Download Introduction: Left ventricular (LV) twist and untwisting rate (LV twist

Left ventricular twist mechanics during exercise in trained and untrained
men
By
Samuel Cooke
A report submitted in partial fulfilment of the requirements for the Degree
of Master of Science Physical Activity and Health
Cardiff School of Sport
Cardiff Metropolitan University
March 2016
This report has been produced as a ‘Journal Article Format’.
The target Journal is ‘Journal of Applied Physiology’.
The word count is: 5640 not including abstract and references.
Samuel Cooke
Left ventricular twist mechanics during exercise in trained and untrained
men.
Left ventricular twist mechanics during exercise in
trained and untrained men.
Samuel Cooke1
1Department of Physiology & Health, Cardiff
School of Sport, Cardiff Metropolitan University, Cardiff, Wales, United Kingdom.
Running title: Cooke et al. LV twist mechanics during exercise.
Cooke et al. LV twist mechanics during exercise.
Abstract
Introduction: Left ventricular (LV) twist
and untwisting rate (LV twist mechanics)
play a crucial role during myocardial
deformation. It is suggested that exercise
training alters resting LV twist mechanics.
However, it is unknown whether LV twist
mechanics respond differently during
exercise in trained and untrained
individuals. Aim: To compare LV twist
mechanics in trained and untrained
individuals at rest and during exercise.
Methodology: 11 trained male runners
(Peak oxygen uptake (VO2peak): 46.2 ± 6.1
ml.kg-1.min-1 SD) and 13 untrained healthy
males (VO2peak: 36.4 ± 6.4 ml.kg-1.min-1
SD) were examined at rest and during
supine cycling exercise at 30%, 40%, and
50% peak power output (PPO). Blood
pressure and heart rate (HR) were measured
continuously using photoplethysmography.
Echocardiographical images were collected
at rest and during the last 3 minutes of each
exercise stage. Speckle tracking technology
was used post-hoc to quantify LV twist
mechanics. Results: There were no
significant differences between the two
cohorts in HR, blood pressure, end-systolicvolume (ESV), cardiac output (CO), LV
twist or circumferential strain at rest or
during exercise (P > 0.05). However, the
trained cohort had a significantly lower LV
untwisting rate and sphericity index during
exercise, as well as a greater end-diastolicvolume (EDV) and stroke volume (SV) (P
< 0.05). Conclusion: In trained and
untrained individuals LV twist and
circumferential strain are similar at rest and
respond similarly to exercise. The lower LV
untwisting rate during exercise in trained
individuals may reflect a more efficient
diastolic function when the cardiovascular
system is challenged.
2
New and Noteworthy

This is the first study to investigate LV
twist mechanics in trained and
untrained males in response to
progressive submaximal exercise.

The novel data in the present study
showed LV twist and circumferential
strain to respond similarly to exercise in
trained and untrained males. However,
the trained group was shown to have a
significantly lower LV untwisting rate
in response to exercise which may
reflect a more efficient diastolic
function.
Key words
Left ventricular, twist, untwisting rate,
exercise.
Introduction
LV twist and untwisting rate have been
identified in playing a significant role with
respect to resting systolic and diastolic
myocardial deformation, influencing both
LV ejection and early diastolic filling,
respectively (44, 11, 38). Specifically, early
modeling studies suggest that LV twist acts
to reduce fiber stress during ventricular
contraction by equalizing the distribution of
stress across the myocardial wall (4, 10),
thus maximizing the efficiency of systolic
ejection (44). In addition, LV twist also acts
as a mechanism whereby the deformation
of the subendocardial and subepicardial
fiber matrix during ejection results in stored
potential energy that is utilized during
diastolic recoil (5, 44, 46). During the
subsequent untwisting of the apex and base,
the stored potential energy is released
which assists in generating a negative
intraventricular pressure gradient, initiating
the passive suction of blood from the atrium
to the ventricle and thus contributing to
early diastolic filling (11, 18). Taken
Cooke et al. LV twist mechanics during exercise.
together, LV twist and the subsequent
untwisting rate have been identified as
important markers of LV function within
both healthy and diseased population
groups (41, 9, 18), whereby LV twist
mechanics have shown to be reduced within
various disease states (50, 8, 14).
In addition to the previous evidence
concerning diseased populations, recent
research has also observed LV mechanical
parameters, including LV twist, untwisting
rate and strain (longitudinal, radial, and
circumferential), to be significantly reduced
within highly trained individuals in
comparison to untrained individuals at rest
(57, 37, 47). Yet, taking into consideration
the adaptive characteristics associated with
the athlete’s heart, e.g. increased LV mass,
chamber size and thickness of the
ventricular wall (29, 6), such reductions in
LV twist mechanics are suggested to reflect
a physiological adaptation to exercise
training (57). However, it is important to
highlight that there is evidence that
contradicts these findings, whereby several
longitudinal studies have shown LV twist
mechanics to remain unchanged (56) and
even increase (54, 1) in response to exercise
training. Such findings have therefore led
researchers to suggest that the behavior of
LV twist mechanics at rest may be
dependent upon the training status of an
individual (54, 56).
Although the alterations in resting LV twist
mechanics are suggested to reflect a
physiological adaptation to exercise
training, there is also evidence to suggest
that not all cardiac adaptations associated
with exercise training are entirely
beneficial. (39, 24). Therefore, in order to
further understand the relationship between
adaptive myocardial mechanics and heart
function, it is crucial to measure LV twist
mechanics under the stress of exercise.
Research had previously observed LV
twist, untwisting rate and strain to
progressively increase with exercise
intensity within both trained (47) and
untrained cohorts (36, 17, 48, 51).
3
However, as to whether the biomechanical
behavior of the LV responds differently
during exercise in trained and untrained
individuals is yet to be fully elucidated.
