Title Page

Correlations and Analysis of Kinematic and Physiological Kinetic Data During Repeated High-Intensity
Contemporary Dance Bouts

By

Michael Doolan

Submitted to the Department of Dance Science Trinity Laban Conservatoire of Music and Dance

In partial fulfilment of the requirements for the degree of

Master of Fine Arts in Dance Science

September 2021

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 Abstract

The development of fatigue causes metabolic and biomechanical efficiency to be negatively

affected. Dancers are frequently required to perform at high intensities often without sufficient
physiological preparation. This study aimed to analyse and correlate physiological and kinematic
variables during high intensity dance bouts. Participants (n=4) completed two sessions, consisting of
four, four-minute, high-intensity dance bouts with an equal work to rest ratio while wearing three
accelerometers at specific locations on the body: above the sacrum at L5, the midpoint between the
lateral epicondyle and the lateral styloid process on the right arm, and the midpoint between head
of the fibula and the lateral malleolus on the right leg. By modelling the kinetics of the heart rate
(HR) and oxygen uptake (V̇ O2), the change in relative energy demand in each bout could be assessed.
Perceptual responses to each bout were also recorded to assess the change in effort within each
session. The changes in cardiopulmonary function were correlated with the change in the kinematic
variable jerk recorded by the accelerometers. Results of the paired t-tests showed that participants’
HR responses significantly increased in all trials (p < 0.01) while the V̇ O2 response only increased
significantly in the first two trials (p < 0.05). The kinematic data showed consistent increases within
trials but only reached significance in two out of twelve measurements. Neither HR nor V̇ O2
significantly correlated with the changes in jerk within trials. Due to the small sample size, and
erratic nature of the jerk responses, individual physiological data from two participants were
presented and observationally discussed to explore the results further. The findings of this study
highlight the varied physiological responses dancers can have to the same choreographic stimulus
and demonstrate the effects fatigue has on the cost and quality of performance. Further research
into dance-specific methods of cardiorespiratory training are discussed in conjunction with the
potential of wearable technology for use in the field.

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 Acknowledgements

The past two years have presented many challenges and surprises and I ask that the future
holds many more. Though, I wish it to be brighter than it has been.

I’m extremely grateful to my supervisors, Emma Redding, and James Brouner for keeping me
on track throughout this thesis. I would not have had the courage to dive as deep without your
support, advice and reason. Many thanks to Scott for your assistance and giving the time to discuss
things. I’m also grateful to Catherine for all the tech support you gave on this project, it was really
invaluable.

A holla at my COVID-housemates, Kylo, Ana and Santiago. We made a bad time more
beautiful. Also, a big shout out to my cohort, especially Amelia, Victoria, and Kendall. Vic, thank you
for providing the illustrations you are a super-talented human!

Lauren, thank you for being my light at the end of the tunnel.

A huge thank you to my Mum for sharing with me the gift of music and dance, I would not
be here without you. Finally, cheers to my old man who was always there when others weren’t. I
love you both dearly and wish you both a long, content retirement together.

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 Tables of Contents

Title Page...........................................................................................................................................1
Abstract.............................................................................................................................................2
Acknowledgements...........................................................................................................................3
List of Figures.....................................................................................................................................7
List of Tables......................................................................................................................................9
List of Abbreviations........................................................................................................................11
Chapter 1: Introduction and Literature Review.................................................................................12
Introduction.....................................................................................................................................12
Energy Systems................................................................................................................................13
Cardiovascular Response to Exercise and the V̇ O2 Max...................................................................14
Skeletal Muscle Fibre Types.............................................................................................................15
Metabolic Threshold Concepts and Modelling of Oxygen Kinetics..................................................15
The V̇ O2 Slow Component................................................................................................................18
The V̇ O2 Slow Component and Non-Linear activity..........................................................................19
Cardiovascular Drift.........................................................................................................................20
Peripheral and Central Fatigue........................................................................................................21
Recovery..........................................................................................................................................22
Demands of Contemporary Dance..................................................................................................23
The Effects of Fatigue in Dance........................................................................................................25
Kinematic Analysis and Fatigue Detection.......................................................................................26
Study Objectives..............................................................................................................................27
Experimental Hypotheses............................................................................................................27
Null Hypotheses...........................................................................................................................27
Chapter 2: Methods............................................................................................................................28
Participants......................................................................................................................................28
Exclusion Criteria.........................................................................................................................28
Preparation and Pilot Phases...........................................................................................................28
Preparation..................................................................................................................................28
Pilot..............................................................................................................................................28
Testing Protocols.............................................................................................................................29
Adapted DAFT (ADAFT)................................................................................................................29
Treadmill Test..............................................................................................................................29
Experimental Design........................................................................................................................30

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 Pre-test............................................................................................................................................33
Familiarisation Session................................................................................................................33
Calibration...................................................................................................................................33
Control Parameters and Procedures................................................................................................33
Metabolic.....................................................................................................................................33
ADAFT Choreography...................................................................................................................34
Inertial Measurement Units.........................................................................................................34
Data Collection................................................................................................................................34
Ethical Considerations.....................................................................................................................34
Data analysis....................................................................................................................................35
Oxygen Data Smoothing and Modelling..........................................................................................35
Treadmill Test..............................................................................................................................35
ADAFT Test..................................................................................................................................35
Heart Rate Data Smoothing and Modelling.....................................................................................38
Treadmill Test..............................................................................................................................38
ADAFT Test..................................................................................................................................38
RPE...................................................................................................................................................38
Accelerometer Data Smoothing and Jerk Calculation......................................................................38
Group Statistical Analysis.................................................................................................................39
Chapter 3: Group Results....................................................................................................................40
Participants Cardiorespiratory Profile..............................................................................................40
T-tests..............................................................................................................................................40
Correlations.....................................................................................................................................45
Chapter 4: Individual Physiological Results........................................................................................48
Participant One................................................................................................................................48
Participant Two................................................................................................................................52
Chapter 5: Discussion..........................................................................................................................56
Group Discussion.............................................................................................................................56
Primary Aim.................................................................................................................................56
Secondary Aim.............................................................................................................................59
Tertiary Aim.................................................................................................................................60
Individual Data Discussion...............................................................................................................61
Impact for Dance and Future Research...........................................................................................62
Limitations.......................................................................................................................................66
Conclusion.......................................................................................................................................66
References..........................................................................................................................................67

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Appendices..........................................................................................................................................86
Appendix 1.......................................................................................................................................86
Appendix 2.......................................................................................................................................87
Appendix 3.......................................................................................................................................88
Appendix 4.......................................................................................................................................89
Appendix 5.......................................................................................................................................90
Appendix 6.......................................................................................................................................93
Appendix 7.......................................................................................................................................94
Appendix 8.......................................................................................................................................95
Appendix 9.......................................................................................................................................96
Appendix 10.....................................................................................................................................97
Appendix 11.....................................................................................................................................98
Appendix 12.....................................................................................................................................99
Appendix 13...................................................................................................................................100
Appendix 14...................................................................................................................................103
Appendix 15...................................................................................................................................106

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 List of Figures

Figure 1. 1. Phases of pulmonary response to exercise in the moderate domain...............................16

Figure 1. 2. Pulmonary response to constant work rate exercise in the moderate, heavy, severe, and
extreme domains.................................................................................................................................18

Figure 2. 1. Representation of work and rest intervals in one session................................................30

Figure 2. 2. Illustration of the placement of the gas analyser and mask, heart rate monitor and IMU’s.
.............................................................................................................................................................31

Figure 2. 3. Representation of time periods for the jerk time point one (TP1) and time point two
(TP2) measurements during ADAFT trial.............................................................................................32

