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The Effect of Swimming Training
on the Cardiac Dimensions in
Thoroughbred Horses
RIRDC Publication No. 08/156
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The Effect of Swimming Training on
the Cardiac Dimensions in
Thoroughbred Horses
by
Associate Professor Allan Davie
Dr C.J. (Kate) Savage
Dr Laura Fennell
October 2008
RIRDC Publication No 08/ 156
RIRDC Project No PRJ-000842
© 2008 Rural Industries Research and Development Corporation.
All rights reserved.
ISBN 1 74151 745 1
ISSN 1440-6845
The Effect of Swimming Training on the Cardiac Dimensions in Thoroughbred Horses
Publication No. 08/156
Project No. PRJ-000842
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Researcher Contact Details
Associate Professor Allan Davie
C/O Southern Cross University
Department of Exercise Science & Sport Management
PO Box 157
Lismore NSW
Phone: 02 66203236
Fax:
02 66203880
Email:
[email protected]
C.J. Savage BVSc(Hons), MS, PhD, Diplomate ACVIM
and L.C. Fennell BVSC (Hons)
Equine Centre, University of Melbourne
250 Princes Hwy.
Werribee VIC 3030
In submitting this report, the researcher has agreed to RIRDC publishing this material in its edited form.
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Level 2, 15 National Circuit
BARTON ACT 2600
PO Box 4776
KINGSTON ACT 2604
Phone:
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Fax: 02 6271 4199
Email:
[email protected].
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Web:
Published in October 2008 by Union Offset
ii
Foreword
Swimming training has been accepted internationally as a modality for improving fitness in horses.
The improvements in fitness in humans is well known, however, actual benefits they obtained for
horses have not been established. Previous research has investigated the effectiveness of a swimming
exercise test for evaluating changes in performance measures, skeletal muscle composition (Misumi
et al. 1994-1995) and respiratory function during swimming (Hobo et al. 1998).
The aim of this study was to examine the potential for altering cardiac dimensions and physical
capacity, and exercise tolerance in horses as a result of swimming training.
There was no significant difference in cardiac wall thickness and fractional shortening (FS) found
between the two training groups either pre- or post-training. The effects of the swimming plus track or
track only training programs had no significant effect both between and within the training groups.
Both groups showed changes in left ventricular internal diameters (mm) from 7.2 to 7.5 and FS (%)
from 37 to 34.6 for swim plus track group and FS from 37.9 to 35.7 for track only group, however,
changes did not reach significance. There was no significant difference between training groups for
resting heart rate, respiratory rates and body temperatures. The results showed that swimming training
at a self determined pace may have a positive effect on training. This was indicated by a reduced
whole blood lactate concentration during treadmill exercise test indicating an improvement in
metabolic efficiency of the muscle. However, it had no significant effect on cardiac dimensional
changes.
This report, an addition to RIRDC’s diverse range of over 1800 research publications, forms part of
our Horse R&D program, which aims to assist with developing the Australian horse industry and
enhancing its export potential.
Most of our publications are available for viewing, downloading or purchasing online through our
website:
•
downloads at www.rirdc.gov.au/fullreports/index.html
•
purchases at www.rirdc.gov.au/eshop
Peter O’Brien
Managing Director
Rural Industries Research and Development Corporation
iii
Acknowledgments
To the Rural Industries Research and Development Corporation for providing the financial support for
this study. Financial support was also provided by Hygain feeds. Kent Racing stables for providing all
horses for the study and to the staff at Kent racing for their support in swimming the horses,
organisation of transport and daily management of horses.
Cranbourne racing centre in Victoria who provided access to the track and swimming facilities for the
study.
Acknowledgement is also given to the staff at Melbourne University Veterinary Hospital for their
assistance in stabling and echocardiographic measurements of horses.
Abbreviations
ANOVA
Analysis of the Variance
b.p.m.
beats per minute
ECG
Echocardiography
FS
Fractional shorting
HLa
Whole Blood Lactate
HR
Heart Rate
HRR
Hearth Rate Reserve
IVS
inter-ventricular septal thickness
IVSd
inter-ventricular septal thickness in diastole
IVSs
inter-ventricular septal thickness in systole
L
Litre
LV
left ventricular
LVFWd
Left ventricle free wall thickness
LVID
Left ventricular internal diameter
LVIDd
Left ventricular internal diameter in diastole
LVIDs
Left ventricular internal diameter in systole
RR
Resting Respiratory Rate
SD
Standard Deviation
SV
stroke volume
VO2max
maximal oxygen uptake
iv
Contents
Foreword ............................................................................................................................................... iii
Acknowledgments................................................................................................................................. iv
Abbreviations........................................................................................................................................ iv
Contents ................................................................................................................................................. v
List of Tables......................................................................................................................................... vi
Executive Summary ............................................................................................................................ vii
Introduction ........................................................................................................................................... 1
Cardiac Hypertrophy-Pathological versus Physiological in Humans...................................................1
Cardiac Adaptations to Training in Humans ........................................................................................1
M-Mode Echocardiographic Analysis..................................................................................................1
Swim Training and Adaptations...........................................................................................................2
General Adaptations to Training in Horses ..........................................................................................3
Treadmill Training ...............................................................................................................................3
Methodology .......................................................................................................................................... 5
Statistical Analysis ...............................................................................................................................6
Results .................................................................................................................................................... 7
Discussion............................................................................................................................................... 9
Implications for Industry ....................................................................................................................11
Recommendations ..............................................................................................................................11
Future Research..................................................................................................................................11
References ............................................................................................................................................ 12
v
List of Tables
Table 1. The mean ± SD for age (yrs), weight (kg), resting heart rate (b.p.m.), resting respiratory rate
(RR b.p.m) and temperature (Temp °C) for groups A (Swim plus track) and B (track only) pre and
post training..............................................................................................................................................7
Table 2. The mean ± SD for whole blood lactate (mmol/L) and heart rates for groups A (swimming
plus track training) and B (track only training) for the treadmill exercise test. Whole blood lactate was
taken one minute post exercise and Peak HR was recorded during the gallop using a polar heart rate
monitor. ....................................................................................................................................................7
Table 3. The mean ± SD for IVSd (mm), IVSs (mm), LVDd (mm), LVDs (mm) and FS for groups A
and B pre and post training.......................................................................................................................8
vi
Executive Summary
What the report is about
This study examined swimming training in relation to its impact on structural development of the
heart.