Stöhr and colleagues (47) had recently
shown LV twist mechanics to be
significantly lower during submaximal
exercise in individuals with higher levels of
aerobic fitness in comparison to individuals
with moderate levels of aerobic fitness. Yet,
it is important to note that these findings
were established in a heterogeneous
population, and that LV twist mechanics
were examined in response to a single bout
of exercise only.
Therefore, to determine whether the
observed alterations in myocardial
mechanics at rest bear any functional
significance during exercise, we aimed to
examine the differences in LV twist
mechanics at rest and in response to
progressive submaximal exercise in trained
and untrained individuals. Conducting this
study would help to provide a greater
insight into identifying and understanding
differences in biomechanical behavior of
the LV between individuals with
contrasting levels of aerobic fitness.
Furthermore, knowledge acquired from this
study could support future research in
further understanding the differences in LV
mechanics between the heart of an athlete
and a pathological heart, thereby potentially
contributing to the treatment of various
pathological states. It was hypothesized that
LV mechanical parameters would be
significantly lower at rest and throughout
progressive submaximal exercise in trained
individuals in comparison to untrained
individuals.
Methodology
Ethical approval and study population
Cooke et al. LV twist mechanics during exercise.
Upon attaining ethical approval from the
Cardiff Metropolitan University School of
Sport Research Ethics sub-committee, 13
healthy untrained males (Age: 20 ± 1 years
± SD; Height: 178.1 ± 6.5 cm ± SD; Body
mass: 79.0 ± 11.3 kg ± SD) and 11 healthy
trained runners (Age: 26 ± 6, years ± SD;
Height: 181.3 ± 4.8 cm ± SD; Body mass:
74.1 ± 6.5 kg ± SD) voluntarily enrolled to
participate in this research study. All
participants provided both written and
verbal informed consent, and completed a
health questionnaire sheet prior to testing.
Participants were excluded if: 1) any
structural or functional myocardial
abnormalities were suspected using
echocardiography, 2) were known or
suspected to have any underlying medical
conditions e.g. systematic diseases, high
blood pressure, and 3) were currently
smoking during the past 6 months. An a
priori sample size calculation suggested
that a sample of n = 13 per group was
required in order to identify significant
differences using an α value of 0.05. This
study conformed to the standards
established by the most recent amendment
of the Declaration of Helsinki. Untrained
males were recruited using an eligibility
criteria stating that individuals must be
male, aged 18 – 35 years, and undertake no
more than 2 hours of structured exercise per
week. Trained runners were recruited using
an eligibility criteria stating that individuals
must be male, aged 18 – 35 years, and
compete in either an endurance discipline
performing no less than 40km running per
week, or as a 400m sprinter with a personal
best of sub 50 seconds.
Research design
This study utilized a cross sectional
research design in order to investigate the
differences in LV twist mechanics between
trained and untrained individuals at rest and
during progressive submaximal exercise.
Participants were requested to attend the
physiology laboratory, located at Cardiff
Metropolitan University, Cyncoed campus,
on two separate occasions: 1) to attain
4
measurements of PPO and VO2peak, and 2)
to undergo a cardiovascular assessment
during submaximal exercise in order to
assess LV twist, untwisting rate and
circumferential strain. The purpose of the
first visit was to assess PPO and VO2peak and
calculate submaximal exercise intensities
relative to each participant in preparation
for visit 2.
Experimental procedure
Visit 1: Initial height and body mass
measurements were taken using an
electronic weighing scale and stadiometer,
and were recorded to the nearest millimeter
and 100g respectively. A standardized
incremental exercise test was then
performed in order to determine both
VO2peak and PPO. Exercise was performed
on a supine cycle ergometer, on which
participants were placed in the left lateral
position at a 45-degree angle (Angio 2003,
LODE, Groningen, Netherlands). The
exercise protocol consisted of an initial 3minute exercise period at an intensity of 40
Watts at a cadence between 60 – 65
revolutions per minute (RPM). The
exercise intensity then increased in 40 Watt
increments every 3 minutes thereafter until
the point of maximal volitional fatigue.
Breath-by-breath VO2 was measured
throughout the exercise protocol using a
fitted gas mask attached to a computer gas
analysis system (OxyconPro, JAEGER at
Viasys Healthcare, Warwick, UK). HR was
recorded throughout the exercise protocol
using a wireless HR monitor (Polar T31,
POLAR ELECTRO, Kempele, Finland).
VO2peak was recorded as the greatest 5
second average value obtained during the
exercise protocol, and both PPO and
maximal HR (HRmax) were recorded at the
point of task failure. For the purpose of
blood lactate analysis, capillary blood
samples (20μL) were extracted from the
right index finger into a capillary tube
containing an anti-hemolyzing solution at
rest, during the remaining 30 seconds of
each 3-minute interval, and at 3-minute post
exercise cessation. All blood lactate
Cooke et al. LV twist mechanics during exercise.
samples were calculated using an offline
lactate analysis system (Biosen, C-Line
Sport, EKF DIAGNOSTICS, Magdeburg,
Germany).
Visit 2: Upon arrival, participants were
briefed with regards to the intended
procedure of visit 2. Both height and body
mass were measured and recorded to the
nearest millimeter and 100g respectively.
Participants were then positioned upon a
supine ergometer (Angio 2003, LODE,
Groningen, Netherlands) and prepared for
the attachment of test equipment. A finger
cuff was placed around the right middle
finger and an arm cuff around the right
upper arm in order to provide an estimation
of the brachial blood pressure waveform as
part of a non-invasive beat-to-beat arterial
blood
pressure monitoring system
(FinometerPRO, FINAPRES, Arnhem,
Netherlands). The brachial blood pressure
waveform was recorded in real time
throughout the protocol for the purpose of
off-line analysis using a data capture
system (PowerLab; ADINSTRUMENTS,
Chalgrove, UK). Electrocardiogram leads
inherent to the ultrasound system (Vivid
E9, GE Vingmed Ultrasound, Horten,
Norway) were attached to provide a
continuous measurement of HR. A nose
clip and a separate mouthpiece comprising
of a two-way respiratory valve attached to a
respiratory turbine were fitted. The
respiratory turbine was connected to a
computer gas analysis system (OxyconPro,
JAEGER at Viasys Healthcare, Warwick,
UK) in order to record continuous breathby-breath ventilatory data.
