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Clinical Science (2002) 103, 249–257 (Printed in Great Britain) Left ventricular long-axis diastolic function is augmented in the hearts of endurance-trained compared with strength-trained athletes Dragos VINEREANU, Nicolae FLORESCU, Nicholas SCULTHORPE, Ann C. TWEDDEL, Michael R. STEPHENS and Alan G. FRASER Department of Cardiology, University of Wales College of Medicine, Heath Park, Cardiff CF14 4XN, Wales, U.K. A B S T R A C T In order to determine left ventricular global and regional myocardial functional reserve in endurance-trained and strength-trained athletes, and to identify predictors of exercise capacity, we studied 18 endurance-trained and 11 strength-trained athletes with left ventricular hypertrophy (172p27 and 188p39 g/m2 respectively), and compared them with 14 sedentary controls. Global systolic (ejection fraction) and diastolic (transmitral flow) function, and regional longitudinal and transverse myocardial velocities [tissue Doppler echocardiography (TDE)], were measured at rest and immediately after exercise. In endurance-trained compared with strength-trained athletes, resting heart rate was lower (59p11 and 76p9 beats/min respectively ; P 0.001), and the increase at peak exercise was greater (j211 % and j139 % respectively ; P 0.001). In addition, exercise duration, workload, maximal oxygen consumption and global systolic functional reserve (but not peak ejection fraction) were higher in the endurance-trained athletes, and resting global diastolic function (E/A ratio 1.62p0.40 compared with 1.18p0.23 ; P 0.01) (where E-wave is peak velocity of early-diastolic mitral inflow and A-wave is peak velocity of mitral inflow during atrial contraction) and long-axis diastolic velocities (ETDE/ATDE ratio 2.2p1.2 compared with 1.1p0.3 ; P 0.01) (where ETDE and ATDE represent peak early- and late-diastolic myocardial or tissue velocity respectively) were augmented. Systolic velocities were similar. Exercise capacity was best predicted from end-diastolic diameter index and E/A ratio at rest, and end-diastolic volume index and diastolic longitudinal velocity during exercise (r l 0.74, n l 43, P 0.001). In conclusion, endurance-trained athletes had higher left ventricular long-axis diastolic velocities, augmented global early diastolic filling, and greater chronotropic and global systolic functional reserve. Maximal oxygen consumption was determined by diastolic loading and early relaxation rather than by systolic function, suggesting that dynamic exercise training improves cardiac performance by an effect on diastolic filling. INTRODUCTION Two morphological forms of ‘ athlete’s heart ’ can be distinguished : a strength-trained heart, present in athletes undertaking mainly isometric exercise such as weight- lifting, and an endurance-trained heart, present in athletes involved in sports with a high dynamic component such as running [1,2]. Strength-trained athletes are presumed to develop concentric hypertrophy secondary to pressure overload, whereas endurance-trained athletes develop Key words : athlete’s heart, cardiac function, tissue Doppler echocardiography. Abbreviations : A-wave, peak velocity of mitral inflow during atrial contraction ; A , peak late-diastolic myocardial or tissue TDE velocity ; EDDI, end-diastolic diameter index ; EDVI, end-diastolic volume index ; EDVI.ex, EDVI immediately after exercise ; E-wave, peak velocity of early-diastolic mitral inflow ; E , peak early-diastolic myocardial or tissue velocity ; met, TDE metabolic equivalent ; TDE, tissue Doppler echocardiography ; V} o max, peak oxygen consumption. # Correspondence : Dr Alan Fraser (e-mail fraserag!cf.ac.uk). # 2002 The Biochemical Society and the Medical Research Society 249 250 D. Vinereanu and others eccentric hypertrophy related to volume overload. Although cardiac structure and global function have been investigated extensively, mainly at rest, there are few data regarding regional function at rest and exercise in the two groups of athletes [3]. Tissue Doppler echocardiography (TDE) allows the quantification of myocardial velocities from different ventricular segments. Tissue Doppler data can be acquired in digital format from every region of the ventricles at the same time as grey-scale images are acquired, and the data can then be analysed off-line after an