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The effects on left and right ventricular (LV, RV) volumes during physical exercise remains controversial. Furthermore, no previous study has investigated the effects of exercise on longitudinal contribution to stroke volume (SV) and the outer volume variation of the heart. The aim of this study was to determine if LV, RV and total heart volumes (THV) as well as cardiac pumping mechanisms change during physical exercise compared to rest using cardiovascular magnetic resonance (CMR). 26 healthy volunteers (6 women) underwent CMR at rest and exercise. Exercise was performed using a custom built ergometer for one-legged exercise in the supine position during breath hold imaging. Cardiac volumes and atrio-ventricular plane displacement were determined. Heart rate (HR) was obtained from ECG. HR increased during exercise from 60+/-2 to 94+/-2 bpm, (p<0.001). LVEDV remained unchanged (p=0.81) and LVESV decreased with -9+/-18% (p<0.05) causing LVSV to increase with 8+/-3% (p<0.05). RVEDV and RVESV decreased by -7+/-10% and -24+/-14% respectively, (p<0.001) and RVSV increased 5+/-17% during exercise although not statistically significant (p=0.18). Longitudinal contribution to RVSV decreased during exercise by -6+/-15% (p<0.05) but was unchanged for LVSV (p=0.74).THV decreased during exercise by -4+/-1%, (p<0.01) and total heart volume variation (THVV) increased during exercise from 5.9+/-0.5% to 9.7+/-0.6% (p<0.001). Cardiac volumes and function are significantly altered during supine physical exercise. THV becomes significantly smaller due to decreases in RVEDV whilst LVEDV remains unchanged. THVV and consequently radial pumping increases during exercise which may improve diastolic suction during the rapid filling phase.
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R E S E A R C H Open Access
Moderate intensity supine exercise causes
decreased cardiac volumes and increased outer
volume variations: a cardiovascular magnetic
resonance study
Katarina Steding-Ehrenborg
, Robert Jablonowski
, Per M Arvidsson
, Marcus Carlsson
, Bengt Saltin
and Håkan Arheden
Background: The effects on left and right ventricular (LV, RV) volumes during physical exercise remains
controversial. Furthermore, no previous study has investigated the effects of exercise on longitudinal contribution
to stroke volume (SV) and the outer volume variation of the heart. The aim of this study was to determine if LV, RV
and total heart volumes (THV) as well as cardiac pumping mechanisms change during physical exercise compared
to rest using cardiovascular magnetic resonance (CMR).
Methods: 26 healthy volunteers (6 women) underwent CMR at rest and exercise. Exercise was performed using a
custom built ergometer for one-legged exercise in the supine position during breath hold imaging. Cardiac
volumes and atrio-ventricular plane displacement were determined. Heart rate (HR) was obtained from ECG.
Results: HR increased during exercise from 60±2 to 94±2 bpm, (p<0.001). LVEDV remained unchanged (p=0.81)
and LVESV decreased with 9±18% (p<0.05) causing LVSV to increase with 8±3% (p<0.05). RVEDV and RVESV
decreased by 7±10% and 24±14% respectively, (p<0.001) and RVSV increased 5±17% during exercise although
not statistically significant (p=0.18). Longitudinal contribution to RVSV decreased during exercise by 6±15%
(p<0.05) but was unchanged for LVSV (p=0.74). THV decreased during exercise by 4±1%, (p<0.01) and total heart
volume variation (THVV) increased during exercise from 5.9±0.5% to 9.7±0.6% (p<0.001).
Conclusions: Cardiac volumes and function are significantly altered during supine physical exercise. THV becomes
significantly smaller due to decreases in RVEDV whilst LVEDV remains unchanged. THVV and consequently radial
pumping increases during exercise which may improve diastolic suction during the rapid filling phase.
Keywords: Physiology, Total heart volume variation, Ventricle, Cardiac pumping, Cardiovascular magnetic resonance
Total heart volume at rest has a strong correlation to
peak exercise capacity in healthy normal subjects and
athletes [1,2]. When going from rest to exercise the nor-
mal heart in a sedentary individual can increase its cardiac
output from 5 L/min to 2025 L/min [3]. This change has
been attributed to an increase in heart rate and stroke
volume. In turn, the stroke volume can increase either by
an increase in end-diastolic volume (EDV), decrease in
end-systolic volume (ESV), or both. The effects on left
ventricular (LV) volumes during physical exercise remain
controversial. Previous studies using radionuclide angiog-
raphy or echocardiography have shown both unchanged
and increased LV end-diastolic volumes (LVEDV) during
upright and supine exercise compared to resting values
in the same position [4-12]. Although most studies show
a decrease in ESV during exercise, Sundstedt et al. [12]
showed unchanged ESV during supine exercise using
echocardiography. Few studies have investigated the
* Correspondence:
Department of Clinical Physiology, Lund University, Lund University Hospital
Lund, Lund, Sweden
Full list of author information is available at the end of the article
© 2013 Steding-Ehrenborg et al.; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the
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distribution, and reproduction in any medium, provided the original work is properly cited.
Steding-Ehrenborg et al. Journal of Cardiovascular Magnetic Resonance 2013, 15:96
effects of exercise on the right ventricle [13,14] and further
studies are needed to understand how physical exercise af-
fects left and right cardiac volumes and subsequently the
stroke volume (SV).
Ventricular stroke volume is ejected by a combination
of longitudinal and radial contraction of the ventricle
[15-18]. At rest the longitudinal contribution to SV has
been shown to be 60% for the LV and 80% for the RV
and radial contribution is 40% and 20% respectively
[15,17,19]. It has been shown that during exercise there
is a significant increase in the mitral valve displacement
during exercise [20]. Longitudinal pumping is calculated
as the atrio-ventricular plane displacement (AVPD) multi-
plied by the short-axis area of the ventricle and an increase
in AVPD may therefore affect the longitudinal contribu-
tion to SV. Several studies have suggested that at higher
heart rates a larger longitudinal contribution may keep the
outer volume variation of the heart to a minimum render-
ing less energy to be wasted on moving surrounding tis-
sues [21-23]. However, this remains to be explored.
Therefore, the aim of this study was to determine left
and right ventricular volumes, left and right atrial vol-
umes and total heart volumes as well as longitudinal and
radial pumping during rest and physical exercise using
cardiovascular magnetic resonance (CMR).
This study was approved by the Regional Ethical Review
Board in Lund, Sweden and follows the Declaration of
Helsinki. All participants provided written informed con-
sent. All CMR examinations were performed at Skane
University Hospital Lund, Sweden.
