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Left ventricular response to dynamic exercise in young cyclists


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Medicine & Science in Sports & Exercise: April 2002 - Volume 34 - Issue 4 - p 637-642
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Superior cardiac functional capacity, or the ability to generate cardiac output (𝑄̇max), is the predominant factor accounting for the greater maximal oxygen uptake (V̇O2max) in endurance athletes compared with nonathletes (21). In turn, the higher 𝑄̇max of the athlete reflects a greater maximal stroke volume (2,11,13,28). Because ventricular preload, contractility, and afterload define stroke volume, it should be expected than an understanding of these influences during exercise would provide insights into the physiological mechanisms that distinguish cardiac output and aerobic fitness in endurance athletes from nontrained individuals. The current body of research data has failed, however, to provide a clear delineation of these exercise responses.

In the nontrained subject, stroke volume rises by approximately 30–40% at the onset of upright progressive exercise. After reaching an intensity of about 40% V̇O2max, values level off and then remain stable to the point of exhaustion (9,14,27,34). These stroke volume responses to upright progressive exercise are associated with changes in left ventricular chamber size. Diastolic dimension typically rises slightly at low intensities and then declines slowly with increasing workloads, reaching values at peak exercise which are equal to or less than those observed preexercise (14,16,20,22,34). Systolic dimension declines more precipitously, resulting in a progressive increase in left ventricular shortening fraction.

The greater maximal stroke volume of the endurance athlete has traditionally been ascribed to a larger ventricular size at rest. Although the pattern of stroke volume response to exercise in the endurance athlete mimics that of the nonathlete, the curve of stroke volume values is displaced above and parallel to that of the nontrained individual (2,9,10,28). This implies that the athlete’s greater maximal stroke volume is simply a reflection of a greater value at rest. By this explanation, factors influencing resting left ventricular size (plasma volume, inherent cardiac dimensions, chronic volume overload from training, and vagal-induced bradycardia) should account for the greater resting and maximal stroke volume—and consequently 𝑄̇max and V̇O2max—of the endurance athlete.

Other information, however, has suggested that the pattern of stroke volume response to progressive exercise in the endurance athlete may differ from nonathletes. Gledhill et al. (11) and others (8,22,32) have reported a progressive rise in stroke volume throughout progressive exercise in highly trained subjects rather than the plateau observed in nonathletes. This finding suggests that the larger maximal stroke volume in the endurance athlete might reflect dynamic influences on stroke volume during the course of exercise (such as augmented diastolic filling or enhanced contractility). Some studies have indicated a larger increase in left ventricular diastolic dimension with exercise in athletic subjects, suggesting that greater preload during the course of exercise might be important (9,29,30).

Cardiac dimensional changes with exercise have been described in adult athletes, and no data have previously been available to assess these responses in trained child competitors. This study investigated changes in left ventricular chamber size and contractility during the course of maximal upright cycle testing with two-dimensional echocardiography in a group of highly trained young cyclists. These responses were related to parallel changes in stroke volume and cardiac output estimated using the Doppler echocardiographic technique. The goal of this investigation was to examine factors that define differences between young endurance athletes and untrained subjects in maximal stroke volume as the critical determinant of 𝑄̇max and V̇O2max.


Eight highly trained young male cyclists (mean age 13.7 ± 1.0 yr) were recruited for exercise testing from cycling clubs in the San Francisco Bay area. All were in good health and taking no medications. Six reported year-round training. Average training regimens were 4.5 ± 1.6 sessions per week, 10.6 ± 4.0 h·wk−1, and 148 ± 45 miles·wk−1 (range 75–225). All were competing regularly in state and national races. By questionnaire, five of the eight reported appearance of pubic hair or voice change, indicative of early puberty.

After determination of stature and mass, scapular and triceps skin-fold thicknesses were determined on the right side by using standard techniques. Values in triplicate were averaged and summed to create a skin-fold score.