Who is the report targeted at?
If cardiac adaptations are occurring with swimming, this understanding of the potential benefits will
assist horse trainers in being able to more fully structure training programs to maximise the benefits
obtained with the potential of reducing training based injuries.
Background
Swimming historically has been used in both humans and horses as a means of stimulating adaptations
with the goal of improving fitness. In the human area the benefits of swim training have long been
known (Fry 1986). However for the horse actual benefits obtained have not been established.
Swimming studies in horses have been done by Thomas et al. (1980) looking at cardiorespiratory
responses to tethered-swimming, Misumi et al. (1994-1995) in which they investigated the
effectiveness of a swimming exercise test for evaluating changes in performance measures and Hobo
et al. (1998) who looked at respiratory function during swimming.
As the horse is predominantly an aerobic athlete and one of the major components of aerobic
performance is cardiac function, this study investigated whether traditional pool swimming would
provide a sufficient stimulus to the heart, in addition to that experienced by normal race training,
resulting in a structural adaptation to the cardiac muscle.
Aims/objectives
The project examined the changes in cardiac dimensions in horses involved in traditional training
compared to those in traditional training coupled with swimming.
It was hypothesised that swimming training would have a positive effect on the heart by inducing an
adaptation in the left ventricular mass and dimensional volume.
Methods used
Fourteen Thoroughbred horses, including seven fillies, two mares, three geldings and two colts were
used in the study. Seven of the horses were un-raced. All horses were stabled at the same racing
complex (Cranbourne Victoria). Horses were paired based on age, sex and racing experience. Each
pair of horses followed the same base training program, with variation existing between pairs
depending on racing experience and age. One horse from each pair was randomly allocated to one of
two groups (swim plus track training Group A and track only training Group B). Diet composition was
kept constant for each pair of horses. Horses were fed a Hygain Sustainer (Hygain Feed Co., Australia)
depending on each horse’s dietary needs. All horses received hay daily.
Prior to echocardiography, both pre and post training, each horse underwent a physical examination,
echocardiography (ECG) and cardiac troponin analysis.
Echocardiography was performed in the week before and the week after completion of the nine week
swimming program. All M-Mode echocardiography was performed at the Equine Centre at the
Werribee Veterinary Department by the same experienced researcher. The procedure followed the
methodology outlined by Young (1999) and Young et al. (2002). M-Mode echocardiography imaging
techniques were used to obtain the data for measurements of inter-ventricular septal thickness in
diastole and systole (IVSd and IVSs) and left ventricular internal diameter in diastole and systole
(LVIDd and LVIDs). Fractional shorting (%FS) was calculated using the measurements LVIDd and
LVIDs.
vii
In the pre and post training phase, each horse completed a three stage submaximal treadmill test
consisting of three one minute gallops at 32 km/hr at six degrees incline with five minutes walking
between each gallop. The physiological responses of heart rate (HR) and whole blood lactate (HLa)
were assesssed during each test. Training included a combination of track and treadmill work six days
per week. The training work loads were increased by progressively increasing the working distance
while keeping the speed constant. Swim training horses completed race training in the morning plus
additionally completed swimming training in afternoons. Total time swimming was increased
gradually commencing with approximately four minutes (four laps) with additional laps added
depending on each horses fitness level. Total number of laps completed ranged from six to eight.
Horses were trained for nine weeks. However due to difficulties with outbreak of Equine Influenza
virus training was stopped for a period of ten days after three weeks of training. Heart rate and whole
blood lactate concentrations were taken immediately after swimming session at week nine. Each horse
had a blood sample collected one minute after leaving the water to determine whole blood lactate
concentrations.
Results/key findings
There was no significant difference in wall thickness and FS between the two training groups both pre
or post training. The effects of the swimming plus track or track only training programs had no
significant effect both between and within the training groups.
Both groups A and B showed changes in LVIDs from 7.2 to 7.5 (mm) and FS (%) from 37 to 34.6 for
group A (swim plus track group) and FS from 37.9 to 35.7 for group B (track only group), however,
changes did not reach significance.
For whole blood lactate and heart rate measures for the treadmill test there was no significant
difference between groups A and B before and after the training program.
