Download Edwards, Daniel - Cardiff Metropolitan University

DANIEL EDWARDS
09001727
SCHOOL OF SPORT
CARDIFF METROPOLITAN UNIVERSITY
CHANGES IN LEFT VENTRICULAR FUNCTION AND MORPHOLOGY IN
RESPONSE TO HIGH-INTENSITY, CROSS-TRAINING.
Acknowledgements
I would like to thank Professor Robert Shave for his continued support
throughout the entire dissertation process. Special thanks go to Dr Eric Stohr
for his invaluable contribution of collecting all of the echocardiographic images
required for this study. I would also like to thank PurePharma Ltd for their
generosity in providing their ultra-pure fish oil product to all participants
involved in this study.
i
Abstract
It is a widely accepted concept that different exercise modalities produce
different effects of myocardial hypertrophy in athletes; a sport-specific
hypothesis proposed by Morganroth et al. (1977). The literature would also
suggest that left ventricular function is altered by endurance and resistance
type exercise and that there are distinct differences between the functioning of
an endurance- and resistance trained heart (Mantziari et al. 2010 & Spence et
al. 2011). However, there is a distinct lack of research examining the effects
that high intensity cross-training has on left ventricular function and
morphology. A group of CrossFit athletes (8 males, mean age 27 ± 4 years)
who had been training using the CrossFit modality for over a year and a half
were included in the study. Written informed consent was approved by the
Cardiff Metropolitan University ethical committee. A group of sex-matched,
healthy individuals who perform ≤ 2 hours of physical activity per week served
as controls. All participants underwent a complete echocardiographic
evaluation and completed a 𝑉̇ O2 maximum test on a cycle ergometer to
determine aerobic fitness. The trained participants had significantly increased
left ventricular cavity dimensions at end diastole (P < 0.05) in comparison to
sedentary controls (5.3 ± 0.6 cm vs 4.5 ± 0.5 cm, respectively) this was also
evident with left ventricular cavity dimensions at end systole (3.5 ± 0.6 cm vs
2.9 ± 0.5 cm (P < 0.05)). Left ventricular posterior wall thickness at end
diastole also proved to be significantly increased (P < 0.05) in comparison to
controls (1.7 ± 0.4 cm vs 1.1 ± 0.3 cm, respectively). Left ventricular posterior
wall thickness at end systole in trained individuals was significantly greater (P
< 0.05) than in controls (2.1 ± 0.3 cm vs1.6 ± 0.2 cm). Stroke volume was
significantly increased in the trained participants (P < 0.05) when compared
with controls (105 ± 16 ml vs 71 ± 15 ml). Ejection fraction was also
significantly increased in trained participants (P < 0.05) in comparison to
controls (54 ± 8 % vs 43 ± 4 %). In conclusion, these findings demonstrate
that high intensity, mixed modality cross-training produce significant
adaptations to the morphology and function of the left ventricle when
compared to sex-matched controls. The findings from this study provide some
support for the Morganroth hypothesis.
ii
Contents
Chapter Number
ONE
Chapter Title
Page number
Literature Review
1.1Introduction
1
1.2 Changes in Cardiac Structure with
Endurance Exercise
2–4
1.3 Changes in Cardiac Function with
Endurance Exercise
4–5
1.4 Changes in Cardiac Structure and
Function with Resistance Exercise
6–8
1.5 Changes in Cardiac Structure and
Function with High-Intensity, Mixed-
8 – 10
Modality Exercise
1.6 High intensity, Mixed-Modality Cross-
10 - 11
Training
TWO
Method
2.1 Study population
12
2.2 𝑉̇ 02 Maximum cycle ergometer test
13
2.3 Echocardiographic evaluation
2.4 Statistical analyses
THREE
13 – 15
16
Results
3.1 Reliability of the Data
3.2 Baseline Characteristics
17 – 18
19
3.3 Baseline Echocardiographic
Measurements
FOUR
20 - 24
Discussion
4.1 Principal Findings
25 – 26
4.2 Left Ventricular Morphology
26 – 28
4.3 Left Ventricular Function
28 – 29
4.4 Limitations
30
4.5 Conclusions
31
LIST OF TABLES
Title
Cross-sectional studies examining left ventricular
hypertrophy in various athletic populations. Adapted from
Naylor et al. (2008).
Page Number
3
Longitudinal studies examining training effects on the left
ventricle. Adapted from Naylor et al. (2008).
8
t-test conducted on all variables for test-retest
measurements.
17
Data summary for all measured variables.
18
Baseline characteristics for study group (n = 15)
19
Baseline echocardiographic measurements presented as
absolute and scaled values.
20
LIST OF FIGURES
Title
Mean left ventricular mass indexed to body surface area
Page Number
4
(LVMi) in 947 elite Italian athletes divided according to
sporting events (Pellicia et al. 1991).
M-mode echocardiography of the left ventricle; Standard
15
parasternal long axis view; Standard apical four chamber
view; Normal transmitral Doppler providing information on
valvular function and left ventricular filling; Standard apical
two chamber view (Images taken from Oxborough, 2008).
A comparison of absolute values in trained (T) participants
21
and controls (C). LVIDd, left ventricular cavity dimensions at
end diastole; LVPWd, left ventricular posterior wall
thickness at end diastole; LVIDs, left ventricular posterior
wall thickness at end systole; LVPWs, left ventricular wall
thickness at end systole.
Differences in stroke volume (SV) between trained
22
participants and controls.
Differences in ejection fraction (EF) between trained
22
participants and controls.
A comparison of scaled variables between trained (T)
23
participants and controls (C). LVIDd, left ventricular cavity
dimensions at end diastole; LVPWd, left ventricular
posterior wall thickness at end diastole; LVIDs, left
ventricular posterior wall thickness at end systole; LVPWs,
left ventricular wall thickness at end systole.
Differences in stroke volume (SV) between trained
participants and controls when scaled to BSA.
23
CHAPTER ONE
LITERATURE REVIEW
Literature review
1.1 Introduction
The term ‘athlete’s heart’ is used in modern sport and exercise medicine to
describe the hypertrophy of the myocardium in response to repeated bouts of
exercise (Maron, 1986). This hypertrophy of the myocardium allows for
increased maximal stroke volume (SV ) and cardiac output (Q), both of which
increase the ability of the heart to deliver more oxygen to the working muscles
(Sharma et al., 2002). It is a widely accepted concept that different exercise
modalities produce different effects of myocardial hypertrophy in athletes; a
sport-specific hypothesis proposed by Morganroth et al. (1977). The
‘Morganroth Hypothesis’ states that there are two morphological forms of the
‘athlete’s heart’ and that this is a result of the haemodynamic stimuli
generated by either endurance or resistance exercise. Due to a greater
volume of blood returning to the ventricles during exercise, purely aerobic or
endurance athletes subject the left ventricle (LV) to repetitive increases in
cardiac preload thus leading to ‘eccentric LV hypertrophy’ (Morganroth et al.,
1975) which is characterised by an increase in LV internal dimensions (LVID)
and a proportional increase in LV wall thickness (LVWT). However, due to
increases in peripheral vascular resistance caused by the pressure of the
external weights being lifted by the limbs and a larger volume of blood
remaining in the ventricles after systole, known as cardiac afterload,
resistance trained individuals experience ‘concentric LV hypertrophy’. This is
manifested as an increased LVWT (Morganroth et al., 1975). The law of La
Place states that the tension (T) on the wall of a sphere is a product of the
pressure (P) times the radius (R) of the chamber and the tension is inversely
related to the thickness of the wall (M), T = (P*R)/M. The Law of La Place
therefore provides logical support for the ‘Morganroth Hypothesis’ which
suggests that cardiac muscle grows to match the workload experienced by
the LV in order to maintain a constant relationship between chamber
pressures and the ratio of wall thickness to ventricular radius.
1.2 Changes in Cardiac Structure with Endurance Exercise
1
There is a general consensus in the literature that suggests that LVM
measured using echocardiography is increased in endurance-athlete
populations (Abergel et al., 2004., Fisman et al., 2001., Karjalainen et al.,
1997 & Pela et al., 2004. See Table 1). In addition to this, the majority of data
from authors who have studied endurance athletes also implies that LVID
during diastole (LVIDd) and/or LVWT is increased when compared with
sedentary controls (Scharhag et al., 2002 & Schmidt-trucksass et al., 2000).
It has been demonstrated by Spence et al. (2011) that 6 months of endurance
training caused a significant increase in LVM and intraventricular thickness
(IVS) when compared to pre-training values. It was also apparent that LV enddiastolic volume (LVEDV) increased with endurance training. The
LVM:LVEDV ratio remained unchanged which is indicative of eccentric
hypertrophy which remains consistent with the Morganroth Hypothesis
(Morganroth et al., 1975). Similarly, Baggish et al. (2008) studied a group of
university level rowers and found that 90 days of endurance type training
produced significant increases in LVM and biatrial enlargement. There have
been additional studies that have examined cardiac remodeling occurring as a
result of rowing based endurance training (Naylor et al., 2005 & Urhausen et
al., 1997) which showed that rowers had increased LVM, IVS, LVPWT and
LVIDd when compared to controls (see Table 1).
Post-mortem evidence has been put forward displaying the excessive cardiac
remodelling that occurs due to repetitive bouts of prolonged endurance type
exercise. Whyte et al. (2007) found that the heart of a highly trained marathon
runner whom died suddenly whilst running displayed clear signs of cardiac
hypertrophy. The weight of the heart was well above the expected values as
were other structures within the heart; LV lateral and anterior free walls and
the septum and posterior walls. Grimsmo et al. (2011) also found that upon
the echocardiograhic evaluation of 48 middle-aged and old former or still
active cross-country skiers that >80% of subjects displayed hypertrophy and
dilation of the left atrium and hypertrophy of the LV.
2
Table 1. Cross-sectional studies examining left ventricular hypertrophy in various athletic populations. Adapted from Naylor et al.
(2008).
Study
Abergel et al. 2004
Baggish et al. 2008
Fisman et al. 2002
George et al. 1998
Karjalainen et al. 1997
Pavlik et al. 2001
Pela et al. 2004
Pelliccia et al. 1993
Scharhag et al. 2002
Schmidt-Trucksass et al.
2000
No. of athletes
286 road cyclists
40 endurance athletes
24 strength athletes
47 long-distance runners
11 elite male weightlifters
32 runners
88 soccer players
77 various sports
262 various sports
12 various sports
20 soccer players
100 weight and power lifters
21 endurance athletes
30 athletes
No. of controls
52
N/A
LVIDd


