Left ventricular filling profiles and angiotensin system activity in elite baseball players

Left ventricular filling profiles and angiotensin system activity in elite baseball players

International Journal of Cardiology 67 (1998) 155–160 Left ventricular filling profiles and angiotensin system activity in elite baseball players a a...

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International Journal of Cardiology 67 (1998) 155–160

Left ventricular filling profiles and angiotensin system activity in elite baseball players a a, b b b Zhi-Yang Lai , Nen-Chung Chang *, Ming-Chuan Tsai , Chuen-Sheng Lin , Sioh-Hue Chang , Tze-Che Wang a a

Section of Cardiology, Department of Internal Medicine, Taipei Medical College Hospital 252, Wu-Hsing St., Taipei 10502, Taiwan b Research Center for Sports Medicine, Taipei Medical College, Taipei, Taiwan Received 14 July 1998; accepted 10 September 1998

Abstract Left ventricular (LV) filling profiles in elite baseball players has not been reported in the literature. Also, angiotensin system activity in athletes has never been reported. We used echocardiography to compare 20 male elite baseball players (aged 21.961.0 years) with those of age- and sex-matched healthy sedentary subjects. Compared with the normal group, the athlete group showed a significant increase in LV mass, LV diastolic and systolic dimension, and left atrial dimension (P,0.05, ,0.001, ,0.001, and ,0.001, respectively). No differences in relative wall thickness or fractional shortening were found between these two groups. Diastolic filling profiles, including peak early diastolic filling velocity (E), peak late diastolic filling velocity (A), E:A ratio, early time–velocity integral (Ei ), atrial time–velocity integral (A i ), Ei :A i ratio, early filling time, deceleration time of early filling, and isovolumic relaxation time, were similar in both groups. Angiotensin system activity, including plasma renin activity, plasma aldosterone, and 24-h urinary aldosterone excretion, showed no difference between these two groups. Conclusion: This study suggests that normal LV filling profile, which is mediated partly by normal angiotensin system activity, is not related to increase in LV dimension and mass in elite baseball players.  1998 Elsevier Science Ireland Ltd. All rights reserved. Keywords: Echocardiography; Baseball players; Left ventricular diastolic function; Angiotensin system

1. Introduction In his 1986 review of structural features of the athletic heart on echocardiography, Maron [1] analyzed numerous studies of competitive athletes. Since that time, a number of additional studies investigating this subject have been reported [2–10]. Maron [1] concluded that left ventricular (LV) mass and volume are increased in athletes. Recent articles continue to support this view. Different patterns of hypertrophy have been described in association with enduranceversus strength-type exercise. LV dimension and mass *Corresponding author. Fax: 1886-2-23911200.

are found to be increased in subjects who participate in predominantly endurance-type exercises, such as running [2–6], cycling [2,3,7,8], soccer [2,3], or swimming [2,3], in contrast to a pattern of selective elevation of LV mass in athletes who participate in strength-type exercises, such as weight lifting [2]. Most ball sports predominantly involve endurancetype exercise. Reliable data are available for male basketball [2,9], female softball [2,10] and field hockey players [2,11]. Besides cardiac structure, differences in cardiac function and particularly LV diastolic function in athletes have been studied by use of Doppler echocardiography [4,5,7,8,12–16]. However, to the best of our knowledge, LV diastolic filling

0167-5273 / 98 / $ – see front matter  1998 Elsevier Science Ireland Ltd. All rights reserved. PII: S0167-5273( 98 )00303-9

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profiles in elite baseball players have not been reported. Furthermore, angiotensin system activity, considered to be related to the development of cardiac adaptation in athletes’ hearts, has never been reported. This study evaluates the LV diastolic filling profile and angiotensin system activity in highly trained elite baseball players and compares them with those of sedentary subjects.

2. Methods

2.1. Study population The study population consisted of all members of the baseball team of a physical education college. Subjects included 20 elite male baseball players, ranging in age from 21 to 25 years (mean, 21.961.0 years). Documented baseball training periods ranged from 8 to 12 years (mean, 10.962.1 years). Documented training intensity was seven times a week (3 h / time). A group of age- and sex-matched healthy, sedentary individuals was randomly selected from the database of our echocardiographic laboratory to serve as a control group. This study conformed to the ethical guidelines of the 1975 Declaration of Helsinki as reflected in a priori approval by the Human Research Committee of our institution. Informed consent was obtained from all subjects.