Study population and experimental setup
Twenty-six healthy volunteers (six women) aged 30±8 years
(mean±SD) (range 1959) underwent CMR at rest and
during exercise with one-legged knee extensions. A custom
built MR-compatible ergometer provided concentric re-
sistance during knee extension by a rope and pulley sys-
tem which was integrated with a mechanically braked
flywheel. A strap connected to a variable weight system
provided resistance and weight was added to achieve an
exercise level at approximately 40 beats per minute
(bpm) higher than the subjectsresting heart rate. The
subjects were connected at the ankle to the axle of the
flywheel by a rope and the extension phase of the exer-
cise turned the flywheel. Gravity returned the leg to the
starting position and a gearing system on the axle
returned the rope to the starting position at the end of
each duty cycle.
Reproducibility of exercise measurements
Six subjects underwent a total of five CMR scans to in-
vestigate the reproducibility of volumetric measurements
during exercise and the potential effects of different re-
spiratory phases as well as differences in exercising muscle
mass. The scans were divided into two sessions with a
1.5 hour rest outside the scanner between them. Session 1
included a) CMR at rest; b) CMR with 1-legged exercise
at end-expiratory breath hold; and c) CMR with 2-legged
exercise at end-expiratory breath hold. Session 2 in-
cluded a) CMR with 1-legged exercise at end-expiratory
breath hold; and b) CMR with 1-legged exercise at end-
inspiratory breath hold with the instructions to keep an
open glottis and avoid Valsalva-like increases in intra-
thoracic pressures.
Cardiac magnetic resonance imaging
A 1.5T scanner (Philips Achieva, Philips, Best, The
Netherlands) with a 5 channel cardiac coil was used to
scan all subjects in the supine position. A balanced
steady-state free-precession (bSSFP) sequence with
retrospective ECG gating was used to acquire images of
the heart (repetition time typically 3.0 ms, turbo factor
16, echo time 1.5 ms, flip angle 60°, reconstructed to a
spatial resolution of 1.4 × 1.4 mm, acquired temporal
resolution typically 50 ms reconstructed to 30 ms, and
slice thickness 8 mm with no slice gap). After defining
the long-axis orientation of the heart, short-axis images
covering the heart from the base of the atria to the apex
of the ventricles were obtained. Breath-hold during
imaging during exercise was typically 6 s for long-axis
images and 810 s for each short-axis slice. An ECG-
triggered phase-contrast sequence was used to measure
blood flow in the aorta (repetition time 8.6 ms, echo
time 6.4 ms, 150 cm/s velocity encoding, slice thickness
8 mm). The measurement plane was positioned perpen-
dicular to the vessel. Heart rate was obtained from the
ECG during image acquisition.
Atrial and ventricular volumes
All measurements were done using the software Segment
1.8 ( [24]. Left and right atrial
volumes were measured in short-axis images at the time of
ventricular end-diastole and ventricular end-systole. Left
ventricular mass (LVM), end-diastolic volume (LVEDV),
end-systolic volume (LVESV) and stroke volume (LVSV)
were measured in short-axis images using planimetry, by
manual delineation of endocardial and epicardial borders
of the left ventricle. Papillary muscles were not included in
LVM measurements. Right ventricular end-diastolic vol-
ume (RVEDV), end-systolic volume (RVESV) and stroke
volume (RVSV) were measured in short-axis images by
manual delineation of the right ventricular endocardial and
epicardial border.
Total heart volume (THV) was measured in short-axis
images by planimetry [22] and was defined as the vol-
ume of all structures within the pericardium, including
Steding-Ehrenborg et al. Journal of Cardiovascular Magnetic Resonance 2013, 15:96 Page 2 of 8
myocardium, blood pool, atria, pericardial fluid and the
proximal parts of the great vessels.
Ventricular pumping
Atrio-ventricular plane displacement (AVPD) was deter-
mined from CMR long-axis images as previously de-
scribed [15]. Longitudinal pumping of the left and right
ventricle was calculated as the distance travelled by the
AV-plane multiplied by epicardial short-axis area of the
ventricle [25]. Radial pumping was determined from the
total heart volume variation (THVV) [15]. Longitudinal
and radial contribution to SV (%) was calculated as lon-
gitudinal pumping divided by SV and radial pumping di-
vided by SV.
Statistical analysis
Statistical analysis was performed using SPSS statistics
20 (IBM, Chicago, IL, USA) and a p-value <0.05 was
considered statistically significant. Paired t-tests were used
to test for changes between rest and exercise. Wilcoxon
non-parametric test was used to test for differences be-
tween rest and exercise in the subgroup of six subjects
who underwent a total of five scans to investigate the re-
producibility of measurements. Results are presented as
mean ±SEM unless stated otherwise. Inter-observer vari-
ability was determined for the left ventricular measure-
ments in ten subjects during rest and exercise.
Subject characteristics are presented in Table 1. All sub-
jects reported to be healthy and none of the subjects
showed any signs of cardiac disease on the CMR scan.
In three subjects the same short-axis slice was imaged
twice due to difficulties in breath holding during exer-
cise. These extra slices were identified and removed be-
fore the images were analysed. Figure 1 and Additional
files 1, 2, 3 and 4 show typical examples of the image
quality during exercise.
Heart rate and cardiac volumes
Heart rate increased significantly during exercise from
60±2 to 94±2 bpm (p<0.001). Left atrial volumes at end-
diastole decreased from 39±3 to 35±3 mL (p<0.05) as did
right atrial end-diastolic volumes from 65±5 to 56±4 mL
(p<0.05). At ventricular end-systole, where the atria reach
their largest volumes, left atrial volumes were unchanged
(84±4 and 85±5 mL, p=0.72) and right atrial volume de-
creased significantly from 124±7 to 103±7 mL (p<0.001)
with exercise.
Left ventricular EDV remained unchanged during ex-
ercise (186±8 to 185±8 mL, p=0.81) and LVESV de-
creased from 82±4 to 74±4 mL (p<0.05) (Figure 2A-B).
Left ventricular SV increased from 104±4 to 111±5 mL
(p<0.05, Figure 2C). For the right ventricle, both RVEDV
and RVESV decreased from 203±9 to 185±10 mL for
RVEDV and from 100±6 to 77±6 mL for RVESV
(p<0.001 for both) (Figure 2D-E) but the increase in
right ventricular SV from 104±4 to 108±5 mL was not
significant (p=0.18) (Figure 2F). Both left and right ven-
tricular ejection fraction (LVEF and RVEF) increased dur-
ing exercise from 56±1 to 60±1% and from 52±1 to 59±1%
respectively (p<0.01 for both). Cardiac output increased
from 6.2±0.3 to 10.4±0.5 L/min (p<0.001) mainly due
ingly, total heart volume decreased significantly during
exercise by 30±8 mL, (p<0.01) corresponding to a 4±1%
decrease of volume (example shown in Figure 4 and in
Additional file 4). As expected, LVM was unchanged from
rest to exercise (115±6 to 114±6 g, p=0.62).
