Major Project final draft

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IN EXERCISE MEASURES OF CARDIAC STRUCTURE AND FUNCTION VERSUS
RESTING RECOVERY IN THE ASSESSMENT OF EXERCISE INDUCED
CARDIAC FATIGUE
by
Mark McCormick
A Major Project submitted to the School of Sport and Exercise Sciences, Liverpool
John Moores University, in partial fulfilment of the degree of B.Sc (Hons) Sport and
Exercise Science, April 2016
Acknowledgements: David Oxborough, Ben Brown.
Abstract:
The purpose of this study was to examine the effects of a prolonged 2 hour exercise
protocol on RV structure and function in healthy competitive cyclists. Methods:
Subjects (n = 6) were cyclists that were competing regularly in endurance and time
trial events. Measures includes Heart Rate (bpm), Height (cm), Body mass (kg), BMI
and 13 cardiac parameters obtained from a cardiac assessment. Participants
performed a 2 hour exercise protocol on a cycle ergometer. Cardiac assessments
were carried out at rest (pre rest), during the start of exercise (pre exercise), when
the 2hr exercise protocol is finished (post exercise), and after exercise when the
participant has had a prolonged rest (post rest), all assessments were performed on
a Lode angiobed. Results: Subject means are as followed: age (years old): 24.5 ±
4.81, height (cm): 175.5 ± 6.75, body mass (kg): 72.1 ± 4.39 and BMI: 23.52 ± 3.
Significant (P<0.05) differences were seen at Pre/Post for Right Ventricular Fraction
Area Change (RVFAC) Right Atrial Area (RAarea) and S’. Conclusion: A prolonged 2
hour bout of exercise at 60% max power promotes symptoms of EICF.

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Introduction
Right ventricular (RV) impairment has been observed in the early recovery periods
after intense prolonged endurance exercise. Recent studies have considered the
features of the recovery state and they may have concluded that when comparing
the Left Ventricle (LV) and the RV, it is the RV that shows a fatigue in function
(Claessen, 2014). It is proposed that this injury to the RV is due to a greater
haemodynamic load and wall stress during intense prolonged exercise (La Gerche,
2010; La Gerche, 2011), also, these discussed injuries are subject to much research
as they are proposed as potential mechanisms for RV arrhythmias in endurance
athletes (Heidbuchel, 2003; Oxborough, 2011). Intense exercise has been
acknowledged to profoundly affect RV function and remodelling, and La Gerche
(2011) has stated that RV recovery may not be complete during a lengthy rest after
an intense prolonged bout of exercise. Along with the work of Heidbuchel and
colleagues (2003), Le Gerche (2010) deliberated the potential for the development of
an arrhythmogenic RV cardiomyopathy phenotype. Additionally, Sharma and Zaidi
(2011) agreed with the previous study, declaring that research in this project would
be enormous due to participating rates in endurance exercise. Although these
injuries have been discussed to cause cardiac abnormalities, it is important to note
that in the absence of any other cardiovascular issues, these effects are nothing to
be concerned about when considering a person’s cardiovascular health. Furthermore,
these issues are attributed to a condition known as Exercise Induced Cardiac
Fatigue (EICF) (Frank, 2011).
The product of heart rate and stroke volume is cardiac output and as the duration of
exercise goes on, there will be an increased requirement for oxygen production. This
increase of oxygen supply could cause a transient impairment which may cause
EICF. RV dysfunction during the recovery periods of intense prolonged endurance
exercise has been named “exercise induced cardiac fatigue” by many researchers,
this term is described as an immediate depression in ventricular diastolic or systolic
following an intense bout of exercise (Oxborough, 2010). It has been discussed that
this cardiac fatigue may be intensified when exposed to acute hypoxia and the
cardiovascular system may be placed under a greater strain. Exposure to hypoxia
has been associated with pulmonary vasoconstriction, which therefore accompanies
an increased pulmonary artery pressure because of this (Ghofrani, 2004; Huez, 2007;

