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1 Central Military Hospital and
Research Institute of Military Medicine, ABSTRACT Karjalainen, Jouko, Matti Mäntysaari, Matti
Viitasalo, and Urho Kujala. Left ventricular mass, geometry,
and filling in endurance athletes: association with exercise blood
pressure. J. Appl. Physiol. 82(2):
531-537, 1997.
left ventricular hypertrophy; athletes' heart; endurance training
INTRODUCTION LEFT VENTRICULAR (LV) mass is greater in competitive
athletes by 45% on average compared with matched control subjects
(20). The expansion in mass is due to growth in end-diastolic
dimensions of the LV, LV wall thickness, or both. Diastolic function is
preserved or even "supernormal" in athletes' heart (10, 17) in
contrast to pathological LV hypertrophy, e.g., in hypertension, in
which altered LV filling is detected early (26).
There is considerable variation among endurance athletes in the
development of changes typical to athletes' heart, but it is not clear
why the same type of training produces more hypertrophy in some
athletes than in others and why the induced hypertrophy is more
concentric in some than in others. Earlier studies (18, 20) have
suggested that alterations in cardiac structure are mainly dependent on
the type of training and/or athletic activity. Thus athletes participating in dynamic-type endurance sports tend to
develop larger LV cavity dimensions without significant increase in
wall thickness, whereas athletes involved in static exertion and
exposed to a pressure load are more likely to develop greater LV wall
thickness without significant increase in cavity dimensions. In
contrast, echocardiographic studies have shown greater LV wall thickness to be common in endurance athletes (20), whereas this is
often undetectable in athletes engaged in intense power training (25).
Exercise blood pressure (BP) is a more powerful determinant of LV
hypertrophy in hypertensive patients than is BP at rest (28), and an
exaggerated BP response to exercise is associated with LV hypertrophy
in normotensive men, too (12). In this study we set out to
explore the relationship between BP during dynamic and static exercise
and LV hypertrophy, geometry, and filling in endurance athletes.
METHODS
We studied whether left ventricular (LV) mass and
concentricity [relative myocardial volume (RMV)] are
associated with exercise blood pressure (BP) in athletes. LV structure
and filling were evaluated by Doppler echocardiography and BP in
maximal bicycle ergometry and isometric handgrip tests on 32 male
endurance athletes and 15 age-matched controls. Indexed LV mass was 145 ± 14 (SD) g/m in athletes and 93 ± 20 g/m in
controls. Mass was not associated with BP at rest or in
low-grade exercise, but with heavier exercise loads this association
strengthened in athletes, being maximal at peak exercise
(r = 0.65 for mass and 0.58 for
indexed mass; P < 0.001). Multivariate analysis indicated that BP at peak
exercise accounted for 34% and the amount of training for an
additional 11% of the variance in indexed LV mass. RMV was 21% larger
in athletes. Only the increase in systolic BP during handgrip explained
significantly (19%) the variance in RMV. LV filling velocities were
not associated with mass, RMV, or BP. We conclude that in endurance
athletes LV mass is associated with BP in heavy dynamic exercise and LV
concentricity with BP response in static exercise.
1 · min1
(range 69-89
ml · kg1 · min1)
and did not differ significantly between orienteering and long-distance runners. The control group consisted of 15 age-matched sedentary men,
Finnish army conscripts and physicians, none of whom exercised over 2 h/wk. Their mean result in the Cooper test (distance run in 12 min) was
2,730 m, an average Cooper test result in Finnish Army conscripts, and
none of them ran over 3,000 m. All athletes and control subjects were
free of known cardiac disease. Because anabolic steroid abuse and some
other medications may cause cardiac muscle hypertrophy (21) and our aim
was to study physiological responses, we selected subjects who used no
medications.
end-diastolic
diameter3] + 0.6 g.
LV length was measured at end diastole from the apical window at a view
maximizing the ventricular length. Measurements were made from the
mitral valve plane to the apical epicardium
(L1) and to the apical endocardium
(L2).