IVS

NR
PWT


LVMi

NR
24
45
15
13
10
44
12
15
26
21
16
NR



















NR










NR

NR










LVIDd = left ventricular cavity dimensions; LVMi = left ventricular mass indexed to body surface area; PWT = posterior wall
thickness, IVS = inter-ventricular septum; NR = not reported; N/A = not applicable;  = indicates significantly higher in athletes;
 = indicates no difference.
3
The evidence for the Morganroth Hypothesis when considering endurance
type exercise was added to by Pellicia et al. (1991) who assessed 947
national or international level athletes from 25 different sports using
echocardiography (see Figure 1). It was shown by Pellicia et al. (1991) that
LVM indexed to body surface area (LVMi) was greatest in rowers (121 ± 22
g/m2). This was further supported by a recent meta-analysis conducted by
Fagard (2003) who found that LVM is greater in endurance athletes when
compared with controls. The endurance athletes’ LVM was increased by 67 g
compared to that of controls and this was due to increases in LVWT and
LVID.
Figure. 1. Mean left ventricular mass indexed to body surface area (LVMi) in
947 elite Italian athletes divided according to sporting events (Pellicia et al.
1991)
1.3 Changes in Cardiac Function with Endurance Exercise
The literature would suggest that the function of the LV changes in response
to endurance exercise (Baggish et al., 2008a & Spence et al., 2011). Baggish
et al. (2008a) found that after 90 days of endurance training that these
athletes experienced a significant increase in LV diastolic tissue velocities and
provided direct evidence that endurance training increases LV longitudinal
4
strain rates and produces LV dilation with accompanying augmentation of LV
diastolic function, whilst one prior study found that LV relaxation rates were
enhanced in elite rowers after 3 months of training (Naylor et al., 2005).
However, Spence et al. (2011) found there to be no significant increase in
longitudinal strain after 6 months of endurance training and Nottin et al. (2008)
showed no differences in global longitudinal strain and strain rates between
elite cyclists and sedentary controls.
Mantziari et al. (2010) measured tissue Doppler systolic velocities at the
lateral and septal mitral annulus and found increased systolic velocities when
compared with sedentary controls. In a study of endurance-trained athletes,
D’Andrea et al. (2002) suggested that systolic function may be enhanced by a
more efficient diastolic stretching of myocardial fibres induced by LV volume
overload, through the Frank-Starling mechanism.
Diastolic function has also been shown to improve after endurance training
(Mantziari et al., 2010). Septal and lateral early diastolic velocities were
increased when compared with sedentary controls and moreover, lateral early
diastolic peak myocardial velocity correlated with lateral systolic peak velocity
revealing a direct relationship and parallel enhancement of diastolic and
systolic function in endurance trained athletes (Mantziari et al., 2010). It has
also been shown that lateral early diastolic peak myocardial velocity / lateral
late diastolic peak myocardial velocity was also increased, showing an
improvement in diastolic function despite the greater wall thicknesses in
endurance trained athletes (Mantziari et al., 2010). Stoylen et al. (2003)
developed the theory of a ‘suction’ mechanism of LV filling that functions due
to decreased stiffness and increased compliance in an endurance trained
heart. This reduction in the stiffness index was shown in Mantziari et al’s.
(2010) study.
5
1.4 Changes in Cardiac Structure and Function with Resistance Exercise
Whilst the literature provides a vast amount of support for the endurancetrained heart of the Morganroth Hypothesis, there is significantly less
evidence proving the hypothesised effects on the heart of a resistance trained
individual. It is clear from the majority of the studies that have been presented
that resistance trained athletes have increased LVWT and LVM values when
compared to sedentary controls (Longhurst et al., 1980) but have not
observed differences in LVIDd relative to controls (Pavlik et al., 2001., Pellicia
et al., 1993., MacFarlane et al., 1991).
Deligiannis et al. (1988) found that LVIDd, IVS, LVWT and LVMi were all
elevated in 15 male body builders and 15 male weightlifters when compared
to controls. These findings were also partially supported by George et al.
(1998) and Fisman et al. (2002) who displayed that IVS, LVWT (measured as
posterior wall thickness, PWT) and LVMi increased in elite male weightlifters
in comparison to controls. However, the Morganroth Hypothesis states that
due to the concentric hypertrophy experienced during resistance training that
these individuals should have greater LVWT when compared to endurance
athletes not just to controls. Several studies have attempted to address the
impact of different training modalities on cardiac structure by directly
comparing strength- and endurance-trained athletes. The majority of the
findings from these studies show that LVM and LVMi was increased in
endurance athletes when compared to strength athletes (Wernstedt et al.,
2002 & Longhurst et al., 1980), whereas one study reported that LVM was
significantly greater in power lifters in comparison to swimmers and this was
suggested to be due to the increased LVWT in the power lifters (Colan et al.,
1985).
Fisman et al. (2002) and Roy et al. (1988) have both concluded that a
difference does not exist between the endurance- and strength trained
athletes in their studies. There were no significant differences in LVM between
weightlifters and long-distance runners in Fisman et al’s. (2002) study,
6
however, scores were not corrected to BSA and so only absolute scores were
presented. Roy et al. (1988) displayed scores scaled to BSA for weightlifters
and endurance runners and found that the groups had similar LVM values. In
support of these findings, a meta-analysis conducted by Pluim et al. (1999)
found there to be no statistically significant differences between strength and
endurance athletes.
The literature also suggests that the alterations in cardiac function in response
to resistance training appear to be restricted to the LV only as opposed to the
both the LV and right ventricle (RV) after periods of endurance training. In
Baggish et al’s. (2008b) study strength trained athletes experienced a
significant reduction in diastolic tissue velocities thus suggesting that
concentric hypertrophy, caused by the increase in cardiac after load and the
slight increase in systolic blood pressure resulted in a decrease in diastolic
function. Whyte et al. (2000) showed that despite increased LV wall
thicknesses that diastolic function, ejection fraction and stroke volume all
remained within normal limits.
7
Table II. Longitudinal studies examining training effects on the left ventricle.
Adapted from Naylor et al. (2008).
Reference
Training
No. of
LVIDd
IVS
PWT
LVMi
protocol
subjects