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Kjaergaard, 2007). These conditions will be further exacerbated when exercise has
been commenced and can further be intensified if an athlete is exposed to
temperatures that exceed 37oC during prolonged endurance exercise. EICF can be
identified through such symptoms as septal wall motion irregularities; altered
diastolic function and decreased cardiac contractility.
The study of EICF has mainly been researched through using endurance athletes
such as marathon runners, cyclists, and triathlon runners. Individuals that may not
participate in some type of endurance exercise programme may experience EICF
after a shorter time period, this is the case as they have a lower threshold and
cannot engage in prolonged exercise as long as endurance athletes. Therefore due
to this lower engagement, they will show exercise induced cardiac fatigue after a
shorter time period while also at a lower intensity (Vanoverschelde et al., 1991).
Many researchers have attributed cardiac impairment (in the absence of any other
cardiovascular issues) to problems such as fatty acid accumulation, prolonged
tachycardia and catecholamine elevations (Rifai et al., 1999). Research from
Douglas et al, 1997 has suggested that a reduction in systolic function is attributed to
a depressed inotropic state (Frank, 2011), while Vanoverschelde et al. (1991)
explained that a decrease in diastolic function was due to altered volume loading.
In a performance perspective, cardiac muscle is unable to attain the recovery period
that skeletal muscle has, this is due to the considerable level of work the heart must
maintain constantly, in order to preserve life. In healthy young athletes, the
dysfunction of the RV after prolonged exercise is not enough to have a significant
effect on their health, but this prospect of EICF could have a detrimental effect on
performance at the highest intensity/duration (Starnes and Bowles, 1995).
To date, there hasn’t been any studies that have assessed cardiac structure and
function during exercise; this would provide a valuable insight to discover how the
heart fatigues over time. Hence, dysfunction of the right ventricle is unable to be
determined throughout exercise, opposed to just being a side effect of prolonged
endurance exercise.
The Right Ventricle (RV) is a key component in the cardiovascular system and its
primary function is to transport blood to the lungs for gas exchange to occur. After
prolonged exercise the RV may become fatigued, therefore the aims of this study

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were to examine if there is exercise fatigue of the RV in cyclists after a 2 hour bout of
exercise, when a pre and post echo scan has been performed. If this aim can be
observed, will this EICF be present during a post exercise scan maintaining the heart
rate (HR) at 100bpm rather than just being present during rest. It is hypothesised
that changes will been seen in functional parameters of the RV following exercise,
whilst also maintaining a heart rate of 100bpm.
Methods
Participants
Six healthy male cyclists were recruited from the Liverpool John Moores University
cycling team and advertisements posted in local cycling clubs (age (years old): 24.5
± 4.81, height (cm): 175.5 ± 6.75, body mass (kg): 72.1 ± 4.39 and BMI: 23.52 ± 3).
Participants were free from any underlying cardiovascular problems and they have
all took part in long distance cycling for >2 years. Informed written consent was
received from all participants to agree that they will take part in this study and that
they understood what risks this research involved. This experimental design and
protocol was approved by the Liverpool John Moores University ethics committee.
Experimental Design
In advance, participants were told that they had to refrain from training, drinking
alcohol, smoking or consuming medication (unless prescribed) before the exercise
session. All participants took part in two exercise sessions; these sessions included
a familiarisation (control) session and a 2 hour endurance session which involved
four echocardiography assessments, analysing 13 cardiac parameters which follow:
Right ventricular outflow tract – parasternal long axis (RVOTplax), Right ventricular
outflow tract – 1 (RVOT1), Right ventricular outflow tract – 2 (RVOT2), Right
ventricular diameter(RVD1, RVD2, RVD3), Right Ventricular Area (diastolic and
systolic area – RVDarea and RVSarea), RV Fractional area change (RVFAC), Right
atrium area (RAarea), S’, E’ and A’.
Experimental Protocols
The participants attended two exercise sessions (cycle ergometer - Excalibur), with
the first test being a familiarisation (control) that involved cycling to find out the
participant’s maximal aerobic capacity. Exercise intensity on the cycle ergometer