The myocardial cross-sectional area of the LV was the difference
between total LV area subtended by the epicardium
(A1)
and LV cavity area
(A2)
traced by using a midventricular short-axis view at the level of
papillary muscle tips. The concentricity or eccentricity of the LV
myocardium was evaluated by calculating the relative myocardial volume
(RMV) by the following formula: RMV = (A1 · L1 A2 · L2)/A2 · L2.
This describes the relationship of the end-diastolic
myocardial volume to end-diastolic chamber volume and is derived from
the area-length model (31). Thus the measurements obtained for the
calculation of RMV were independent of the measurements obtained for
the calculation of LV mass. The sphericity of the LV chamber was
evaluated by calculating the ratio of LV end diastolic diameter to
ventricular length. In all two-dimensional measurements, the
endocardial-LV cavity (white-black) interface was used for endocardial
border definition (31).
Measurements of LV diastolic filling velocities were obtained in an
apical four-chamber view by positioning the pulsed Doppler volume
sample ~1 cm below the mitral annulus. Early peak flow velocity
(VE)
and peak atrial flow velocity
(VA)
were measured and the ratio
VE/VA
calculated.
All echocardiographic measurements were made by the same observer and
obtained directly from the screen monitor with the aid of calipers and
the instrument's trackball.
Handgrip test.
In the isometric handgrip test the subjects squeezed a rubber ball in
their dominant hand at 30% of the maximal squeezing force for 3 min.
The test was done in the supine position. Heart rate and systolic and
diastolic BPs were measured before and after 3 min of squeezing just
before the release of handgrip.
Exercise test.
A maximal exercise test was performed by the subjects on an
electrically braked bicycle ergometer until exhaustion. The initial load was 50 W with subsequent increments of 50 W every 3 min. During
the exercise test, a 12-lead electrocardiogram, heart rate, BP, and
perceived exertion were recorded. BP was monitored in the subjects at
rest after 5 min in the supine position, during exercise at 3-min
intervals, and at peak exercise immediately before the subject was
allowed to stop cycling. BP was measured sphygmomanometrically by the
same observer in all tests.
Statistical methods.
Results were expressed as means ± SD when appropriate. The strength
of the associations between BPs and LV measurements was assessed by
least- squares linear correlation. Comparison between athletes and
control subjects, and between subgroups of athletes with differing LV
mass index and RMV, was made by using the unpaired two-tailed
t-test and by calculating the 95%
confidence intervals. We also studied the predictors of indexed LV mass
and RMV by using stepwise regression models (2R, BMDP Statistical
Software, Berkeley, CA).
RESULTS
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To investigate the simultaneous effects of background factors on indexed LV mass in athletes, we included physical characteristics, amount of training, rest BP, rise in handgrip BP, and systolic BP at peak exercise as independent variables into a stepwise regression analysis. The two factors entering the model were systolic BP during peak exercise, accounting for 34%, and amount of training (hours/week), accounting for an additional 11% of the variance in indexed LV mass. When RMV was correlated with BP measurements, significant correlations were found in athletes with systolic (r = 0.43, P < 0.05) and diastolic (r = 0.40, P < 0.05) BP increases in the handgrip test, and with peak exercise systolic BP (r = 0.42, P < 0.05). RMV in athletes was associated with myocardial mass (r = 0.55, P < 0.001), as shown in Fig. 2, but not with the shape (sphericity) of the LV chamber. The sphericity of the LV was associated with the LV end-diastolic diameter (r = 0.64, P < 0.001). In athletes, myocardial mass, RMV, and exercise BP responses were not associated with diastolic Doppler velocities of LV filling. In stepwise regression analysis, only the rise in systolic BP during handgrip entered the model, accounting for 19% of the variance in RMV.
, Control subjects; 
, endurance athletes.