Abergel et al. Cyclists in
37 cyclists
1995 and 1998
Tour de France
training
variable


Ehsani et al.
9 wk of
8 swimmers 
NR
training
following 2-9
mo off-training




Naylor et al.
6 mo of rowing 22 rowers
season
following 6 wk
off-training


Wieling et al. Rowing season 9 freshmen
NR

(7 mo)
14 senior
NR



Spence et al. 6 months
13 resistance 
2011
resistance or
10
endurance
endurance
training
followed by 6
weeks detraining
LVIDd = left ventricular cavity dimensions; LVMi = left ventricular mass indexed
to body surface area; IVS = inter-ventricular septum; PWT = posterior wall
thickness; NR = no result;  = significant increase after training;  = significant
decrease after training;  = no change after training.
1.5 Changes in Cardiac Structure and Function with High-Intensity, MixedModality Exercise
Whilst considering strength and endurance exercise modalities separately it is
necessary to pay attention to the effects of high intensity and interval type
training on the structure and function of the left ventricle as this is linked to
cardiac remodelling (Morganroth et al. 1975). It has been noted by Naylor et
al. (2003), Baggish et al. (2008b) and Mantziari et al. (2010) that a training
regime that incorporates both resistance and endurance elements is likely to
be the most potent stimulus for eliciting the greatest morphological and
functional adaptations to the heart. Slordahl et al. (2004) showed that aerobic
8
interval training at 90-95% of maximal heart rate increased 𝑉̇ O2 max by 18%,
LV mass by 12% and increased LV contractility during exercise by 13% in
previously untrained female participants. Studies by Burgomaster et al. (2008)
and Warburton et al. (2005) have demonstrated that short duration, high
intensity anaerobic interval training is more beneficial for improving aerobic
fitness when compared to moderate intensity, longer duration type exercise.
However, other studies have found no such evidence that would suggest high
intensity training to provide such a vast amount of alteration to cardiac and LV
function (Foster et al. 1999 & George et al. 2004). Foster et al. (1999) studied
8 male cyclists during interval and steady state exercise and measured HR,
LV volumes, LVEF, Q and SV. They discovered that there was augmented
emptying of the LV during recovery and no evidence for enhanced filling
during “hard” periods of interval exercise. It was also noted that the
haemodynamic response and LV function was similar between steady state
and interval exercise. The cross-sectional evidence for high intensity training
and its effects on the heart suggests that it is likely to cause a reduction in
diastolic function (George et al. 2004 & Baggish et al. 2008a) and does not
cause enhanced filling or a significant depression in systolic function (Foster
et al. 1999 & George et al. 2004). However, more recent longitudinal data
suggests that 10 weeks of concurrent strength and endurance training caused
an increase in LV systolic function due to a heightened LV contractile reserve
(duManoir et al. 2007).
High intensity, anaerobic, interval type training has already been shown to
increase aerobic fitness (Burgomaster et al. 2008 & Warburton et al. 2005)
which is closely linked to cardiovascular health (Keteyian et al. 2008). Regular
high intensity aerobic interval training at 85-90% of 𝑉̇ O2max. improves the
maximal extent of shortening in unloaded cardiomyocytes during electrical
field stimulation and contraction and relaxation rates improve by 20-40%
(Kemi et al. 2004 & Wisloff et al. 2002). According to Wisloff et al. (2009)
exercise training improves cardiomyocyte calcium handling. A component of
this improved handling due to exercise training results in a faster diastolic
decay and systolic rise of the Ca2+ transient and these effects depend on the
9
exercise intensity (Kemi et al. 2005). Although the contractile function of the
cardiomyocyte depends a great deal on Ca2+ induced Ca2+ release and the
contractility of the myofillaments it should also be considered that
physiological cardiomyocyte hypertrophy is an important factor too. High
intensity interval training at 85-90% of 𝑉̇ O2max. induces hypertrophy in the
cardiomyocytes that is observable after just a few weeks of training. The
magnitude of the hypertrophy depends on the intensity of exercise because
high intensity exercise training induced a significantly larger response when
compared to moderate intensity exercise; 14% versus 5% longer cells,
respectively (Kemi et al. 2005).
1.6 High intensity, Mixed-Modality Cross-Training
Whilst there appears to be some support for increased cardiac hypertrophy
with high-intensity training (Kemi et al., 2005) there has been very little
research conducted into the adaptations to cardiac function and morphology
caused by high intensity, mixed modality training.
Mixed-modality training uses a combination of resistance and endurance
exercise, however, many studies have looked at rowers when considering
cardiac adaptations to exercise and have failed to consider other training
modalities that a rower may be completing (e.g. resistance) or have failed to
control for this and have focused purely on endurance exercise (Baggish,
2008a & Baggish, 2009). Due to the fact that mixed-modality training uses this
constantly varied method of exercise the purpose of this study is to determine
what effects this type of cross-training has on the function and morphology of
the heart when compared to a group of sedentary controls.
Due to the high-intensity and mixed-modality nature of cross-training it is
hypothesised that the trained participants will show a greater amount of
structural cardiac adaptation when compared to sedentary controls due to a
combination of an increased pre-load as a result of more blood returning to
the heart during the endurance type activities and an increased after-load and
10
systolic pressure. This would lead to both eccentric and concentric
hypertrophy of the myocardium and would result in increased LVPW, LVWT
and LVID.
It is also hypothesised that the trained participants will display increased
diastolic function in comparison to controls due to increased compliance and
decreased stiffness of the myocardium thus allowing for greater filling due to
the ‘suction’ this creates (Stoylen et al. 2003).
Finally, it is hypothesised that the trained participants will display improved
systolic function due to increased contractility and therefore a higher
contractile reserve.
11
CHAPTER TWO
METHODS
Method
2.1 Study population
In order to study a group of participants who were trained using high intensity,
mixed modality cross-training, a group of CrossFit athletes (8 males, mean
age 27 ± 4 years) who had been training using the CrossFit modality for over
a year and a half were included in the study. Written informed consent was
obtained as approved by the University of Wales Institute, Cardiff (UWIC)
ethical committee. A group of sex-matched, healthy individuals who perform ≤
2 hours of physical activity per week served as controls. All of the athletes
were involved in CrossFit competition at a high level and at the time of the
study followed a high intensity and high volume CrossFit training programme