Once test equipment was attached,
participants were placed in the left lateral
position at a 45-degree angle and a blood
capillary sample (20μL) was drawn from
the right ear lobe for the purpose of blood
lactate analysis. Echocardiographic images
were then recorded by an experienced
sonographer using a 2D and 4D probe
(M5S-D and 4V-D, GE VINGMED
ULTRASOUND, Horten, Norway) as part
of a commercially accessible ultrasound
5
system (Vivid E9, GE VINGMED
ULTRASOUND, Horten, Norway). Images
were recorded for three to five consecutive
cardiac cycles during brief periods of endexpiratory breath holds that participants
were made familiar with, prior to the
recording of data. Echocardiographic
images were recorded from the following
anatomical windows; parasternal short-axis
at the base and apex, parasternal long-axis,
and apical triplane images. To ensure the
reproducibility
of
echocardiographic
images throughout each exercise interval,
the transducer location on the chest at rest
was marked with a marker pen and used as
a reference point to reproduce the same
image during the three exercise stages. This
allowed for easier identification of a similar
apical imaging window, enabling the
sonographer to amend and obtain visually
comparable cross-sectional views. As
outlined in previous publications (47),
parasternal short-axis images at both the
base and apex were obtained at a rate of 80
frames per second. Both the frame rate as
well as the image depth remained consistent
throughout within-subject acquisition.
Recorded images were attained in
agreement with existing guiding principles
(26), and as summarized by similar
methodologies undertaken by the same
research group (48, 47).
Following the collection of baseline data,
the participant’s feet were strapped to the
supine cycle ergometer and the ergometer
adjusted according to the participant’s
height. Each participant then performed an
exercise protocol identical to the one during
the first visit up to the point of completion
of the initial warm up period. Participants
then proceeded to complete three
consecutive 5-minute exercise bouts
performed at 30%, 40% and 50% of each
participant’s PPO at a cadence of 60 – 65
RPM. Echocardiographic images were
recorded during the last 3 minutes of each
5-minute exercise bout. For the purpose of
blood lactate analysis, capillary blood
samples were extracted from the right ear
Cooke et al. LV twist mechanics during exercise.
lobe at the last 30 seconds of each 5-minute
increment, and at 3-minute post exercise
cessation.
Data analysis
Conventional echocardiography: Recorded
echocardiographic images were saved
within the ultrasound machine and then
exported to commercially accessible data
analysis software for the purpose of offline
echocardiography analysis (EchoPAC
Version 112 revision 1.0, GE VINGMED
ULTRASOUND, Horten, Norway). LV
parasternal long axis images were analyzed
for the purpose of attaining dimensional
measurements including LV posterior wall
thickness (LVPW), LV internal diameter
(LVID) and intraventricular septum (IVS)
at both diastole and systole. As defined by
previous research (58), sphericity index
was quantified by dividing the maximal LV
length over the maximal LV diameter at
end-diastole. As previously described (26)
the area length method was used to
calculate LV mass. Manual tracing of the
apical triplane images at both the enddiastolic and end-systolic phase was
performed in order to obtain EDV, ESV and
SV. CO values were quantified through the
calculation of HR multiplied by SV. All
dimensional measurements, SV and CO
were indexed to body surface area (BSA)
using the Du Bois and Du Bois formula (20,
53) (see equation section). The final values
reported for each variable represent the
average value taken from three cardiac
cycles.
Speckle
tracking
echocardiography:
Parasternal short-axis images at both the
base and apex were obtained for the
purpose of quantifying LV twist mechanics
and circumferential strain. The endocardial
border of both the apical and basal
parasternal short-axis images were traced
post-hoc, and a region of interest formed to
incorporate
the
whole
contractile
myocardium whilst eliminating any valves
and trabeculations. The data analysis
software (EchoPAC Version 112 revision
6
1.0, GE VINGMED ULTRASOUND,
Horten, Norway) produced raw speckle
tracking data, in which cubic spline
interpolation was applied using custom
software (2D Strain Analysis Tool, Version
1.0beta14, Stuggart, Germany) in order to
intercalate raw data to 600 points during
both systole and diastole. As described in
previous research (36, 45, 47), frame by
frame values of twist and untwisting rate
were acquired by subtracting the apical
rotation data from the basal rotation data.
LV twist and untwisting rate were reported
as the peak systolic and early diastolic
values respectively. The relative change in
LV twist and untwisting rate were
expressed as the percentage change from
baseline to each exercise intensity and
calculated using a simple formula (see
equation section). All LV mechanical
parameters documented were established
through interpolated results and constitute
the mean of all the myocardial segments.
Statistical analyses
Normal distribution was assessed for all
data sets using the Sharpio-Wilk test.
Differences in baseline characteristics
between the trained and untrained group
were determined using an unpaired t-test,
provided that the data were identified as
normally distributed. In the event that the
data were non-parametric, the MannWhitney U test was applied. To determine
the influence of exercise and training status,
along with the interaction between the two
factors, a two-way repeated measures
ANOVA was utilized followed by a
Bonferroni post-hoc test when significant
main effects were detected. Unless
otherwise stated, all data are reported as
means ± SD. All statistical analyses were
carried out using GraphPad prism 6
(version 6.00 for Windows; GRAPHPAD
SOFTWARE, San Diego, California,
USA).
Results
Baseline data and cardiac measurements
Cooke et al. LV twist mechanics during exercise.
All data is reported as trained vs. untrained.