Before testing, supine measurements of left ventricular chamber dimensions were made with M-mode echocardiography by using two-dimensional guidance (Hewlett Packard Sonos 5500, Andover, MA). Measurements were recorded in triplicate in the parasternal long-axis view immediately distal to the tips of the mitral valve leaflets. The left ventricular end diastolic dimension (EDD) was measured from the posterior edge of the ventricular septum to the endocardial surface of the left ventricular posterior wall coincident with the Q wave of the electrocardiogram. The left ventricular end-systolic dimension (ESD) was recorded as the shortest distance from the ventricular septum to the endocardial surface of the ventricular free wall during systole. Left ventricular shortening fraction was calculated as (EDD − ESD)/EDD × 100. Averaged dimension values were expressed relative to the square root of the body surface area (12).

Subjects performed a progressive maximal exercise test in the upright position on a mechanically braked Monark cycle ergometer (model 818, Varberg, Sweden). Toe clips were not permitted, and subjects were required to remain seated throughout the test (to mimic testing conditions of the control group). Exercise was performed with a cadence of 50 rpm with initial and incremental loads of 25 W. Stage duration was 3 min. During the final 1–2 min of the test, the subjects were permitted to increase the pedal cadence to 60–70 rpm. The test was terminated when subjects could no longer sustain a constant pedal cadence. Peak work capacity (PWC) was defined as the highest load achieved (in W), prorated for partial stages completed.

Heart rate was measured by electrocardiogram. Cardiac output was estimated using standard Doppler echocardiographic techniques (5). A 1.9-Mhz continuous wave Doppler transducer was positioned in the suprasternal notch to estimate ascending aorta blood flow velocity. The integral of velocity over time (velocity-time integral; VTI) was recorded by tracing the velocity curve for individual beats both on-line and off-line. VTI values for the 4–10 curves with greatest consistent values and most distinct spectral envelopes were average at rest, during the final minute of each 3-min workload and in the final minute of exercise.

Aortic cross-sectional area was calculated from measurements of the maximal diameter at the level of the sinotubular junction, assuming the aorta to be circular. Aortic diameter was determined from the average of 5–10 preexercise measurements with the subject seated on the cycle by using two-dimensional echocardiography (parasternal long-axis view). It was assumed that any changes in aortic diameter from rest to exercise are similar in athletes and controls subjects. Stroke volume was then estimated as the product of VTI and aortic cross-sectional area, and cardiac output was calculated as the product of stroke volume and heart rate. Both cardiac output and stroke volume were expressed relative to body surface area (cardiac index and stroke index). Reliability and validity of this technique have been previously documented (18,22,25,26).

Left ventricular dimensions were estimated by two-dimensional echocardiography (parasternal long-axis view) at rest, in the last minute of each work stage, and during the final minute of exercise. Measurements of diastolic and systolic chamber dimensions were made off-line from videotape. All measurements were made perpendicular to the long axis of the left ventricle and only from frames in which the left ventricular cavity, both aortic and mitral valve rings, and the aortic root were visible. Measurements of diastolic dimensions were taken in the first frame of mitral valve closure at the onset of ventricular contraction, and systolic dimension was measured in the last frame before mitral valve opening at the end of ventricular contraction.

Dimensions were recorded as the shortest distance from septal to posterior wall endocardial surface, 1–2 cm distal to the closed mitral valve, perpendicular to the long axis. Average values were calculated from 5–10 measurements made at each stage. We have previously published test-retest reliability for this technique during maximal cycle exercise (22). Coefficients of variation of 6.0% and 13.8% were found for diastolic and systolic dimensions, respectively, at peak exercise.

Indices measured as indicators of myocardial performance during exercise included left ventricular shortening fraction, peak aortic velocity, and average aortic acceleration. The latter was determined as the slope of the line connecting initiation of flow to peak flow velocity for individual velocity-time curves.

Anthropometric values and hemodynamic data for the cyclists were compared to those previously published for 39 nontraining boys (control group 1) (24). This group included individuals with a wide range of fitness, as 10 boys were recruited from each quartile of finish times in a physical education class for a mile run test (one failed to complete testing). The group was physically active (69% had recently participated on a community sports team), but none was involved in regular exercise training. Fourteen of the 39 (36%) were in early puberty by questionnaire. The patterns of ventricular dimensional changes, shortening fraction, average aortic acceleration, and peak aortic velocity in the cyclists were compared with those previously reported in a separate control set of 10 healthy nontraining boys (mean age 11.8 ± 0.8 yr) (control group 2) (22).