for ≤ 20 hours per week. All of the participants attended one laboratory
session and were subjected to an echocardiographic evaluation immediately
followed by a VO2 maximum test on a cycle ergometer. None of the subjects
had received any vasoactive medication and none had systemic arterial
hypertension, diabetes mellitus, dyslipidemia, obesity [body mass index (BMI)
430 kg/m2), coronary artery disease or a family history of premature coronary
artery or cerebrovascular disease or sudden death. Before each
echocardiographic study, resting heart rate, height and weight for each
participant was measured, and body surface area (BSA) were calculated.
BSA (m2) was defined as 0.20247 x Height(m)0.725 x Weight(kg)0.425 using the
Du Bois and Du Bois formula (Du Bois & Du Bois, 1915). The anthropometric
characteristics of CrossFit athletes and controls are presented in Table 1.
CrossFit athletes had a significantly lower resting heart rate than controls (58
± 4 vs 73 ± 3 beats/min, P < 0.001).
2.2 𝑉̇ 02 Maximum cycle ergometer test
The trained participants began cycling (name of bike, make, country) at 75 W
for 3 minutes, following this warm up period the workload increased by 30 W
every minute until volitional exhaustion. The control subjects started cycling
12
(LODE ergometer, Corival, Lode Medical Technology, Groningen, The
Netherlands) at 50 W for 3 minutes and following this period the workload
increased by 20 W every minute until volitional exhaustion. Participants
selected their own cadence throughout the test and RPE was measured using
a Borg scale every minute throughout the test. Maximal oxygen uptake, 𝑉̇ 02
max
was measured continuously throughout the test (OXYCON Pro, Jaeger,
Kempele, The Netherlands), and the average of the three highest values was
determined as the maximum value. Heart rate was monitored throughout the
test and the participant’s maximum heart rate was recorded at exhaustion
(Polar F1, Polar Electro, Finland). Prior to and after each test, the ventilometer
and gas analyser were calibrated according to the manufacturers instructions
using a 1 litre syringe and gases of known concentration (Servomex Gas
Analyser, Model 1440C, Servomex Group Ltd, United Kingdom).
2.3 Echocardiographic evaluation
All subjects underwent a complete echocardiographic evaluation, including
two-dimensional (2D), and spectral Doppler as well as TDI using a GE
Vingmed Vivid 7 system (GE Vingmed Ultrasound, Horten, Norway). All
images were saved digitally in raw data format to a DVD disc for offline data
analysis (figure 2).
Standard 2D Doppler images were obtained using the parasternal long- and
short-axis and apical views. Three consecutive cycles were averaged for
every parameter. Left ventricular (LV) dimension at end diastole and end
systole (LVIDd and LVIDs, respectively), Intraventricular septal thickness at
diastole and systole (IVSd and IVSs, respectively) and left ventricular
posterior wall thickness at diastole and systole (LVPWTd and LVPWTs,
respectively) were measured using 2D-targeted M-mode echocardiography.
Resting LV ejection fraction was measured using Simpson’s Biplane method.
End-diastolic and end-systolic volumes (EDV and ESV, respectively) were
measured using the apical four-chamber and apical two-chamber views.
13
Pulsed Doppler echocardiography for the assessment of the LV diastolic filling
and systolic emptying velocities were performed using the apical fourchamber view. Thus, the peak early diastolic filling velocity (E-wave), peak
late diastolic filling velocity (A-wave) and their ratio (E/A) were recorded. All
measurements were averaged over the final 3 complete cardiac cycles.
Pulsed-wave TDI was used to assess mitral annular velocities. Gains were
minimised in order to allow for a clear tissue signal with minimal background
noise. All TDI recordings were obtained during normal respiration in the apical
four-chamber view. A 5 mm sample volume was placed at the septal and
lateral corner of the mitral annulus. The peak myocardial velocities during
systole (S’), early diastole (E’) and late diastole (A’) were recorded.
14
Fig. 2. M-mode echocardiography of the left ventricle; Standard parasternal
long axis view; Standard apical four chamber view; Normal transmitral
Doppler providing information on valvular function and left ventricular filling;
Standard apical two chamber view (Images taken from Oxborough, 2008).
15
2.4 Statistical analyses
All statistical analyses were conducted using Minitab 15 (Minitab Inc, State
College, Pennsylvania) and the Statistical Package for the Social Sciences
(SPSS for Microsoft, SPSS inc., Chicago, IL). The reliability of the data
analysis procedure was conducted on test and retest scores. Residuals were
tested for normality using the Anderson-Darling test. Bias and random
variation were calculated using 95% limits of agreement (Bland & Altman,
1986). The residuals between test and retest were also subjected to a t-test
and the interclass correlation (ICC) (3,1) and 95% standard error of
measurement (SEM) was calculated for all variables. All data in tables is
presented as means and standard deviations. Differences between groups
were assessed using two-tailed, Independent t-tests and were conducted on
all variables between CrossFit athletes and controls. Relationships between
the variables and the V02 max results were assessed using Pearson’s
correlation co-efficient.
16
CHAPTER 3
RESULTS
Results
3.1 Reliability of the Data
Two separate data analyses (test-retest) were conducted upon ESV, EDV,
MV E Vel, MV A Vel and SV. Due to time constraints it would have been
impractical to conduct a reliability study on all variables. Table 5 shows that
the dependent t test conducted to test the hypothesis of no difference
between the mean score for the test and the mean score for the retest
showed no significant difference for all variables.
Table 5. t-test conducted on all variables for test-retest measurements
Variable
Sample Size
t-test
ESV
15
0.307
EDV
15
0.397
MV E Vel
15
0.294
MV A Vel
15
0.165
SV
15
0.895
P < 0.05
The residual errors between scores on the rest and retest were calculated
using the Anderson-Darling test and were found to be normally distributed (P
= 0.065, 0.45, 0.015, 0.097, 0.044 for ESV, EDV, MV A VEL, MV E VEL and
SV respectively) and all data was found to be heteroscedasctic by plotting
absolute differences against means.
From the Bland-Altman plots it was possible to calculate the 95 % limits of
Agreement (LoA) for all the variables using the equation; Mean diff ± (1.96 x
Sdiff). The systematic bias and random variation was analysed for all variables
using the Bland-Altman plot and there was found to be a negative bias for all
variables and a fair amount of random variation. Using the upper and lower
limits of agreement it is possible to contextualise these results. For example, if
a new player had an ESV of 60 ml it would be acceptable to say that upon a
retest the participants ESV value could be as high as 61.1 ml or as low as
17
58.6 ml. Figure 10 provides a graphical illustration of a Bland-Altman plot for
one of the variables with superimposed upper and lower limits of agreement.
95 % Standard error of measurement (SEM) was calculated for all variables