Implications for industry
One of the goals of the horse program is to ensure the animal safety in relation to health and welfare,
with an objective of reducing the injury and breakdown rates for horses in training. This study
addressed part of this in providing an insight into cardiac adaptations with swimming in relation to the
effectivness of swimming as a stimuli for adaptation. With this understanding trainers may be able to
structure swimming programs to be a more effective component for stimulating training adaptations.
An understanding of this will now assist the trainer in training program design by providing a better
understanding of the intensity of swimming to provide fitness benefits.
Recommendations
This study was unique in that it was the first to investigate the effects of traditional swimming training
in Thoroughbred horses on training responses as cardiac dimensional changes and general fitness
measures. The study examined swimming, at a self determined intensity, that is commonly utilized in
the industry, to examine if this intensity was sufficient to stimulate changes in the cardiovascular
system. The study reported that swimming at a self determined intensity, five days per week, was not
sufficient to provide an additional stimullii above that experienced by normal training, to induce
further adaptations in the cardiovascular system. In relation to obtaining the maximum fitness value
from swimming, trainers need to consider the intensity and duration they swim horses. Therefore it
seems that a program that involves higher intensity work periods over short periods may be more
benifical for obtaining improvements in fitness.
Future Research
The information provided by this study has set the foundation, by the use of a tethered swimming pool,
to examine firstly the degree of hypoxia and secondly the degree of muscle metabolic enzyme changes
occurring during swimming at different intensities.
viii
Introduction
Cardiac Hypertrophy-Pathological versus Physiological in Humans
Cardiac hypertrophy is a cellular response to an increased stress. Hypertrophy, depending on the type
of stress can be pathological or physiological in nature. Physiological hypertrophy as a response to
training differs in structural and molecular profile to pathological that results predominately from
disease. In humans hypertrophy in relation to pathological stress has been considered an essential
adaptation to maintain cardiac output, however, prolonged hypertrophy has been associated with
increased risk of death (Frey & Olsen 2003). This hypertrophy stimulus can be in the form of
hypertension, valve disease, myocardial infarction and genetic mutations (McMullen and Jennings
2007; Zar 1984; Levy et al. 1988).
Physiological hypertrophy is a result of the large increase in venous return resulting from the
vasodilation and muscle activity that occurs during exercise. This hypertrophy is an eccentric
hypertrophy which is characterised by increased chamber size and a proportional change in wall
thickness (Pluim et al. 2000; Zar 1984).
Cardiac Adaptations to Training in Humans
Training has been associated with providing the desired stimuli to bring about morphological changes
in the heart such as increases in muscle mass, left ventricular wall thickness and chamber size. Cardiac
adaptations have been shown to respond to both preload and afterload training stimuli however, the
nature of cardiac hypertrophy differs in response to a volume (preload, eccentric) versus a pressure
(afterload, concentric) overload. In humans training has been shown to cause moderate left ventricular
hypertrophy with the intensity of training playing a key factor in the degree and type of adaptation
(Pluim et al. 2000). Intense anaerobic, strength or sprint training results in a more concentric left
ventricular (LV) hypertrophy. In comparison aerobic or endurance training results in enlargement of
LV diameter (Morganroth et al. 1975; Fagard 2003). The changes in LV diameter are believed to be
the result of the increased haemodynamic load associated with endurance training (George et al. 1991).
In human studies of athletes that are involved in training modes that create high after loads (weight
training) there have been reported increases in left ventricular wall thickness (Peronnet et al. 1980) left
ventricular mass (Morganroth et al. 1975) and interventricular septum thickness (Menapace et al.
1982). Research in both humans and horses supports the existence of a relationship between left
ventricular mass and maximal oxygen uptake (VO2max) with equine studies using echocardiography
also showing a correlation between heart score and maximal oxygen uptake (Young et al. 2002).
Hypertrophy provides for an increased heart capacity (endurance), as a result of an increased volume
of blood being pumped per heart beat (stroke volume). A higher stroke volume provides for a more
efficient heart as more blood is being pumped per beat. This response is the major adaptation that can
determine performance capacity.
Cardiac output is the product of heart rate and stroke volume and as maximal heart rate does not
change with training, cardiac performance at sub-maximal levels is largely dependant on the
determinants of stroke volume, including preload, afterload and contractility. An increased preload
(volume overload) results in an increased end diastolic volume and increased stroke volume (FrankStarling Law). In contrast an increased afterload (pressure overload) increases the resistance to blood
leaving the heart, resulting in a decreased stroke volume.
M-Mode Echocardiographic Analysis
Cardiac function has been evaluated in the horse with the quantitative two-dimensional
echocardiograph being introduced in the early 1990’s (Voros 1997; Reef 1990). Standardised
techniques have now been established for quantification of cardiac size and assessing valvular
integrity (Long et al. 1992; Lord & Croft, 1990; Reef 1991). In addition echocardiology has been used
to examine the correlation between heart score and maximal oxygen uptake (Young et al. 2002) to
1
examine cardiac dimensions in Standardbreds (Bakos et al. 2002) and recording changes in cardiac
dimensions during deconditioning in horses (Kriz et al. 2000).