echo study [4]. This allows rapid acquisition of data and much more detailed study of regional function than has been possible previously during exercise. Functionally, there are two major myocardial layers in the left ventricle, with fibres in the subepicardial layer being orientated in a circumferential direction, and those in the subendocardial layer being aligned longitudinally between apex and base. The first group of fibres is responsible principally for short-axis shortening, and the second group is responsible principally for long-axis dynamics [5]. Since longitudinal fibres are connected anatomically to the mitral annulus, long-axis function can be measured from the mitral annular velocities by tissue Doppler [6]. In comparison, short-axis function is measured from tissue Doppler sampling of the septum and posterior wall. The aims of the present study were to assess short-axis and long-axis function of the left ventricle in strengthtrained and endurance-trained athletes, at rest and at peak exercise, in order to determine differences in regional myocardial function or cardiac reserve between the two groups, and by comparison with normal subjects to identify which aspects of myocardial function correlate best with peak exercise capacity. METHODS Subjects A total of 43 male subjects were enrolled into the study : 29 competitive club athletes (11 weight-lifters and 18 long-distance runners) and a control group of 14 agematched sedentary, normal subjects. Athletes were included if they had an increased left ventricular mass index 131 g\m# [7]. Each participant had trained for at least 7 h\week (aerobic and anaerobic exercise) for the last 5 years (11p2 h\week for 10p5 years). Three of the weight-lifters admitted to the use of anabolic steroids for a period of between 2 and 12 months during their training. All athletes and control subjects were normotensive and non-smokers. All subjects were studied after abstention from caffeine for 12 h. The protocol was approved by the Local Research Ethics Committee, and each subject gave informed consent. # 2002 The Biochemical Society and the Medical Research Society Figure 1 Representative recording showing measurement of the velocities of lateral mitral annular motion from digitally acquired data Off-line velocities were : systolic velocity, 11.30 cm/s ; E-wave velocity, k13.34 cm/s ; A-wave velocity, k6.76 cm/s. Baseline echocardiography Studies were performed using a commercially available ultrasound system equipped with tissue Doppler capabilities (Vingmed System 5), using a 2.5 MHz transducer, with subjects in the left lateral decubitus position. The electrocardiogram was recorded simultaneously. Standard echocardiographic studies consisted of Mmode, cross-sectional and Doppler blood flow measurements. M-mode tracings from the parasternal long-axis view were used to measure the diameter of the aortic root, the diameter of the left atrium, the end-diastolic diameter of the right ventricle, and septal thickness, left ventricular diameter and posterior wall thickness, in systole and diastole. Pulsed-wave Doppler echocardiography of transmitral flow was used to assess global diastolic filling. The sample volume was placed at the tips of the mitral leaflets in the apical four-chamber view. The following Doppler indices were measured : peak velocity of early-diastolic mitral inflow (E-wave), peak velocity of mitral inflow during atrial contraction (A-wave), E-wave deceleration time and isovolumic relaxation time. The E\A ratio was calculated. Left ventricular inflow was also recorded by colour M-mode echocardiography, and flow propagation velocity was measured [8]. For TDE, digital image loops containing two complete cardiac cycles were recorded during passive held endexpiration, with colour tissue Doppler superimposed on grey-scale images and downloaded directly to a Macintosh computer. Tissue Doppler data were analysed offline using customized software (Echopac TVI GE Diastolic function in athletes Vingmed, version 6.0). Grey-scale images of apical fourand two-chamber views were displayed for the measurement of end-diastolic and end-systolic cross-sectional areas, and left ventricular cavity length. Colour tissue Doppler cine! -loops were displayed of the parasternal long-axis view for measurements of shortaxis function at the mid-septum and mid-posterior wall ; of the four-chamber view for measurements of long-axis function at the lateral and medial sites of the mitral annulus and the lateral tricuspid annulus ; and of the twochamber view for the anterior and inferior sites of the mitral annulus. The sample volume was positioned in systole over each investigated site of the annulus. For each location, a tissue velocity profile was displayed and the following parameters were measured as the average from two beats : peak systolic velocity, and peak early (ETDE) and late (ATDE) diastolic myocardial or tissue velocities (Figure 1). The ETDE\ATDE ratio was calculated. Doppler traces were rejected for analysis, and an alternative adjacent site for the sample volume on the computer screen was sought if the velocity profiles of the two heartbeats differed considerably. Right ventricular function was assessed by measuring tricuspid annular velocities. Exercise protocol Graded treadmill exercise testing was performed using an extended Bruce protocol, until exhaustion. Blood pressure (by sphygmomanometer), heart rate, ECG and cardiopulmonary function were monitored. Breath-by-breath gas exchange analysis was performed using a commercially available metabolic cart (MedGraphics Corp., St. Paul, MN, U.S.A.). The pneumotachygraph was calibrated using a 3-litre syringe at five different flow rates. Respiratory gas was sampled continuously from a mouthpiece, and analysed using a zirconia cell oxygen analyser and a single-beam IR carbon dioxide analyser. The signals underwent analogue-todigital conversion for the calculation of peak oxygen consumption (VI O max). This was defined as the highest # measured oxygen consumption value over the last 10 s of exercise. Immediately after exercise, the subjects were placed in the left lateral decubitus position. Tissue Doppler loops from the apical views and parasternal long-axis view were acquired digitally and stored, within 2 min of the termination of exercise, for the subsequent measurement of immediate post-exercise ejection fraction and exercise myocardial velocities ; calculations of cardiac output were made from measurements of the apical images recorded from 30 s to 60 s after maximal exercise. Echocardiography data analysis Left ventricular volumes and mass were indexed by body surface area. Left ventricular volumes and ejection fraction were calculated by the modified biplane Simpson’s method [9]. End-systolic wall stress (ESWS), in units of 10$ dyn\cm#, was calculated according to the following validated formula : ESWS l 0.334iSBPioLVESD\ [(1jLVSPW\LVESD)iLVSPW]q where SBP is systolic blood pressure (mmHg) measured by a cuff sphygmomanometer, LVESD is left ventricular end-systolic diameter and LVSPW is left ventricular endsystolic posterior wall thickness (cm) [10]. Left ventricular (LV) mass was estimated by the method of Devereux [7] with the application of the Penn convention : LV mass (g) l 1.04i[(IVSDjLVDPWjLVEDD)$ kLVEDD$]k13.6 where IVSD is septal thickness, LVDPW is posterior wall thickness and LVEDD is left ventricular diameter, all measured at the end of diastole [7]. Reproducibility Detailed studies of inter-observer agreement have been reported elsewhere [11]. Ten randomly selected studies were analysed by nine observers, and each pooled S.D. was divided by its corresponding mean value, to give a coefficient of variation (in %). Coefficients of variation for measurements of peak systolic long-axis velocities were 9–14 % at rest. For measurements of myocardial E velocities in basal segments at rest, coefficients of variation were 11–22 %. Statistical analysis Statistical analysis was performed with SPSS software (version 9.0). Results are presented as mean values p S.D. Differences between groups were tested for significance using ANOVA, with post-hoc analysis by the Scheffe' F test. Changes in variables from baseline to exercise were compared by paired-sample t tests. Correlations between variables were performed using the Pearson bivariate two-tailed test. Univariate linear regression analysis was performed, and also stepwise multiple linear regression analysis (criteria : probability-of-F-to-enter 0.05 ; probability-of-F-to-remove 0.10) to identify the best predictors of VI O max. The variables that were tested are # given in the Results section. P 0.05 for a two-tailed test was considered significant. RESULTS