and was found to be 1.9 ml or 1.9 m/s for the respective variables. These
figures can be seen for all variables in table 6.
By correlating the test and retest scores using the ICC (3,1) it was found that
there was a significant relationship between test and retest scores for all of
the variables analysed. The P value was found to be significant to 0.005 by
calculating a t ratio using the equation; ICC/√[(1-ICC2)/(n-k)] and then testing
the t value for significance using a critical values table.
Table 6. Data summary for all measured variables
Variable
Sample
95 % CI
95 % SEM
ICC (3,1)
95 % LoA
size
EDV
15
-5.8, 2.4 ml
1.9 ml
0.986*
12.8, -16.2
ESV
15
-3.2, 1.1 ml
1.9 ml
0.991*
6.6, -8.7
MV A
15
-0.02, 0.01
1.9 m/s
0.972*
0.04, -0.06
1.9 m/s
0.984*
0.05, -0.07
1.9 ml
0.968*
11.5, -11.1
Vel
MV E
m/s
15
Vel
SV
-0.03, 0.01
m/s
15
-3.0, 3.4 ml
* = P < 0.005
18
3.2 Baseline Characteristics
Fifteen (n = 15) participants were enrolled on to the study (Trained = 9,
Controls = 6). Baseline characteristics are displayed in table 3 and are
presented as means ± standard deviations. The mean age for the group was
24 ± 5 years and there was a significant difference (P < 0.05) between the
mean age of the trained participants and the controls (27 ± 4 years VS 20 ± 1
year, respectively). The trained participants displayed significantly lower
resting HR (P < 0.001) when compared to controls (58 ± 4 bpm VS 73 ± 3
bpm, respectively) and significantly higher (P < 0.05) 𝑉̇ O2max. scores (52.4 ±
7.6 ml/kg/min VS 41.9 ± 2.7 ml/kg/min, respectively). There were no
significant differences between groups when comparing BSA, height and
weight.
Table 3. Baseline characteristics for study group (n = 15)
Group
Age
Height
Weight
VO2 max.
Resting
BSA
(n=15)
(years)
(cm)
(kg)
(ml/kg/min)
HR
(m2)
(bpm)
Trained
27 ± 4*
(n=9)
Controls
(n=6)
177.8 ± 4.1 85.8 ±
52.4 ± 7.6*
58 ± 4**
2.04 ± 0.11
41.9 ± 2.7
73 ± 3
1.91 ± 0.14
8.3
20 ± 1
178.9 ± 7.2 73.1 ±
9.9
* - significant difference between trained and controls, P < 0.05; ** - significant
difference between trained and controls, P < 0.001.
19
3.3 Baseline Echocardiographic Measurements
All baseline echocardiographic measurements for diastolic and systolic
function are detailed in table 4 as absolute values and are presented as
means ± standard deviations.
Table 4. Baseline echocardiographic measurements presented as absolute
and scaled values.
Absolute values
Scaled values
Variable
Trained
Controls
Trained
Controls
IVSd (cm) (cm/m2)
1.2 ± 0.3
1.1 ± 0.1
0.6 ± 0.1
0.5 ± 0.1
2
IVSs (cm) (cm/m )
1.8 ± 0.3
1.6 ± 0.1
0.9 ± 0.1
0.8 ± 0.1
MV E Vel (m/s)
0.82 ± 0.17
0.84 ±
0.08
MV A Vel (m/s)
0.49 ± 0.12
0.45 ±
0.08
MV E/A Ratio
1.77 ± 0.42
1.93 ±
0.39
S’ v (m/s)
0.09 ± 0.01
0.10 ±
0.01
E’ v (m/s)
0.13 ± 0.01*
0.12 ±
0.02
A’ v (m/s)
0.08 ± 0.02
0.08 ±
0.01
*significantly different between trained and controls P < 0.05; IVS,
interventricular septum; MV, Mitral Valve; S, systole; E, early diastole; A,
late diastole.
The trained participants had significantly increased LVIDd (t(13) = 2.379, P =
0.033) in comparison to sedentary controls this was also evident with LVIDs
(t(13) = 2.190, P = 0.047). LVPWd also proved to be significantly increased
(t(13) = 3.347, P = 0.005) in comparison to controls. LVPWs in trained
individuals was significantly greater (t(13) = 3.780, P = 0.002) than in controls
(see figure 2).
20
ID
d
(C
LV
)
PW
d
(T
LV
)
PW
d
(C
)
LV
ID
s
(T
)
LV
ID
s
(C
LV
)
PW
s
(T
LV
)
PW
s
(C
)
d
ID
LV
LV
(T
)
Measurement of absolute variable (cm)
7.0
6.5
6.0
5.5
5.0
4.5
4.0
3.5
3.0
2.5
2.0
1.5
1.0
0.5
0.0
Variable
Fig. 3. A comparison of absolute values in trained (T) participants and controls
(C). LVIDd, left ventricular cavity dimensions at end diastole; LVPWd, left
ventricular posterior wall thickness at end diastole; LVIDs, left ventricular
posterior wall thickness at end systole; LVPWs, left ventricular wall thickness
at end systole.
SV was significantly increased in the trained participants (t(13) = 4.182, P =
0.001) when compared with controls (figure 3). EF was also significantly
increased in trained participants (t(13) = 2.905, P = 0.012) in comparison to
controls (figure 4).
21
150
SV (ml)
125
100
75
50
25
C
on
tr o
ls
Tr
ai
ne
d
0
Training Status
Fig. 4. Differences in stroke volume (SV) between trained participants and
controls.
80
70
EF (%)
60
50
40
30
20
10
C
on
tro
Tr
ai
ne
d
ls
0
Training Status
Fig. 5. Differences in ejection fraction (EF) between trained participants and
controls.
When scaled to BSA, LVPWd remained significantly (t(13) = 2.709, P = 0.018)
greater in trained participants when compared to controls (figure 5). SV also
remained significantly (t(13) = 4.297, P = 0.001) higher in trained participants
in comparison to control participants (figure 6).
22
3
2
1
(T
LV
)
PW
d
(C
)
LV
ID
s
(T
)
LV
ID
s
(C
LV
)
PW
s
(T
LV
)
PW
s
(C
)
)
d
LV
LV
P
ID
ID
LV
W
d
(C
(T
)
0
d
Measurement of scaled variable (cm/m2)
4
Variable
Fig. 6. A comparison of scaled variables between trained (T) participants and
controls (C). LVIDd, left ventricular cavity dimensions at end diastole; LVPWd,
left ventricular posterior wall thickness at end diastole; LVIDs, left ventricular
posterior wall thickness at end systole; LVPWs, left ventricular wall thickness
at end systole.
80
70
SV (ml/m2)
60
50
40
30
20
10
C
on
t
ro
l
Tr
ai
ne
d
s
0
Training Status
Fig. 7. Differences in stroke volume (SV) between trained participants and
controls when scaled to BSA (body surface area).
23
IVSd (t(13) = 1.603, P = 0.133) and IVSs (t(13) = 1.450, P = 0.171) proved to
show no statistical significance between trained participants and controls. No
statistical significance existed (t(13) = -0.166, P = 0.871) between trained
participants and controls when considering MV E Vel. The same was true
when considering the difference in MV A Vel (t(13) = 0.697, P = 0.498) of
trained participants and controls. EDV (t(13) = 1.963, P = 0.071) and ESV
(t(13) = 0.431, P = 0.673) also proved to be insignificant when comparing
trained participants and controls. S’ v displayed no significant difference (t(13)
= -1.196, P = 0.253) between trained participants and controls. There was no
significant difference (t(13) = -2.290, P = 0.390) between trained participants
and controls when considering E’ v. There was also no significant difference
in A’ v (t(13) = 0.957, P = 0.356) between trained participants and controls.
24
CHAPTER FOUR
DISCUSSION
Discussion
4.1 Principal Findings
The purpose of this study was to examine the effects that high-intensity,
mixed modality cross-training, using the CrossFit method of training, has on
left ventricular function and morphology in comparison to sex-matched
controls who perform ≤ 2 hours of physical activity per week.
It was hypothesised that due to the high-intensity and mixed-modality nature
of CrossFit that the trained participants would show signs of both eccentric
and concentric hypertrophy of the myocardium and that this would result in
increased left ventricular posterior wall thickness and left ventricular cavity
dimensions.
It was also hypothesised that the trained participants would display increased
diastolic function as assessed by the E:A ratio in comparison to controls due