Age (26 ± 6 vs. 21 ± 1 years; P < 0.05),
VO2peak (46.2 ± 6.1 vs. 36.4 ± 6.4; ml.kg1
.min-1 P < 0.001), PPO (251 ± 20 vs. 193 ±
33; Watts P < 0.001), and the point at which
lactate threshold occurred (13.6 ± 2.1 vs.
10.2 ± 2.0; Min P < 0.05) were significantly
higher in the trained group. In addition, the
trained group also demonstrated a
significantly greater LV mass (180.20 ±
28.31 vs. 141.20 ± 18.10; g P < 0.001), and
EDV (147 ± 20 vs. 130 ± 19; ml P < 0.05),
yet, a significantly lower IVS index (0.5 ±
0.01 vs. 0.6 ± 0.08; cm.m2 P < 0.001). In
contrast, height, body mass, BSA, systolic
blood pressure (SBP), diastolic blood
pressure (DBP), and mean arterial blood
pressure (MAP) were not significantly
different between the two groups (P >
0.05). Similarly, no significant differences
were observed in any remaining parameters
associated with LV wall thickness, cardiac
dimensions or LV mechanics (P > 0.05).
All baseline data are presented in Table 1.
Response to submaximal exercise
Cardiovascular parameters including HR,
SBP, DBP, MAP, ESV and CO
significantly increased in response to
exercise, and were shown to increase to the
same extent in both groups. In addition, the
absolute and relative change in LV twist
(Figure 1 and 3, respectively), absolute LV
untwisting rate (Figure 2), and both apical
and basal circumferential strain also
increased to a similar degree in response to
exercise in both cohorts. In contrast,
exercise significantly increased VO2, SV,
SV index, sphericity index and the relative
change in LV untwisting rate, but not to the
same extent in both groups. Post-hoc
analysis revealed the trained group to have
a significantly higher VO2 at 30% (P <
0.05), 40% (P < 0.01), and 50% (P < 0.001)
exercise intensity. Similarly, the trained
group were shown to have a greater SV
(108 ± 10 vs. 94 ± 11 ml; P < 0.01) and SV
index (56 ± 6 vs. 48 ± 8 ml.m2; P < 0.05) at
50% exercise intensity, whereas, the
relative change in LV untwisting rate was
7
significantly lower in the trained group
(246 ± 107 vs. 332 ± 110 %; P < 0.05) at
50% exercise intensity (Figure 4). EDV
was significantly higher in the trained
group during exercise, but did not
significantly change from resting values.
All exercise data are presented in Table 2.
Discussion
Main findings
It has previously been suggested that
exercise training induces significant
alterations in resting LV twist mechanics.
However, it is unknown as to whether LV
twist mechanics respond differently during
exercise in trained and untrained
individuals. The primary aim of the current
study was to examine the differences in LV
twist mechanics in trained and untrained
individuals in response to exercise. To the
best of the author’s knowledge, this is the
first study to investigate the effect of
training status/aerobic fitness on LV twist
mechanics in response to progressive
submaximal exercise. There were two
novel findings from this investigation: 1) no
significant differences were identified in
LV twist or circumferential strain at rest or
during exercise between the trained and
untrained individuals, and 2) although the
differences in absolute values of LV
untwisting rate were non-significant, the
relative change in LV untwisting rate was
significantly lower during exercise in
trained individuals. Thus the present data
suggests that LV twist and circumferential
strain are similar at rest and change in a
similar manner from rest to moderate
exercise. However, the lower LV
untwisting rate in trained individuals may
reflect a more efficient diastolic function
under conditions of exercise stress.
Baseline data
It is evident that there is a clear division in
training status between the trained and
untrained cohorts as manifested by the
distinct differences in VO2peak, PPO and
lactate threshold. However, an interesting
Cooke et al. LV twist mechanics during exercise.
observation was the similar values in
resting HR and peripheral blood pressure
between the two cohorts. In particular, the
relatively low resting HR in the untrained
group was unexpected, and disputes
previous evidence (21, 13, 19); though this
may be reflective of the untrained group
representing a young and healthy
population, not a sedentary population. In
contrast, taking into consideration the
chosen study cohorts, it was expected that
the trained group had a greater LV mass in
addition to a concomitant increase in EDV.
It is widely acknowledged that dynamic
exercise training induces morphological
adaptations to the heart including an
increase in LV mass, chamber size and wall
thickness, caused by volume overload
associated with the sustained elevation in
CO during endurance training (40, 30, 55).
However, a notable finding showed both
trained and untrained individuals to have a
similar LV wall thickness. It is understood
that the increase in LV mass and chamber
size associated with eccentric hypertrophy
is accompanied by a proportional increase
in LV wall thickness (40, 23). Yet, there is
evidence to suggest that exercise training
can augment LV mass and chamber size
without any significant changes in LV wall
thickness (56). Specifically, it was
proposed that individuals experience a
phasic response to exercise induced cardiac
remodeling, whereby acute exercise
training is associated with an increase in LV
mass and EDV, whereas, adaptations in LV
wall thickness occur in response to chronic
exercise training (56). Although the
individuals recruited in the trained cohort
are considered to be experienced athletes, it
could be suggested that there is potential for
further cardiac remodeling.
In addition to the non-significant
differences in LV wall thickness, resting
LV mechanical parameters were also
similar in both cohorts. These findings
dispute the proposed hypothesis suggesting
that LV twist mechanics are significantly
reduced in trained individuals at rest and
8
contradicts the majority of previous
evidence showing either a reduction (57,
37, 47) or an increase (54, 1) in parameters
of LV twist mechanics as a result of
exercise training. Yet, there is existing
evidence that complements the findings of
the present study (56), and may help
explain why no significant differences were
evident between the trained and untrained
cohorts. Specifically, the longitudinal study
by Weiner and colleagues (56) suggested
that short term exercise training is
associated with an increase in LV twist
mechanics, whereas, long term exercise
training is accompanied by a regression in
LV twist mechanics back to baseline
values. It was therefore concluded that the
duration of training is a major determinant
of the degree of LV twist mechanics (56).