Echocardiography is used routinely in equine practice to assess changes in cardiac dimensions and
valvular integrity. M-mode analysis of the left ventricle allows for measurement of the myocardial
thickness and also the diameter of the cardiac chambers in systole and diastole. Furthermore, the
fractional shortening is used to assess the degree of contractility of the left ventricle. The expected
cardiac changes in response to exercise training include an increase in the left ventricular internal
diameter in diastole as a result of increased stroke volume. A recent study has also demonstrated
subclinical valvular regurgitation, also thought to be a result of chamber dilation in response to
training (Young et al. 2008). Fractional shortening has also been shown to decrease (Young et al.
1999).
Swim Training and Adaptations
In human and mice studies swimming training has long been recognised as having the potential to
induce myocardial hypertrophy and left ventricular volume (Evangelist et al. 2003; Kaplan et al.
1994). The changes in cavity dimensions or wall thickness resulting from training have been reported
to be greatest in the sports of rowing, cycling and swimming (Maron & Pelliccia 2006). In
approximately 50% of trained athletes some evidence of cardiac remodelling exists, however, a large
change in LV chamber occurs in only approximately 15% of athletes (Pelliccia et al. 1999).
Previous swim studies in horses have examined the effects of swimming on cardiorespiratory
responses. Asheim et al. (1970) examined swimming for three periods of four minutes with three
minutes rest between swims and reported lactate ranges from 3.0 to 9.3 mmol/L after the third swim
with heart rates ranging from 158-210 b.p.m. Thomas et al. (1979) used tethered swimming and found
that stroke volume decreases at low intensity and only returned towards resting values when intensity
increased to high levels. Misumi et al. (1994) investigated the effectiveness of a swimming exercise
test for evaluating changes in performance measures, Hobo et al. (1998) who looked at respiratory
function during swimming, found respiratory rates to be around 25 breaths per minutes with changes
also in blood gases and significant increases in intra-tracheal pressures. Jones et al. (2002) found peak
expiratory pressures to be higher during swimming than galloping and that horses’ breathed at rates
five times slower during swimming than galloping.
Swimming a horse is quite different from humans in relation to physiological responses to the
exercise. Human studies have shown that the highest VO2 attained during swimming averages
approximately 90% of that attained during cycling. Blood lactates during maximum swimming have
been shown to be in the same order as that during maximum cycling (10mmol/L). The major factor
preventing the use of high intensity swimming as in humans for the horse is the restrictions on their
breathing capacity. As a result most trainers allow horses to swim at the horses own pace.
The performance of the horse is largely a function of its maximum oxygen uptake which itself is the
product of cardiac output and arterio-venous oxygen difference. The cardiac output (HR x SV) is a
function of the effectiveness of the heart whose performance is measured in several ways. Heart rate is
under the control of both the sympathetic and parasympathetic nervous systems in combination with
circulating catecholamines. Stroke volume (SV), the second component of cardiac output is under the
influence of end diastolic and end systolic volumes. There is an inverse relationship between after load
on the heart and stroke volume. In consideration of the increased expiratory pressures and reduced
stroke volumes reported during swimming, the horse during swimming could be working at a greater
physiological stress compared to land activities at a given work output.
2
General Adaptations to Training in Horses
Training provides the stimuli for an adaptation to occur. The stimulus needs to be of sufficient
intensity and/or duration to provide an overload to the system for a response to occur with an
adaptation generally occurring after several responses. These adaptations can be in the form of central
or cardiovascular changes or cellular metabolic changes.
The central changes are mainly in the form of increased blood volume and cardiac adaptations such as
increased ventricular capacity, increased myocardial thickness, increased stroke volume and
myocardial contractility. The metabolic changes being at the cellular level are in the form of changes
in the concentration of enzymes that control the rate of metabolism resulting in a more efficient energy
system.
The improvements in metabolic efficiency with training are the result of increased concentrations of
the key regulatory enzymes within the different metabolic pathways. The responses and adaptations of
these enzymes to training stimuli are very specific with high intensity exercise stimulating changes in
glycolytic regulators and endurance based work stimulating changes in the aerobic pathway.
The type of training therefore is an important factor in eliciting for specific adaptations.
Long slow aerobic work stimulates increases that improve oxygen carrying capacity and at the cellular
level, increases in myoglobin, number of mitochondria and activity levels of enzymes involved in
energy production. High intensity training stimulates changes in strength and speed with changes in
muscle mass and enzymes involved in anaerobic metabolism.
For the horse the importance of the level of the stimulation providing for a specific adaptation has
been highlighted in the literature. Von Wittke et al. (1994) in examining the training programs of
several training establishments showed that the number of days of workouts showed a significant
correlation with performance. Evans et al. (1995) compared the effects of high versus low intensity
treadmill training for nine weeks, with VO2 increasing by 20% in both groups indicating that intensity
is not important in the early phases of training. Geor et al. (1999) exercised horses for ten consecutive
days at a moderate-intensity of 55% VO2max for 60 minutes per day (13-14 km/day) which resulted in
8.9% increase in VO2max and 24% increase in run time to exhaustion. These finding were reinforced by
the work of Tyler et al. (1999) who proposed that endurance based moderate intensity training is more
important in inducing adaptations in VO2max than high intensity training.