5
was increased every two minutes by 30W until the participant could not continue.
Oxygen and carbon dioxide levels were monitored throughout the test and the
results were used to establish a cycling velocity of 60% of the participant’s VO2max
to be used for the next visits. During the next visit participants arrived in the lab at
the time they were allocated for and were asked to prepare for exercise. When
participants were dressed appropriately, they were weighed using calibrated scales
(seca) and their height was measured using a stadiometer (seca). Once these
measurements were completed, a cardiac assessment (Pre Rest) was carried out
using a transthoracic echocardiography approach, this method was used to view the
chambers of the heart and investigate cardiac function. Images were taken of the
participant’s heart for further interpretation, these measurements were recorded by
an advanced sonographer. This evaluation took place on a Lode angiobed. After this
procedure, blood pressure was recorded and the Heart Rate monitor (Polar monitor
FT1) was fitted and participant was prepared for exercise. The participant then
engaged in exercise of 60W to raise their HR to ~100BPM, they were once again
scanned using the same echocardiographic technique (Pre Exercise).
When the participant was ready, they began exercising at their allocated 60% of
maximal power which was found in the familiarisation (control) test, the participants
maintained a cycling pace of above 100RPM. During exercise, Rate of Perceived
Exertion (RPE) and Heart Rate (HR) were measured at 15 minutes, 30 minutes, 1
hour, 1 hour 30 minutes and 2 hours. After two hours of exercise the participants
stopped exercising and were removed from the cycle ergometer. The participant’s
blood pressure was taken and the HR monitor was then removed, the participant
was then asked to rest on a Lode angiobed for a period of 5 minutes, when this rest
period had ended another cardiac assessment was then undertaken (Post Exercise).
During this assessment the participant was asked once again asked to cycle on the
angiobed maintaining their HR at 100bpm.Finally, the participant was told to rest for
20 minutes and once this period had finished, one last cardiac assessment was
undertaken (Post Rest). Table 1 and Figure 1 have outlined the schedule for
measurements throughout the study.
Echocardiography Measurements

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Using a commercial VividQ ultrasound (GE healthcare), 2D and tissue Doppler
images were recorded, in accordance with the American Society of
Echocardiography (ASE) patients were oriented in the left lateral decubitas positon
and placed in the semiprone positon (Rudski et al., 2010). A minimum of three
cardiac cycles were recorded by an experienced sonographer, then analysed at a
later time after the cardiac assessment had ended by a trained observer using an
EchoPAC, Version 7, GE Healthcare. Parameters observed can be noted in Table 2.
M Mode and 2D echocardiography techniques were used to assess RV internal
dimensions. Pulse wave Doppler recordings facilitated the assessment of diastolic
function using peak early (S’) and late atrial (A’) myocardial tissue velocities (Banks
et al., 2011).
Statistical Analysis
Information that was collected was inputted into IBM SPSS 22 software, with data
being represented as means. For the analysis of differences between Pre Rest, Pre
Exercise, Post Exercise and Post Rest for the 13 parameters shown in Table 2, a
Two way Mixed ANOVA was used.
Results
HR
There was a significant main effect for condition (F3,15 = 40.04, P = 0.000). There
was also a significant increase of 38bpm between the Pre Rest echo scan and the
Pre Exercise echo scan (P < 0.05). Additionally there was a significant increase of
47bpm from the Pre Rest echo scan and the Post Exercise echo scan (P<0.02).
RVOTplax
There was no significant main effect for condition (F3,15 = 0.74, P = 0.973). Overall
there was no significant difference when comparing RVOTplax during four different
time points.
RVOT1
there was no significant difference when comparing RVOT1 during four different time
points.