Figure 2. 4. Representation of V̇ O2 and HR time point one (TP1) and time point one (TP2)
measurements during ADAFT trial.......................................................................................................37

Figure 3. 1. Combined V̇ O2 values at TP1 and TP2 from both sessions................................................41

Figure 3. 2. Combined HR values at TP1 and TP2 from both sessions..................................................42

Figure 3. 3. Combined jARM values at TP1 and TP2 from both sessions.................................................43

Figure 3. 4. Combined jLEG values at TP1 and TP2 from both sessions..................................................44

Figure 3. 5. Combined jCOM values at TP1 and TP2 from both sessions.................................................45

Figure 4. 1. P01 Session one V̇ O2 with anaerobic thresholds and V̇ O2 peak.……………………………………49

Figure 4. 2. P01 Session one heart rate with heart rate peak..............................................................50

Figure 4. 3. P01 Session two V̇ O2 with anaerobic thresholds and V̇ O2 peak.........................................51

Figure 4. 4. P01 Session two heart rate with heart rate peak..............................................................52

Figure 4. 5. P02 Session one V̇ O2 with anaerobic thresholds and V̇ O2 peak.........................................53

Figure 4. 6. P02 Session one heart rate with heart rate peak..............................................................54

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Figure 4. 7. P02 Session two V̇ O2 with anaerobic thresholds and V̇ O2 peak........................................55

Figure 4. 8. P02 Session two heart rate with heart rate peak..............................................................55

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 List of Tables

Table 1. 1. Muscle fibre type classifications and properties................................................................15

Table 2. 1. Outline of jerk TP1 and TP2 measurements in a whole session.........................................32

Table 2. 2. Time points corresponding to the O2 and HR measurements in each trial.........................37

Table 3. 1. Cardiorespiratory profile of participants............................................................................40

Table 3. 2. Paired t-test results on V̇ O2 of TP1 and TP2 for each trial..................................................40

Table 3. 3. Paired t-test results on HR TP1 and TP2 for each trial........................................................41

Table 3. 4. Mean rating of perceived exertion for all trials displaying a gradual increase...................42

Table 3. 5. Paired t-test results on jARM of TP1 and TP2 for each trial...................................................42

Table 3. 6. Paired t-test results on jLEG of TP1 and TP2 for each trial....................................................43

Table 3. 7. Paired t-test results on jCOM of TP1 and TP2 for each trial..................................................44

Table 3. 8. Pearson’s product-moment correlation coefficient between ΔΟ2 and ΔARM in the same trial.
.............................................................................................................................................................45

Table 3. 9. Pearson’s product-moment correlation coefficient between ΔΟ2 and ΔLEG in the same trial.
.............................................................................................................................................................46

Table 3. 10. Pearson’s product-moment correlation coefficient between ΔΟ2 and ΔCOM in the same
trial......................................................................................................................................................46

Table 3. 11. Pearson’s product-moment correlation coefficient between ΔHR and ΔARM in the same
trial......................................................................................................................................................47

Table 3. 12. Pearson’s product-moment correlation coefficient between ΔHR and ΔLEG in the same trial.
.............................................................................................................................................................47

Table 3. 13. Pearson’s product-moment correlation coefficient between ΔHR and ΔCOM in the same
trial......................................................................................................................................................47

Table 4. 1. Time periods corresponding to the mean HR and V̇ O2 baseline calculations.....................48

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Table 4. 2. P01 anaerobic thresholds and V̇ O2 peak............................................................................48

Table 4. 3. P01 session one V̇ O2 linear regression calculations with peak and mean respiratory
exchange ratio.....................................................................................................................................49

Table 4. 4. P01 session one RPE scores................................................................................................49

Table 4. 5. P01 Heart rate peak value from treadmill test...................................................................49

Table 4. 6. P01 Session one heart rate linear regression calculations.................................................50

Table 4. 7. P01 session two V̇ O2 linear regression calculations with peak and mean respiratory
exchange ratio.....................................................................................................................................50

Table 4. 8. P01 session two RPE scores................................................................................................51

Table 4. 9. P01 Session two heart rate linear regression calculations.................................................51

Table 4. 10. P02 anaerobic thresholds and V̇ O2 peak..........................................................................52

Table 4. 11. P02 session one V̇ O2 linear regression calculations with peak and mean respiratory
exchange ratio.....................................................................................................................................52

Table 4. 12. P02 session one RPE scores..............................................................................................52

Table 4. 13. P02 Heart rate peak value from treadmill test.................................................................53

Table 4. 14. P02 Session one heart rate linear regression calculations...............................................53

Table 4. 15. P02 session two V̇ O2 linear regression calculations with peak and mean respiratory
exchange ratio.....................................................................................................................................54

Table 4. 16. P02 session two RPE scores..............................................................................................54

Table 4. 17. P02 Session two heart rate linear regression calculations...............................................55

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 List of Abbreviations

3D Three dimensional IMU Inertial Measurement Unit

ADAFT Adapted dance aerobic fitness test J Jerk

ADP Adenosine diphosphate K+ Potassium

AMP Adenosine monophosphate L Lactate

AT Anaerobic threshold LIHIIT Long intensity high intensity interval training

ATP Adenosine triphosphate LT Lactate threshold

BPM Beats per minute MEMS Micro-Electromechanical system

Ca2 Calcium Na+ Sodium

CNS Central nervous system NADH Nicotinamide adenine dinucleotide

CO Cardiac output O2 Oxygen

CO2 Carbon dioxide PCr Phosphocreatine

COM Centre of mass Pi Inorganic phosphate

CP Critical power RER Respiratory exchange ratio

DAFT Dance aerobic fitness test RMS Root mean square

EMG Electromyography RPE Rating of perceived exertion

FADH Hydrogenated flavin adenine dinucleotide SSC Stretch shortening cycle

FMS Functional movement screen SV Stroke volume

GET Gas exchange threshold TP1 Time point one

GPS Global positioning system TP2 Time point two

H Hydrogen V̇ O2sc Slow component of oxygen uptake

HIDPFT High intensity dance performance fitness test VT Ventilatory threshold

HIIT High intensity interval training W’ W prime

HR Heart rate ΔHR Rate of change in heart rate

HRsc Heart rate drift ΔV̇ O2 Rate of change in oxygen uptake

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 Chapter 1: Introduction and Literature Review

Introduction

Dance practice is largely based on tradition and sports/dance medicine and science is not
widely or consistently applied in dance training (Redding, 2009; Rafferty, 2010). Only two Elite
classical dance institutions in the United Kingdom have recently incorporated multi-disciplinary
healthcare teams into their organisations (Redding, 2019). However, it is still not commonplace
which may be in part due to the disproportional split in arts funding that is typically seen between
classical and contemporary works and organisations (Harvie, 2013). Supporting medical staff within
the vast majority of arts organisations and institutions are either limited or non-existent with many
health professionals lacking the knowledge to deal with this unique population (Dick et al., 2013).
Dancers are now seen as artistic-athletes yet injury rates are extremely high in dance with fatigue
and overtraining are thought to be key factors (Liederbach et al., 2013; Redding, 2019). Therefore,
methods of monitoring dancers’ fatigue in the field would be beneficial to investigate.