There have been several studies that have examined the type of physiological responses and
adaptations to training and racing in Thoroughbred horses. Studies have looked at the correlation of
racing ability and physiological variables (Evans et al. 1993; Harkins et al. 1993) validity of training
measures on fitness prediction (Valette et al. 1996) effects of slope on muscle adaptations (Miyata
et al. 1999) and metabolic adaptations to intermittent maximal exercise (Snow et al. 1985). Changes in
blood lactate-running speed relationship (Von Wittke et al. 1994) training experience and
physiological responses to training (Ohmura et al. 2002) adaptations to training, overtraining and
detraining (Foreman et al. 1990; Tyler et al. 1998) influence of training and the correlation of ATPase
activity and myosin heavy chain composition (Rivero et al. 1996) work intensity effects on lactate
accumulation (Harris et al. 1987; Harris et al. 1991; Linder et al. 1992) and cardio and respiratory
responses to sub-maximal exercise training (Evans & Rose 1988; Davie & Evans 2000).
Treadmill Training
The treadmill provides an ideal tool for interval training, in that both distance and speed can be
accurately controlled and time greatly reduced in comparison to track interval work. The uniqueness of
the treadmill is that the intensity, volume and duration of the work interval can be controlled.
Several studies have investigated the effectiveness of the treadmill in stimulating physiological
responses similar to those experienced on the training track. Courouce et al. (2000) in examining the
physiological responses of track versus treadmill, found that at 2% incline on the treadmill horses
3
produced similar responses to those reported following training on the track. Harkins et al. (1993)
found a negative correlation between track running speed over distances of 1200, 1600 and 2000m and
treadmill gallop variables with the stronger correlation being between 1600m and 2000m with VLa4,
VO2max and V200 measured on the treadmill. Further Lucia & Greppi (1996) also found a correlation
between racing performance and fitness parameters after exercise tests both on the treadmill and track
in Standardbred racehorses. However, the fitness parameters calculated on the treadmill occurred at a
significantly lower speed than for the same variable on the track. This variation in parameters between
treadmill and track was also reported by Werkmann et al. (1996). He looked at the conditioning effects
in Thoroughbred horses exercising on the treadmill and reported that the specific blood lactates
concentrations used for training on the track may not be sufficient to stimulate adaptations in blood
lactate responses when treadmill training. The research to date suggests that the intensity of exercise
needed to stimulate adaptations on the treadmill may be different than that on the track and to equate
work on the track with the treadmill needs to be treated with caution.
4
Methodology
The study consisted of fourteen Thoroughbred horses, including seven fillies, two mares, three
geldings and two colts. Seven of the horses were un-raced. All horses where stabled at the same racing
complex (Cranbourne Victoria). Horses were matched paired based on age, sex and racing experience.
Each matched pair of horses followed the same base training program, with variation existing between
pairs depending on racing experience and age. One horse from each pair was randomly allocated to
one of two groups (swimming plus track training and track only training).
The study was conducted according to the ethical principles in research adopted by both Southern
Cross and Melbourne University animal experimentation.
Diet composition was kept constant for each pair of horses. Horses were fed a Hygain Sustainer
(Hygain Feed Co., Australia) depending on each horse’s dietary needs. All horses received hay daily.
Prior to echocardiography both pre and post training each horse underwent a physical examination
including rebreathing, auscultation, ECG and cardiac troponin analysis to assess general, pulmonary
and myocardial health. Echocardiography was performed following physical examination.
Echocardiography was performed prior to and the week after completion of the nine week swimming
program. All M-Mode echocardiography were performed at the Equine Centre Werribee, by the same
experienced researcher who was blind to each horses’ training group.
The procedure followed the procedure outlined by Young (1999) and Young et al. (2002). As
recommended by Young et al. (2002) images were recorded only when the resting heart rate was
stable and approximately 40 b.p.m. All images were taken from the right hemithorax using a short axis
view of the left ventricle. M-Mode echocardiography imaging techniques were used to obtain the data
for measurements of inter-ventricular septal thickness (IVS) left ventricular internal diameter (LVID)
in diastole (d) and systole (s) and left ventricle free wall thickness (LVFWd), diastole and systole.
Fractional shorting (%FS) is calculated using the following measurements.
%FS = LVIDdiastole -- LVIDsystole
------------------------X 100
LVID diastole
Training: All horses completed four weeks of trot and canter work prior to the commencement of the
study. Pre and post training each horse completed a three stage submaximal treadmill test consisting of
three one minute gallops at 32 km/hr @ six degrees incline with five minutes walking between each
gallop. The physiological responses of heart rate (HR) and whole blood lactate (HLa) were assesssed
during each test. Whole blood for lactate measurement was taken one minutes post final stage with
peak HR recorded during each stage and recovery heart rate taken one and half minutes into each
recovery period. Heart rate was measured using a Polar horse heart rate monitor. Blood was collected
aseptically via jugular venipuncture using vacutainers and 21 gauge needles. Blood for whole lactate
assays was collected into 3ml lithium heparin tubes. Samples were analysed immediately using a
Lactate Pro portable analyser.
Training included a combination of track and treadmill work six days per week. The track training
work loads were increased by progressively increasing the working distance while keeping the speed
constant.
Swim training horses completed race training in the morning plus additionally swimming training in
afternoon. This design has been adopted to enable the study to fit as closely as possible into the normal
training regimen total time swimming was incresed gradually commencing with approximately four
5
minutes (four laps) with one additional lap added every second week depending on each horses fitness
level. Total number of laps swum ranged from six to eight. All swimming training was conducted in
the Cranbourne training centre swimming pool. However due to difficulties with outbreak of Equine.