2.2. Echocardiography We directed all subjects to quit physical exercise and maintain a normal diet without sodium restriction for 48 h before visiting our laboratory. Chest X-ray and resting EKG were taken on the morning of this visit followed by an echocardiographic examination and then a treadmill exercise test. Echocardiographic examination was performed on an ATL (Advanced Technology Laboratories, Bothell, WA, USA) Ultramark 7, phased-array, ultrasound system with a 2.5-MHz transducer. Mitral inflow velocity was recorded from apical four-chamber view by pulsed Doppler technique with patients in passive end-expiration. Sample volume was placed at the level of mitral leaflet tips. Images were recorded on a 0.5-inch S-VHS video tape recorder. Tapes were analysed on a

Panasonic editing controller system with a Panasonic AG-7350 video recorder. All parameters were calculated by averaging five successive cardiac cycles. We measured LV mass (LVM) and relative wall thickness (RWT) to determine whether subjects had hypertrophy of LV. LVM (g) was calculated as (Vepi 2 Vend )31.05. LV epicardial enclosed volume (Vepi ) and endocardial enclosed volume (Vend ) were measured at end-diastole (the R-wave peak of simultaneously recorded EKG). Volume measurements were calculated from apical four-chamber (A 1 ) and twochamber (A 2 ) views by use of biplane area–length formula [V58A 1 A 2 /(3p L)], where L is the lesser of the lengths of long axis of these two views. RWT was calculated as 23(PWT / LVD d ), where PWT and LVDd are LV posterior wall thickness and LV diastolic dimension, respectively. These values were measured at end-diastole from parasternal long axis view of a two-dimensional image. Systolic function was expressed in terms of fractional shortening (FS). FS was calculated as (LVD d 2LVD s / LVD d )3100, where LVDs represents LV systolic dimension and was defined as the shortest systolic dimension taken from parasternal long-axis view of a two-dimensional image. Left atrial dimension (LAD) was defined as the largest systolic dimension taken from the parasternal long axis view of a two-dimensional image. LV diastolic filling indices [17] included: peak early diastolic filling velocity (E) (cm / s), peak late diastolic filling velocity (A) (cm / s), E:A ratio, early time–velocity integral (Ei ) (cm), atrial time–velocity integral (A i ) (cm), Ei :A i ratio, early filling time (EFT, ms), and deceleration time of early filling (DT, ms). In addition, isovolumic relaxation time (IVRT, ms) was defined as the time interval from aortic valve closure artifacts on Doppler sampling to onset of mitral valve flow. Pulmonary venous flow velocity pattern recording [18] was obtained after mitral flow velocity pattern recording. This examination was also performed by apical four-chamber view. Left atrial filling from the pulmonary vein was represented by red signals along the interatrial septum in the upper part of the left atrium in color Doppler image. The orifice of the right pulmonary vein was visualized at the bottom of flamelike red signals, and sample volume for pulsed Doppler measurements was set just at the orifice of the right pulmonary vein. Peak systolic forward flow velocity (S) (cm / s), peak

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diastolic forward flow velocity (D) (cm / s), and S:D ratio were measured. Echocardiograms were carried out and analyzed by the same operator (N.-C.C.) throughout this study, who was blinded with regard to other data of all subjects. All subjects in this study were young without concomitant lung disease or chest wall deformity. Thus, we had satisfactory echocardiographic measurements, including all parameters of two-dimensional LV measurements, transmitral flow Doppler and pulmonary venous flow Doppler measurements in all subjects.

2.3. Angiotensin system activity Angiotensin system profiles were evaluated in all subjects. We instructed all subjects to maintain a normal diet without training for 48 h, take nothing at home after midnight prior to the day of examination, and sit quietly for 30 min in the early morning after arriving at our laboratory. A blood sample was drawn for measuring plasma renin activity (PRA) and aldosterone. On the same day, we ordered all subjects to collect urine for measuring 24-h urinary aldosterone after drawing blood. These measurements were performed within 2 weeks of the echocardiographic examination.

2.4. Statistics Values were expressed as means6standard deviation. Comparisons were done using paired t-test. A value of P,0.05 was considered statistically significant.