Left and right atrio-ventricular plane displacement
Left ventricular AVPD and RVAVPD remained unchanged
during exercise. Left ventricular AVPD was 14.6±0.3 mm
at rest and 15.3±0.5 mm during exercise (p=0.06) and
the RV AVPD was 20.9±0.6 mm for both rest and ex-
ercise (p=0.90).
Longitudinal and radial pumping
Left ventricular longitudinal contribution to SV (%)
remained unchanged at approximately 60% (59±1% at
rest and 60±2% at exercise, p=0.74). Right ventricular
longitudinal contribution (%) decreased from 81±2 to
75±2% (p<0.05) (Figure 5A-B) due to the decrease in
RV end-diastolic volume. Total heart volume variation
increased during exercise from 5.9±0.5 to 9.7±0.6%
(p<0.001) (Figure 5C).
Table 1 Subject characteristics and cardiac volumes at
rest for men and women (mean±SD)
Men n=20 Women n=6
Age (years) 30±9 29±8
Weight (kg) 78±12 61±14
Height (m) 1.80±0.07 1.68±0.07
THV (mL) 861±145 586±123
LVEDV (mL) 197±34 148±36
RVEDV (mL) 219±37 149±39
LVSV (mL) 109±19 87±22
RVSV (mL) 110±17 84±23
LVM (g) 126±22 79±17
LAes (mL) 89±19 65±24
RAes (mL) 134±33 90±22
g = gram, kg = kilogram, LAes = left atrial volume measured at ventricular
end-systole, LVEDV = left ventricular end-diastolic volume, LVM = left ventricular
mass, LVSV = left ventricular stroke volume, m = metre, mL = millilitre,
RAes = right atrial volume measured at ventricular end-systole, RVEDV = right
ventricular end-diastolic volume, RVSV = right ventricular stroke volume,
THV = total heart volume, THVV = total heart volume variation.
Steding-Ehrenborg et al. Journal of Cardiovascular Magnetic Resonance 2013, 15:96 Page 3 of 8
Reproducibility of exercise measurements
For the six subjects participating in repeated scans there
were no differences in THV, RVEDV or left and right SV
between the first and second exercise session with one
leg. Left ventricular EDV increased more during the
second exercise session when compared to rest; a 5±5%
increase during the first session and a 11±4% increase
during the second session (p<0.05). When comparing end-
expiratory breath hold with end-inspiratory breath hold,
only LVEDV differed between sessions. When compared
Figure 1 Short-axis images showing the typical image quality during exercise. These images were acquired at a heart rate of 119 bpm. The
top left image shows the most basal short-axis slice showing the roof of the atria and the bottom right image shows the most apical slice of the
ventricles. Ao aorta, LA left atrium, LV left ventricle, Pulm pulmonary trunk, RA right atrium, RV right ventricle.
Figure 2 Left and right ventricular volumes and stroke volumes at rest and exercise. Upper panel shows no changes in left ventricular
end-diastolic volumes (A) and a small but significant decrease in end-systolic volume (B), leading to an increased stroke volume (C). Lower panel
show a significant decrease in right ventricular end-diastolic volume (D) and end-systolic volume (E). Right ventricular stroke volume increased
during exercise, however not statistically significant (F). Error bars denote mean and standard error of the mean (SEM).
Steding-Ehrenborg et al. Journal of Cardiovascular Magnetic Resonance 2013, 15:96 Page 4 of 8
to rest there was a 5±5% increase at end-expiratory
breath hold and a 15±7% increase at end-inspiratory
breath hold (p<0.05). During exercise using two legs,
left and right ventricular EDV did not differ when com-
pared to one-legged exercise. Left ventricular EDV in-
creased by 5±5% and 7±7% respectively (p=0.35), and
RVEDV decreased by 4±6% and 2±7% respectively
(p=0.17). Right ventricular SV, however, increased more
during exercise using two legs. When compared to rest the
increase was 3±10% with one leg and 12±9% with two legs.
Inter-observer variability and validation
Results are presented as mean ±SD. At rest, inter-
observer variability for LVM was 9±5 g, EDV 1±4 mL
and SV 2±5 mL. During exercise imaging was more
difficult and the image quality was lower, which is
reflected by a slightly larger variability; LVM 7±10 g,
EDV 3±16 mL and SV 0±9 mL.
The present study has shown that the total heart vol-
ume decreases in healthy normal subjects during
moderate exercise in the supine position. This de-
crease is caused by reduced right atrial and ventricu-
lar volumes whilst left atrial and ventricular volumes
remain unchanged during exercise. With regards to
pumping function there is an increase in outer vol-
ume changes during exercise and thus, an increased
radial contribution to stroke volume. AV-plane move-
ment is unchanged during exercise but a smaller
short-axis area of the right ventricle causes the lower
longitudinal contribution to RVSV. Left ventricular
longitudinal contribution to SV is unchanged during
exercise. Total left and right ventricular SV were only
slightly increased (LVSV) or unchanged (RVSV) dur-
is best explained by the rise in heart rate.
Figure 3 Heart rate and cardiac output at rest and exercise. Heart rate (A) and cardiac output (B) increased significantly from rest to
exercise. Error bars denote mean and standard error of the mean (SEM).
Figure 4 Mid-ventricular short axis slices in end-diastole (ED) and end-systole (ES) during rest and exercise with the corresponding
4-chamber (4 ch) view to illustrate the location of the slice. The solid line indicates delineations for total heart volume. In the exercise
images, the dashed line shows the total heart volume delineation copied from the corresponding resting image. The right ventricular volume is
decreased whereas the left ventricle remains unchanged.
Steding-Ehrenborg et al. Journal of Cardiovascular Magnetic Resonance 2013, 15:96 Page 5 of 8
Ventricular volumes and stroke volume
The inconsistent results of previous studies [4-7,11,12,14,26]
may be explained by differences in imaging modalities
and, perhaps most important, body position. The results
of this study are in line with other studies of supine exer-
cise showing unchanged LVEDV [5,9,10,27,28]. The sig-
nificant decrease in RVEDV differs from previous studies
of RV volumes during supine exercise using radionuclide
ventriculography [13] and CMR [14,28] where RVEDV
remained unchanged during moderate intensity exercise
(mean HR in these studies were 112,120 and 100 bpm re-
spectively). However, in line with our results the study by
Mols et al. [13] used radionuclide ventriculography and
showed a decreased RVEDV at workloads at a HR of
127 bpm and above. The differences between the present
study and previous CMR studies may be explained by dif-
ferences in exercise protocol where we acquired breath-
hold images during leg exercise whilst Holverda et al. [28]
used non-breath hold imaging and Roest et al. [14]
allowed the subjects to rest for the short period of image
acquisition. Free-breathing may decrease image quality
and rest during image acquisition will allow HR to de-
crease making interpretation of results more difficult.