General clinical and resting echocardiographic characteristics of the three groups are given in Table 1. There were no differences between weight-lifters and runners # 2002 The Biochemical Society and the Medical Research Society 251 252 D. Vinereanu and others Table 1 General characteristics of the study groups at rest RV, right ventricle ; LV, left ventricle ; ED, end-diastolic ; ES, end-systolic ; ESWS, end-systolic wall stress. Significance of differences : *P 0.05 compared with endurance-trained athletes ; †P 0.05 compared with controls. Table 2 Parameter Strength-trained athletes (n l 11) Endurance-trained athletes (n l 18) Controls (n l 14) Age (years) Body surface area (m2) Systolic blood pressure (mmHg) Diastolic blood pressure (mmHg) Aortic root diameter (mm) Left atrial diameter (mm) RV ED diameter (mm) Septal thickness (mm) LV posterior wall thickness (mm) LV ED diameter index (mm/m2) LV ES diameter index (mm/m2) LV mass index (g/m2) ESWS (103 dyn/cm2) 36p6 2.06p0.19*† 139p12 83p9 34p2 41p5 28p4† 13p1† 13p1*† 27p3* 17p3 188p39† 52p16 40p10 1.89p0.15 140p19 81p9 33p4 40p4 26p3† 13p1† 12p1† 29p3† 18p2† 172p27† 58p21 39p12 1.99p0.11 136p11 80p9 35p3 37p4 21p3 10p1 9p1 26p1 15p2 106p14 56p14 Resting and exercise systolic myocardial velocities ST, strength-trained athletes ; ET, endurance-trained athletes ; IVS, ventricular septum ; PW, left ventricular posterior wall ; LMA, lateral mitral annulus ; MMA, medial mitral annulus ; AMA, anterior mitral annulus ; IMA, inferior mitral annulus ; TA, lateral tricuspid annulus. All results are quoted as meanspS.D. Velocity (cm/s) Rest Immediate post-exercise Site ST ET Controls ST ET Controls IVS PW LMA MMA AMA IMA TA k3.6p1.6 5.1p1.8 7.1p2.3 7.7p1.3 7.6p2.0 8.3p1.6 11.7p2.3 k3.3p1.6 5.2p1.4 8.4p1.6 7.3p1.1 7.8p1.8 7.8p1.5 10.7p2.2 k3.0p1.1 5.7p1.3 8.3p2.7 7.3p1.5 8.2p1.9 8.0p1.4 10.3p1.3 k7.1p1.5 10.8p2.3 16.1p1.3 16.6p1.8 16.3p2.1 16.8p1.2 21.0p6.9 k7.3p3.2 11.3p3.5 17.8p2.7 15.7p2.9 16.3p3.0 16.1p3.0 21.0p5.0 k6.0p2.5 10.2p3.0 16.6p5.2 13.7p3.4 15.4p4.4 15.1p2.5 19.5p6.1 with regard to duration of training (10 p 2 h\week for 9 p 3 years and 11 p 2 h\week for 10 p 5 years respectively). Resting heart rate was significantly lower in endurance-trained athletes (59 p 11 beats\min) than in strength-trained athletes (76 p 9 beats\min ; P 0.001). Resting blood pressure was similar in the three groups. Exercise data The increase in heart rate from rest to peak exercise was greater in endurance-trained athletes (j121p13 beats\ min ; j211 %) than in strength-trained athletes (j103p 16 beats\min ; j139 %) (P 0.001). However, the peak exercise heart rate was not different between the two groups of athletes (runners, 180p18 beats\min ; weight-lifters, 179p11 beats\min). Peak exercise blood pressure was also similar in the three groups (runners, 229p15 mmHg ; weight-lifters, 223p16 mmHg ; con# 2002 The Biochemical Society and the Medical Research Society trols, 221p18 mmHg). Exercise duration, exercise workload and VI O max were significantly higher in # endurance-trained athletes [15p2 min, 18p3 metabolic equivalents (mets) and 51p8 ml : min−" : kg−" respectively] than in strength-trained athletes (12p2 min, 14p3 mets and 36p7 ml : min−" : kg−" respectively ; all P 0.01 compared with endurance-trained athletes) and in normal subjects (13p2 min, 14p2 mets and 32p7 ml : min−" :kg−" respectively ; all P 0.01 compared with endurance-trained athletes). Global systolic function There were no significant differences between the groups in resting ejection fraction (61p5 %, 62p6 % and 66p 6 % respectively for runners, weight-lifters and normal subjects). On exercise, the ejection fraction increased by 18 % from resting values in runners (to an absolute value Diastolic function in athletes of 71p7 % ; P 0.05), by 12 % in weight-lifters (to 70p5 % ; P 0.05), and by 8 % in controls (to 71p6 % ; P 0.05) (P 0.05 for runners compared with controls). The ejection fraction on exercise did not differ significantly between the groups. In both groups of athletes, the end-diastolic volume index (EDVI) did not change significantly from rest to peak exercise (j2.6 % in runners ; j0.5 % in weight-lifters), whereas the end-systolic volume index decreased by 22 % in runners and by 18 % in weight-lifters (P 0.05). In normal subjects, both volume indices decreased at peak exercise (end-diastolic