Influencza virus training was stopped for a period of ten days bewteen weeks three and five. Heart rate
and whole blood lactate concentrations were taken immediately after swimming session at week nine.
Heart rate was measured using a Polar horse heart rate monitor. Measurements were taken as the horse
came out of the water. Each horse had a blood sample collected one minute after leaving the water to
determine whole blood lactate concentrations. Blood was collected aseptically via jugular
venipuncture using vacutainers and 21 gauge needles. Blood for whole lactate assays was collected
into 3ml lithium heparin tubes. Samples were analysed 30 minutes post swim using a Lactate Pro
portable analyser.
Statistical Analysis
All data is reported as mean ± SD. For all cardiac dimension data analysis the pre score for each
measure was subtracted from the post score to get a change score.
Statistical analysis using SPSS was carried out using multivariate ANOVA on the different change
scores for cardiac dimensions.
Weight, resting heart rate, respiratory rates and temperatures were compared pre and post training
using repeated measures ANOVA.
6
Results
The aim of this project was to determine if swim training in addition to normal track training would
stimulate changes in left ventricular dimensions and performance.
There was no significant difference between training groups for resting heart rate, respiratory rates and
body temperatures.
Table 1. The mean ± SD for age (yrs), weight (kg), resting heart rate (b.p.m.), resting respiratory rate (RR
b.p.m) and temperature (Temp °C) for groups A (Swim plus track) and B (track only) pre and post
training.
Group
A
Mean
SD
Age
(yrs)
3.0
1.15
B
Mean
SD
2.6
0.79
Weight
Pre
(kg)
504.1
28.58
Weight
Post
(kg)
492.7
34.60
Rest
HR Pre
(b.p.m)
30.3
3.35
Rest HR
Post
(b.p.m)
37.1
3.80
RR
Pre
(b.p.m)
10.0
2.00
RR
Post
(b.p.m)
9.1
1.95
Temp
Pre
(°C)
37.6
0.24
Temp
Post
(°C)
37.7
0.31
477.7
22.87
459.7
31.27
36.0
4
37.7
4.54
12.0
2
11.4
1.51
37.8
0.21
38.0
0.33
The mean heart rate and lactate concentration for swimming taken 30 seconds and one minute post
swim respectively were 109±18.75 (b.p.m.) and 1.8±0.57 (mmol/L).
After training, in both group A and group B there was a reduction in whole blood lactate production
during the treadmill exercise test. The reduction in whole blood lactate reflects an improvement in
metabolic efficiency of the horses. Although the change from pre to post training was greater in group
A than group B, this difference between groups was not significant.
Five of the seven two year old Thoroughbreds and one three year old experienced higher heart rates at
end of the third treadmill test gallop, however, all horse were in their first preparation.
Table 2. The mean ± SD for whole blood lactate (mmol/L) and heart rates for groups A (swimming plus
track training) and B (track only training) for the treadmill exercise test. Whole blood lactate was taken
one minute post exercise and Peak HR was recorded during the gallop using a polar heart rate monitor.
Group
Lactate
(mmol/L)
Lactate
(mmol/L)
HR
(b.p.m)
HR
(b.p.m)
Mean
SD
Pre
7.6
4.41
Post
4.8
3.21
Pre
200
9.2
Post
204
16.1
B
Mean
SD
Pre
6.3
5.22
Post
5.7
4.59
Pre
198
9.67
Post
214
14.71
A
7
There was no significant difference in wall thickness and FS between the two training groups both pre
or post training. The effects of the swimming plus track or track only training programs had no
significant effect both between and within the training groups.
Both groups showed changes in LVIDs (mm) from 7.2 to 7.5 mm) and FS (%) from 37 to 34.6 for
group A (swim plus track group) and from 37.9 to 35.7 for group B (track only group); however,
changes did not reach significance.
Table 3. The mean ± SD for IVSd (mm), IVSs (mm), LVDd (mm), LVDs (mm) and FS for groups A and B
pre and post training
Group A
Group B
3.4 ± 0.37
3.4 ± 0.34
11.4 ± 0.67
11.5 ± 0.90
4.5 ± 0.34
4.7 ± 0.32
7.2 ± 0.60
7.5 ± 0.47
37 ± 4.21
34.6 ± 4.84
3.3 ± 0.56
3.2 ± 0.42
11.5 ± 0.68
11.6 ± 0.67
4.9 ± 0.39
4.9 ± 0.36
7.2 ± 0.69
7.5 ± 0.39
37.9 ± 2.72
35.7 ± 1.56
Left Ventricle
IVSd Pre (mm)
IVSd Post (mm)
LVDd Pre (mm)
LVDd Post (mm)
IVSs Pre (mm)
IVSs Post (mm)
LVIDs Pre (mm)
LVIDs Post (mm)
FS % Pre
FS % Post
Mean Troponin I values for pre and post training were 0.01 µg/L and 0.02 µg/L respectively for group
A and 0.01 µg/L and 0.01 µg/L respectively for group B.
8
Discussion
The horses in the swimming component of this study failed to demonstrate any additional evidence of
changes in cardiac dimensions, above those that were experience by horses in normal training that
potentiates the myocardial responses to training. The changes experienced were mild increases in
LVIDs and %FS without significant changes in any variable.