In line with studies by Bevegård et al. [29] the present
study showed that CO increased significantly due to in-
creased HR whilst SV only increased by 8%. During the
early stages of exercise in healthy subjects, the increase in
HR is primarily caused by a decreased parasympathetic
tone whereas the sympathetic effects are not seen until
later stages [30]. As the exercise bouts of the study were
short, the increased HR with only a small increase in SV is
likely caused by parasympathetic withdrawal. Further-
more, the increased venous return caused by the supine
position lead to maximal filling of the ventricles already at
rest, which would explain the discrepancy between our
study and exercise studies performed in the upright pos-
ition. Our study would then be more representative of ex-
ercise in the supine position such as swimming or perhaps
in micro gravitational environments such as space flight.
Longitudinal and radial contribution to stroke volume
In contrast to a previous study of upright exercise on an
ergometer cycle where the left ventricular valve displace-
ment was significantly increased during exercise [20],
our results showed unchanged LV AVPD and longitudinal
contribution to LVSV. Right ventricular valve displace-
ment (RV AVPD) remained unchanged but together with
the decreased volume of the right ventricle, the right ven-
tricular longitudinal contribution to SV was significantly
decreased. Furthermore, total cardiac pumping became
significantly more radial during exercise as shown by the
increased THVV when exercising both with one and two
legs, as well as during end-expiratory and end-inspiratory
breath hold. This is in contrast to a hypothesis previously
suggested by our group [22] where we expected cardiac
longitudinal pumping to increase and radial pumping to
decrease. Increased radial pumping as seen in the present
study may theoretically increase the amount of energy
spent on moving surrounding tissues and thus decrease
the energy efficiency of the heart. However, for the left
ventricle, Riordan and Kovács [31] showed that radial
pumping may actually be important for diastolic suction
during the rapid filling phase. Exercise requires rapid mass
transfer from the atria to the ventricle, and it is possible
that the increased radial pumping seen in the right ven-
tricle may actually improve cardiac pumping efficiency
due to enhanced diastolic suction.
It is possible that our findings of increased THVV only
relates to exercise in the supine position such as swim-
ming, and it would be of interest to perform similar
studies during upright exercise.
Reproducibility of exercise measurements
Ventricular volumes and THV were reproducible between
the first and second exercise session, and also when im-
aging was performed at end-inspiratory breath hold as
well as during exercise with two legs. The differences seen
in LVEDV between the first and second exercise session
with one leg as well as between end-expiratory and end-
Figure 5 Longitudinal and radial contribution to stroke volume at rest and exercise. Left ventricular longitudinal contribution increased
(A) whereas the right ventricular contribution decreased (B). Total radial contribution calculated as total heart volume variation THVV (C) increased
significantly indicating an overall increase in radial pumping of the heart during exercise. Error bars denotes mean and standard error of the
mean (SEM).
Steding-Ehrenborg et al. Journal of Cardiovascular Magnetic Resonance 2013, 15:96 Page 6 of 8
inspiratory breath hold is probably best explained by indi-
vidual variations that are more distinguishable in the small
population. As shown in Figure 2 there is some variability
between individuals for all variables and when only asses-
sing six subjects results may fall out as statistically signifi-
cant although not physiologically relevant.
Clinical implication
Heart failure is a complex syndrome and diagnosis can
be especially challenging at early stages. Cardiac MR
during physical exercise may become useful for assessing
patients with normal ejection fraction and suspected
heart failure to investigate if cardiac function and filling
are affected during low and medium intensity exercise.
Furthermore, exercise CMR may also be used to asses
patients with congenital heart disease such as Tetralogy
of Fallot before and after surgery.
Exercise heart rate in our healthy volunteers only in-
creased by approximately 40 bpm over resting HR and it
is possible that a higher exercise HR may yield different
results. The study population included to test for repro-
ducibility of exercise measurements was small (n=6) and
the results of the statistical tests of this subpopulation
on reproducibility should be interpreted with caution.
Furthermore, the study was performed in the supine
position limiting the interpretation of our results to su-
pine exercise such as swimming, but it may also be ap-
plicable for conditions of microgravity, such as space
Moderate intensity exercise in the supine position sig-
nificantly decreases the total heart volume. This is due
to decreases in right atrial and ventricular volumes at
end-diastole whilst the LVEDV remains unchanged. The
contribution of longitudinal pumping to stroke volume
is unchanged in the left ventricle but decreased in the
right ventricle in exchange for an increase in radial
pumping. In contrast to previous belief, THVV and con-
sequently radial pumping increases which may improve
diastolic suction of the ventricles.
Additional files
Additional file 1: Short-axis image of a healthy heart during
exercise at a heart rate of 108 bpm.
Additional file 2: Two-chamber long-axis view of a healthy heart
during exercise at a heart rate of 102 bpm.
Additional file 3: Three-chamber long-axis view of a healthy heart
during exercise at a heart rate of 117 bpm.
Additional file 4: Four-chamber long-axis view of a healthy heart
during exercise at a heart rate of 124 bpm.
Competing interests
The authors declared that they have no competing interest.
KSE: Conception of study, data inclusion and analysis, interpretation of data,
drafting and revising the manuscript. RJ: Data inclusion and critical revision
of the manuscript. PMA: Data inclusion and analysis, critical revision of the
manuscript. MC: Conception of study, data inclusion and critical revision of
the manuscript. BS: Conception of study, construction of MR ergometer,
critical revision of manuscript. HA: Conception of study, critical revision of
manuscript. All authors read and approved the final manuscript.
The authors wish to thank FlemmingJessen at the Copenhagen Muscle
Research Centre for design and construction of the ergometer and Ance
Kreslin for help with data collection and analysis. This study was supported
by the Swedish Research Council, the Swedish Heart and Lung Foundation,
Region of Scania, the Medical Faculty at Lund University, Sweden, the
Swedish Heart Association and Novo Nordisk Foundation, Denmark.
Author details
Copenhagen Muscle Research Centre, Copenhagen, Denmark.
Research Centre for Magnetic Resonance, Hvidovre Hospital, Copenhagen,
Department of Clinical Physiology, Lund University, Lund
University Hospital Lund, Lund, Sweden.
Received: 26 April 2013 Accepted: 1 October 2013
Published: 24 October 2013
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Cite this article as: Steding-Ehrenborg et al.:Moderate intensity supine
exercise causes decreased cardiac volumes and increased outer volume
variations: a cardiovascular magnetic resonance study. Journal of
Cardiovascular Magnetic Resonance 2013 15:96.