volume by 12 % and endsystolic volume by 27 % ; both P 0.01). The cardiac index increased by 274 % (from 4.1p1.4 to 13.9p 2.2 litres : min−" : m−#) in runners and by 165 % (from 5.5p1.4 to 14.2p3.5 litres :min−" : m−#) in weight-lifters (P 0.001 for the relative increases ; peak values not significantly different), in comparison with 142 % in normal subjects (from 4.5p1.3 to 10.4p1.9 litres : min−" : m−#). Regional systolic function Resting and peak exercise systolic velocities were not significantly different between the three groups, for either left ventricular long-axis or short-axis contraction, or for tricuspid annular motion (Table 2). Long-axis systolic velocities averaged at four annular sites increased at peak exercise by 115p37 % in runners, by 111p44 % in weight-lifters and by 101p42 % in normal subjects, whereas averaged short-axis systolic velocities increased by 115p49 % in runners, by 131p85 % in weight-lifters and by 91p50 % in normal subjects ; none of these changes was significantly different between groups. Global diastolic function Resting global diastolic function differed between endurance-trained and strength-trained athletes. Although E-wave velocity was not different between the two groups (runners, 83p16 cm\s ; weight-lifters, 84p 18 cm\s), the runners had a lower A-wave velocity (53p13 cm\s compared with 72p11 cm\s ; P 0.001), and an increased E\A ratio (1.62p0.40 compared with 1.18p0.23 ; P 0.01). At rest, E-wave deceleration time, isovolumic relaxation time and flow propagation velocity were not significantly different between the two groups of athletes or between them and the normal subjects : the E-wave deceleration times were 119p37 ms in the runners, 174p33 ms in the weight-lifters and 176p38 ms in the control subjects ; isovolumic relaxation times were 103p18, 78p26 and 84p15 ms respectively ; and mitral inflow propagation velocities were 61p12, 61p10 and 63p15 cm\s respectively. Regional diastolic function Endurance-trained athletes had augmented long-axis diastolic function at rest compared with strength-trained Figure 2 Graphs showing early diastolic myocardial velocities (top), late diastolic velocities (middle), and myocardial ETDE/ATDE ratio (bottom), measured at rest by tissue Doppler across the four sites of the mitral annulus LMA, lateral mitral annulus ; MMA, medial mitral annulus ; AMA, anterior mitral annulus ; IMA, inferior mitral annulus. Open bars, strength-trained athletes ; Closed bars, endurance-trained athletes ; hatched bars, normal subjects. Significance of differences : * P 0.05 for comparison between the two groups of athletes. athletes (Figure 2). The mean ETDE\ATDE ratios at the four annular sites at rest were 2.22p1.17 in runners, 1.09p0.26 in weight-lifters, and 1.64p0.54 in controls (P 0.01). The only difference between the groups for the short-axis diastolic velocities at rest was a lower myocardial ATDE wave in the left ventricular posterior wall in endurance-trained athletes, resulting in a higher ETDE\ATDE ratio in this segment. Immediately after exercise, diastolic mitral annular velocities were similar for runners and weight-lifters : 16.8p3.3 compared with 13.3p3.7 cm\s, 14.8p3.2 compared with 16.7p 3.5 cm\s, 15.5p3.6 compared with 12.6p3.0 cm\s, and 15.8p3.3 compared with 15.9p2.6 cm\s respectively for the lateral, medial, anterior and inferior mitral annulus, # 2002 The Biochemical Society and the Medical Research Society 253 254 D. Vinereanu and others when ETDE and ATDE velocities could be measured separately. achieved a greater increase in heart rate than did the weight-lifters. Overall, exercise capacity was determined by diastolic rather than systolic function. Oxygen consumption The strongest univariate predictors of VI O max, analysed # in all 43 subjects together, were : from the haemodynamic measurements, percentage increment in heart rate from baseline to peak exercise (r l 0.63, P 0.001) ; from Mmode echocardiographic indices, resting end-diastolic diameter index (EDDI) (r l 0.57, P 0.001) ; from the biplane cross-sectional echocardiographic data, EDVI immediately after exercise (EDVI.ex) (r l 0.47, P 0.01) ; from the conventional Doppler indices of global ventricular filling, the mitral E\A ratio at rest (r l 0.46, P 0.01) ; and from the off-line tissue Doppler parameters of regional myocardial function, the four-site averaged