The study was conducted on Thoroughbred race horses in training for commercial racing. Horses were
matched based on age and racing history. Training incorporated a combination of treadmill and race
track work. All pairs completed the same training program however, the volume of training was
different between pairs. For two year olds the volume and intensity of training was not as high as
horses with prior racing history.
The significance of cardiac hypertrophy can be viewed in relation to its impact on cardiac output.
Cardiac hypertrophy has been shown to be occurring in response to both pressure (concentric) and
volume overload (eccentric). Volume overload is a factor of venous return where as pressure overload
is a result of increased resistance to flow. It has been suggested that swimming is related to volume
overload induced cardiac eccentric hypertrophy. In humans it has been suggested that a higher venous
return, lower heart rate and higher stroke volume during swimming is a result of the horizontal
position of the body during swimming (Triposkiadis et al. 2002). In horses however, a reduced stroke
volume has been reported with swimming, and that it only returns towards on land standing rates if the
intensity of exercise was increased (Thomas et al. 1980). The heart rates ranges of 150 to 200 (b.p.m.)
reported by Thomas et al. (1980) are superior to those reported in this study suggesting that swimming
at a self determined pace may not be providing a sufficiently high heart rate stimuli to the
cardiovascular system, therefore a volume overload was unlikely to have occurred. An increased
respiratory stress may be occurring during swimming as the horse is unable to develop an ideal
breathing pattern during swimming. The breathing rate in horses swimming has been shown to be
around 25-28 breaths/minute in comparison to racing at approximately 120 breaths /min. Further peak
expiratory pressure is higher during swimming (68-79 torr) compared to galloping (26-32 torr) (Jones
et al. 2002). Such a breathing effect, plus the increased pressure from the water, may create an
increased pressure overload. These pressure changes may have the potential to create an hypoxic
environment placing a respiratory stress on the horses. Hypoxia is known to be key stimuli for certain
physiological adaptations and it may be a player in stimulating adaptations to swim training.
In human studies training in a hypobaric chamber resulted in increases in citrate synthase activity and
increases in myoglobin concentrations (Terrados et al. 1990) and increases in muscle volume and
muscle fibre cross sectional area. Hypoxia has also been shown to stimulate changes in muscle mRNA
levels of proteins. Hypoxia-inducible factor (HIF-1) which is involved in oxygen sensing in skeletal
muscle is activated by hypoxia. Hoppeler & Vogt (2001) reported mRNA levels of HIF-1 increased
after hypoxic training and that these changes were irrespective of training intensity.
Cardiac function was evaluated in the horse in the early 1990’s using the quantitative two-dimensional
echocardiograph (Voros K 1997). Standardised techniques have now been established for
quantification of cardiac size and assessing flow (Long et al. 1992; Lord & Croft 1990; Reef 1991). In
more recent studies echocardiography has been used to examine the correlation between heart score
and maximal oxygen uptake (Young et al. 2002) and in examining cardiac dimensional changes during
deconditioning in horses (Kriz et al. 2000).
The cardiac dimensions measured in this study were within the reference ranges reported in the
literature. Previous research has reported cardiac dimensions for LVIDs of 7.35 ± 0.72, LVIDd of
11.90 ± 0.72, IVSs of 4,55 ± 0.66, IVSd of 3.02 ± 0.39 and FS of 38.76 ± 4.59 (Lescure et al. 1984;
Long et al. 1992; Patteson et al.1995).
In a study by Young, (1999) in which they examined cardiac changes in a group of seven two year old
Thoroughbreds after 18 weeks of training, they reported a significant reduction in %FS from 39 ± 9%
9
to 31 ± 3%, EF from 0.76 ± 0.08 to 0.67 ± 0.04 and LVIDd (cm) which increased from 11.38 ± 0.56 to
12.16 ± 0.70.
The percentage change in FS (8%) are double (4%) those reported in the present study in which the
mean %FS for the two groups was decreased from 37 ± 4.21 to 34.6 ± 4.84 and from 37.9 ± 2.72 to
35.7 ± 1.56 in groups A and B respectively. Changes in both %FS and LVIDs, however, were not
significant.
Training has been shown to increase aerobic performance. The traditional marker of changes in
performance capacity with training has been VO2max. As we were unable to measure VO2max a
traditional marker of skeletal muscle efficiency, whole blood lactate concentrations were measured
during a standardized treadmill performance test. The measurement of whole blood lactate
concentrations post exercise have been used to measure fitness in Thoroughbred horses both on the
track and treadmill (Miller & Lawrence (1987) . A decrease in heart rate at a specific sub-maximal
work load following conditioning is also a typical response reported in the literature (Miller &
Lawrence 1987; Evans 1994). The decreased lactate concentrations reported in both training groups in
this study is consistent with the training effects reported in the literature (Miller & Lawrence 1987).
The accumulation of lactate in the blood reflects a difference between production and removal. There
is debate as to which of these factors is affected most by training, however, it is most likely a balance
of the two. In the present study both training programs provided improvements in metabolic efficiency
as determined by the reduced lactate concentrations during the final work load of the three stage
performance test, with the decrease being greater for the swim group, however, the differences were
not significant.