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... Invasive pressure-volume (PV) loops are gold standard to assess hemodynamic function and cardiac performance [1] and can provide information on both load-dependent and load-independent parameters such as myocardial contractility, ventricular efficiency, and arterial elastance [2]. Thus, PV loops may provide additional information in patients with decreased cardiac function and potentially explain the enhanced cardiac function seen in endurancetrained (ET) athletes during exercise [3][4][5][6][7][8]. However, measuring PV loops during exercise has been challenging, likely due to the invasive nature previously needed to acquire the measurements. ...
... This is the first study to show feasibility of non-invasive PV loops using CMR during exercise for hemodynamic assessment, adding to prior work by Seemann et al. [9] and Sjöberg et al. [10]. The physiological exercise response of LV volumes are in line with previous studies, demonstrating increased LVSV through increased LVEDV and decreased LVESV in ET, and increased LVSV through maintained or decreased LVEDV and decreased LVESV in healthy volunteers [3,5,6]. Furthermore, the physiological exercise response of hemodynamics is also in line with previous studies, demonstrating decreased SVR and increased contractility [30,31], indicating that non-invasively obtained PV loops during exercise can be used to assess hemodynamic changes. ...
Full-text available
IntroductionPressure-volume (PV) loops can be used to assess both load-dependent and load-independent measures of cardiac hemodynamics. However, analysis of PV loops during exercise is challenging as it requires invasive measures. Using a novel method, it has been shown that left ventricular (LV) PV loops at rest can be obtained non-invasively from cardiac magnetic resonance imaging (CMR) and brachial pressures. Therefore, the aim of this study was to assess if LV PV loops can be obtained non-invasively from CMR during exercise to assess cardiac hemodynamics.Methods Thirteen endurance trained (ET; median 48 years [IQR 34-60]) and ten age and sex matched sedentary controls (SC; 43 years [27-57]) were included. CMR images were acquired at rest and during moderate intensity supine exercise defined as 60% of expected maximal heart rate. Brachial pressures were obtained in conjunction with image acquisition.ResultsContractility measured as maximal ventricular elastance (Emax) increased in both groups during exercise (ET: 1.0 mmHg/ml [0.9-1.1] to 1.1 mmHg/ml [0.9-1.2], p
... Dobutamine dose was set as 5-10 µg/kg/min and adjusted every 2 min, until reaching a HR ∼60% higher than the one at rest. This target HR was chosen in order to achieve HR in the range of those from previous studies on stress testing with MRI (31)(32)(33)(34). HR was monitored continuously throughout the study and blood pressures were measured at rest and after dobutamine. ...
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The total kinetic energy (KE) of blood can be decomposed into mean KE (MKE) and turbulent KE (TKE), which are associated with the phase-averaged fluid velocity field and the instantaneous velocity fluctuations, respectively. The aim of this study was to explore the effects of pharmacologically induced stress on MKE and TKE in the left ventricle (LV) in a cohort of healthy volunteers. 4D Flow MRI data were acquired in eleven subjects at rest and after dobutamine infusion, at a heart rate that was ∼60% higher than the one in rest conditions. MKE and TKE were computed as volume integrals over the whole LV and as data mapped to functional LV flow components, i.e., direct flow, retained inflow, delayed ejection flow and residual volume. Diastolic MKE and TKE increased under stress, in particular at peak early filling and peak atrial contraction. Augmented LV inotropy and cardiac frequency also caused an increase in direct flow and retained inflow MKE and TKE. However, the TKE/KE ratio remained comparable between rest and stress conditions, suggesting that LV intracavitary fluid dynamics can adapt to stress conditions without altering the TKE to KE balance of the normal left ventricle at rest.
... Reliability of LV volumetric and mass measurements between all completed RT short-axis stack constructions was tested using ICC to further evaluate necessary image acquisition time. For reliability during exercise, only LVM was compared to ECG-gated images as volumes, but not mass, were expected to differ between these two physiological conditions 17,33,34 . Similarly, RT CMR images analyzed at end inspiration were not used for volumes as ventricular volumes may differ depending on the respiratory state [17][18][19] . ...
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Exercise cardiovascular magnetic resonance (CMR) can unmask cardiac pathology not evident at rest. Real-time CMR in free breathing can be used, but respiratory motion may compromise quantification of left ventricular (LV) function. We aimed to develop and validate a post-processing algorithm that semi-automatically sorts real-time CMR images according to breathing to facilitate quantification of LV function in free breathing exercise. A semi-automatic algorithm utilizing manifold learning (Laplacian Eigenmaps) was developed for respiratory sorting. Feasibility was tested in eight healthy volunteers and eight patients who underwent ECG-gated and real-time CMR at rest. Additionally, volunteers performed exercise CMR at 60% of maximum heart rate. The algorithm was validated for exercise by comparing LV mass during exercise to rest. Respiratory sorting to end expiration and end inspiration (processing time 20 to 40 min) succeeded in all research participants. Bias ± SD for LV mass was 0 ± 5 g when comparing real-time CMR at rest, and 0 ± 7 g when comparing real-time CMR during exercise to ECG-gated at rest. This study presents a semi-automatic algorithm to retrospectively perform respiratory sorting in free breathing real-time CMR. This can facilitate implementation of exercise CMR with non-ECG-gated free breathing real-time imaging, without any additional physiological input.
... Several investigators demonstrated exercise stress CMR using an in-room treadmill system followed by a rapid transfer of the subject into the scanner with subsequent imaging [7][8][9][10][11][12]. On the other hand, MR-compatible equipment enabling imaging at 1.5 tesla (T) while the patient is at peak exercise stress was shown to be feasible for the evaluation of blood flow dynamics and ventricular function in healthy volunteers [13][14][15][16][17][18][19][20]. Another proof-of-concept study reported on a 3T compatible ergometer, which allowed the assessment of cardiac morphology and function in healthy subjects [6]. ...
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Background: Cardiac magnetic resonance imaging (CMR) remains underutilized as an exercise imaging modality, mostly because of the limited availability of MR-compatible exercise equipment. This study prospectively evaluates the clinical feasibility of a newly developed MR-conditional pedal ergometer for exercise CMR METHODS: Ten healthy volunteers (mean age 44 ± 16 years) and 11 patients (mean age 60 ± 9 years) with known or suspected coronary artery disease (CAD) underwent rest and post-exercise cinematic 3T CMR. Visual analysis of wall motion abnormalities (WMA) was rated by 2 experienced radiologists, and volumes and ejection fractions (EF) were determined. Image quality was assessed by a 4-point Likert scale for visibility of endocardial borders. Results: Median subjective image quality of real-time Cine at rest was 1 (IQR 1-2) and 2 (IQR 2-2.5) for post-exercise real-time Cine (p = 0.001). Exercise induced a significant increase in heart rate (62 [62-73] to 111 [104-143] bpm, p < 0.0001). Stroke volume and cardiac index increased from resting to post-exercise conditions (85 ± 21 to 101 ± 19 mL and 2.9 ± 0.7 to 6.6 ± 1.9 L/min/m², respectively; both p < 0.0001), driven by a reduction in end-systolic volume (55 ± 20 to 42 ± 21 mL, p < 0.0001). Patients (2/11) with inducible regional WMA at high-resolution post-exercise cine imaging revealed significant coronary artery stenosis in subsequently performed invasive coronary angiography. Conclusion: Exercise-CMR using our newly developed 3T MR-conditional pedal ergometer is clinically feasible. Imaging of both cardiac response and myocardial ischemia, triggered by dynamic stress, is rapidly conducted while the patient is near their peak heart rate.