mitral annular ETDE\ATDE ratio at rest (r l 0.49, P 0.001) and the averaged maximal diastolic velocity immediately after exercise (r l 0.45, P 0.01). End-systolic volume index at rest was a less strong predictor (r l 0.39, P 0.05), whereas end-systolic volume index immediately after exercise did not show a significant correlation (r l 0.26). Left ventricular mass index was a weak predictor (r l 0.32, P 0.05). All of these variables, both at rest and on exercise, and also age, blood pressure, systemic pulse pressure and cardiac index, were included in a stepwise multiple linear regression analysis. The best prediction of VI O max was # obtained from a combination of resting EDDI and resting mitral E\A ratio (E\A), EDVI.ex and averaged maximal diastolic longitudinal velocity (meanE.ex) (r l 0.74, r# l 0.55, F l 11.0, P 0.001) : VI O max l k34.36j(1.02iEDDI)j(8.58iE\A)j # (0.28iEDVI.ex)j(1.38imeanE.ex) Since the morphological pattern is different in strengthtrained athletes (marked left ventricular hypertrophy without cavity enlargement), the linear regression analysis was repeated for the endurance-trained athletes and normal controls only. Three variables predicted VI O max # well ; these were EDDI at rest, EDVI.ex and averaged maximal diastolic longitudinal velocity after exercise (meanE.ex) (r l 0.79, r# l 0.63, F l 14.8, P 0.001) : VI O max l k43.25j(1.42iEDDI)j(0.40iEDVI.ex) # j(1.73imeanE.ex) DISCUSSION Our study showed that endurance-trained athletes had augmented left ventricular long-axis early diastolic filling velocities compared with strength-trained athletes, resulting in better global diastolic function. The runners # 2002 The Biochemical Society and the Medical Research Society Strength-trained compared with endurancetrained athletes Morganroth et al. [1] were the first to suggest that two different forms of ‘ athlete’s heart ’ can be distinguished : the strength-trained heart and the endurance-trained heart. Adaptation of the heart to strength training can be accounted for by the blood pressure response during weight-lifting, which can increase to levels as high as 320\250 mmHg [12]. Strength-trained athletes usually develop a large increase in left ventricular wall thickness, but only a slight increase in left ventricular diameters [3,13]. In contrast, during long-distance running, the heart has to adapt to both volume and pressure loads, and endurance-trained athletes develop an increase in both left ventricular diameter and wall thickness (usually described as ‘ eccentric ’ hypertrophy) [3,13]. At baseline, we found only minor structural differences between the two groups of athletes (Table 1), which was in accordance with a recent meta-analysis [3]. Global ejection fraction and regional systolic function, measured from the velocities of myocardial segments, were also similar in the two trained groups and in normal subjects. However, endurance-trained athletes had evidence of increased early diastolic filling compared with strengthtrained athletes, whether this was assessed globally or regionally from long-axis velocities. Diastolic function in athletes Athlete’s heart is associated with normal or supranormal diastolic function at rest, and better diastolic performance than normal subjects during exercise [14,15]. Moreover, the left ventricular diastolic dysfunction associated with ‘ normal ’ ageing is less pronounced in exercise-trained individuals [16]. Endurance-trained athletes have better global diastolic function than strength-trained athletes, as we have confirmed, but measurements of transmitral flow have shown only small differences (E\A ratio 2.20 compared with 2.11 ; not significant) [3]. Regional diastolic function can now be assessed by measuring myocardial diastolic velocities by tissue Doppler. For example, a ratio of early\late velocities of mitral annular motion of 1 has been shown to have fairly good sensitivity and specificity ( 70 %) for detecting diastolic dysfunction, even in patients with a pseudonormal E\A ratio [17]. It has been suggested that myocardial diastolic velocities may be useful as less loaddependent indices [18,19], but this requires further investigation. Using TDE, we have shown that endurance-trained athletes had better long-axis diastolic function at rest than strength-trained athletes, whereas short-axis di- Diastolic function in athletes astolic