Thus, the similar values in LV twist
mechanics in the present study may in part,
be explained by the fact that the individuals
recruited in the trained cohort have been
exercise training for an extensive period of
time.
Conversely, whilst the data presented by
Weiner and colleagues (56) may
complement the outcomes of the current
study, it must be considered that the
findings were established in young rowers.
There is strong evidence to suggest that
different modalities of exercise impose
differential hemodynamic loads upon the
right and left ventricle, thus producing
diverging patterns of exercise induced
cardiac remodeling (33, 32, 35, 27).
Similarly, LV twist mechanics have also
been shown to differ in response to a variety
of different exercise modalities (15, 42). To
the best of the author’s knowledge, this is
the first study to examine LV twist
mechanics involving trained runners. There
is, therefore, a distinct possibility that our
findings apply specifically to the running
population and that differences in findings
between studies may in part be explained by
the differences in the studied population
groups.
Cooke et al. LV twist mechanics during exercise.
Cardiovascular responses and LV twist
mechanics during exercise
It is understood that LV twist mechanics
play an integral role in augmenting cardiac
function during exercise (18). Previous
evidence suggests that in response to
physiological stimuli LV twist is increased,
resulting in a greater amount of stored
potential energy in compressed titin (5).
Consequently, titin expands with greater
force during diastolic recoil, which in turn,
augments LV untwisting rate and facilitates
a more rapid diastolic filling in order to
maintain CO (36, 18). As anticipated, the
majority of LV functional parameters
including LV twist mechanics increased in
response to exercise in both groups. This is
primarily a result of the body’s need to
increase LV output in order to meet the
increased oxygen demands of the
exercising skeletal muscles (22, 43, 49).
However, a notable observation was the
non-significant differences in CO between
the two groups despite a differential
response in SV. Although a similar HR
response throughout the exercise protocol
was evident, the trained cohort presented a
significantly greater EDV and SV. Clearly
the magnitude of difference in EDV and SV
between the trained and untrained groups
was insufficient in producing any
significant differences in either the absolute
or relative values of CO.
Similarly, with respect to the response in
LV twist mechanics to exercise, LV twist
and circumferential strain were also
identified as non-significant. These
findings, in part, disprove our stated
hypothesis that LV twist mechanics would
be significantly lower in trained individuals
during exercise, and further disagrees with
recent evidence showing LV twist to be
significant lower in trained individuals in
response to submaximal exercise (47).
However, these findings may advance the
proposed theory that parameters of LV
twist mechanics may be dependent upon the
duration of exercise training (56),
suggesting that the training status of an
9
individual may provide a good indication as
to the degree of LV twist during low to
moderate exercise intensities. Yet, further
research is warranted in order to strengthen
this theory. Conversely, although such
findings may advance the theory proposed
by Weiner and colleagues (56), it is also
important to interpret the findings with
respect to LV twist in the context of several
functional parameters. Numerous studies
have implicated various physiological
factors including preload, afterload, HR and
myocardial contractility to have a
significant influence upon the degree of LV
twist during exercise. Specifically, a
directly proportional relationship was
suggested to exist between EDV and LV
twist, whereas the relationship between
ESV and LV twist was proposed to be
inversely related (28, 16). Similarly, an
increase in HR as well as myocardial
contractility has been shown to directly
correlate with LV twist (31, 12). Therefore,
taking into consideration that LV twist has
been suggested to be volume- and HRdependent, the non-significant differences
in LV twist during exercise in the present
study, may in part, be explained by the nonsignificant differences in HR and ESV;
along with the minor changes in EDV from
rest to exercise. In addition, considering
that both the trained and untrained cohort
demonstrated a similar amount of blood
being delivered to the periphery as
manifested
by
the
non-significant
differences in CO, it is logical that LV twist
was similar during exercise.
In contrast, although the absolute values of
LV twist mechanics were non-significant
between the two groups, the relative change
in LV untwisting rate was significantly
lower in the trained group in response to
exercise. This finding, in part, agrees with
the stated hypothesis that LV twist
mechanics would be significantly lower in
trained individuals in response to
progressive submaximal exercise; and may
suggest that trained individuals have a more
efficient diastolic function when the
Cooke et al. LV twist mechanics during exercise.
cardiovascular
system
is
stressed.
Specifically, data in the present study
showed the trained cohort to have a greater
EDV and a lower untwisting rate in
response to exercise, whereas, the untrained
cohort were shown to have a lower EDV
and a greater LV untwisting rate. This
suggests therefore, that trained individuals
are able to draw a larger amount of blood to
the LV for a lower LV untwisting rate
during exercise, which may be reflective of
a more efficient diastolic suction and
relaxation. This would fall in agreement
with previous evidence that also proposes
that exercise training enhances parameters
of diastolic function including LV suction,
relaxation and filling within trained (40)
and diseased populations (2, 3, 7).
However, although the lower untwisting
rate in trained individuals could be regarded
as a highly novel finding, it is not exactly
clear as to how this has occurred. Thus,
further discussion is warranted with respect
to the potential mechanisms behind this
finding.
Potential mechanisms for a lower LV
untwisting rate
Taking into consideration that LV twist
mechanics have been shown to play a
crucial role in overall LV performance
within several disease states, the small
number of studies investigating the
adaptive response in LV twist mechanics to
exercise training is somewhat surprising.
Consequently, the underlying mechanisms
behind the adaptive response in LV twist
mechanics to physiological stimuli are
poorly understood. Despite this, there is
existing evidence that may, in part, help
explain the findings in the current study. It
is known that the strength of restoring
forces play an important role in the
magnitude of LV untwisting rate (36, 38).