At present in sports, many athletes are regularly monitored during training and competition
(Laursen & Buchheit, 2019). External workload can be recorded with wearable devices such as heart
rate (HR) monitors, accelerometers and global positioning systems (GPS) while internal bodily
responses can be ascertained from perceptual ratings such as rating of perceived exertion scales
(RPE) or physiological markers such as blood lactate (Fox et al., 2017; Gómez-Carmona et al., 2020).
In the case of RPE, this subjective measure is prone to variation (Chen et al., 2002) and physiological
markers such as blood lactate are invasive meaning their use in the field is limited. However, the
technological development of MEMS (micro-electromechanical systems) devices mean that in many
cases, these non-invasive devices giving objective data can be used on a daily basis in-the-field and
during performance (Camomilla et al., 2018). Using these measures, coaches can make real time,
informed decisions on each athlete regarding their training load or team selection (Gómez-Carmona
et al., 2020).

Twenty first century ‘contemporary’ dance is constantly expanding and changing, with
increased exposure through mainstream and social media accelerating the process (Kwan, 2017;
Wyon et al., 2018). The physiological demands of team sports such as football have increased since
the late 20th century (Drust & Green, 2013) and it seems logical to consider the demands of dance to
be following a similar trend (Rafferty, 2010). Consequently, it is of importance to investigate current
methods of monitoring in relation to biomechanical and physiological variables with contemporary
dancers. In this thesis, the relationship between movement smoothness and internal and perceptual
physiological indices will be explored using telemetric and MEMS technology during high intensity
dance activity. However, before defining the demands of contemporary dance and introducing the
measurements used, it is necessary to explore the physiological mechanisms and systems that
operate in healthy, human movement.

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Energy Systems

For the body to move it performs mechanical work through muscular contraction to displace
its mass through space (Ferretti, 2015). Once and action potential is triggered at the neuromuscular
junction, it rapidly spreads across the plasma membrane (Davis et al., 2019). This change in voltage
causes calcium to be released from the sarcoplasmic reticulum initiating contraction (Davis et al.,
2019). The energy needed for muscular contraction is produced from the high-energy molecule
adenosine triphosphate (ATP) during ATP hydrolysis (McArdle et al., 2015). Myosin proteins bind ATP
and actin proteins resulting in adenosine diphosphate, inorganic phosphate (Pi) and energy (Davis et
al., 2019). ATP is stored in the muscle in limited supply (McArdle et al., 2015). Therefore, to maintain
the work ATP must be continuously synthesized or resynthesized in the working muscle.

Current understanding dictates that there are three main energy systems in the body
contribute to the supply – demand of ATP:

(i) The anaerobic ATP-PCr (Adenosine Triphosphate-Phosphocreatine) system

(ii) The anaerobic lactic/glycolytic system

(iii) The aerobic system (Ferretti, 2015 p. 13)

The ATP-PCr system is responsible for immediate energy at the onset of exercise (McArdle et
al., 2015). It uses the high energy bonds from the phosphate molecules in both ATP and PCr to
produce energy. PCr also provides a mechanism for the resynthesis of ATP from ADP (adenosine
diphosphate) or AMP (adenosine monophosphate) catalysed by creatine kinase and is considered a
‘reservoir’ of high energy phosphate bonds (McArdle et al., 2015). While muscle PCr stores are
greater than those of ATP, both are limited and this system has a capacity between 8-10 seconds
(Wyon, 2009). The use of the anaerobic lactic/glycolytic system demarcates a shift in metabolic
function but can also indicate a lack of oxygen supply or the depletion of the ATP-PCr system
(Janssen., 2001; Wyon., 2009). This occurs during ADP phosphorylation where muscle glycogen is
broken down in the cytosol in rapid anaerobic glycolysis (McArdle et al., 2015). Anaerobic glycolysis
involves a series of reactions that enable the catabolism of glucose to produce pyruvate where two
ATP molecules are synthesised releasing hydrogen (H) and NADH (nicotinamide adenine
dinucleotide) (McArdle et al., 2015). Lactate formation occurs in this instance where non-oxidized H
atoms combine with pyruvate, catalysed by lactate dehydrogenase (McArdle et al., 2015). Lactate
accumulation is dependent on the rate of production to rate of clearance ratio (McArdle et al., 2015)
of which the physiological determinants will be discussed later in more detail. Finally, the aerobic
system oxidizes glucose, glycogen, or triacylglycerol. Glycolysis, in aerobic conditions, occurs in the
mitochondria and converts pyruvate into acetyl-CoA where it enters the citric acid cycle (McArdle et
al., 2015). This process releases H, which is removed through carbon dioxide (CO 2) transport,
simultaneously resynthesizing ATP (McArdle et al., 2015). H released in anaerobic processes enter
the electron transport chain, transported via NADH and FADH 2 (Flavin Adenine Dinucleotide)
(McArdle et al., 2015). Through the process of oxidative phosphorylation, ATP is synthesised in
oxidation-reduction reactions (Spinelli & Haigis, 2018).

Through these metabolic processes the chemically bound energy is converted into
mechanical work and heat (Latash & Zatsiorsky, 2016). The most efficient system is the oxidative

13
system which provides a much larger ATP yield and therefore has a greater capacity to sustain
muscular contraction (Wasserman et al., 2012). Physical activity always utilises a combination of the
three systems and the modality, work rate, intensity, and duration of the activity determines the
magnitude of each energy system used (Wyon, 2009). To examine the ramifications of this more
closely in dance, it is necessary to understand the mechanisms underlying the energy systems in the
human body.

Cardiovascular Response to Exercise and the V̇O2 Max

The rise in ATP demand during exercise means oxygen delivery to the muscle cells is a
primary factor in the response and tolerance to physical activity (Poole & Jones, 2012). “The
cardiovascular system provides an integrative response to any increase in energy expenditure and
rapid adjustments in blood flow that impact the entire cardiovascular system are made” (McArdle et
al., 2015 p. 335). Initially, energy demands within the muscle cells increase but there is a delay in the
required blood supply while cardiac output (CO) (heart rate (HR) and stroke volume (SV) where: CO =
HR x SV) increases to meet the demand, and blood flow is optimised (McArdle et al., 2015). The
increase in heart rate and stroke volume is driven initially by parasympathetic withdrawal while
vascular control is largely sympathetically mediated (Fisher et al., 2015). Vasodilation in the local
arterioles, relative to the working muscles, is coupled with visceral vasoconstriction that diverts a
large flow of blood into the central circulation (McArdle et al., 2015). Reflexes such as the pressor
reflex, baroreflex and metaboreflex respond to afferents from receptors in skeletal and visceral
muscle and their vasculature (Fisher et al., 2015). Regulated in the ventrolateral medulla, with input
from higher brain areas (ie. motor cortex), these afferents are crucial in the adjustment of the
cardiovascular system at rest, and in the transition to and during exercise (McArdle et al., 2015).
Ventilatory drive increases, oxygen consumption rises exponentially towards the rate of ATP
production within the working muscle and carbon dioxide (CO 2) produced through anaerobic
processes is removed (Behnke et al., 2005). The point at which V̇ CO2 equals V̇ O2 is known as the gas
exchange threshold (GET) and marks a transition in the V̇ CO2 - V̇ O2 relationship in the venous blood
returning to the lungs (Pettitt et al., 2013). At rest, 75% of the blood’s oxygen load remains bound to
the haemoglobin and acts as an oxygen reserve (McArdle et al., 2015). During maximal exercise
however, the amount of oxygen utilised from the haemoglobin can increase more than three times
its resting rate and the blood flow in the muscle tissue up to 10 times that of resting levels (McArdle
et al., 2015).