velocities were similar. Both global and long-axis diastolic function at rest were correlated with VI O max, # suggesting that increased exercise capacity in runners might be explained by augmented diastolic functional reserve in the long axis. The greater E\A ratio in endurance-trained athletes, without any increase in absolute E-wave velocity, suggests less dependence in trained hearts on the atrial contribution to global diastolic filling at rest, because of ‘ supranormal ’ early diastolic relaxation or ventricular suction. If this is true, endurance-trained athletes would demonstrate a greater increase in atrial-phase filling on exercise ; however, assessment of myocardial diastolic function on exercise was limited because of fusion of the E and A velocities. Maximal long-axis filling velocities were similar in all three groups of subjects. Systolic function in athletes during exercise Our study showed that endurance-trained athletes increase their cardiac output on exercise through a more prominent augmentation of their heart rate and ejection fraction than do strength-trained athletes. Immediately after exercise, the ejection fraction was increased due to a reduction of end-systolic volume, whereas end-diastolic volume remained unchanged. These findings differ from results reported at submaximal exercise in endurancetrained athletes, when end-diastolic volume was increased by 14 % [20,21]. In our study, there were no significant differences between the types of athlete with regard to left ventricular systolic velocities, either at rest or immediately after exercise. Weight-lifters had the highest mean left ventricular mass index, but, on average, their systolic myocardial velocities and their peak exercise capacity were similar to those of sedentary controls. Exercise capacity The volunteers recruited for this study were club athletes rather than elite international athletes, but we nevertheless observed changes, e.g. in resting EDVI and left ventricular mass index, that were similar to those reported previously [3]. In our view, the subjects constituted a suitable population in which to test for correlations between haemodynamic parameters and VI O max ; the # range of VI O max was from 21.9 to 60.3 ml : min−" : kg−". # The major cardiac determinants of VI O max that were # observed in the present study were all related to diastolic loading or to early diastolic filling. Increases in the early diastolic lengthening velocity of the long-axis of the left ventricle (ETDE) were correlated with increased VI O max, # implying that ventricular suction is augmented in endurance-trained athletes. In normal subjects, the left ventricular stroke volume index increases linearly at low levels of exercise, but then reaches a plateau, so that any further increases in cardiac index at peak exercise have to come from an increase in heart rate [22]. EDVI reaches its peak at approx. 40 % of VO max ; beyond this level of exercise, it remains # unchanged or decreases slightly, so stroke volume is maintained by a fall in end-systolic volume index [22]. These data, and the findings in our study, suggest that left ventricular filling becomes constrained during exercise, perhaps when ventricular interaction occurs. In experimental studies in animals, maximal cardiac output is limited by the development during exercise of pericardial constraint [23], and maximal end-diastolic volumes and cardiac output at peak exercise are increased following pericardiectomy [23,24]. Our data in humans are consistent with the hypothesis that endurance-trained athletes, but not strength-trained athletes, augment cardiac performance by increasing early diastolic filling, through chronic adaptive enlargement of the pericardial cavity in response to repeated volume overload during training. The strength-trained athletes in our study had the greatest mean left ventricular mass index, but this adaptive hypertrophy caused by isometric exercise did not translate into better total exercise capacity compared with the normal subjects. Resting systolic myocardial velocities were similar in the athletes and normal subjects, but the endurance-trained athletes had better dynamic exercise capacity. Our study has demonstrated that this correlates instead with increased end-diastolic volume and with myocardial E\A velocities. Two previous studies have also