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RVOT2
there was no significant difference when comparing RVOT2 during four different time
points.
RVD1
there was no significant difference when comparing RVD1 during four different time
points.
RVD2
points.
RVD3
points.
RVDarea
there was no significant difference when comparing RVDarea during four different
time points.
RVSarea
there was no significant difference when comparing RVSarea during four different
time points.
RVFAC

8
There was no significant main effect for condition (F3,15 = 2.208, P = 0.129).
However there was a significant decrease of 8% in RVFAC when comparing at Pre
Exercise and Post Rest (F1,5 = 218.725, P < 0.05).
RAarea
was also a significant decrease of 3mm when comparing RAarea from Pre Rest and
Pre Exercise (F1,5 = 1468.566, P < 0.05). Additionally there was a significant
decrease of 4mm during the conditions Pre Rest and Post Exercise. (P<0.02).
S’
was also a significant 5.5cm/s decrease when comparing S’ at condition Pre
Exercise and Post Rest (F1,5 = 381.176, P < 0.05). Additionally, there was a
significant decrease of 5.5cm/s when comparing Pre Exercise and Post Exercise
conditions (P<0.05).
E’
there was no significant difference when comparing E’ during four different time
points.
A’
there was no significant difference when comparing A’ during four different time
points.
Discussion
The current study provides a comprehensive insight into how cardiac function is
effected after a 2 hour prolonged bout of exercise. This study consisted of two aims,
the first aim was to consider if there was any exercise induced cardiac fatigue
observed after a two hour bout of exercise at 60% maximal power, the second aim
was to observe if there was any EICF seen when the participant was maintaining

9
their HR at 100bpm. The four echocardiography scans consisted of a resting
echocardiography assessment, another assessment with the participant maintaining
their HR at 100bpm, a third cardiovascular evaluation when the participant has
finished the 2 hour cycle ergometer protocol (also maintaining their HR at 100bpm)
and then a final echocardiography assessment when the participant has had a 20-30
minute rest. All assessments took place on a Lode angiobed. The hypothesis of this
study was that changes would been seen in functional parameters of the RV
following exercise, whilst also maintaining a heart rate of 100bpm. The findings show
that the hypothesis was correct and this can be seen in Table 2, Figure 6, 7 and 8.
It is not the first time this approach of assessing EICF has been used, many
researchers have used the method of examining RV dysfunction which involves a
resting cardiac evaluation comparing the results to a post exercise resting
cardiovascular assessment. However it is, to the best knowledge of the researcher,
the first study that analyses cardiac functional parameters while the participant is
maintaining exercise, immediately at the start and at the end of the exercise protocol,
while also carrying an assessment out during rest and after a period of rest when
exercise has been completed.
As mentioned previously, researchers have utilised the protocol of assessing cardiac
structure before and after exercise. A study conducted by La Gerche et al. (2011)
investigated cardiac function after prolonged exercise, using 40 well trained athletes,
concluded that intense prolonged exercise causes acute dysfunction of the RV, they
also stated that RV arrhythmias and chronic RV remodelling is commonly found in
highly trained endurance athletes, which may constitute a risk of cardiac injury.
However a study by Ruiz, Joyner, and Lucia, (2013) concluded that currently there is
no “strong evidence” of permanent or pathological damage due to prolonged
endurance exercise stating that regular prolonged exercise offsets the chance of any
type of cardiac irregularities.
From table 2 and figure 5 it can be seen that there is a small decrease in RV systolic
and diastolic size, this data contradicts recent research from Oxborough et al. (2011).
This study used 16 ultra-endurance athletes during a 161km endurance race and
concluded that the cause of this increase in RV size could be due to an increase of
RV afterload or an intrinsic reduction in myocardial function (Oxborough et al., 2011).