to increased compliance and decreased stiffness of the myocardium thus
allowing for greater filling due to the ‘suction’ this creates (Stoylen et al. 2003)
and that the trained participants will display improved systolic function as
assessed by ejection fraction and stroke volume due to increased contractility
and therefore a higher contractile reserve.
To my knowledge this is the only study that has considered the effects that
CrossFit, as a form of high intensity mixed modality training, has on left
ventricular morphology and function. The principal findings of this study were
that left ventricular cavity dimensions, interventricular septal thickness and
posterior wall thickness were increased in participants who trained using the
high intensity, mixed modality method of training known as CrossFit when
compared to untrained individuals. The trained participants displayed
significantly larger values for LVIDd, LVIDs, LVPWd and LVPWs in
comparison to controls. An increase in left ventricular cavity dimensions
(LVIDd and LVIDs) is indicative of the ‘eccentric’ hypertrophy pattern that the
‘Morganroth’ hypothesis states occurs as a result of prolonged endurance
training. Increased thickness of the LVPWd and LVPWs would suggest that
‘concentric’ hypertrophy of the myocardium is evident when individuals
25
partake in high intensity, mixed modality training, which the ‘Morganroth’
hypothesis describes as occurring as a result of resistance type training. Once
the absolute values were scaled to BSA it became less evident that a clear
difference existed between trained participants and controls with only LVPWd
remaining significantly greater in trained participants. When considering left
ventricular function, ejection fraction and stroke volume were significantly
greater in trained participants in comparison to controls, however, no
significant difference existed in any other function-related variables between
the trained and untrained participants.
4.2 Left Ventricular Morphology
The increased wall thicknesses and ventricular septal thicknesses in trained
participants within the current study are consistent with those findings from
other studies that display signs of cardiac remodeling as a result of exercise
training. Baggish et al. (2009) examined differences in cardiac parameters
between elite rowers and sedentary controls and found interventricular septal
thickness to be significantly (P < 0.05) greater in the trained individuals in
comparison to the controls (5.5 ± 0.3 mm/m2 vs. 4.9 ± 0.3 mm/m2,
respectively). Posterior wall thickness was also significantly greater in elite
rowers (5.4 ± 0.6 mm/m2) when compared to sedentary controls (4.9 ± 0.6
mm/m2). The findings from the current study show increased wall thicknesses
and ventricular septal thickness in response to a training stimulus. These
findings are consistent with those observed by Scharhag (2002) who
compared endurance athletes compared to matched non-athletic controls and
observed enlarged wall thicknesses and ventricular septal thicknesses in
endurance athletes in comparison to the controls (PWT, 11.2 ± 0.9 mm vs. 9.5
± 0.9, respectively. IVS, 11.4 ± 0.9 mm vs. 10.2 ± 0.9, respectively). The
mechanistic underpinning of the increased cavity dimensions and wall and
septal thicknesses observed in the trained group may be explained by the
haemodynamic stress caused by increased wall pressures and peripheral
vascular pressure and the transduction of that stress to increase protein
synthesis, which could involve number of signaling pathways including growth
factors, Akt andP13K(Ruwhof & van der Laarse, 2000). According to Di Mauro
26
et al. (2009) the presence of a polymorphism of angioensin-converting
enzyme (ACE) known as ACE-DD and a polymorphism of angiotensin type 1
receptor gene (AGTR1) called AGTR1-AC/CC were correlated to the highest
blood plasma and tissue levels of ACE. This produced a significant increase
in LVM indexed to body size (LVMi) with greater prevalence of concentric
hypertrophy in endurance athletes due to ACE stimulating the production of
angiotensin II which in turn stimulates cardiac protein synthesis. The findings
from Di Mauro et al. (2009) suggest that genetics may influence the
differential myocardial hypertrophy demonstrated in athletes rather than the
training stimulus and haemodynamic stress alone. Due to the mixed-modality
nature of CrossFit it is difficult to attribute the hypertrophy of the myocardium
to either solely resistance or endurance training or a combination of the two.
Many studies have shown that resistance training may not be associated with
marked morphological change. For example, it was observed by Spence et al.
(2011) that after a 24-week ‘Olympic’ weightlifting programme no significant
difference existed between pre- and post-training cavity dimensions and wall
and septal thicknesses. Similarly, strength training or a combination of aerobic
and strength training both failed to induced cardiac morphological adaptations
in older women over a 12 week training period (Haykowsky et al. 2005). It is a
common belief in the sport cardiology literature that increased arterial
pressure during the lifting of weights is the key stimulus for increasing left
ventricular mass. However, it has been shown using invasive haemodynamic
and transthoracic echocardiography, that submaximal and maximal resistance
efforts performed with a brief Valsalva manoeuvre (a natural response to
repetitive submaximal and maximal exercise) do not increase wall stress
(Haykowsky et al. 2001). This apparent lack of wall stress during weightlifting
may explain why concentric left ventricular hypertrophy is not an obligatory
adaptation to strength training and why the adaptations seen in this cohort of
cross-trained athletes may be caused by the endurance component of the
training regime . Conversely, and in agreement with the current study, it has
been reported by Baggish et al. (2008b) that endurance and power training
elicited effects which were entirely consistent with the ‘Morganroth
hypothesis’. This study assessed rowers and American-footballers, sports
which may be described as ‘mixed’, involving a combination of aerobic and
27
resistive components (duManoir et al. 2007) which have been said to
generate unique hemodynamic loads (Naylor et al. 2008). Rowers and
American-footballers experienced increases in wall thicknesses, ventricular
septal thicknesses and volumes during a 3-month period of team training.
4.3 Left Ventricular Function
The trained participants in this study displayed increased ejection fraction.
This data would suggest that CrossFit training improves systolic function.
However, a consideration of left ventricular ejection fraction and more direct
measurements of systolic function would suggest that left ventricular ejection
fraction has inherent limitations for the assessment of systolic function
(Baggish et al. 2008a). This is due to the fact that ejection fraction does not
account for geometric changes and thus lacks sensitivity to track left
ventricular function in the presence of significant changes in cardiac
remodeling. In contrast with this data, several previous studies have
examined the impact of exercise training on left ventricular systolic function. A