Oxygen utilisation in the muscle is thought to be a key limiting factor in the rate at which
ATP can be synthesised through oxidative pathways (Poole & Jones, 2012). However, it has also been
shown to depend on the exercise modality (isolated or whole-body) and cardiovascular oxygen
transport (Feretti, 2015). Individual muscle cells’ ability to generate energy aerobically depends on
factors such as the size and number of mitochondria available and oxidative enzyme activity
(McArdle, et al., 2015). The V̇ O2 max therefore, represents the maximal rate at which ATP can be
synthesised aerobically (Wasserman et al., 2012). Graded exercise tests can be used to determine an
individual’s V̇ O2 max where O2 consumption plateaus despite an increase in workload and exercise
tolerance becomes extremely limited (Wasserman et al., 2012). The V̇ O2 max achieved will always
depend upon both O2 delivery and peripheral O2 extraction (which is determined by the O2 diffusing
capacity of the active muscle), and the limiting factor in the pathway of oxygen conductance from
the mouth to the mitochondrion will depend also on the exercise mode (i.e., engagement of small vs

14
large muscle mass) (Poole & Jones, 2005 p. 14). Skeletal muscles however are a mosaic of different
fibres that have differing metabolic properties in relation to the energy production.

Skeletal Muscle Fibre Types

According to current theory, skeletal muscle contains at least four distinct fibre types that
differ in the primary mechanisms they use to produce ATP and the type of motor neuron innervation
that precedes contraction (McArdle et al., 2015). The distribution of an individual’s fibre type profile
is primarily dependant on genetic factors and age (McArdle et al., 2015). However, there is a certain
homogeneity regarding the location of certain fibre types in humans (ECSS.tv, 2016). For example,
the lower limbs have a higher proportion of type-I fibres comparatively to the upper limbs
(Schneider et al., 2002). Fibre type composition amongst athletes has been shown to align with the
demands of the sport due to either training or genetics (McArdle et al., 2015). For example, an
endurance athlete will have a high percentage of type-I fibres in the vastus lateralis (>90%)
compared to a sprinter (23-30%) or an untrained person (~50%) (Wasserman et al., 2012). There are
no studies that have specifically analysed fibre type in contemporary dancers but ballet dancers have
been shown to have a high percentage (~64%) of type-I fibres in the lower limbs (Dahlstrom et al.,
1997). The complexities of muscle phenotype and its relation to contemporary dance is beyond the
scope of this study. However, an outline of the different fibre types and their metabolic and
functional properties that will be discussed in relation to the major topics of this thesis can be found
in Table 1. 1.

Table 1. 1. Muscle fibre type classifications and properties (From McArdle et al., 2015 p. 378)

Metabolic Threshold Concepts and Modelling of Oxygen Kinetics

Oxygen kinetics in steady state exercise can been described with a three-phase model
(Figure 1. 1). As discussed previously, at the onset of exercise there is an increase in neural drive that
stimulates respiration and heart rate (McArdle et al., 2015). This initial exponential stage is known as

15
phase-I or the cardiodynamic phase and lasts for roughly 15 seconds (Wasserman et al., 2012).
Phase-II, or the primary phase where the curve begins to approach its nadir, has been shown to
reflect 85% of the oxygen utilisation in the muscle cells and lasts up to three minutes (Wasserman et
al., 2012). The speed of this phase is related to the training status of the person in general and in the
selected modality (Jones & Poole, 2005a). It is also affected by factors such as muscle fibre type and
the position of the heart in relation to the working muscle (Poole & Jones, 2012). Faster phase-II
kinetics are associated with a lower O2 deficit and intracellular perturbation such as acidosis and
increased Pi (Jones & Poole, 2005). In steady state activity, the phase-III component is dependent on
the metabolic pathways utilised and can reach an immediate or delayed steady state or will continue
to rise to the individuals V̇ O2 max where fatigue ensues (Wasserman et al., 2012).

Current understanding defines exercise intensity in relation to physiological thresholds that

relate to the pathways of ATP resynthesis, metabolite accumulation, and depletion rate of energy
stores such as ATP, PCr and glycogen (Poole & Jones., 2012; Wyon., 2009). Research has indicated
the gas exchange threshold (GET) and the critical power (CP) are the most important thresholds in
determining exercise tolerance in endurance activity (Poole et al., 2016). Different physiological
behaviour characterises each intensity (Jones & Poole, 2005b). The intensity of an activity for an
individual is influenced by factors such as their physical condition and skill level in that modality
making it highly variable (McArdle et al., 2015).

Figure 1. 1. Phases of pulmonary response to exercise in the moderate domain from Jones and
Poole, 2005 p. 17.

Steady state exercise below the GET is deemed ‘moderate’ exercise where the dominant
pathway is the aerobic metabolism and there is a negligible amount of metabolite build up and the
rate of lactate clearance matches the rate of production (Whipp, 1996). Moderate exercise can be
sustained for long periods, due to the metabolic efficiency of oxidative pathways, such that
endurance athletes like runners and cyclists will have a high threshold in relation to their overall
capacity (≥80%) (Jones & Poole, 2005a). The pulmonary response to moderate exercise can be

16
described with a mono-exponential function model where a steady state is achieved in the phase-III
component (Figures 1. 1 & 1. 2).

Above the lactate threshold indicates ‘heavy’ exercise where muscle and blood lactate rise
above basal levels through use of anaerobic glycolytic pathways (Jones & Poole, 2005). This domain
is situated between the GET and the critical power where V̇ O2 and lactate illicit delayed and elevated
steady state responses (Poole et al., 2016). During a graded exercise test, the GET can be determined
by plotting the V̇ O2/time response and identifying the first rise in V̇ O2 without a concomitant rise in
V̇ CO2 (Wasserman et al., 2012). The kinetics of oxygen uptake in this domain can be modelled with a
bi-exponential function where the phase three component has a steady increase, termed the V̇ O2
slow component (V̇ O2sc), until steady-state is achieved (Figure 1.1) (Jones & Burnley, 2009). This rise
in V̇ O2 is usually seen ~ 120 – 180 seconds after the onset of exercise (Poole & Jones, 2012). The
critical power concept therefore represents the highest intensity possible where metabolic
homeostasis is attainable (Poole et al., 2016). This has distinct implications for individual exercise
tolerance therefore work in this domain can be sustained but is limited to <20-30 minutes (Jones et
al., 2011).

According to Poole and Jones (2005), work >CP can be divided into the ‘severe’ and
‘extreme’ domains where the work rate either coincides with or exceeds V̇ O2 max, respectively.
These domains have been studied less than the lower domains due to the complex analysis and
intense work rate for the athlete. Though, they cover a huge range of work rates ranging from power
outputs corresponding to sub-maximal and supra-maximal efforts (Figure 1.1) (Balci et al., 2020).
Like the heavy and moderate domains, these intensities have been modelled with exponential
functions (Jones & Poole, 2005b). However, Balci and colleagues’ (2020) research suggested that
there are different response characteristics in the lower limits of the extreme domain (~98% V̇ O2
max). Certainly, there is more to learn regarding the nuances of the anaerobic intensity domains but
above a certain threshold, proton accumulation has reached a level that causes hyperventilation and
V̇ CO2 expiration to surpass V̇ O2 (Wasserman et al., 2012).

In a meta-analysis by Galán-Rioja and colleagues (2020), metabolic thresholds such as the

maximal lactate steady state (MLSS), the second ventilatory threshold (VT 2) and the respiratory
compensation point (RCP), often considered synonymous with the CP, were compared. It was found
that CP denotes the heavy-severe exercise intensity transition with relatively little error, while MLSS
to underestimated CP ~ 11% and RCP and VT 2 overestimated CP by 6 and 21%, respectively. Still,
these measures represent an upper limit in constant work rate exercise tolerance. The CP is
considered the ‘gold standard’ however (Jones et al., 2019), where rates exceeding the CP are time
bound by the W’ concept (Poole et al., 2016). The W’ represents the curvature constant of the
hyperbolic curve corresponding to an individual’s CP profile with exhaustion occurring when W’ is
depleted (Craig et al., 2019). Methods for ascertaining the CP and calculating the W’ can taxing for
participants, even for well-trained endurance athletes (All-Out Physiology, 2021).