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However, similar structural results were seen in another study by La Gerche et al.
(2008), this study used 27 ultra-endurance triathlon athletes to compare structural
changes of the RV. They concluded that there was no difference in RV diastolic size,
although, there was a significant difference in RV systolic size. These researchers
stated that this reduction of the RV systolic area constitutes a valid reduction of the
right ventricular function. Furthermore, this reduction is possibly due to an increase
in afterload or a reduction in contractility, this contractility impairment may also be
able to explain the small reduction of E’ seen in Table 2 (La Gerche et al., 2011).
There was an 8% reduction in RVFAC when comparing Pre Exercise and Post Rest
(P = 0.021), this decrease can be seen in Table 7. This data agrees with the findings
found from Oxborough et al. (2011), who showed a similar decrease of 12% stating
the reason behind this was associated with an increase in HR post-race. Another
study from Welsh et al. (2005) found similar results once again using a five day
echocardiography assessment protocol during an ultra-endurance event.
Even though there is increasing evidence of EICF after prolonged exercise, there
seems to be a limited body of research involving the mechanisms of it and that the
mechanisms are not fully understood. However the case, Oxborough et al. (2010)
has proposed two main hypothesise for Exercise Induced Cardiac Fatigue. The first
of which is a down regulation of cardiac beta-adrenergic receptors, and secondly
there is a reversible process of damage to cardiomyocytes, referred to as stunning.
This term was first coined by Saltin and Stenberg. (1964) several years after their
original study. These researchers found a decrease in submaximal stroke volume
(SV) after 3 hr of exercise at 75% of maximal oxygen consumption. This term was
defined by them as a contractile dysfunction without the presence of myocardial
necrosis (Starnes and Bowles., 1995). This process of stunning can affect the
metabolism of calcium, and for this reason contractile function is compromised. The
theory of stunning is that it does not result in necrosis or permanent cell damage,
whilst it is also transient in nature (Dawson et al., 2003). Once again, this theory of
stunning is supported by such research from Douglas et al. (1987), these scientists
found no lasting EICF symptoms 24 – 48 hours after exercise.
The next mechanism, which is beta-adrenergic downregulation, was supported by
the research of Friedman, Ordway, and Williams. (1987), who aimed to test if high
levels of catecholamines, associated with strenuous exercise, produced beta

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adrenergic desensitisation. They concluded that a single bout of exercise would be
significant enough to decrease chronotropic responsiveness to isoproterenol, which
would in turn cause a transient desensitisation of cardiac adrenergic receptors
(Friedman, Ordway, and Williams., 1987). This theory is difficult to confirm as the
assessment of inotropic responses to beta-adrenoceptor stimulation is problematic,
although saying this, prolonged exercise elevates catecholamines, exposing athletes
to them for a lengthy period and it is possible that this prolonged exposure could
provide a post exercise beta-adrenoceptor downregulation (Fraser et al., 1981).
Even though it is difficult to confirm this theory, Banks et al. (2009) conducted a
study with 18 well trained individuals measuring the effect of intensity during
prolonged exercise. These researchers found that LV and RV dysfunction after
prolonged exercise was related to beta adrenergic desensitisation. This was also
supported by a decreased strain, strain rate and ejection fraction (Banks et al., 2009).
One other study that supports this information was Welsh et al. (2005), they
investigated transient impairment of the ventricles caused by prolonged strenuous
exercise and they found that their results provided evidence that EICF may be
caused by altered beta – receptor function.
Other researchers have provided two different factors to consider; elevated free fatty
acid levels (Liedtke, Nellis, and Neely, 2005) and increased free radical production
(Starnes and Bowles., 1995). Additionally, other mechanisms have been proposed
and provide a different insight to the reasons behind EICF, they include prolonged
tachycardia and elevated levels of cardiac enzymes such as creatine kinase MB and
cardiac troponin – T. However, there is limited research to provide a clear and
concise confirmation to whether these are mechanisms of exercise induced cardiac
fatigue.
When considering increased free fatty acid (FFA) concentration as a mechanism for
EICF it is important to note the work of both McKechnie et al. (1979) and Seals et al.
(1998), both researchers proposed that ventricular dysfunction discovered in their
study was caused by an increased level of FFAs. This increase of FFAs resulted in a
decreased efficiency of electron transport and more specifically mitochondrial
respiration.