For the heart rate analysis the results were contrary to the literature. At the final stage of the treadmill
test mean heart rates was higher post than pre testing. These higher mean heart rates were a result of
increased heart rates occurring in five of the seven two year olds. This change may be associated with
the fact that the horses were experiencing shin soreness during the final week of the program.
Previous research on swimming training in horses has examined the effects of swimming for 900m
lasting approximately four minutes with three minutes rest between each swim on physiological
responses as heart rates during the swim and lactate immediately post swim. Peak heart rates during
the periods of four minutes swimming (900 m) averaged 189 (b.p.m.) with mean lactate concentrations
of 5.3 mmol/L after swim one 190 (b.p.m.) and lactate of 5.6 mmol/L after swim two. For a continuous
swim of 1200m at a lower speed, heart rate ranged form 144-183 (b.p.m.) and lactate of 2.5 to 5.6
mmol/L (Asheim et al. 1970).
As heart rate in the present study was only measured immediately post swimming, a comparison with
the literature is difficult. Treadmill studies have shown HR can be returned to 110 (b.p.m.) within one
minute post exercise (Foreman et al. 1990). Therefore it is very difficult to extrapolate to the heart rate
during swimming from post exercise responses. However whole blood lactate concentration is known
to peak within five minutes post exercise therefore lactate is a good representation of metabolic stress
and enables comparative analysis with other studies. The range of lactate concentrations of one to 2.6
mmol/L are low relative to the values reported by Asheim et al. (1970) indicating that horses allowed
to swim at their own pace are not producing a large metabolic stress.
In considering the general guidelines for humans to obtain a training effect it outlines that there needs
to be an overload on the cardiovascular system for an adaptation to occur. The literature describes an
intensity of between 50 to 85% VO2max depending on the fitness levels of the individuals (Powers and
Howley 2002) or a target heart rate range of 60 to 80% of heart rate reserve (HRR). The Karvonen
formula is used to calculate training zones based on calculated HRR. If exercising at 60% of HRR then
(0.6 x maximum HR minus resting HR) + resting HR.
The application of this concept to a horse with a VO2 max of 150 ml/kg/minute and max heart rate of
240 (b.p.m.) will provide a heart rate training zone of 150 to 200 (b.p.m.). In comparison to the present
10
study the mean heart rate of 109 (b.p.m.) is well short of the minimum heart rate for obtaining
cardiovascular training stimuli.
The aim of this study was to determine if traditional swimming training, as used by trainers, in which
horses are allowed to swim at their own pace for a designated distance or time period, had a sufficient
stimuli on cardiac muscle or muscle metabolism to stimulate an adaptation.
The results have shown that allowing horses to swim at their own pace for up to six to eight minutes
appears to have little additional impact on cardiac dimensional changes than that attained from
conventional training.
Implications for Industry
One of the goals of the horse program is to ensure the animal safety in relation to health and welfare,
with an objective of reducing the injury and breakdown rates for horses in training. This study
addressed part of this in providing an insight into cardiac adaptations with swimming in relation to the
effectivness of swimming as a stimuli for adaptation. With this understanding trainers may be able to
structure swimming programs to be a more effective component for stimulating training adaptations.
An understanding of this will now assist the trainer in training program design by providing a better
understanding of the intensity of swimming to provide fitness benefits.
Recommendations
This study was unique in that it was the first to investigate the effects of traditional swimming training
in Thoroughbred horses on training responses as cardiac dimensional changes and general fitness
measures. The study examined swimming, at a self determined intensity, that is commonly utilized in
the industry, to examine if this intensity was sufficient to stimulate changes in the cardiovascular
system. The study reported that swimming at a self determined intensity, five days per week, was not
sufficient to provide an additional stimullii above that experienced by normal training, to induce
further adaptations in the cardiovascular system. In relation to obtaining the maximum fitness value
from swimming, trainers need to consider the intensity and duration they swim horses. Therefore it
seems that a program that involves higher intensity work periods over short periods may be more
benifical for obtaining improvements in fitness.
Future Research
The information provided by this study has set the foundation, by the use of a tethered swimming pool,
to examine firstly the degree of hypoxia and secondly the degree of muscle metabolic enzyme changes
occurring during swimming at different intensities.
11
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15
The Effect of Swimming Training on the Cardiac
Dimensions in Thoroughbred Horses
RIRDC Publication No. 08/156
RIRDC Publication No. INSERT PUB NO. HERE
Swimming historically has been used in both humans and
horses as a means of stimulating adaptations with the goal
of improving fitness. In the human area the benefits of swim
training have long been known. However for the horse actual
benefits obtained have not been established. As the horse
is predominantly an aerobic athlete and one of the major
components of aerobic performance is cardiac function, this
study investigated whether traditional pool swimming would
provide a sufficient stimulus to the heart, in addition to that
experienced by normal race training, resulting in a structural
adaptation to the cardiac muscle.
This study examined swimming training in relation to its
impact on structural development of the heart.
This publication can be viewed at our website—
www.rirdc.gov.au. All RIRDC books can be
purchased from:.
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Cover photos: Courtesy The Canberra Racing Club
If cardiac adaptations are occurring with swimming, this
understanding of the potential benefits will assist horse trainers
in being able to more fully structure training programs to
maximise the benefits obtained with the potential of reducing
training based injuries.
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