Unsurprisingly, there are no dance studies that have used the CP, W’ concept or modelled
the kinetics of pulmonary response to dance activity. This could largely be since it would be difficult
to accurately measure as they require a constant power output or work rate (Beck et al., 2018).
However, in previous dance studies, graded treadmill tests have been used to determine the GET
(Beck et al., 2018) and VT1 and VT2 (Rodrigues-Krause et al., 2014) in contemporary and ballet
dancers, respectively and used these values to indicate the relative intensity of dance activity. Beck
and colleagues (2015) state the importance of relating dance activity to metabolic thresholds due to
the complex interplay between aerobic and anaerobic systems. The relative intensity of an activity is

17
dependent on many factors that relate to efficiency and will be discussed in more detail throughout
this thesis. Dance requires sub-maximal, maximal and supra-maximal levels of exertion (Guidetti et
al., 2007; Needham-Beck et al., 2019; Redding et al., 2009). Therefore, it is important to further
explore the mechanisms that govern the changes in energy production and muscular function during
work >GET.

Figure 1. 2. Pulmonary response to constant work rate exercise in the moderate (60% and 90% of
GET), heavy (40% Delta), severe (100% and 80% Delta) and extreme (120%) domains. Delta = %
between GET and V̇ O2max. (from Jones and Poole, 2005 p. 18).

The V̇O2 Slow Component

As discussed, the on-transient kinetics of the V̇ O2 response to steady-state exercise >GET

elicits a gradual increase in oxygen consumption deemed the V̇ O2sc. The mechanistic bases for the
V̇ O2sc is still a subject of debate to the present day (Colosio et al., 2020). Traditionally, the V̇ O2sc has
been associated with a loss of efficiency in the working muscle and the fatigue process (Jones &
Burnley, 2009). This loss of efficiency was initially thought to be associated with an increase in
recruitment of type-II muscle fibres to meet the energetic demands and rate of the work being done
(Jones & Poole, 2005b). A larger V̇ O2sc had also been shown to positively correlate with a larger
percentage of type-II fibres in the contracting muscle and are also related to slower primary kinetics
(Barstow et al., 1996). However, Vanhatalo and colleagues (2010) showed that a V̇ O2sc was present in
all-out and constant rate cycling work bouts >CP despite decreasing electromyographic values in the
all-out test. Their conclusions were that the fatigued type-II muscle fibres efficiency is severely
impaired relative to their power output which is either diminished or energetically expensive. These
fibres still consume oxygen for Ca2+ and Na+/K+ pump activities and in the case of a constant work
rate, more muscle fibres would have to be recruited to maintain the work rate (Zoladz et al., 2008).
Grassi and colleagues (2015) proposed that the shortening velocity/efficiency and force/efficiency
relationships of type-I and type-II fibres mean that as peak force and velocity are reduced during
muscle fatigue, the force or velocity at which efficiency reductions occur also is reduced. This offers

18
an alternative view to the mechanistic basis of the V̇ O2sc that may not lie solely in type-II muscle
fibres. Colosio and colleagues (2020) measured the ventilatory, anaerobic and aerobic contributions
to work in the moderate, heavy, and severe domains. They hypothesize that the V̇ O2sc in the heavy
domain was associated with a ‘metabolic shift’ to the aerobic system rather than an increase in the
overall cost of work and only a true loss of efficiency was observed in the severe domain. This
suggests that there is a distinct difference in the physiological foundations of the V̇ O2sc when the
glycolytic contribution, and consequently proton accumulation, to ATP resynthesis is greater.

Muscle fibres become less efficient as they approach the metabolic characteristics of fatigue,
where decreases in the Gibbs free energy of ATP hydrolysis, phosphocreatine, and glycogen
concentrations, as well as increases in muscle metabolites all contribute (Zoladz et al., 2008).
According to Poole and Jones (2012), ~ 85% of the V̇ O2sc is occurring in the muscle. Contractile
properties have been postulated to be affected by the decrease in free energy and increases in
metabolites that affect ion transport and release processes mediated by sarcoplasmic reticulum Ca 2+
and myosin ATPase (Grassi et al., 2015; Sundberg & Fitts, 2019). This may lead to increased
resistance in the mechanical coupling process, requiring further ATP for internal work which does
not contribute to the force output increasing the ATP:Power output ratio (Zoladz et al., 2008).
Concurrently, the development of peripheral fatigue and its relation to the V̇ O2sc was shown by Keir
and colleagues (2016) where a larger V̇ O2sc resulted in further reductions in muscle torque in
electrically stimulated muscle when increasing the duration of very heavy work bouts. Evidently,
efficiency, the V̇ O2sc and the process of fatigue are inexorably linked (Grassi et al., 2015) and will be
discussed further throughout this thesis.

The V̇O2 Slow Component and Non-Linear activity

Clearly, the V̇ O2sc has important applications for endurance activities. However, its
significance in intermittent team sports, such as basketball and football, where irregular supra and
sub-maximal efforts are required, should not be overlooked (Jones & Vanhatalo, 2017). Indeed, the
V̇ O2sc has been shown in response to a high-intensity tennis test protocol using non-steady-state,
intermittent activity (Sanchez et al., 2018). The relative intensities and duration of each effort along
with the rest interval, will determine the extent to which the V̇ O2sc and changes in neural and
muscular function are altered. This will therefore depend on the individuals’ anaerobic thresholds
and exercise economy in the specific modality. Exercise economy is the ability of an individual to
perform a task at a lower metabolic requirement than someone else (McArdle et al., 2015). This is
thought to be a highly relevant concept in dance due to its highly skilled nature (Wyon, 2009; Beck et
al., 2018). Dancers with a lower technical ability have been shown to work at a higher intensity
(>GET) when compared with experienced dancers doing the same choreography (Guidetti et al.,
2007). In team-sports such as football, movement economy is seen to be advantageous as delayed
fatigue and improved recovery mitigate the drop in performance usually seen during a match (Dolci
et al., 2018). To perform optimally, footballers need the ability to accelerate, decelerate and change
direction efficiently while also possessing high aerobic power (Dolci et al., 2020). Efficiency of
movement is therefore related to both metabolic and biomechanical factors so the physical
condition along with the technical ability of the dancer will underlie the physiological response to
movement.

Furthermore, the V̇ O2sc is affected by the nature of the activity itself. Body position (in
relation to gravity) has been shown to change slow and fast components of cardiorespiratory

19
responses (Koga et al., 1999). Koga and colleagues (1999) showed reduced phase-II and increased
phase-III components in supine compared to upright exercise. Similar changes were observed when
comparing the pulmonary kinetics of heavy arm and leg exercise meaning the location, and
subsequently fibre type, of the working muscles have an effect on the V̇ O2sc (Schneider et al., 2002).
Contemporary dance involves a multitude of diverse movements, with frequent direction and
orientation changes, utilizing the limbs in a dynamic, non-linear fashion (Redding et al., 2004). While
the V̇ O2sc has not been previously studied in dance, its relation to the fatiguing process and
subsequent effects on movement quality would seem relevant given the increased injury risk
associated with fatigue (Liederbach et al., 2013). However, fatigue is explained by both central and
peripheral factors (Morales-Alamo et al., 2015). Therefore, the following section will explore
intensity-dependent mechanistic responses that are linked to the cardiovascular system.

