Major Project final draft

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.

1

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,

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2007; 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

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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

7

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

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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.,

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2011). 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

10

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 they

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

13

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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17

Appendix

18

Figure 1. Schedule for both visits during study.

Table 1. Diagram of Experimental Protocols

RPE

Height/Weight

Heart RateCardiac Assessment Rest

SpO2

Blood Pressure

Time: -30 -15 0 15 30 1hr 1hr 30 2 hr 2hr 15 2hr 30

PRE 2 HOUR CYCLE POST 2 HOUR CYCLE

Pre RestPre

Exercise Post Rest Post ExerciseRVOTpla

x 26.67 26.12 26.00 26.33RVOT1 31.42 28.83 27.15 27.42RVOT2 23.75 22.28 23.67 23.30RVD1 40.92 41.83 41.47 38.75RVD2 31.33 34.06 31.83 31.42RVD3 92.67 89.60 94.33 92.42

RVDarea 26.55 24.98 24.73 24.52RVSarea 14.17 12.95 14.90 14.00RVFAC 0.47 0.48 0.40 0.43

RA_AREA 19.97 16.68 18.00 16.02S' 18.50 21.50 16.00 16.00E' 17.83 19.67 17.67 16.50A' 13.67 13.83 19.83 17.67

19

Table 1. Experimental Protocol undertaken during Visit 2.

20

Heart Rate 0

20

40

60

80

100

120

Pre Rest Post Rest Pre Exercise Post ExerciseHR

(BPM

)

Table 2. Standard RV indices for Pre Rest, Pre Exercise, Post Rest and Post Exercise Echocardiography testing.

RVOTplax RVOT1 RVOT20.00

5.00

10.00

15.00

20.00

25.00

30.00

35.00

Pre Rest Post Rest Pre Exercise Post Exercise

RV Outflow Tract, Proximal, Distal

Dim

ensio

ns (m

m)

Figure 3. Mean ± SD RV outflow, proximal and distal measurements of Pre Rest, Post Rest, Pre Exercise and Post Exercise Echocardiography Scans.

Figure 4. Mean ± SD RV dimensions (RVD 1, RVD2 and RVD3) at Pre Rest, Post Rest, Pre Exercise

Significant RV functional parameters which include Mean ± SD

21

RVD1 RVD2 RVD30.00

10.00

20.00

30.00

40.00

50.00

60.00

70.00

80.00

90.00

100.00 Pre Rest Post Rest Pre Exercise Post Exercise

Right Ventricular Dimensions

Dim

ensio

n (m

m)

Figure 4. Mean ± SD RV dimensions (RVD 1, RVD2 and RVD3) at Pre Rest, Post Rest, Pre Exercise

RVDarea RVSarea0.00

5.00

10.00

15.00

20.00

25.00

30.00 Pre Rest Post Rest Pre Exercise Post Exercise

RV diastolic and systolic areas

Dim

ensio

n (m

m)

Figure 5. Mean ± SD RV diastolic and systolic areas (RVDarea and RVS area) at Pre Rest, Post Rest, Pre Exercise and Post Exercise Echocardiography Scans.

RA AREA0.00

5.00

10.00

15.00

20.00

25.00Pre Rest Post Rest Pre Exercise Post Exercise

Dim

ensio

n (m

m)

Figure 6. Mean ± SD Right Atrial area (RA area) at Pre Rest, Post Rest, Pre Exercise and Post Exercise Echocardiography Scans.

Prerest Pre Exercise Postrest Post Exercise0

5

10

15

20

25S' E' A'

S' E' and A' measurements

TDI S

' E' A

' (cm

/s)

22

Pre Rest Post Rest Pre Exercise Post Exercise0

0.1

0.2

0.3

0.4

0.5

0.6

0.7Pe

rcen

tage

Cha

nge

(%)

Figure 7. RV fractional area change for individual participants during different echo scans. Significant main effect can be seen when comparing Pre Exercise and Post Rest(P = 0.021).

Figure 8. Mean TDI S’ E’ and A’ for participants during different echo scans.

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