Comparison of athletes with LV mass index below or above the group median of 143 g/m. When athletes were divided into two groups on the basis of a median LV mass index of 143 g/m, the groups differed significantly only in exercise systolic BP (Table 6). Figure 3 shows that the difference in exercise BPs increased with the rise in exercise load. Heart rate during exercise and exercise duration were similar. Athletes with a larger myocardial mass index tended to have larger RMV. BP responses to the handgrip test, as well as LV diastolic filling velocities, were similar between the groups.
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Comparison of athletes with RMV below or above the group median of 1.26. Although athletes with larger RMV tended to have smaller LV end-diastolic diameter and bigger myocardial mass index, these differences were insignificant (Table 7). Athletes with more concentric LV hypertrophy had larger increases in both systolic and diastolic BPs during the handgrip test, whereas there were no significant differences in BPs during dynamic exercise or resting systolic BP. Resting diastolic BP was lower in the group with larger RMV. Diastolic LV filling velocities were not affected by the concentricity of the LV hypertrophy.
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DISCUSSION
Our study shows that, despite similar training and exercise capacity, there are considerable differences in the LV mass and geometry among top-level endurance athletes. Greater LV mass was associated with higher systolic BP in exercise, and the more strenuous the dynamic exercise, the stronger the association. Moreover, the concentricity of the LV hypertrophy was associated with the BP response in static exercise. Whereas athletes had higher peak exercise BPs than sedentary control subjects, exercise BPs were similar at similar exercise loads. In athletes, greater LV mass or concentricity did not impair LV velocities.
Earlier studies. Our results in endurance athletes resemble findings by Gottdiener et al. (12) in normotensive sedentary men with exaggerated BP responses to exercise. They found a corresponding association (r = 0.65) between LV mass and peak exercise systolic BP but no significant association with BP at rest or in low-grade exercise. However, they did not study the LV diastolic function in these normotensive men with LV hypertrophy, leaving unresolved whether the hypertrophy mimicked that found in athletes or resembled the pathological hypertrophy seen in hypertension. Similarly, Cigarroa et al. (3), in a study of cocaine abusers, found that subjects with LV hypertrophy had an exaggerated pressor response in exercise, in contrast to those without LV hypertrophy. However, this study did not measure the diastolic filling of the LV. Douglas et al. (7) measured mean exercise BP during an 8-h exercise test in 14 triathletes and found a strong correlation (r = 0.88) with LV mass, whereas diastolic function remained normal. They did not study control subjects, however. In contrast, Fagard and co-workers (8) did not find that exercise BP explained the variance in LV mass better than did rest BP. However, their subjects had the exercise test only up to 160 W, and most of them did not have LV hypertrophy. Their subjects thus resembled our control subjects, in whom no significant association was found between LV mass and rest or exercise BPs. Thus earlier studies and our study suggest that exercise BP is more strongly associated with LV mass in subjects with LV hypertrophy than in subjects with normal-sized hearts. Further, the association is strong only during strenuous exercise. Adaptive vs. pathological LV hypertrophy. There are differences between the pathological LV hypertrophy and the adaptive hypertrophy of athletes. Diastolic filling is impaired in pathological hypertrophic states, in which the heart is under a pressure load such as in aortic stenosis (9). In arterial hypertension, the degree of pathological LV hypertrophy is directly related to the impairment of diastolic filling (11). On the other hand, because LV hypertrophy may precede the appearance of arterial hypertension (27, 32), it has been suggested that factors other than increased systemic vascular resistance are underlying LV hypertophy in this disease. These hormonal factors would also affect nonmyocyte cell populations such as fibroblasts in the myocardium, leading to remodeling of the interstitium (34) and thereby to an altered compliance of the myocardium reflected in diastolic filling velocities. Concentric LV hypertrophy in hypertension is associated with increased cardiovascular morbid event rate in subsequent years (14). There is no evidence, however, that the geometric pattern of LV hypertrophy in athletes would affect later cardiovascular morbidity. Although LV hypertrophy often precedes hypertension in sedentary subjects, and