Cardiovascular Drift

Similar to the V̇ O2sc, cardiovascular drift (HRsc) is observed in prolonged exercise and has
received comparatively less attention in the literature (Zuccarelli et al., 2018). HRsc has been
associated with a drop in SV which in turn demands an increased HR in order to maintain CO (Wingo
et al., 2012). The HRsc has been shown at even in moderate intensities with either immediate or a
delayed (~ 10-15 min) responses (Zuccarelli et al., 2018; McArdle et al., 2015). Exercise induced heat
stress leading to a rise in core body temperature and, during prolonged exercise, dehydration are
major contributors to the development of the HR sc (Wingo et al., 2012). The decrease in SV has been
attested to peripheral blood displacement thereby increasing cutaneous blood flow, facilitating
thermoregulation, leading to a drop in blood volume and pressure (Wingo et al., 2012). However,
the HRsc has been shown to be present despite stable measurements in cutaneous blood flow
(Fritzsche et al., 1999). It is likely to represent sympathetic nervous system activity affected by core
temperature, central command components and neural reflex mechanisms such as, the exercise
pressor reflex’ (Fisher & Secher, 2019). Direct measurement of autonomic adjustments during
exercise is challenging but increases in sympathetic activity 30 to 60s after the onset of exercise,
possibly due to metabolite accumulation, have been shown to stimulate an increase in HR (Fisher et
al., 2015). Similarly, heart rates upward of 100bpm have been shown to increase sympathetic
activity (Bernard et al., 1997). Consequently, the increase in HR is thought to reduce ventricular
filling time, thus reducing SV (McArdle et al., 2015). This has important implications on both exercise
prescription and tolerance especially as the HR sc has been shown to be more pronounced in
comparison to the V̇ O2sc at the same work rate (Zuccarelli et al., 2018). The findings from that study
were from steady state activity. HR/V̇ O2 relationships during intermittent activity are not linearly
related and possibly have different adjustment mechanisms at low and high intensities (Redding et
al., 2004; Bernard et al., 1997). Repeated changes in direction and alternating work to rest ratios also
affect SV due to the variations in muscular venous pump action (Buchheit & Laursen, 2013). In
healthy humans, autonomic adjustments to exercise appear to work interactively to orchestrate an
appropriate neural-cardiovascular response to exercise in an intensity dependent manner (Fisher et
al., 2015).

20
Peripheral and Central Fatigue

Fatigue is a multifaceted phenomenon that incorporates metabolic, neural, and

neuromuscular components, among others (Wyon & Koutedakis, 2013). It is still the topic of much
debate as reliable and accurate measurement in vivo presents many challenges (Place, 2021).
However, Place (2021) states; “There is a general consensus around the idea that an acute reduction
in the force generating capacity is caused by alterations located above and/or beyond the
neuromuscular junction, i.e., central (neural) and/or intramuscular (peripheral) processes,
respectively”. Central and peripheral mechanisms both contribute proportional reductions in
performance, motivation and eventually, exercise termination in relation to mode, intensity,
duration and volume (Hureau et al., 2018). The mechanisms of fatigue are therefore believed to
interact to protect the body from catastrophic damage (Hureau et al., 2018).

As previously discussed, the V̇ O2sc and muscular fatigue appear to be related, manifesting as
perturbations in innervation and contraction function from intracellular metabolites (Grassi et al.,
2015). As the rate of ATP turnover increases and the ATP-PCr and glycolytic systems are further
called upon, the rate of metabolite accumulation such as, Pi, ADP, L- and H also increases (Grassi et
al., 2015). The accumulation of Pi is linked to the decline in Gibbs free energy increasing the cost of
contraction as previously discussed (Grassi et al., 2015). Force production and myofibrillar Ca2+
sensitivity have also been shown to be reduced by H, Pi, and K + accumulation (Davis et al., 2019;
Grassi et al., 2015). Other muscular action potentials such as reduced Ca2+ release and sarcoplasmic
sensitivity can also be affected by intramuscular ionic concentrations and Na + and K+ content
(Gandevia, 2001). These cumulative responses can all contribute to the declining efficiency of
contraction as exercise continues.

Metabolic conditions from muscle biopsies at the cessation of exercise >CP have been
shown to be similar irrespective of duration but heavy exercise and moderate display different
metabolic profiles at exercise termination (Black et al., 2017). During severe exercise, Black et al.
(2017) hypothesised that increases in metabolic milieu severely impaired the muscle fibre action
potential leading to task failure. However, heavy exercise was thought to end from ionic changes on
muscle membrane excitability, muscle metabolite accumulation and the decrease of energy
substrate which all act collectively to impair excitation-contraction coupling. Moderate exercise had
a negligible metabolite accumulation and termination related to the depletion of muscle glycogen
which itself affects neuromuscular excitability and transmission. Lactate (L-) formation would be
present in intensities above the GET. Changes in intracellular pH were historically and commonly
thought to be the main cause of fatigue through acidosis (Ferguson et al., 2018). More recently
though, acidosis (accumulation of H and L-) and task failure have been shown to be dissociated and
L- has been postulated to aid recovery after exhaustive exercise (Morales-Alamo et al., 2015).
Morales-Alamo and colleagues’ (2015) study took muscle biopsies of the vastus lateralis pre, post
and one minute after a graded cycling test to exhaustion and compared normoxic and hypoxic
conditions with and without bilateral occlusion immediately following the graded test. Participants
also completed a ten-second all out sprint test before the graded test and after the final muscle
biopsy. The results showed that despite a further increase in muscle lactate and decreases in ATP,
PCr and muscle pH, after occluded recovery in normoxic and hypoxic conditions, participants were
able to achieve ~48% and ~53% (10 seconds recovery), and ~62% and ~64% (60 seconds recovery),
of their pre-test mean 10 second sprint speed, respectively. Therefore, these authors concluded that
central factors were more dominant in participants’ decision to stop exercise.

21
 Central fatigue describes the changes in the ability to deliver force efficiently and is related
to mechanisms occurring proximal to the neuromuscular junction (Taylor et al., 2016). During
sustained fatiguing contractions increases in EMG (electromyography) have been associated with the
recruitment of new motor units as previously recruited motor units gradually lose neuromuscular
propagation potential (Taylor et al., 2016). Similarly, the onset of central fatigue is associated with
an increase in corollary discharge which increases ‘effort’ perception (Hureau et al., 2018). Effort
always increases before the force begins to decline in sustained contractions (Enoka, 2008). If
submaximal efforts are prolonged, the increase in EMG will cease and then decline (Taylor et al.,
2016). EMG activity decreases as a result of propagation fatigue or inhibited descending motor drive
due to supraspinal fatigue (Taylor et al., 2016). The difficulty in determining the exact cause-effect
relationship in fatigue is what makes it so interesting but also incredibly difficult to research.
However, there are several peripheral and central mechanisms that are thought to provide an
integrative and protective response to exercise (Hureau et al., 2018).

The interaction of peripheral and central factors differ in relation to exercise mode and
intensity where different mechanisms of fatigue are observable (Taylor et al., 2016). For example,
Thomas and colleagues (2016) found greater indices of peripheral fatigue during short duration, high
intensity cycling when compared to long duration, low intensity work. This occurrence was observed
to be inversely related with central indices demonstrating that the mechanisms of exercise
termination are duration and intensity dependent. As the body expends energy, afferent and
efferent information through the CNS (central nervous system) is regulating the response through
sensory neurons such as those located the skeletal muscles, visceral muscles and the vasculature
(Black et al., 2017; Zoladz et al., 2019). Type III receptors respond to muscular contraction and/or
stretch whereas type IV, to changes in intramuscular metabolites and noxious levels of mechanical
strain (Hureau et al., 2018). Their inhibition has a whole-body effect, even when the peripheral
fatigue is localised (Amann et al., 2013). Pharmacological inhibition of both these afferents can cause
greater peripheral fatigue (Blain et al., 2016). Hureau and colleagues (2018) therefore
conceptualised a ‘sensory tolerance limit’ by which an individual’s relative proximity to the ‘limit’
determines their time to fatigue. They postulate that sum of all feedback and feedforward signals is
processed in the CNS and regulates the intensity of an activity to ensure it remains tolerable.