Physiological and anthropometric differences between cyclists and untrained children were analyzed by independent Student t-test. Intragroup differences between resting and maximal values were examined by paired t-test. Comparison of stroke index responses to exercise between the cyclists and nonathletes in control group 1 was performed by ANCOVA with repeated measures using stroke index as the covariate. Statistical significance as defined as P < 0.05.

Informed consent was obtained from a parent of each child. This study was approved by the Institutional Review Board for the Protection of Human Subjects of the University of San Francisco.


The cyclists averaged 1.5 yr older than the nonathlete control group 1 (13.7 ± 1.0 vs 12.2 ± 0.5 yr, respectively, P < 0.05) and were taller (164 ± 8 vs 153 ± 9 cm, P < 0.05) and more lean (skin-fold sum 13.3 ± 2.6 vs 21.2 ± 9.1 mm, P < 0.05). The somewhat younger mean age and less advanced sexual maturation of the control subjects were not considered to influence their value as a comparison group. Age and biological maturation do affect stroke volume values with exercise as well as resting left dimensions, but not when adjusted for body surface area (12,27). The two groups were similar in body mass (50.1 ± 8.1 and 45.6 ± 10.1 kg for cyclists and controls, respectively, P > 0.05) and body surface area (BSA) (1.51 ± 0.15 m (2) for the cyclists and 1.40 ± 0.18 m2 for the controls, P > 0.05). Mean PWC per kg values were 3.77 ± 0.25 W·kg−1 for the cyclists and 3.04 ± 0.45 W kg−1 for the nonathletes (P < 0.05). All subjects were considered to have provided a maximal exhaustive effort by a) subjective observation and b) having achieved a peak heart rate equal to or greater than 190 bpm.

Resting supine echocardiograms revealed significantly greater left ventricular diastolic and systolic dimension (expressed relative to body size) in the cyclists compared with the boys in control group 1. Mean left ventricular end diastolic dimension was 4.10 ± 0.23 cm BSA−0.5 in the cyclists and 3.64 ± 0.31 cm BSA−0.5 in the nonathletes, whereas end systolic dimension measured 2.52 ± 0.27 and 2.19 ± 0.30 cm BSA−0.5 in the two groups, respectively. There was no significant difference in resting supine ventricular shortening fraction (38.8 ± 4.0% and 39.1 ± 5.7% for cyclists and controls, respectively).

Table 1 outlines values for heart rate, stroke volume, and cardiac output at preexercise and maximal exercise in the cyclists and nonathletes (control group 1). The cyclists demonstrated a significantly lower preexercise heart rate, but at maximal exercise the mean value was not different from that of the controls. The athletes had larger stroke volumes and cardiac output (both absolute and adjusted for BSA) compared with the controls both preexercise and at maximal exercise.

Table 1
Table 1:
Resting and maximal data for cyclists (N = 8) and nonathletic subjects (N = 39) (from ref. 24) in control group 1, values are mean (SD).

The pattern of stroke volume response to progressive exercise was similar in the two groups (Fig. 1). In the cyclists, mean values rose from rest by 22% at the second workload and then remained virtually unchanged to exhaustion. A 27% rise to plateau in the nonathletes was also achieved by the second workload (a work intensity approximately 37% of maximal). ANCOVA controlling for resting stroke index indicated a significant main effect for stroke index with increasing workloads but not for group. No significant interaction between group and stroke index was observed.

Stroke index responses to progressive exercise in trained young male cyclists and untrained control boys (from ref. 24). Data are mean values (SD). The abscissa is work rate in W.

The ratio of maximal:preexercise stroke index was 1.29 ± 0.13 and 1.41 ± 0.23 for the cyclists and controls, respectively (P > 0.05). Average maximal stroke volume was significantly greater than the resting value in both groups.

Echocardiographic measurements of left ventricular diastolic and systolic dimensions are depicted in Figure 2. The pattern of change in diastolic dimension with increasing work intensity mimicked that previously reported in nonathletic children. Values rose slightly at the onset of exercise and then gradually declined to levels that were significantly less than those observed preexercise (P = 0.03).