... Animal studies initially showed that LA relaxation rate, reservoir volume, and mean and V-wave pressures increase during exercise (198). In humans, the LA volume response to exercise remains unclear; several studies using two-dimensional (2D) volumes or diameters have shown increased maximal and stable minimal LA size (199)(200)(201), whereas others demonstrate the opposite (166,202,203), which may reflect differences in study design. However, both perspectives support an expanded reservoir volume proportionate to increases in SV (59) during exercise along with reservoir phase LA strain (172,195). ...
With each heartbeat, the right ventricle (RV) inputs blood into the pulmonary vascular (PV) compartment which conducts blood through the lungs at low pressure and concurrently fills the left atrium (LA) for output to the systemic circulation. This overall hemodynamic function of the integrated RV-PV-LA unit is determined by complex interactions between the components that vary over the cardiac cycle but are often assessed in terms of mean pressure and flow. Exercise challenges these hemodynamic interactions as cardiac filling increases, stroke volume augments, and cycle length decreases, with PV pressures ultimately increasing in association with cardiac output. Recent cardio-pulmonary exercise hemodynamic studies have enriched the available data from healthy adults, yielded insight into the underlying mechanisms which modify the PV pressure-flow relationship, and better delineated the normal limits of healthy responses to exercise. This review will examine hemodynamic function of the RV-PV-LA unit using the 2-element Windkessel model for the pulmonary circulation. It will focus on acute PV and LA responses that accommodate increased RV output during exercise, including PV recruitment and distension and LA reservoir expansion, and the integrated mean pressure-flow response to exercise in healthy adults. Finally, it will consider how these responses may be impacted by age-related remodeling and modified by sex-related cardio-pulmonary differences. Studying the determinants and recognizing the normal limits of PV pressure-flow relations during exercise will improve our understanding of cardio-pulmonary mechanisms that facilitate or limit exercise.
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Aims Left ventricular (LV) pressure-volume (PV) loops provide gold-standard physiological information but require invasive measurements of ventricular intracavity pressure, limiting clinical and research applications. A non-invasive method for the computation of PV loops from magnetic resonance imaging and brachial cuff blood pressure has recently been proposed. Here we evaluated the fidelity of the non-invasive PV algorithm against invasive LV pressures in humans. Methods and results Four heart failure patients with EF < 35% and LV dyssynchrony underwent cardiovascular magnetic resonance (CMR) imaging and subsequent LV catheterization with sequential administration of two different intravenous metabolic substrate infusions (insulin/dextrose and lipid emulsion), producing eight datasets at different haemodynamic states. Pressure-volume loops were computed from CMR volumes combined with (i) a time-varying elastance function scaled to brachial blood pressure and temporally stretched to match volume data, or (ii) invasive pressures averaged from 19 to 30 sampled beats. Method comparison was conducted using linear regression and Bland-Altman analysis. Non-invasively derived PV loop parameters demonstrated high correlation and low bias when compared to invasive data for stroke work (R2 = 0.96, P < 0.0001, bias 4.6%), potential energy (R2 = 0.83, P = 0.001, bias 1.5%), end-systolic pressure-volume relationship (R2 = 0.89, P = 0.0004, bias 5.8%), ventricular efficiency (R2 = 0.98, P < 0.0001, bias 0.8%), arterial elastance (R2 = 0.88, P = 0.0006, bias −8.0%), mean external power (R2 = 0.92, P = 0.0002, bias 4.4%), and energy per ejected volume (R2 = 0.89, P = 0.0001, bias 3.7%). Variations in estimated end-diastolic pressure did not significantly affect results (P > 0.05 for all). Intraobserver analysis after one year demonstrated 0.9–3.4% bias for LV volumetry and 0.2–5.4% for PV loop-derived parameters. Conclusion Pressure-volume loops can be precisely and accurately computed from CMR imaging and brachial cuff blood pressure in humans.
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Background: Real-time (RT) exercise cardiac magnetic resonance imaging (exCMR) is an emerging approach for cardiac stress testing as part of a comprehensive cardiovascular imaging assessment. It has advantages over alternative approaches due to its high spatial resolution and use of non-pharmacological stress. As access to exCMR increases, there is a need to establish reference ranges in healthy adults for clinical interpretation. Methods: We analysed data from 162 healthy adults who had no known cardiovascular disease, did not harbour genetic variants associated with cardiomyopathy, and who completed an exCMR protocol using a pedal ergometer. Participants were imaged at rest and after exercise with left ventricular parameters measured using commercial software by two readers. Prediction intervals were calculated for each parameter. Results: Exercise caused an increase in heart rate (64±9 bpm vs 133±19 bpm, P < 0.001), left ventricular end-diastolic volume (140±32 ml vs 148±36 ml, P < 0.001), stroke volume (82±18 ml vs 102±26 ml, P < 0.001), ejection fraction (59±6% vs 69±7%, P < 0.001), and cardiac output (5.2±1.2 l/min vs 10.0±3.1 l/min, P < 0.001), with a decrease in left ventricular end-systolic volume (58±18 ml vs 46±16 ml, P < 0.001). There was an effect of gender and age on response to exercise across most parameters. Measurements showed moderate to excellent intra- and inter-observer agreement. Conclusion: In healthy adults, an increase in cardiac output after exercise is driven by a rise in heart rate with both increased ventricular filling and emptying. We establish normal ranges for exercise response, stratified by age and gender, as a reference for the use of exCMR in clinical practice.