Specifically,
deformation
of
the
subendocardial and subepicardial fiber
matrix during systole results in the
generation of restoring forces known as
potential energy (38). During systole,
potential energy is stored in myocyte
10
components known as titin (5, 38). It is
during diastolic recoil that titin expands and
releases the stored potential energy which
assists LV untwisting (36). It is suggested
that an increased amount of stored potential
energy allows the compressed titin to
expand with greater force during diastolic
recoil, thereby generating a greater amount
of LV untwisting (36, 38). Thus, one
potential mechanism could be that the
trained and untrained group are storing a
different amount of potential energy or
have differential restorative properties
despite similar values in LV twist. This in
turn may be a causative factor for the
observed differences in LV untwisting rate.
Yet, further research is needed to strengthen
this theory.
In addition, another potential mechanism
with respect to the differential response in
LV untwisting rate may be related to the
observed differences in the shape of the LV
between the trained and untrained cohort. It
has previously been suggested that the more
spherical the LV cavity the lesser amount of
LV twist occurs in conjunction with a more
evenly distributed myofiber stress in
diseased populations (58, 34). However, a
limitation of the study by Van Dalen and
colleagues (58) is that the influence that the
shape of the LV has upon diastolic function,
and in particular LV untwisting rate, was
not investigated. Data in the present study
shows that the trained cohort possess a
more spherical LV cavity during exercise,
whereas, the untrained cohort demonstrate
a more elongated LV cavity. It is therefore
possible that the differences in the shape of
the LV cavity may help explain why a lower
LV untwisting rate was observed within the
trained cohort. However, the suggestion
that a more spherical LV cavity may result
in a lower LV untwisting is speculative at
this point in time, and requires the direct
study between LV cavity shape and
diastolic untwisting rate.
Finally, it has also previously been
suggested that the rate of myocardial
relaxation is a strong determinant of peak
Cooke et al. LV twist mechanics during exercise.
LV untwisting rate (38). Specifically, an
increase in LV untwisting rate was shown
to have been associated with a faster
myocardial relaxation rate (38). In the
present
study,
trained
individuals
demonstrate a lower LV untwisting rate,
which was suggested to reflect alterations
in diastolic function. It could therefore be
suggested that the observed differences in
LV untwisting rate in the present study may
be as a result of the trained group having a
more prolonged myocardial relaxation rate
compared to the untrained individuals.
Although a delayed myocardial relaxation
rate is a key feature in various disease states
(52, 25), a prolonged myocardial relaxation
rate in trained individuals may reflect a
physiological adaptation to exercise
training. However, further research into the
adaptive potential of LV mechanics in
relation to heart function is needed to
support this speculation.
Study limitations and future research
It is acknowledged that failing to recruit the
required sample size precludes us from
drawing conclusions that may be
extrapolated to the entire running
population as a whole. Furthermore, it is
important to note that due to recruitment
issues, the trained cohort in the present
study consisted of endurance runners
specializing in long distance disciplines as
well as sprinters competing in events such
as the 400m. As previously indicated, there
is evidence to suggest that different training
modalities elicits diverging patterns of
exercise induced cardiac remodeling (33,
35). Thus, incorporating various exercise
modalities in the trained cohort not only
reduces the generalizability of the data, but
may well have had a significant impact
upon the findings. Another important
limitation to consider is the low ecological
validity of the study. In an ideal scenario,
trained runners would perform an exercise
protocol that is indicative of their
discipline.
However,
taking
into
consideration
current
measuring
techniques, LV twist mechanics could only
11
be obtained in the supine position. In
relation to this, hemodynamics are known
to alter in accordance with the posture in
which one exercises (i.e. supine vs. upright
cycling). Thus, it is also important to note
that supine cycling exercise may be
associated with a differential response in
LV twist mechanics compared to different
modalities of exercise testing. Finally, to
the best of the author’s knowledge,
normative values for LV twist and
untwisting rate at rest and during exercise
are yet to be established. This makes it
difficult to compare findings to previous
studies and prevents the use of LV twist
mechanics in the present study as a marker
of cardiac performance.
It is clear that the number of studies
investigating LV twist mechanics in
response to exercise is extremely limited.
This is somewhat surprising considering
that LV twist mechanics have been shown
to play an integral role in the
pathophysiology of many disease states. It
is still unclear whether alterations in LV
twist mechanics represent a physiological
or pathological adaptation to exercise.
Further investigation into the response of
LV twist mechanics to exercise is needed
and will expand our understanding into the
functional differences between the heart of
an athlete and a pathological heart. In
addition, such research may enhance our
knowledge
with
respect
to
the
pathophysiology of various disease states,
and potentially contribute towards possible
treatment strategies.
Conclusion
In summary, the novel data of this study
suggests that in trained and untrained
individuals LV twist and circumferential
strain are similar at rest and respond in a
similar manner to the stress of exercise.
However, the trained cohort were shown to
have a significantly lower LV untwisting
rate in response to exercise, which may
reflect a more efficient diastolic function
related to LV suction and relaxation when
Cooke et al. LV twist mechanics during exercise.
the cardiovascular system is challenged.
Further research investigating the adaptive
potential of LV twist mechanics in response
to physiological stimuli is needed, and may
help expand our knowledge and further
develop our understanding of the
differences between the heart of an athlete
and a diseased heart.
Appendix
Links to Journal of Applied Physiology
“Author instructions”
Appendix A. Formatting requirements
http://www.theaps.org/mm/Publications/Info-ForAuthors/Formatting
Appendix B. Manuscript composition
http://www.theaps.org/mm/Publications/Info-ForAuthors/Composition
Appendix C. Preparing Figures
http://www.theaps.org/mm/Publications/Info-ForAuthors/Preparing-Figures
Author contributions
S.C. is responsible for the research and
experimental design, collection and
analysis of data, interpretation of results,
and manuscript composition. The author
approves the final form of the manuscript
and is fully accountable for the work.
Acknowledgements
The author would like to take this
opportunity to thank all participants and
coaches for their efforts and commitment to
this project.
