Download Left ventricular long-axis diastolic function is

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.
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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.
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Correspondence : Dr Alan Fraser (e-mail fraserag!cf.ac.uk).
# 2002 The Biochemical Society and the Medical Research Society
249
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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
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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
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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
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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
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range of VI O max was from 21.9 to 60.3 ml : min−" : kg−".
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The major cardiac determinants of VI O max that were
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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. However, subjects in
our study were club and not elite athletes, and our
purpose was not to ascertain VI O max, but to study its
#
main predictors.
# 2002 The Biochemical Society and the Medical Research Society
We measured left ventricular longitudinal function
from the velocities of mitral annular motion, which are
higher than velocities recorded when the sample volume
is placed over the adjacent basal segments of myocardium.
Thus the absolute velocities reported should only be
compared with other data that have been obtained offline, with the same technique.
CONCLUSION
Endurance-trained athletes had augmented left ventricular long-axis diastolic function compared with strengthtrained athletes, resulting in augmented global diastolic
function. They had also a higher chronotropic and global
systolic functional reserve. These changes are responsible
for the increased exercise capacity of endurance-trained
athletes.
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Received 15 January 2002/4 April 2002; accepted 27 May 2002
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