an exaggerated BP response in exercise is regarded as a precursor of established hypertension at rest (19), there is no evidence that athletes with adaptive LV hypertrophy risk developing hypertension later. When elite athletes stopped their training, LV wall thickness reduced by 15-33% in 6-34 wk (21). However, there is some evidence that in older subjects engaged in heavy training, LV hypertrophy may become irreversible (22). On the other hand, former elite athletes, whether or not still in training, do not have an abnormal prevalence of hypertension (15). Is an exaggerated exercise BP response the cause or consequence of LV hypertrophy? Studies reporting an association between LV mass and exercise BP in hypertension (28), normotensive men (12), cocaine abusers (3), and triathletes (7) all assumed greater pressure loads to have induced the hypertrophy. It has been speculated that, although the exaggerated BP response to strenuous exercise is not in itself a sufficient stimulus to induce LV hypertrophy, it could be a marker of similar BP responses to daily emotional and other stimuli (6). An alternative and more plausible explanation in athletes is that exaggerated BP responses are the consequence and not the cause of the LV hypertrophy. Alexander and co-workers (1) found that, in subjects with stable heart rates due to pacemakers, static exercise increased BP by increasing stroke volume, with no change in the systemic vascular resistance. Greater LV mass is associated with larger stroke volume (16), and during exercise competitive athletes increase stroke volume more than do noncompetitive athletes (4). We did not measure stroke volume changes during exercise, but if athletes with larger LV mass were to increase their stroke volume during exercise more than athletes with smaller myocardial mass despite similar heart rates, this might explain the differences in BP responses. Our finding of a gradually widening difference in BP response at comparable heart rates with increasing exercise loads between athletes with larger or smaller LV mass is evidence for this mechanism. Both larger end-diastolic and smaller end-systolic chamber volumes may play a role in stroke volume increases (4). Moreover, because a dynamic exercise, running, was the main training modality in the studied athletes, it is unlikely that the enhanced BP response in static exercise induced the greater concentricity of the ventricular hypertrophy. The normal diastolic filling of even the thickest LVs in athletes is further evidence against the suggestion that higher exercise BP causes the more prominent LV hypertrophy. The reason why some athletes develop larger and more concentric myocardial mass than others, despite similar training, may lay in genetic disposition. Familial aggregation of LV dimensions has been reported and it has been concluded that >60% of the variability in LV mass can be explained by heritable factors (33). Recent evidence implicates genes coding for components of the renin-angiotensin system in the pathogenesis of cardiac hypertrophy (13). In fact, preliminary data suggest that D polymorphism of the angiotensin-converting enzyme gene is strongly associated with the LV growth in response to exercise (23). In rat heart, different patterns of gene expression regulate myocardial hypertrophy in hypertensive hypertrophy as opposed to adaptive hypertrophy in which myocardial catecholamine levels are increased (2). There is much evidence that catecholamines could induce cardiac hypertrophy via direct stimulation of myocardial adrenoceptors (24). One limitation of our study is that we used bicycle ergometry instead of treadmill running to get more reliable BP measurements during exercise. The athletes had trained running and could not achieve their maximal heart rate on bicycle ergometry because of premature fatique of leg muscles. Thus we could not measure the BP in athletes during their true maximal heart rate. It is highly probable, however, that if the true maximal exercise heart rate and BP had been achieved, the association between peak exercise BP and LV mass would have been still stronger, as suggested by Fig. 1. Further, there is the possibility that the hemodynamic response during cycling differs from that during running. Conclusions. The endurance training response of LV hypertrophy is heterogenous. Larger LV mass is associated with higher systolic BP in strenuous dynamic exercise. The concentricity of the LV hypertrophy is associated with BP response in static exercise.ACKNOWLEDGEMENTS
This study was supported by grants from the Finnish Defence Forces and from the Aarne Koskelo Foundation.
FOOTNOTES
Address for reprint requests: J. Karjalainen, Central Military Hospital, PL 50, 00301 Helsinki, Finland.
Received 28 May 1996; accepted in final form 21 October 1996.
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ABSTRACT