Grants
12
The author has no conflict of interest to
report.
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Cooke et al. LV twist mechanics during exercise.
17
LV
Figure captions
untwisting
rate
was
shown
to
significantly increase from rest to moderate
Figure 1. Peak LV twist at rest and during
intensity exercise in both groups, though
exercise in the trained and untrained group.
the relative change in LV untwisting rate
LV twist is shown to significantly increase
from rest to 50% exercise intensity was
in response to exercise in both groups,
significantly lower in the trained group (P
though the observed differences between
< 0.05). Data presented as mean ± SD.
trained and untrained individuals were nonsignificant (P > 0.05). Data are presented as
mean ± SD.
Figure 2. Peak LV untwisting rate at rest
and during exercise in the trained and
untrained group. LV untwisting rate is
shown to significantly increase in response
to exercise in both groups, though the
differences
between
the
trained
and
untrained individuals were non-significant
(P > 0.05). Data are presented as mean ±
SD.
Figure 3. The relative change in LV twist
from rest to 30%, 40% and 50% exercise
intensity in the trained and untrained group.
The percentage change in LV twist was
shown to significantly increase from rest to
moderate intensity exercise, though the
differences between trained and untrained
individuals
were
found
to
be
non-
significant (P < 0.05). Data presented as
mean ± SD.
Figure 4. The relative change in LV
untwisting rate from rest to 30%, 40% and
50% exercise intensity in the trained and
untrained group. The percentage change in
Cooke et al. LV twist mechanics during exercise.
18
Figures
L V T w is t
40
T r a in e d
T w is t (d e g .)
35
U n tr a in e d
30
25
20
15
10
5
%
5
0
%
0
4
0
3
R
E
S
T
%
0
E x e r c i s e w o r k lo a d
Figure 1. Peak LV twist at rest and during exercise in the trained and untrained group. LV
twist is shown to significantly increase in response to exercise in both groups, though the
observed differences between trained and untrained individuals were non-significant (P >
0.05). Data are presented as mean ± SD.
Cooke et al. LV twist mechanics during exercise.
19
L V U n t w is t in g R a t e
U n tw is tin g r a te (d e g /s )
-4 0 0
T r a in e d
-3 5 0
U n tr a in e d
-3 0 0
-2 5 0
-2 0 0
-1 5 0
-1 0 0
-5 0
5
0
%
%
0
4
0
3
R
E
S
T
%
0
E x e r c i s e w o r k lo a d
Figure 2. Peak LV untwisting rate at rest and during exercise in the trained and untrained
group. LV untwisting rate is shown to significantly increase in response to exercise in both
groups, though the differences between the trained and untrained individuals were nonsignificant (P > 0.05). Data are presented as mean ± SD.
Cooke et al. LV twist mechanics during exercise.
20
T w is t % c h a n g e
400
T r a in e d
350
T w is t ( %

)
U n tr a in e d
300
250
200
150
100
50
%
5
0
%
0
4
0
3
R
E
S
T
%
0
E x e r c i s e w o r k lo a d
Figure 3. The relative change in LV twist from rest to 30%, 40% and 50% exercise intensity
in the trained and untrained group. The percentage change in LV twist was shown to
significantly increase from rest to moderate intensity exercise, though the differences between
trained and untrained individuals were found to be non-significant (P < 0.05). Data presented
as mean ± SD.
Cooke et al. LV twist mechanics during exercise.
21
Figure 4. The relative change in LV untwisting rate from rest to 30%, 40% and 50% exercise
intensity in the trained and untrained group. The percentage change in LV untwisting rate was
shown to significantly increase from rest to moderate intensity exercise in both groups, though
the relative change in LV untwisting rate from rest to 50% exercise intensity was significantly
lower in the trained group (P < 0.05). Data presented as mean ± SD.
Cooke et al. LV twist mechanics during exercise.
22
Tables
Table 1. Baseline characteristics of the untrained and trained groups.
Untrained group (n = 13)
Trained group (n = 11)
P value
Age (years)
21 ± 1
26 ± 6
< 0.05
Height (cm)
178.1 ± 6.5
181.3 ± 4.8
> 0.05
Body mass (kg)
79.0 ± 11.3
74.1 ± 6.5
> 0.05
1.97 ± 0.12
1.94 ± 0.09
> 0.05
36.4 ± 6.4
46.2 ± 6.1
< 0.001
PPO (Watts)
193 ± 33
251 ± 20
< 0.001
Lactate threshold (min)
10.2 ± 2.0
13.6 ± 2.1
< 0.05
53 ± 5
51 ± 6
> 0.05
SBP (mmHg)
124 ± 12
130 ± 15
> 0.05
DBP (mmHg)
73 ± 6
79 ± 17
> 0.05
MAP (mmHg)
91 ± 10
99 ± 16
> 0.05
EDV (ml)
130 ± 19
147 ± 20
< 0.05
ESV (ml)
54 ± 15
65 ± 13
> 0.05
74 ± 10
82 ± 14
> 0.05
38 ± 6
42 ± 8
> 0.05
CO (L.min-1)
4.2 ± 0.5
4.2 ± 0.9
> 0.05
CO index (L.min-1.m2)
2.1 ± 0.3
2.1 ± 0.4
> 0.05
141.20 ± 18.10
180.20 ± 28.31
< 0.001
5.0 ± 0.3
5. 2 ± 0.2
> 0.05
2.6 ± 0.2
2.7 ± 2.4
> 0.05
3.5 ± 0.3
3.7 ± 0.3
> 0.05
1.8 ± 0.2
1.9 ± 0.2
> 0.05
LVPWd (cm)
1.00 ± 0.2
1.1 ± 0.2
> 0.05
LVPWd index (cm.m2)
0.5 ± 0.1
0.6 ± 0.1
> 0.05
LVPWs (cm)
1.6 ± 0.2
1.7 ± 0.3
> 0.05
0.8 ± 0.1
0.9 ± 0.1
> 0.05
1.1 ± 0.2
1.2 ± 0.3
> 0.05
0.6 ± 0.08
0.5 ± 0.01
< 0.001
1.5 ± 0.1
1.6 ± 0.2
> 0.05
0.8 ± 0.1
0.8 ± 0.2
> 0.05
1.81 ± 0.19
1.71 ± 0.08
> 0.05
BSA
(m2)
VO2peak(ml.