Left ventricular diastolic and systolic chamber dimensional responses to progressive upright exercise in young cyclists and untrained controls (from ref. 22). Data are mean values (SD). The abscissa is the work rate in W, and the ordinate is left ventricular size in cm.

Systolic dimension declined with exercise progressively and more precipitously than diastolic size, and mean value at maximal exercise was significantly lower than at preexercise. As a result, left ventricular shortening fraction rose steadily as work intensity increased. However, no significant difference in maximal shortening fraction or response of shortening fraction to exercise was observed between cyclists and nonathletes (Fig. 3). Mean shortening fraction rose 13.9 ± 4.3% (from 35.0 ± 3.0% preexercise to 48.9 ± 5.6% at maximal exercise) in the cyclists. The increase was 17.2 ± 3.8% for the nonathletes (29.4 ± 4.9% at rest and 46.6 ± 5.5% at maximal exercise). No significant differences were observed for mean values of average aortic acceleration or peak aortic velocity either at rest or maximal exercise between the cyclists and nonathletes (Table 2).

Changes in left ventricular shortening fraction during progressive cycle exercise in young trained cyclists and untrained controls (from ref. 22). Data are mean values (SD). The abscissa is work rate in W.
Table 2
Table 2:
Indices of myocardial function at rest and maximal exercise in cyclists and nonathletic subjects in control group 2 (from ref. 22); values are mean (SD).


A clear understanding of cardiac dimensional and hemodynamic responses to exercise in athletes has been hampered by conflicting research data. These variations may be explained by differing techniques, variable body position (supine, semisupine), limited stage measurements, and restriction to submaximal exercise. In this echocardiographic study, off-line measurements with selected two-dimensional videotape frames permitted sufficient precision to assess ventricular chamber size during maximal upright exercise. These data, combined with stroke volume values from Doppler echocardiography, provided information regarding the cardiac dynamics of young endurance athletes in response to exercise, the roles of preload and contractility in influencing stroke volume responses, and potential mechanisms that might account for stroke volume differences between athletes and nonathletes. These findings support the following concepts:

The cardiac dynamics during progressive exercise are no different in trained young cyclists than in nonathletes.

Stroke volume increased by 22–27% at the initiation of exercise and then plateaued as exercise intensity increased. Left ventricular diastolic size rose slightly at the onset of exercise but then fell slowly as work intensity increased. These responses of stroke volume and diastolic dimension at the beginning of upright exercise reflect a combination of increased preload from initiation of skeletal muscle pump function augmenting systemic venous return as well as a dramatic decline in peripheral vascular resistance from skeletal muscle arteriolar dilatation (31). Beyond moderate exercise intensity, systemic venous return continued to rise, but stroke volume was stable and ventricular diastolic dimension changed little. This set of observations can be explained by the rise in heart rate, which closely matches venous return, stabilizing stroke volume and ventricular preload above mild-moderate exercise intensities (17).

Although stroke volume remained unchanged as work intensity increased, left ventricular shortening fraction continued to rise. This suggests that augmented contractility serves to maintain rather than increase stroke volume with increasing work, permitting the same volume of blood to be expelled in a shorter systolic ejection time as heart rate increases (4).

The findings in this study suggest that this “scenario” is not different in young endurance athletes than nonathletes. Instead, the greater cardiac functional capacity of the cyclists reflected quantitative differences in resting, submaximal, and maximal stroke volume.

The greater maximal stroke volume of the young endurance athletes reflects a greater ventricular preload (chamber volume at end-diastole) at rest.

The cyclists in this study demonstrated greater values of resting and maximal stroke index. The pattern of stroke volume response paralleled that of the nontrained children but with higher values at all levels of work intensity. In both groups, no significant change in stroke volume was observed beyond the early stages of exercise. Furthermore, when controlling for resting values, the stroke index during exercise was not different between athletes and nonathletes. These observations imply that factors responsible for the greater maximal stroke volume of the athlete are those that influence stroke volume at rest.