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The following factor, that is free radical production, is speculative as there is no data
for human subjects in this area. In this case it is recommended to interpret with
caution. Free radicals are cellular species that have one or more unpaired electrons
and are capable of independent existence, which allows them to react with another
chemical specie. During exercise there is an increase in catecholamine hormones
(adrenaline and dopamine), this oxidation can produce free radicals and can cause a
release of superoxide from neutrophil NADPH oxidase (Cooper et al., 2002).
Prolonged exercise is associated with an elevation of free radicals and that the y
have potential to be an aetiological factor of EICF (Seals et al., 1988)
A final factor that could explain the diastolic dysfunction of the ventricles could be the
alteration of calcium metabolism, although it is unclear, it has been suggested that
altered calcium metabolism could be impaired by an increased pH or inorganic
phosphates that would change myofilament sensitivity, therefore changing both
systolic and diastolic tensions (Ferrari., 2002).
The majority of the previously mentioned studies have utilised the methodical
process of prolonged exercise to further enhance the symptoms of EICF. If the
exercise related factors of EICF are considered, there is a correlation between
prolonged exercise and EICF symptoms. Scientific evidence is very limited when
investigating a brief bout of intense exercise, this suggests that EICF may not be
present after this intensity and duration. However, there is evidence to support that
there are no changes in ventricular structure or function. Research from Seals et al.
(1988) has confirmed that it is not the type of exercise which affects the severity of
EICF but it is the factor of prolonged exercise that causes a dysfunction of the heart.
Exercise duration is a factor that affects EICF, however there are no markers to
decide when the onset of ventricular dysfunction occurs, although this is the case,
there are no specific studies on exercise intensity alone in the field of exercise
induced cardiac fatigue (Dawson et al., 2003). Another researcher that used the
previously mentioned strategy of altering exercise intensity is Banks et al. (2009),
these scientists used two different intensities (60% and 80% VO2max) at different time
points to quantify if there were any effects on the LV and RV when using both
moderate and high intensity exercise, they concluded that diastolic impairment after
prolonged exercise could be observed in both the LV and RV, regardless of what the
intensity of exercise was.

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The field of EICF has progressed steadily with advancements in different
echocardiography methods (such as tissue Doppler and strain rate imaging),
previous researchers have found it extremely problematic when imaging the RV. The
cause of this is due to the geometry, location and excess trabeculation associated
with the RV, therefore causing issues when imaging function and calculating
volumes (Oxborough et al., 2010). Due to this issue, there is very limited data when
assessing overall RV size and function, during rest and also in cardiac diseases. An
increase of quantitative approaches would allow sonographers to carry out a better
cardiac assessment and evaluation, whilst improvements in technology could mean
an increased use of echocardiography methods (Rudski et al., 2010). These
improvements could mean a development in the knowledge of EICF and more
importantly, the mechanisms behind it. The clinical significance of EICF is varied and
some researchers state that further research may be required in order to identify the
implications these investigations might have on a clinical perspective (Banks et al.,
2009). However, Oxborough et al. (2011) has suggested that the significance of a
marked impact on a single endurance event affecting cardiac structure and function
would provide new information to support a theory of RV remodelling and fibrosis.
Furthermore, recent evidence from Wilson et al. (2011) prompted more research to
discover the long term effects endurance exercise has on athletes. (Oxborough et al.,
2011).
As this study has a very small sample size (n = 6), it is important to interpret this data
with caution. Another limitation to this study would be that there are no gender
differences, for future research it would interesting to note the effect of prolonged
exercise on different genders. Previous studies have mainly used prolonged exercise
to stimulate EICF, consequently this study used the same protocol and decided
against using an intensity orientated study to produce symptoms of EICF. This study
limited the variation of echocardiography assessments by using one experienced
and well trained sonographer to limit the variability of information acquired.
In conclusion, the results suggest that a prolonged two hour exercise protocol does
induce functional symptoms of cardiac fatigue, such as significant RVFAC and S’
reductions which can been observed in Figures 6, 7 and 8, while there was also a
reduction in RA area which could be attributed to a decreased preload. These
reductions can also be seen after a 2 hour cycle test when the participant is

14
maintaining their HR at 100bpm, this information suggests there is some type of
mechanism occurring such as beta-adrenergic downregulation due to the lengthy
exposure to catecholamines such as adrenaline. The changes observed after a
prolonged endurance event could provide a trigger for further cardiac adaptation, it is
also possible that the results seen in this study could just be due to an acute
adaptation process after prolonged cardiac stress, however this is speculative.
Therefore, more research should be provided using endurance athletes examining
any cardiac dysfunction and adaptation.
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18
Appendix
Figure 1. Schedule forbothvisitsduringstudy.

