia et al. [7] reported on 947 amateur competitive athletes belonging to Italian national teams from which Olympic athletes were selected and who underwent a mandatory medical evaluation in the Institute of Sports Sciences in Rome during period of intense training. They were free of systemic or cardiovascular disease and blood pressure was consistently or predominantly < 140/90 mm Hg. Age averaged 22 years (range 13–49), 78% were men. They were involved in competitions since 3 to 20 years, in one of 25 different sports; half of the athletes had international recognition. Based on echocardiography left ventricular wall thickness exceeded 12 mm in 16 athletes, all men, aged between 18 and 27 years; the maximal wall thickness was 16 mm. It is noteworthy that all 16 athletes were involved in rowing, canoeing or cyclism. Importantly, left ventricular internal diameter was increased in all of them, ranging from 55 to 63 mm, and systolic and diastolic function were normal; LV fractional shortening was between 33 and 41% and the Doppler E/A ratio averaged 2.2 ± 0.4 (SD). The authors concluded that a left ventricular wall thickness of 213 mm is very uncommon in highly trained athletes, and that it is associated with an enlarged LV cavity. In addition, the upper limit to which the thickness of the LV ventricular wall may be increased by athletic training appears to be 16 mm.
We assessed the upper limit of physiologic left ventricular hypertrophy in 45 male competitive road cyclists, average age 22 years, who cycled 590 km/week on average at the time of the echocardiographic study and had been involved in competitive cycling for a mean of 6.4 years. Left ventricular internal diameter and mean wall thickness (i.e., the average of septal and posterior wall thickness) amounted to 54.0 ± 4.7 (SD) mm and 12.4 ± 1.6 (SD) mm, respectively. LV wall thickness was 213 mm in 14 out of the 45 athletes, but its level never exceeded 16 mm. We furthermore studied whether LV function differed between these 14 athletes and those with LV wall thickness < 13 mm. As can be seen in Table 4, fractional shortening and the Doppler A/E ratio were similar in both groups of athletes.
Table 4.
Left ventricular structure and systolic and diastolic function in competitive road cyclistis, divided in 2 groups, according ro mean wall thickness.
Pelliccia et al. [7] concluded that athletes with wall thickness of more than 16 mm and a nondilated left ventricular cavity are likely to have primary forms of pathologic hypertrophy, such as hypertrophic cardiomyopathy. It has been suggested, based on the comparison of group averages, that Doppler echocardiographic assessments of diastolic function may help to distinguish physiological from pathophysiological hypertrophy, but their value for the individual subject is questionable [11,12].
The author gratefully acknowledges the secretarial assistance of N. Ausseloos.
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