Purpose: Exercise-induced dyspnea caused by lung water is an early heart failure symptom. Dynamic lung water quantification during exercise is therefore of interest to detect early stage disease. This study developed a time-resolved 3D MRI method to quantify transient lung water dynamics during rest and exercise stress. Methods: The method was evaluated in 15 healthy subjects and 2 patients with heart failure imaged in transitions between rest and exercise, and in a porcine model of dynamic extravascular lung water accumulation through mitral regurgitation (n = 5). Time-resolved images were acquired at 0.55T using a continuous 3D stack-of-spirals proton density weighted sequence with 3.5 mm isotropic resolution, and derived using a motion corrected sliding-window reconstruction with 90-s temporal resolution in 20-s increments. A supine MRI-compatible pedal ergometer was used for exercise. Global and regional lung water density (LWD) and percent change in LWD (ΔLWD) were automatically quantified. Results: A ΔLWD increase of 3.3 ± 1.5% was achieved in the animals. Healthy subjects developed a ΔLWD of 7.8 ± 5.0% during moderate exercise, peaked at 16 ± 6.8% during vigorous exercise, and remained unchanged over 10 min at rest (-1.4 ± 3.5%, p = 0.18). Regional LWD were higher posteriorly compared the anterior lungs (rest: 33 ± 3.7% vs 20 ± 3.1%, p < 0.0001; peak exercise: 36 ± 5.5% vs 25 ± 4.6%, p < 0.0001). Accumulation rates were slower in patients than healthy subjects (2.0 ± 0.1%/min vs 2.6 ± 0.9%/min, respectively), whereas LWD were similar at rest (28 ± 10% and 28 ± 2.9%) and peak exercise (ΔLWD 17 ± 10% vs 16 ± 6.8%). Conclusion: Lung water dynamics can be quantified during exercise using continuous 3D MRI and a sliding-window image reconstruction.
While pharmacologic stress cardiovascular magnetic resonance imaging (MRI) is a robust noninvasive tool in the diagnosis and prognostication of epicardial coronary artery disease, clinical guidelines recommend exercise‐based testing in those patients who can exercise. This review describes the development of exercise cardiovascular MRI protocols, summarizes the insights across various patient populations, and highlights future research initiatives. Level of Evidence 5 Technical Efficacy Stage 2
While the phases of left atrial (LA) function at rest have been studied, the physiological response of the LA to exercise is undefined. This study defines the exercise behavior of the normal left atrium by quantitating its volumetric response to graded effort. Healthy subjects (n=131) were enrolled from the Health eHeart cohort. Echocardiograms were obtained at baseline and during ramped supine bicycle exercise. Left ventricular volume index, stroke volume index (LVSVI), left atrial end-systolic volume index (LAESVI), end-diastolic volume index (LAEDVI), emptying fraction (LAEF), reservoir and conduit fraction were analyzed. The LVSVI increased with low exercise, but did not increase further with peak exercise; cardiac output increased through the agency of heart rate. The LAESVI and LAEDVI decreased and the LAEF increased with exercise. As a result, LA reservoir volume index was static throughout exercise. The reservoir fraction decreased from 46% at rest to 40% with low exercise (p<0.001) in association with increased LVSVI, and remained similar at peak exercise. The conduit volume index increased from 20 mL/m ² at rest to 24 mL/m ² at low exercise and stayed the same at peak exercise. Similarly, the conduit fraction increased from 54% at rest to 60% at low exercise (p<0.001) and did not change further with peak exercise. Although atrial function increased with exercise, the major contribution to the augmentation of LV SV is LA conduit fraction, a marker of active ventricular relaxation. Furthermore, the major determinant of raising cardiac output during high level exercise is heart rate.
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Long term endurance training is known to increase peak oxygen uptake (VO2peak) and induce morphological changes of the heart such as increased left ventricular mass (LVM). However, the relationship between and the total heart volume (THV), considering both the left and right ventricular dimensions in both males and females, is not completely described. Therefore, the aim of this study was to test the hypothesis that THV is an independent predictor of VO2peak and to determine if the left and right ventricles enlarge in the same order of magnitude in males and females with a presumed wide range of THV. The study population consisted of 131 subjects of whom 71 were athletes (30 female) and 60 healthy controls (20 female). All subjects underwent cardiovascular MR and maximal incremental exercise test. Total heart volume, LVM and left- and right ventricular end-diastolic volumes (LVEDV, RVEDV) were calculated from short-axis images. was significantly correlated to THV, LVM, LVEDV and RVEDV in both males and females. Multivariable analysis showed that THV was a strong, independent predictor of (R2 = 0.74, p < 0.001). As LVEDV increased, RVEDV increased in the same order of magnitude in both males and females (R2 = 0.87, p < 0.001). Total heart volume is a strong, independent predictor of maximal work capacity for both males and females. Long term endurance training is associated with a physiologically enlarged heart with a balance between the left and right ventricular dimensions in both genders.
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Commercially available software for cardiovascular image analysis often has limited functionality and frequently lacks the careful validation that is required for clinical studies. We have already implemented a cardiovascular image analysis software package and released it as freeware for the research community. However, it was distributed as a stand-alone application and other researchers could not extend it by writing their own custom image analysis algorithms. We believe that the work required to make a clinically applicable prototype can be reduced by making the software extensible, so that researchers can develop their own modules or improvements. Such an initiative might then serve as a bridge between image analysis research and cardiovascular research. The aim of this article is therefore to present the design and validation of a cardiovascular image analysis software package (Segment) and to announce its release in a source code format. Segment can be used for image analysis in magnetic resonance imaging (MRI), computed tomography (CT), single photon emission computed tomography (SPECT) and positron emission tomography (PET). Some of its main features include loading of DICOM images from all major scanner vendors, simultaneous display of multiple image stacks and plane intersections, automated segmentation of the left ventricle, quantification of MRI flow, tools for manual and general object segmentation, quantitative regional wall motion analysis, myocardial viability analysis and image fusion tools. Here we present an overview of the validation results and validation procedures for the functionality of the software. We describe a technique to ensure continued accuracy and validity of the software by implementing and using a test script that tests the functionality of the software and validates the output. The software has been made freely available for research purposes in a source code format on the project home page Segment is a well-validated comprehensive software package for cardiovascular image analysis. It is freely available for research purposes provided that relevant original research publications related to the software are cited.
Whereas ventricular filling has been extensively studied and debated, atrial filling is less well characterized. Therefore, the aim of this study was to quantify atrial filling secured during ventricular diastole and systole, and to investigate whether atrial filling depends on heart rate (HR) and total heart volume (THV). Thirty-two athletes (16 women) and 32 normal subjects (16 women) underwent cardiac magnetic resonance imaging. Cardiac volumes and atrioventricular plane displacement (AVPD) were determined. Longitudinal and radial contribution to stroke volume was calculated using planimetry and used to determine diastolic and systolic atrial filling. Atrial filling during ventricular diastole was 29 ± 10% of the total stroke volume, and during ventricular systole atrial filling was 68 ± 8% of the total stroke volume. There were no differences between groups of different HR (P = 0·70 and P = 0·41 for diastolic and systolic filling, respectively) or THV (P = 0·44 and P = 0·46 for diastolic and systolic filling, respectively). Systolic atrial filling was strongly correlated to longitudinal ventricular pumping (R = 0·76, P<0·001). This study demonstrated that in healthy humans at rest, approximately 30% of the total stroke volume enters the atria during ventricular diastole and approximately 70% during systole, independent of heart rate (HR) or heart size. The atria are filled through suction driven by ventricular longitudinal contraction which aspirates blood from the pulmonary and caval veins. As 70% of the atrial filling occurs during ventricular emptying, the heart volume remains relatively constant over the cardiac cycle, which minimizes pulling on surrounding tissues and therefore optimizes energy expenditure.