meta-analysis of cross-sectional data showed no difference in left ventricular
ejection fraction among trained athletes compared with sedentary controls
(Pluim et al. 1999). An assessment of left ventricular characteristics among
elite distance runners demonstrated a high prevalence of reduced left
ventricular ejection fraction but concluded that this was a secondary effect of
left ventricular dilation (Legaz et al. 2005). In summary, these studies suggest
that endurance training has no significant effect on left ventricular function.
It was recently reported by duManoir et al. (2007) that significant increases in
resting left ventricular cavity dimensions, stroke area, and mass were evident
after 10 weeks of 3 times weekly rowing sessions. As noted by the authors,
athletes in this study performed combined strength and endurance training
that differs from the purer endurance-type rowing training. Several studies
have shown improved LV relaxation rates and therefore improved overall
diastolic function as a result of endurance training (Baggish et al. 2008a;
Naylor et al. 2005). However, diastolic function in the cross-trained individuals
28
from the current study as assessed by the E:A ratio showed no significant
difference when compared to the untrained individuals (1.77 ± 0.42 vs. 1.93 ±
0.39, respectively).
In a recent study, Baggish et al (2008b) observed that strength-trained
participants experienced an increase in left ventricular mass, an increase in
left ventricular wall thickness, but no change in left ventricular chamber
dimensions, volume, or resting cardiac output. The change in left ventricular
mass was positively correlated with the change in left ventricular wall
thickness but was unrelated to chamber volume. In addition, they experienced
a significant reduction in left ventricular diastolic tissue velocities, which were
inversely correlated with rising left ventricular mass. In addition, endurancetrained athletes experienced significant increases in left ventricular diastolic
tissue velocities, which were positively correlated with the magnitude of left
ventricular mass increase. The data from this study suggests that the LV
undergoes significant concentric hypertrophy with a resultant reduction of
diastolic function when exposed to a sustained period of strength training and
that endurance training improves diastolic function. However, the data from
these studies is in contrast to the findings of the current study, which would
suggest that the high-intensity cross-training produces both concentric and
eccentric hypertrophy of the myocardium yet diastolic function remain similar
to the values of the untrained individuals. It is therefore evident from this
cross-sectional study that a reduction in diastolic is not an obligatory training
adaptation to high-intensity mixed-modality training. It is plausible to suggest
that due to the strength and endurance components of this type of training
that the increase in cardiac afterload causes an improvement in systolic
function and the increased preload causes a reduction in diastolic function as
suggested in other studies (Baggish et al. 2008a; Leite-Moreira et al. 1999).
This area requires further study.
29
4.4 Limitations
There are several limitations with the present study. The use of
echocardiography for assessing cardiac morphological adaptations has
recently come under scrutiny (Naylor et al. 2008). It has been noted that
because of the geometrical assumptions made by 2-D echocardiography
when estimating LV mass and volumes that it is no longer the “gold standard”
for cardiac morphologic adaptation assessment due to the amount of error
associated with this measurement. Indeed differences between cardiac
dimensions of athletes and non-athletes lie within the methodological error
range for 2-D echocardiographic assessments, estimated to be ~60 g (at 95
% confidence) (Jenkins et al. 2007).
Secondly, when scaling to BSA it has been stated the using fat-free mass
(FFM) is the “gold standard” measurement (Batterham and George, 1998).
However, due to time constraints it was deemed to be impractical to use this
method within the current study and BSA was used a suitable surrogate as
suggested by Batterham and George (1998).
Most notably, the cross-sectional study design has been criticised by Naylor
et al. (2008) who suggested that the cross-sectional data are limited by
inherent assumptions made that differences between groups are due to a
training effect rather than other between-subject differences such as body
size. Naylor et al. (2008) suggest that sample groups should be matched for
sex, age, height and weight in order to minimize these differences, however,
this was not controlled for in the current study. Sample groups have been
suggested to be ≥ 25 participants which limits study power where betweengroup comparisons, associated with greater group variability, are necessary.
Finally, females were not used in this study but it is acknowledged that
cardiac morphological adaptations to training may be sex dependent
(Wernstedt et al. 2002; Baggish et al. 2008a).
30
4.5 Conclusions
In conclusion, the findings from this study demonstrate that CrossFit as a
method of high intensity, mixed modality cross-training produces significant
adaptations to the morphology of the left ventricle when compared to sexmatched controls. It is also evident that there are certain functional
adaptations, namely increased SV and EF, that occur to the left ventricle as a
result of high-intensity, cross-training. The findings from this study provide
some support for the Athletes Heart hypothesis, however, future studies
should look at high intensity, mixed modality cross-training in a longitudinal
manner and compare to sedentary controls and strength- and endurance
trained individuals.
31
REFERENCE LIST
Reference list
Abergel, E., Chatellier, G., & Hagege, A. Serial left ventricular adaptations in
world-class professional cyclists: implications for disease screening and
follow-up. 2004. Journal of the American College of Cardiology; 44 (1): 144149.
Baggish, L., Yared, K., Wang, F., Weiner, R., Hutter, A., Picard, M., & Wood,
M. The impact of endurance exercise training on left ventricular systolic
mechanics. 2008a. American Journal of Physiology – Heart and Circulatory
Physiology; 295: 1109-1116.
Baggish, L., Wang, F., Weiner, B. Training-specific changes in cardiac
structure and function: a prospective and longitudinal assessment of
competitive athletes. 2008b. Journal of Applied Physiology; 104(4):1121–8.
Baggish, L., Yared, K., Wang, F., Weiner, R., Demes, R., Hagerman, F.,
Picard, M., & Wood, M. Differences in cardiac parameters among elite rowers
and subelite rowers. 2009. Journal of Medicine and Science in Sports and
Exercise; 1215-1220.
Batterham, A., George, K., Whyte, G. Scaling cardiac structural data by body
dimensions: a review of theory, practice and problems. 1999. International
Journal of Sports Medicine; 20 (8): 495-502.
Burgomaster, K., Howarth, K., Phillips, S. Similar metabolic adaptations
during exercise after low volume sprint interval and traditional endurance
training in humans. 2008. Journal of Physiology; 586: 151-60.