Recovery

Recovery is a complex phenomenon involving the progressive return to cellular and system
homeostasis and is intensity dependent (Zoladz et al., 2019). Above the GET, off-transient pulmonary
kinetics can be modelled with (inverse) bi-exponential functions (Özyener et al., 2001)caused by a
decrease in oxygen demand the active muscles (McArdle et al., 2015). Exercise ranging between the
heavy and extreme domains may take up to 24 hours for pulmonary function to reach baseline levels
again (Zoladz et al., 2019). HR is modelled with similar exponential decrease, immediate
parasympathetic reactivation drives down HR and increases in SV are seen (Goldberg & Shephard,
1980) while delayed post exercise sympathetic withdrawal may leave HR elevated for upwards of 90
minutes (Romero et al., 2017). The restoration of energy stores such as PCr and glycogen are also
responding in an intensity dependent manner. Intracellular ion concentrations have a short recovery
time (< 5 minutes) and the recovery of intracellular pH ranges from 5-15 minutes (Seiler & Hetlelid,
2005). Blood lactate can stay elevated upwards of an hour post exercise (Burnley et al., 2006). The
temporal profile of each system returning to homeostasis/baseline is beyond the scope of this
literature review as the focus is the phase-III component of the V̇ O2 and HR kinetics. However, the
importance of recovery, or lack of, will be discussed more in the final chapter.

22
Demands of Contemporary Dance

Ultimately, the duration, type and quality (ie. In normoxia) of recovery and exercise bouts
will determine the time required for complete recovery. Wyon (2009), documented w:r ratios in
class, rehearsal, and performance of a contemporary dance company over the time course of a
creation period. In class, the warm-up section was ~3.5:1 and centre practice, 1:3. However, Wyon
(p. 141) notes, ‘the main factors that affect the work time are the length of the sequence, the
number of people in the class and the floor space’ demonstrating the large variability that w:r ratios
will have in all dance classes. Dance genre also impacts the w:r ratio of the class. For example,
Dahlstrom and colleagues (1996) recorded 1.4:1 and 2:1 for ballet and contemporary warm up
sections and 0.8:1 and 0.9:1 for the centre sections, respectively. Wyon (2009), documented
rehearsal to generally have low w:r ratios comparatively to class and performance due to the
explorative nature of the creative period. In the same study, contemporary dance performance had
a w:r ratio between 2:1 and 1.46:1. Wyon also recorded the HR responses and using the aerobic HR
training zone (120-180bpm) as an indicator. The percentage of time spent >120bpm was calculated
for each condition. Percentage times for performance, rehearsal and class were 53.36%, 44.4% and
52.35%, respectively. Despite the similar values between class and performance, the time spent in
the upper regions of the dancers’ capacities was considerably more for performance demonstrating
the high energy requirements. Intermittent sports such as tennis, basketball and soccer have work to
rest ratios of 1:3-5 (Kovacs, 2007), 1:9 (Bishop & Wright, 2006), 1:7-9 (O’Donoghue, 2002),
respectively. The latter two studies’ ratios are calculated using only high intensity work meaning the
true values may be different. However, in comparison to dance performance, the time spent at high
intensities is still less. Wyon (p. 152), concludes that recovery time between the exercise bouts
during dance performance suggest only partial restoration of cellular energy stores. Therefore,
understanding levels of dancers’ cardiorespiratory fitness is necessary in optimising their
performance.

Monitoring of contemporary dancers’ physiological fitness has been made possible through
the development of fitness tests such as the Dance Aerobic Fitness Test (DAFT) (Wyon et al., 2003),
the High Intensity Dance Performance Fitness Test (HIDPFT) (Redding et al., 2009). The DAFT is a
five-stage, incremental test consisting of a four-minute, repeated, bilateral dance phrase that
increases intensity with each stage. The HIDPFT is a one-minute, supra-maximal intensity, repeated
bi-lateral dance phrase repeated four time with a w:r of 1:2. Both tests were created with scope to
be periodically used in assessing dancers’ cardiovascular and respiratory responses to incremental
(wyon et al., 2003) and high intensity interval dance (Redding et al., 2009). The non-linear nature of
dance means that the kinetics of V̇ O2 ad HR will be prone to fluctuations meaning that achieving a
‘steady state’ will be rare in dance. However, Wyon and colleagues (2003) designed the DAFT to
have minimal variations in V̇ O2 requirement (± 5 ml∙kg-1∙min-1) throughout each stage whereby a
pseudo steady-state can be achieved.

Contemporary dance therefore is classified as intermittent exercise with varying degrees of

intensity that are dictated by the nature of the class, rehearsal, or performance (Wyon, 2009). Class
has been shown to have no significant differences in cardiorespiratory measures at university,
graduate and professional level (Wyon et al., 2002) demonstrating the lack of systemic progressive
overload that exists in the main form of dance training. As a discipline, dance has evolved eclectically
(Rafferty et al., 2009) with a clear focus on skill acquisition in class and rehearsal (Kimmerle & Cote,
2007). The extent to which the many components of dancers’ physical condition are improved is
probably circumstantial and unorganised in many cases. Like dance, many team sports require short

23
bursts of energy with changes of direction requiring accurate, skilled movements and activity-
specific movements (Laursen & Buchheit, 2019). Training the anaerobic and aerobic systems to cope
with the demands they will be required to work under during performance is therefore a large part
training in athletes such as mixed martial artists, footballers, and tennis players (Laursen & Bucheit,
2019). “Anaerobic fitness describes a type of physical fitness in the continuum between aerobic
fitness and muscle strength” (Koutedakis & Jamurtas, 2004 p. 653). Professional contemporary
dancers have been shown to generally have ~15.1% larger V̇ O2 max values (49.1 ml∙kg-1∙min-1) when
compared to ballet dancers, who have similar capacities to untrained individuals (~43.1 ml∙kg -1∙min-1)
(Angioi, 2009). Modern dancers’ similar fitness levels to non-endurance athletes is anecdotally
attributed to them commonly participating in multidisciplinary physical activities prior to starting
dance (Koutedakis et al., 2005). Equally, this may be related to the influence of sport in
contemporary dance and the more athletic approach taken by ‘modern’ choreographers (Koutedakis
et al., 2007). However, Chmelar and colleagues (1988) showed professional contemporary dancers’
indices of leg strength to not differ significantly from their ballet counterparts who have been shown
to have similar fitness levels to untrained individuals (Koutedakis et al., 2005). Similarly, no
significant differences were found between non-dancers, beginner, intermediate students and
professional contemporary dancers in the Wingate anaerobic test or knee and ankle strength and
power (Chatfield et al., 1990). Suggesting that their condition is not adequately maintained by their
training. By now, it is deemed ‘unacceptable’ to employ a dance-only training approach (Rafferty et
al., 2009) at any level of dance training. However, the full extent of this seems yet to be recognised
by the wider dance community (Rafferty, 2010).