We used M-mode echocardiography to measure left ventricular dimensions in diastole (Dd) and systole (Ds) and to assess ventricular performance by computing the percent dimensional shortening (%ΔD) and the normalized rate of dimensional shortening (Vd) during isometric and isotonic exercise in normal subjects. In 27 subjects, isometric handgrip exercise at 50% of maximum grip until fatigue produced a significant increase in Ds (33 ± 3.4 (DS) vs 30.6 ± 3.7 mm, p<0.001), and a reduction in %ΔD (34 ± 4 vs 39 ± 5%, p<0.001) and Vd (1.15 ± 0.15 vs 1.28 ± 0.19 sec-1, p<0.001). Handgrip exercise at 15% of maximum grip produced similar but less marked changes in the 27 subjects, and acute pressure loading with phenylephrine caused similar but more marked changes in 10 of the subjects. In the 20 subjects who performed at least 12 minutes of supine bicycle exercise, Ds decreased significantly (25.6 ± 4.0 vs 31.7 ± 2.8 mm, p<0.001) and %ΔD increased (49 ± 6 vs 36 ± 5%, p<0.001). We observed similar results in the 12 subjects also studied during upright bicycle exercise. Dd was smaller in the upright position but unchanged during either isometric or isotonic exercise. We conclude that: 1) end-diastolic left ventricular size is maintained during isometric exercise and moderate dynamic exercise, even in the upright position; 2) isometric exercise leads to a mild decrease in left ventricular shortening, whereas dynamic exercise results in marked increases in shortening; this difference may be related to the relatively greater increase in blood pressure than in heart rate during isometric exercise; and 3) M-mode echocardiography can be successfully accomplished in selected subjects during various forms of exercise.
Ten healthy men aged 18 to 23 years performed supine bicycle ergometer exercise during continuous echocardiographic recording. Beat to beat analysis of ventricular dimensions revealed that during constant work load exercise end-diastolic dimension did not change and end-systolic dimension decreased insignificantly by 4 percent. The stroke dimension and fractional shortening of the ventricular dimension rose 7 and 5 percent, respectively. During recovery, end-diastolic dimension and stroke dimension increased above the resting value, beginning 26 seconds (range 16 to 45) after cessation of exercise, whereas heart rate fell promptly to resting levels by 37 seconds. The peak increase in end-diastolic dimension and stroke dimension averaged 11 and 35 percent, respectively. Endsystolic dimension coincident with peak end-diastolic dimension decreased 11 percent in 6 of 10 subjects, and was unchanged in four. Fractional shortening of the ventricular dimension increased 8 percent (P < 0.025) in parallel with end-diastolic dimension.These dimensional changes indicate a significant increase in end-diastolic dimension and stroke dimension in all 10 subjects during the recovery phase of supine exercise with a parallel rise in the percent shortening of the ventricular dimensions. During exercise a clear Frank-Starling effect is masked, whereas during recovery the continuing high level of venous return is dissociated from the decreasing heart rate, resulting in a transient increase in end-diastolic volume and a measurable Frank-Starling effect.
This investigation examines the hypothesis that athletes increase stroke volume with submaximal exercise through an augmentation of left ventricular (LV) end-diastolic volume and a reduction of LV end-systolic volume, whereas sedentary adults only increase stroke volume modestly, because LV end-diastolic volume does not increase. Upright bicycle exercise was performed by 17 endurance-trained male athletes and 15 sedentary men. M-mode echocardiograms were obtained during submaximal exercise at predetermined heart rates. Athletes, at a heart rate of 130 beats/min, increased their stroke volume 67% from 72 +/- 18 ml to 120 +/- 26 ml (p less than 0.001). This resulted from an increase of LV end-diastolic volume from 119 +/- 23 to 152 +/- 28 ml (p less than 0.001) and a reduction in LV end-systolic volume from 46 +/- 14 to 31 +/- 9 ml (p less than 0.001). Sedentary men at the same heart rate increased stroke volume 22% from 63 +/- 15 to 77 +/- 21 ml (p less than 0.05). LV end-diastolic volume did not change (96 +/- 20 vs 97 +/- 28 ml) (p = not significant), but LV end-systolic volume decreased (33 +/- 11 vs 20 +/- 9 ml) (p less than 0.001). In conclusion, athletes increased cardiac output through a more prominent augmentation of stroke volume than sedentary subjects at submaximal exercise. This was accomplished through an augmentation of LV end-diastolic volume. This may have a conserving effect on myocardial oxygen consumption at these levels of exercise.
Right ventricular (RV) adaptation to supine exercise has been studied in 10 young male volunteers by 81mKr electrocardiogram (ECG)-gated radionuclide ventriculography. During progressive supine exercise, the ejection fraction gradually increased from a mean value of 46% at rest up to 60% at a maximal exercise level. End-diastolic volume however remained unchanged at a low exercise level and even slightly decreased at a higher exercise level. Little or no change in end-diastolic volume and an increase in ejection fraction produced a significant decrease in end-systolic volume and a net increase in stroke volume. These results indicate that the Frank-Starling mechanism does not contribute to the increase in right ventricular stroke volume during progressive supine exercise, but the increase in right ventricular stroke volume rather seems related to an increased contractility, presumably mediated by an increased sympathetic activity.
To assess left ventricular structure and function at rest and during exercise in endurance athletes, 10 elite marathon runners, aged 28 to 37 years, and 10 matched nonathletes were studied by echocardiography and supine bicycle ergometry. Each athlete's best marathon time was less than 2 h 16 min. Echocardiography was performed at rest, at a 60 W work load and at an individually adjusted work load, at which heart rate was 110 beats/min (physical working capacity 110 [PWC110]). Oxygen uptake at PWC110 averaged (+/- SD) 1.14 +/- 0.2 liters/min in the nonathletes and 2.0 +/- 0.2 liters/min in the runners (p less than 0.001). The left ventricular internal diameter at end-diastole was similar at the three activity levels in the control subjects but increased significantly from rest to exercise in the runners (p less than 0.001). Left ventricular systolic meridional wall stress remained unchanged during exercise in the nonathletes but was significantly higher at PWC110 in the athletes (p less than 0.05). Both the systolic peak velocity of posterior wall endocardial displacement and fractional shortening of the left ventricular internal diameter increased with exercise; at PWC110 the endocardial peak velocity was higher in the runners than in the control subjects (p less than 0.01). The endocardial peak velocity during relaxation was comparable in athletes and control subjects at rest, increased similarly at a 60 W work load, but was higher in the runners at PWC110 (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)