kg--1.min-1)
HR (bpm)
SV (ml)
SV index
(ml.m2)
LV mass (g)
LVIDd (cm)
LVIDd index
(cm.m2)
LVIDs (cm)
LVIDs index
(cm.m2)
LVPWs index
(cm.m2)
IVSd (cm)
IVSd index
(cm.m2)
IVSs (cm)
IVSs index
(cm.m2)
Sphericity Index
All data presented as mean ± SD. d = diastole s= systole
Cooke et al. LV twist mechanics during exercise.
23
Table 2. Systematic cardiovascular responses and peak left ventricular twist mechanics at rest and during submaximal exercise intensities in trained and untrained individuals.
Untrained group (n = 13)
Trained group (n = 11)
Main effects
Rest
30%
40%
50%
Rest
30%
40%
50%
4.5 ± 1.2
16.0 ± 2.4
19.1 ± 2.8
21.6 ± 3.2
5.70 ± 1.3
19.3 ± 2.7*
23.5 ± 3.3**
27.8 ± 4.0***
# † ~
-
58.0 ± 10
77.3 ± 13
97 ± 16
-
75 ± 6***
100.3 ± 8***
125 ± 10***
# † ~
0.77 ± 0.22
1.37 ± 0.43
1.75 ± 0.81
2.42 ± 1.06
1.06 ± 0.54
1.37 ± 0.51
1.69 ± 0.75
2.11 ± 1.07
†
53 ± 5
79 ± 18
83 ± 20
93 ± 24
51 ± 6
77 ± 10
88 ± 12
91 ± 13
†
SBP (mmHg)
124 ± 12
165 ± 16
168 ± 17
171 ± 17
131 ± 15
168 ± 21
173 ± 21
175 ± 22
†
DBP (mmHg)
74 ± 6
91 ± 12
90 ± 11
90 ± 11
79 ± 17
96 ± 22
96 ± 20
93 ± 18
†
MAP (mmHg)
91 ± 10
118 ± 14
118 ± 13
120 ± 13
99 ± 16
123 ± 23
125 ± 21
124 ± 19
†
EDV (ml)
130 ± 19*
133 ± 9
140 ± 17
139 ± 17
147 ± 20
154 ± 23
151 ± 19
157 ± 24
~
ESV (ml)
54 ± 15
49 ± 10
50 ± 15
44 ± 15
65 ± 13
66 ± 20
55 ± 13
49 ± 19
†
SV (ml)
74 ± 10
84 ± 6
90 ± 8
94 ± 11
82 ± 14
88 ± 9
96 ± 10
108 ± 10**
†~
SV index (ml.m2)
38 ± 6
43 ± 5
46 ± 6
48 ± 8
42 ± 8
45 ± 6
50 ± 7
56 ± 6*
†~
CO (L.min-1)
4.2 ± 0.5
8.2 ± 0.9
10 ± 1.0
11.6 ± 1.4
4.2 ± 0.9
7.8 ± 1.3
10.2 ± 2.0
12.6 ± 2.4
†
CO index (L.min-1.m2)
2.1 ± 0.3
4.2 ± 0.6
5.1 ± 0.7
5.9 ± 1.0
2.1 ± 0.4
4.0 ± 0.7
5.3 ± 0.9
6.5 ± 1.2
†
Sphericity index
1.81 ± 0.19
1.54 ± 0.06
1.60 ± 0.14
1.61 ± 0.15
1.71 ± 0.08
1.51 ± 0.15
1.47 ± 0.17
1.49 ± 0.14
# † ~
LV twist (°)
13.9 ± 3.9
20.2 ± 4.2
22.1 ± 5.9
25.9 ± 5.9
12.4 ± 7.2
18.5 ± 6.4
19.8 ± 8.3
21.2 ± 5.9
†
-
156 ± 61
174 ± 90
198 ± 65
-
158 ± 82
166 ± 90
187 ± 114
†
-91 ± 18
-203 ± 61
-242 ± 73
-292.2 ± 65
-114 ± 34
-183 ± 45
-227 ± 66
-265 ± 76
†
-
226 ± 168
271 ± 90
332 ± 110
-
168 ± 50
212 ± 107
246 ± 107*
†~
Basal circ strain (°)
-15.4 ± 2.8
-18.1 ± 3.8
-19.1 ± 4.4
-19.3 ± 3.3
-16.3 ± 2.9
-18.2 ± 2.9
-19.2 ± 3.0
-17.6 ± 3.9
†
Apical circ strain (°)
-19.9 ± 2.8
-26.6 ± 1.6
-29.8 ± 3.6
-31.1 ± 3.7
-22.4 ± 3.4
-27.9 ± 2.8
-30.4 ± 2.2
-32.8 ± 4.4
†
VO2 (ml. kg-1.min-1)
PO (Watts)
Lactate (mmol.L)
HR (bpm)
LV twist (% Δ)
LV untwisting rate (°.sec-1)
LV untwisting rate (% Δ)
All data presented as mean ± SD. * = P < 0.05 ** = P < 0.01 *** = P < 0.001 # = Significant interaction main effects † = Significant exercise effect ~ = Significant group effect
Cooke et al. LV twist mechanics during exercise.
Equations
Du Bois and Du Bois formula
BSA = (Weight 0.425 x Height 0.725) x 0.007184
LV twist and untwisting rate percentage change formula
Percentage change = 100/ baseline value x exercise intensity value
24