Colan, S., Sanders, S., MacPheraon, D., et al. Left ventricular diastolic
function in elite athletes with physiologic cardiac hypertrophy. 1985. Journal of
the American College of Cardiology; 6: 545-549.
Di Mauro, M., Izzicupo, P., Santarelli, F., Stefano, P. ACE and AGTR1
Polymorphisms and Left Ventricular Hypertrophy in Endurance Athletes.
2010. Medicine and Science in Sport and Exercise; 42 (5): 915-23.
Ehsani, A., Hagberg, J., Hickson, R. Rapid changes in left ventricular
dimensions and mass in response to physical conditioning and
deconditioning. 1978. American Journal of Cardiology; 42 (1): 52-6.
Fagard, R. Athlete’s heart. 2003. Heart; 89: 1445-1461.
Fisman, E., Pelliccia, A., & Motro, M. Effect of intensive resistance training on
isotonic exercise Doppler indexes of left ventricular systolic function. 2002.
American Journal of Cardiology; 89: 887-891.
George, K., Batterham, A. Modeling the influence of body size and
composition on M-mode echocardiographic dimensions. 1998a. American
Journal of Physiology; 274 (2): H701-8.
George, K., Batterham, A., & Jones,B. The impact of scalar variable and
process on athlete-control comparisons of cardiac dimensions. 1998b.
Medicine and Science in Sports and Exercise; 30: 824-830.
Haykowsky, M., Chan, S., & Bhambhani, Y. Effects of combined endurance
and strength training on left ventricular morphology in male and female
rowers. 1998. Canadian Journal of Cardiology; 14: 387-391.
Jenkins, C., Bricknell,K., Chan, J. Comparison of two- and three- dimensional
echocardiography with sequential magnetic resonance imaging for evaluating
left ventricular volume and ejection fraction over time in patients with healed
myocardial infarction. 2007. American Journal of Cardiology; 99: 300-6.
Karjalainen, J., Matntysaari, M., Viitasalo, M. Left ventricular mass, geometry,
and filling in endurance athletes: association with exercise blood pressure.
1997. Journal of Applied Physiology; 82: 531-7.
Kemi, O., Haram, P., Loennechen, J. Moderate vs. high exercise intensity:
differential effects on aerobic fitness, cardiomyocyte contractility, and
endothelial function. 2005. Cardiovascular Research; 67: 161-72.
Kemi, O., Haram, P., Wisloff, U., Ellingsen, O. Aerobic fitness is associated
with cardiomyocyte contractile capacity and endothelial function in exercise
training and detraining. 2004. Circulation; 109: 2897-904.
Keteyian, S., Brawner, C., Savage, P. Peak aerobic capacity predicts
prognosis in patients with coronary heart disease. 2008. American Heart
Journal; 156: 292-300.
Laursen, P. Training for intense exercise performance: high intensity or high
volume? 2010. Scandinavian Journal of Medicine and Science in Sports; 20:
1-10.
Legaz,A., Serrano, E., Gonzalez, M., Lacambra, I. Echocardiography to
measure fitness of elite runners. 2005. Journal of the American Society of
Echocardiography;18(5):419–26.
Mantziari, A., Vassilikos, V., Giannakoulas, G., Karamitsos, T., Dakos, G.,
Girasis, C., Papadopoulo, K., Ditsios, K., Karvounis, H., Styliadis, I.,
Parcharidis, G. Left ventricular function in elite rowers in relation to traininginduced structural myocardial adaptation. 2010. Scandinavian Journal of
Medicine and Science in Sports; 20 (3): 428-33.
Maron, B. Structural features of the athlete’s heart as defined by
echocardiography. 1986. Journal of the American College of Cardiology; 7:
190-203.
Mitchell, H., Haskell, W., & Raven, P. Classification of sports. 1994. Medicine
and Science in Sports and Exercise; 26: S242-245.
Morganroth, J., Maron, B., Henry, W. Comparative left ventricular dimensions
in trained athletes. 1975. Annals of Internal Medicine; 82: 521-524.
Morganroth, J., & Maron, B. The athlete’s heart syndrome: a new perspective.
1977. Annals of the New York Academy of Sciences; 301 (1): 931-941.
Naylor, L., Arnolda, L & Deague, J. Reduced diastolic function in elite athletes
is augmented with the resumption of exercise training. 2005. Journal of
Physiology; 563: 957-963.
Naylor, L., George, K., O’Driscoll, G., & Green, D. The Athlete’s Heart. A
contemporary appraisal of the ‘Morganroth Hypothesis’. 2008. Sports
Medicine; 38 (1): 69-90.
Pavlik, G., Olexo, Z., Osvath, P. Echocardiographic assessment of male
athletes of different ages. 2001. British Journal of Sports Medicine; 35: 95-9.
Pela, G., Bruschi, G., Montagna, L. Left and right ventricular adaptation
assessed by Doppler tissue echocardiography in athletes. 2004. Journal of
the American Society of Echocardiogrpahy; 17 (3): 201-11.
Pelliccia, A., Maron, B., Sparato, A., et al. The upper limit of physiological
hypertrophy in highly trained elite athletes. 1991. The New England Journal of
Medicine; 324: 295-301.
Pelliccia, A., Sparato, A., Caselli, G. Absence of left ventricular wall thickening
in athletes engaged in intense power training. 1993. American Journal of
Cardiology; 72: 1048-54.
Pluim, B., Zwinderman, A., & Van der Laarse, A. The athlete’s heart: a metaanalysis of cardiac structure and function. 1999. Circulation; 100: 336-344.
Roy, A., Doyon, M., Dumesnil, J. Endurance vs strength training: a
comparison of cardiac structures using normal predictive values. 1988.
Journal of Applied Physiology; 64 (6): 2552-2557.
Sadaniantz, A., Yurgalevitch, S., & Zmuda, J. One year of exercise does not
alter resting left ventricular systolic or diastolic function. 1996. Medicine and
Science in Sports and Exercise; 28 (11): 1345-1350.
Scharhag, J., Schneider, G., Urhausen, A. Athlete’s heart: right and left
ventricular mass and function in male endurance athletes and untrained
individulas determined by magnetic resonance imaging. 2002. Journal of the
American College of Cardiology; 40 (10): 1856-63.
Schmidt-Trucksass, A., Schmid, A., Haussler, C., et al. Left ventricular wall
motion during diastolic filling in endurance-trained athletes. 2000. Medicine
and Science in Sports and Exercise; 33 (2): 189-95.
Sharma, S., Maron, B., & Whyte, G. Physiological limits of left ventricular
hypertrophy in elite junior athletes: relevance of differential diagnosis of
athlete’s heart and hypertrophic cardiomyopathy. 2002. Journal of the
American College of Cardiology; 40 (8): 1431-1436.
de Simone, G., Devereux, R., & Meyer, R. Left ventricular mass and body size
in normotensive children and adults: assessment of allometric relations and
impact of overweight. 1992. Journal of the American College of Cardiology; 20
(5): 1251-1260.
Urhausen, A., & Kindermann, W. One- and two-dimensional
echocardiography in body builders and endurance-trained subjects. 1989.
International Journal of Sports Medicine; 10: 139-144.
Warburton, D., Mckenzie, D., Haykowsky, M. Effectiveness of high-intensity
interval training for the rehabilitation of patients with coronary artery diease.
2005. American Journal of Cardiology; 95: 1080-4.
Wernstedt, P., Sjostedt, C., Ekman, I. Adaptation of cardiac morphology and
function to endurance and strength training: a comparative study using MR
imaging and echocardiography in males and females. 2002. Scandinavian
Journal of Medicine and Science in Sports; 12: 17-25.
Wieling, W., Borghols, E., Hollander, A. Echocardiographic dimensions and
maximal oxygen uptake in oarsmen during training. 1981. British Heart
Journal; 46 (2): 190-5.