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Table 1 Echocardiographic data of study populations Athletes Two-dimensional LVM (g) 163618 RWT 0.3660.05 FS (%) 3566 LVDs (mm) 3865 LVDd (mm) 5864 LAD (mm) 3964 Doppler Transmitral flow A (cm / s) 44610 E (cm / s) 6568 E:A 1.4860.09 A i (cm) 5.860.8 Ei (cm) 14.566.8 Ei :A i 2.4360.15 EFT (ms) 265648 DT (ms) 174630 IVRT (ms) 76610 Pulmonary venous flow S (cm / s) 52610 D (cm / s) 47612 S:D 1.1260.35

Normals

P

145616 0.3160.06 3868 4865 2964 3264

,0.05 NS NS ,0.001 ,0.001 ,0.001

4868 59610 1.4460.10 6.360.6 14.065.4 2.4860.16 275651 185635 8269

NS NS NS NS NS NS NS NS NS

5369 46610 1.1060.29

NS NS NS

Abbreviations are shown in text. Values are means6standard deviation.

these two groups. Compared with the normal group, the athlete group showed a significant increase in LVM, LVD d , LVD s , and LAD (P,0.05, ,0.001, ,0.001 and ,0.001, respectively). No significant increase in RWT or change in FS could be found in the athlete group (P5NS). No difference in diastolic filling profiles was found between these two groups. Table 2 demonstrates angiotensin system activity in these two groups. Plasma renin activity, plasma aldosterone, and 24-h urinary aldosterone excretion were not significantly different between these two groups.

3. Results Body mass index (BMI) in the athlete and normal groups was 2867 and 2368 kg / m 2 , respectively (P5NS). Heart rate (during echocardiographic examination) in athlete and normal groups was 6368 and 6567 beats / min, respectively (P5NS). All subjects had normal chest X-ray films. All resting EKGs showed no ST-T change. All exercising EKGs showed no significant ischemic ST-T change. Two subjects showed a mild mitral regurgitation and one showed a trivial aortic regurgitation in color Doppler image. Table 1 displays echocardiographic data in

4. Discussion Baseball is a sport with high dynamic and low static demands. Previous studies have found that Table 2 Laboratory data of study populations

PRA (ng / L?S) Plasma aldosterone (mmol / l) Urine aldosterone (nmol / day)

Athletes

Normals

P

0.1960.34 260628 1968

0.2060.48 265625 18610

NS NS NS

Abbreviations are shown in text. Values are means6standard deviation.

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echocardiographic structures of elite athletes have a predominant elevation in LV mass and dimension [2,3,19]. However, these studies found that wall thickness of athletes was proportionate or slightly disproportionate to the size of internal dimensions so that relative wall thickness was not different or slightly increased compared to that of controls [2,3,19]. Echocardiography is a noninvasive technique used to evaluate patterns of filling in athletes. Studies using image echocardiography have reported that peak rates of chamber enlargement or filling, posterior wall movement, or wall thinning are not different from controls in runners [4,14], swimmers [12], cyclists [20], triathletes [13], throwers [21], power lifters [12], and basketball players [9]. Doppler echocardiographic studies have shown that the ratio of transmitral E:A is normal in runners [4,22], swimmers [23], cyclists [24], weight-lifters [1,22], throwers [21], and basketball players [9]. Some investigators, however, have found an enhanced E wave in athletes [7], probably related to the necessity to normalize for absolute volume flow. Moreover, other studies of runners [5] and triathletes [13] have found that A wave is proportionately lower than E wave. An increase in the E:A ratio has also been observed [5,7,13]. This seems to be related to heart rate effect. A lower heart rate prolongs the filling period and has a direct effect on E:A ratio, with a reduced A and higher E:A ratio [15]. Thus, no abnormality of diastolic filling exists that can be attributed to a combination of ventricular dilatation and hypertrophy in athletes. Our present study not only examined E, A waves and E:A ratio, but also evaluated other diastolic filling parameters. Our findings show that resting heart rates in the baseball athlete and normal group did not differ during echocardiographic examination. Our findings are similar to those of many previous reports [2,4,5,7,9,13,16,21,23,24] which have shown that E and A waves as well as their ratio are similar in baseball athletes and controls. Further, we found no differences in other diastolic filling profiles between these two groups. There are complex interactions involved in measuring transmitral velocity profiles as Doppler indices of diastolic function. Many cardiac factors, such as ischemic and valvular heart disease, LV size and