addressed the relationship between diastolic function and exercise capacity, but they were less ‘ physiological ’ than our present study, and neither employed methods that were able to characterize regional myocardial function in detail or immediately after exercise. Levy and colleagues [25] used radionuclide methods during supine bicycle exercise, whereas Vanoverschelde and colleagues [26] compared VI O max during upright bicycle exercise. In the multiple # linear regression analyses to identify predictors of VI O # max, the haemodynamic variables selected were peak early filling rate [25] ; and the ratio of early to late transmitral filling velocities (E\A ratio) as well as left ventricular end-systolic volume index at rest [26]. After endurance exercise training, mitral A velocity decreased [25], similar to the findings in endurance-trained athletes in the present study, and also suggesting improved early diastolic filling rather than the development of a mild restrictive filling pattern. Our study extends the observations of these previous reports by demonstrating that the predominant effect of endurance training is on longitudinal diastolic function, and by identifying that regional diastolic function during exercise is also a significant predictor of VI O max. # Study limitations Three of the weight-lifters admitted that they were taking anabolic steroids, but we did not confirm this objectively. The use of anabolic steroids during physical training by # 2002 The Biochemical Society and the Medical Research Society 255 256 D. Vinereanu and others intensive resistance exercise probably exacerbates the development of left ventricular hypertrophy, but effects on diastolic function have not been proven [27–30]. In our study none of the weight-lifters taking anabolic steroids had diastolic dysfunction, defined as an E\A ratio of 1 and\or an ETDE\ATDE ratio of 1, and therefore they were not excluded. Furthermore, on removing these three cases from the analysis, differences between groups remained significant. It is not possible to perform detailed echocardiographic studies of regional myocardial function during upright dynamic exercise. Treadmill exercise was chosen for the present study, since it provides the most ‘ normal ’ physiological stress, leading to the unavoidable compromise that changes in heart function could be recorded only immediately after exercise. Acquisition of data was limited to those recordings that could be made within 2 min of the end of exercise, and in each subject recordings were obtained in the same sequence (apical views before parasternal views). The storage of digital loops containing full echocardiographic data allowed regional function to be studied in detail by subsequent post-processing. Myocardial early diastolic velocities correlate inversely with heart rate, and thus higher long-axis ETDE velocities in endurance-trained athletes might be related to their lower resting heart rate and increased end-diastolic volume. However, in adults without sinus tachycardia, this difference is unlikely to be a confounding factor for our results. Immediately after exercise (i.e. within 1 min), there are substantial and significant decreases from peak values in heart rate, systolic blood pressure and cardiac output [31]. There is an acute but transient increase in ejection fraction, due predominantly to a sudden reduction in end-systolic volume, caused by an immediate fall in venous return as the pumping effect of skeletal muscle contraction is lost and as splanchnic vasoconstriction is reversed. At 2 min, haemodynamic loading and performance remain significantly different from baseline [31]. Thus the measurements that we obtained will have underestimated peak changes ; nonetheless ‘ peak ’ cardiac index was 14 litres : min : m−# on average, in runners who had reached a VI O max of approx. 50 ml : min−" : kg−". # However, there are no published data to suggest that there might be any differences between groups in the rates of change of haemodynamic parameters after exercise, and so we consider that the comparisons between groups remain valid. There are some concerns about the equipment that we used, in that it may not accurately measure VI O max in # elite athletes because of the delay between volume and expired gas fraction measurements. 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