19
Table 1. Diagram of Experimental Protocols
RPE
Height/Weight
Heart Rate
Cardiac Assessment Rest
SpO2
BloodPressure
Time: -30 -15 0 15 30 1hr 1hr 30 2 hr 2hr 15 2hr 30
Table 1. Experimental ProtocolundertakenduringVisit2.

20
PRE 2 HOUR CYCLE POST2 HOUR CYCLE
Pre Rest
Pre
Exercise Post Rest PostExercise
RVOTplax 26.67 26.12 26.00 26.33
RVOT1 31.42 28.83 27.15 27.42
RVOT2 23.75 22.28 23.67 23.30
RVD1 40.92 41.83 41.47 38.75
RVD2 31.33 34.06 31.83 31.42
RVD3 92.67 89.60 94.33 92.42
RVDarea 26.55 24.98 24.73 24.52
RVSarea 14.17 12.95 14.90 14.00
RVFAC 0.47 0.48 0.40 0.43
RA_AREA 19.97 16.68 18.00 16.02
S' 18.50 21.50 16.00 16.00
E' 17.83 19.67 17.67 16.50
A' 13.67 13.83 19.83 17.67
0
20
40
60
80
100
120
Heart Rate
HR(BPM) Pre Rest Post Rest Pre Exercise Post Exercise
Table 2. Standard RV indicesforPre Rest,Pre Exercise,PostRestandPostExercise Echocardiographytesting.
Figure 2. Heart rate (Mean ± SD) for Pre Rest,PostRest,Pre Exercise andPostExercise EchoScans.
SignificantRV functional parameters which include Mean± SD

21
0.00
5.00
10.00
15.00
20.00
25.00
30.00
35.00
40.00
RVOTplax RVOT1 RVOT2
Dimensions(mm)
RV Outflow Tract, Proximal,Distal
Pre Rest Post Rest Pre Exercise Post Exercise
Figure 3. Mean ± SD RV outflow,proximalanddistal measurementsof Pre Rest,PostRest,Pre
Exercise andPostExercise Echocardiography Scans.
0.00
20.00
40.00
60.00
80.00
100.00
120.00
RVD1 RVD2 RVD3
Dimension(mm)
Right Ventricular Dimensions
Figure 4. Mean ± SD RV dimensions(RVD1,RVD2 and RVD3) at Pre Rest,PostRest,Pre Exercise
and PostExercise EchocardiographyScans.

22
0.00
5.00
10.00
15.00
20.00
25.00
30.00
35.00
RVDarea RVSarea
Dimension(mm)
RV diastolic and systolic areas
Figure 5. Mean ± SD RV diastolicandsystolicareas(RVDareaandRVSarea) at Pre Rest,PostRest,
Pre Exercise andPostExercise EchocardiographyScans.
0.00
5.00
10.00
15.00
20.00
25.00
RA AREA
Dimension(mm)
Figure 6. Mean ± SD RightAtrial area(RA area) at Pre Rest,PostRest,Pre Exercise andPost
Exercise EchocardiographyScans.

23
0
0.1
0.2
0.3
0.4
0.5
0.6
0.7
PercentageChange(%)
Figure 7. RV fractional areachange forindividual participantsduringdifferentechoscans.
Significantmaineffectcanbe seenwhencomparingPre Exercise andPostRest(P=0.021).

24
0
5
10
15
20
25
Prerest Pre Exercise Postrest Post Exercise
TDIS'E'A'(cm/s)
S' E' and A' measurements
S' E' A'
Figure 8. Mean TDI S’ E’ and A’for participantsduringdifferentechoscans.

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