mass, LV systolic function, heart rate, and LA size, as well as some extracardiac factors such as age, sex, obesity, and hydration state complicate interpretation [25,26]. However, the characters of our study population can exclude these confounding factors. None in our study had mitral or aortic regurgitation of more than a mild degree on color flow mapping study. The treadmill exercise test showed no significant ischemic ST-T change in any subject. All participants showed a normal systolic function of LV on echocardiographic examination and had regular sinus rhythm on resting EKG. Heart rates were similar during echocardiographic examination in these two groups without tachycardia or bradycardia. We selected ageand gender-matched individuals. Obesity is another confounding factor in the determination of LV filling profiles. In our present study, none of the baseball athletes had a BMI more than the mean12 SD of that of the age-matched normal subject. Impaired diastolic function after strenuous exertion has been described [6,27]. This finding is quite difficult to interpret because of reduced state of hydration after extreme exertion and reduction in preload in these individuals. In our study, adequate hydration in all subjects was promoted by quitting exercise 48 h before echocardiographic examination. Elevated LA pressure presented with an E-dominant mitral flow pattern can mimic a normal LV diastolic filling profile despite the coexistence of diastolic dysfunction [28]. In our present study, however, for all individuals with normal systolic function who also had a normal LA pressure shown by a normal pulmonary venous flow velocity pattern, being well hydrated with no concomitant congestive heart failure, LV presented a normal diastolic function [28]. Angiotensin system profiles are thought to be related to LV mass and LV diastolic function. Weber and Brilla [29] suggested that aldosterone directly stimulates LV remodeling in hypertensive patients. Chang and associates [30] reported a significant correlation between 24-h urinary aldosterone level and LV diastolic filling profile, specifically transmitral E:A ratio, in white-coat hypertensive subjects. In animal studies with spontaneously hypertensive rats, it has been demonstrated that myocardial angiotensin II leads to a change in ratio of collagen phenotypes and an increase in collagen content, resulting in a deterioration of diastolic function [31–33]. Ex-

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trapolating from results of studies on hypertensive hearts, we can postulate that normal LV diastolic filling profile is mediated at least partially by normal activity in the renin–angiotensin–aldosterone system, and is not related to increases in LV dimension and mass in highly trained baseball players. There are several possible explanations for the increased LV dimension and mass in elite baseball players. First, in athletes there is an increase in parasympathetic tone and a resultant bradycardia [34]. Diastolic filling time is increased, and LV dilatation occurs. Second, during endurance-type exercise, athletes experience a vast increase in cardiac output without large pressure loads, and LV is exposed to an additional volume load. This can lead to cardiac hypertrophy characterized by an increase in myofibrils in series [35]. The stimulus for series growth is an increase in preload (i.e., diastolic wall stress), resulting in a pattern of eccentric hypertrophy. There are several limitations in our present study. Frequency, duration, and intensity of training influence cardiovascular response in athletes. However, quantification of exercise is controversial. Although individual response would be different, ideally stimuli should be both uniform and measurable. Unfortunately, this type of study design seems to be unrealizable. An impartial measure of training level, such as maximal oxygen consumption, anaerobic threshold, or power-duration product is necessary to recognize a significant training effect and to compare groups. These indices appear to correlate with some cardiac changes associated with training. Also, a group of measurably and uniformly sedentary individuals is necessary for controlled study. Altered cardiac structure and function may be detected in those individuals who had been engaged in different sports for variable periods previously. The possibility of involvement of genetic factors in cardiac modification of an individual may be an important indication that some of the features of athletic heart are not acquired. Sensitivity of diastolic filling indices for detection of abnormalities may be inadequate because of the complex and variable relationship between myocardial properties and diastolic filling. Studies involving angiotensin II measurement may be essential for a clearer assessment of the causality between the renin–angiotensin–aldosterone axis and diastolic function. It is not clear whether long-term physically

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strenuous exercise, for example more than 20 years, can induce a diastolic dysfunction. Longitudinal study is probably required to address this problem.

5. Conclusion Our present study clearly demonstrates that LV diastolic filling profiles in highly trained baseball athletes do not differ from those of sedentary individuals. A normal LV diastolic filling profile, which is mediated partly by normal activity in angiotensin system, is not related to increases in LV dimension or mass in elite baseball players.

Acknowledgements The authors wish to express their thanks to Mr Hu Cheng (President) and Mr Ming-Cheng Lin (Director of the Department of Sports Training Science), Taipei Physical Education College, Taipei, Taiwan for providing cases for this study.

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