At rest, left ventricular diastolic dimension (relative to body size) was significantly greater in the cyclists. However, no differences were observed in left ventricular shortening fraction, aortic velocity, or average aortic acceleration, suggesting that myocardial contractility and afterload were similar in athletes and nonathletes. Consequently, the larger stroke index at rest in the athletes can be attributed to factors that influence resting ventricular filling or preload.

The magnitude of changes in preload and contractility that cause stroke volume to rise at the onset of upright exercise were similar in the athletes and controls. As exercise intensity and systemic venous return increased, stroke volume remained stable, indices of contractility rose, and left ventricular diastolic size slowly decreased, all these findings being equal in the two groups. These findings suggest that changes in ventricular preload, contractility, and afterload during exercise play no role in defining differences in maximal stroke volume (and thus 𝑄̇max and V̇O2max) between young endurance athletes and controls. The greater maximal stroke volume in the cyclists resulted from their larger ventricular size and preload, factors that were present at rest.

Previous studies both support and refute these conclusions. A plateau in stroke volume with increasing work intensity in endurance athletes has been observed by some authors (2,9,10,15,28–30), whereas others have described a progressive rise (8,11,33). We found that stroke volume plateaued in a previous study of young cyclists (28) but not in child runners (tested on a cycle ergometer) (23). The explanation for these different findings is not immediately clear.

Three previous studies assessing cardiac dimensions during upright exercise have indicated a larger increase in diastolic dimension in athletes compared with nonathletes (9,29,30). However, none measured dimensions at maximal exercise. Schairer et al. (30) found that a group of swimmers and cyclists increased their end diastolic volume (as estimated by M-mode echocardiography) from a mean of 119 to 152 mL when cycling to a heart rate of 130 bpm compared with no change in nonathletes. Rubal et al. (29) described a greater increase in end diastolic dimension with cycling to 150 bpm in a group of pentathletes compared with controls. DiBello et al. (9) reported a mean preexercise end diastolic volume of 143 mL in a group of elite cyclists, whereas immediately after peak exercise the value was 168 mL.

Consistent with findings in the present study, previous investigations have consistently failed to show differences in myocardial performance (rise in ventricular ejection fraction or shortening fraction) during exercise in athletes and nonathletes (1,3,6,30). Afterload was not directly assessed in this study, but no differences have previously been observed in response of blood pressure or peripheral vascular resistance to exercise in trained and nontrained individuals (1,9,13).

Enhanced resting left ventricular size (the “athlete’s heart”) is unlikely to reflect chronic volume overload from endurance training.

Highly trained endurance athletes typically exhibit a large left ventricular diastolic size, part of a set of clinical findings termed the “athlete’s heart” (7,19). The young cyclists in this study clearly demonstrated this characteristic, indicating that cardiac enlargement in endurance athletes can be observed at a young age.

Considerable controversy surrounds the etiology of the “athlete’s heart” (19). It has been proposed that the greater diastolic ventricular size of the athlete results from long-term repetitive volume overload that occurs with training. The myocardial stretch and ventricular enlargement associated with this recurrent diastolic overload would stimulate the addition of myocardial fibers in series and augment chamber size (7). The findings in the present study suggest that this concept is incorrect, because the rise in cardiac output in response to acute high-intensity exercise was not accompanied by an increase in left ventricular diastolic size. Based on this finding, there is no stimulus from ventricular enlargement during acute training episodes that would trigger chronic left ventricular chamber dilatation seen in the “athlete’s heart.” This study suggests that other training-induced factors affecting resting ventricular size (particularly enhanced plasma volume and decreased resting heart rate) are more likely to contribute to the clinical manifestations of the “athlete’s heart” as well as the greater resting and maximal stroke volume observed in endurance athletes (17).

It should be recognized that this study is limited to the characterization of cardiac responses to exercise in young, circumpubertal male cyclists. Although highly trained, no assumptions can be made regarding the projection of these findings to those of more mature cyclists with additional years of intense training and competition.

The authors are grateful to Agilent Technologies, which graciously supplied the echocardiographic equipment for this study. This study was supported by a Faculty Development Grant from the University of San Francisco.

Address correspondence to: Thomas Rowland, M.D., Department of Pediatrics, Baystate Medical Center, Springfield, MA 01199.


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© 2002 American College of Sports Medicine