The apparent preparatory discrepancy may have implications for the extent of fatigue
experienced by dancers throughout the season. For training and performance to be optimal, specific
adaptations designed to match or exceed the demands of performance occur after a cycle (or cycles)
of training and adequate recovery is given (Zatsiorsky et al., 2021). Tapering allows for the effects of
fatigue to decline and facilitates the adaptation period, peaking in tandem with performance or a
performance period (Haff et al., 2016). This type of periodisation isn’t a methodology that is largely
used in dancers’ scheduling possibly to the detriment of performances and the dancer’s longevity
(Wyon, 2010). Consequently, little thought is given to the structure of dancers training and readiness
to perform possibly leaving dancers at an increased risk of overtraining in comparison to other
athletes. Wyon and Redding (2005) monitored cardiorespiratory adaptations throughout a rehearsal
and performance period. They found no significant differences in dancers’ physiological responses
(mean HR, max HR and blood lactate) during stage five of the dance aerobic fitness test (Wyon et al.,
2003) in pre-rehearsal and pre-performance measures. However, significant differences from pre-
performance were measured in all parameters post-performance. Therefore, the relative intensity of
performance was high and the degree to which fatigue may have been present during the execution
of the performance itself is increased. Furthermore, Koutedakis and colleagues (1999) showed
professional ballet dancers to increase fitness indices after an extended rest period (3-4 week
summer break) and attributed them to recovery from end of season overtraining syndrome. Similar
findings have been shown in athletes from individual and team sports (Koutedakis, 1995). However,
the culture of monitoring the fitness-fatigue relationship in athletes is now commonplace in high-
performance sports (Coutts et al., 2018) meaning their findings may not be as applicable to today.

24
The Effects of Fatigue in Dance

As previously discussed, fatigue is a multifactorial concept that compromises central and

peripheral mechanisms occurring proximally and/or distally to the neuromuscular junction (Place,
2021). The effects of fatigue on dance performance have not been studied in detail (Jarvis & Abergel,
2019) therefore, understanding the effects fatigue has on neuromuscular function in dancers is
important. Armstrong and colleagues (2018a) predicted fatigue to have a negative effect on
movement quality in dancers. Dancers’ functional movement scores (FMS) were tested before and
after completing the DAFT test. Their mean composite, deep squat, dominant inline lunge, and non-
dominant inline lunge FMS scores were all significantly impaired. In other findings, fatigue altered
neuromuscular actions in the lower limbs during simple, isokinetic (Lin et al., 2016) and plyometric
(Abergel et al., 2021; McEldowney et al., 2013) tasks. Both Lin and colleagues’ (2016) and Abergel
and colleagues’ (2021) found greater mediolateral centre of mass displacement during fatigue in
repetitive relevés and sautés, respectively. Altered agonist-antagonist muscle activation between the
quadriceps and hamstrings during drop landings were observed (McEldowney et al., 2013) and
similar results with subsequent movement compensations detected in a relevé action (Lin et al.,
2016). Therefore, fatigue negatively affects motor control during prolonged exercise above a certain
threshold, the impact of which is likely increase mechanical loading and cost (Armstrong et al.,
2018a) and the risk of injury (Liederbach et al., 2013). In contrast, Armstrong and colleagues (2018b)
failed to show any significant changes in star excursion balance test scores and similarly, no changes
in a dance-specific balance task (arabesque) in fatigued dancers (Coutts et al., 2006). This may have
been be due to the time between finishing the fatigue protocol and the measurements taken
allowing the dancers to recover (Coutts et al., 2006) or suggest a ‘fatigue resistance’ that may be
specific to dancers neuromuscular capabilities in a fatigued state (Armstrong et al., 2018b).

However, the previously mentioned studies adopt pre-post designs that use either non-
dance-specific test protocols (Armstrong et al., 2018b; Armstrong et al., 2018a; McEldowney et al.,
2013) or isolated, dance-specific movements (Abergel et al., 2021; Coutts et al., 2006; Lin et al.,
2016) to study the change in dancers’ neuromuscular function. Consequently, the applicability of the
findings to dynamic dance performance are questionable. The interaction of peripheral and central
mechanisms during high intensity movement is ultimately what alters neuromuscular control
(Batson, 2013). Impaired concentration, co-ordination and postural stability lead to compensatory
movement strategies and the ability to perform skilled tasks is reduced (Batson, 2013). Furthermore,
central fatigue has been shown to be greater in people with joint hypermobility syndrome (To et al.,
2019); a condition which has a high prevalence in dance and is associated with impaired autonomic
function (Foley & Bird, 2013). Given the large eccentric component seen in dance movement and
therefore the high level of neuromuscular control needed during dynamic dance combinations
(Paschalis et al., 2012), studying fatigue during dynamic dance movement may be more relevance
than in experimental conditions. There is currently no dance-specific study exploring the effects of
fatigue during dynamic dance activity and on the activity itself. Thus, this provides a basis for the
methodological approach of this study which will adopt a similar pre-post design, but using a
dynamic, high intensity dance phrase with a w:r ratio that emulates the demands of dance
performance.

25
Kinematic Analysis and Fatigue Detection

Methods of fatigue detection and monitoring in dance therefore could be of use to coaches,
choreographers, and directors. Experimentally, 3D motion analysis is largely considered the ‘gold
standard’ for kinematic analysis (Zhang et al., 2019). However, usually the equipment is expensive
and has to be used under controlled laboratory conditions (i.e. eliminating natural light) (Winter,
2009). Wearable technology such as IMU’s (inertial measurement units), used in regular athlete
monitoring, has expanded in recent years (Gómez-Carmona et al., 2020). IMU’s are comprised of
either one, or multiple micro-sensors such as accelerometers, gyroscopes, magnetometers, and
global positioning systems and are small, lightweight, and non-invasive making them ideal for in-field
use (Camomilla et al., 2018; Gómez-Carmona et al., 2020). Measurements can be taken and used for
kinematic analysis (Winter, 2009) or, sensors can combine data (i.e. data fusion from accelerometer,
gyroscope magnetometer and GPS sensors) in order to provide real time metrics such as an athletes
external workload (Camomilla et al., 2018). High-end IMU’s with many sensors, and their supporting
software are marketed at sports teams may be too expensive for most dance schools and
companies. However, due to the massive growth in the use of micro-sensors in recent years in an
array of fields such as smartphones, gaming and healthcare research, affordable IMU’s exist that can
give objective data about dancers and their movement (Rasras et al., 2019; Park, 2016). IMU’s have
been used to quantify mechanical loading during the DAFT and were found to be sensitive to
changes in intensity of dance movement (Brogden et al., 2018).

Jerk, the time derivative of acceleration, can provide qualitative information about the
execution of motor tasks (Choi et al., 2014). The jerk is proposed to measure deviations from
optimally executed, natural movements that would illicit a bell-shaped curve when plotted as a
function of time (Latash & Zatsiorsky, 2016b). This may have special importance in contemporary
dance where the efficiency of mechanical energy transfers directly affect the aesthetic of the
performance (Winter, 2009). Efficient movement can described as smooth and fluid (Montero, 2011;
Winter, 2009). Indeed, jerk has been shown to decrease as skill level increases in dance (Park, 2016;
Spriggs et al., 2002; Bronner & Shippen 2015), golf (Choi et al., 2014), climbing (Seifert et al., 2014),
and running (Hreljac, 2000). Therefore, as jerk can objectively distinguish between different levels of
motor control, it stands to reason that it could provide a useful measure of fatigue. As fatigue ensues
and degrades motor control the central and peripheral efficiency of movement production decreases
(Grassi et al., 2015; Batson, 2013). Despite this however, jerk has not been widely employed as a
measure of fatigue (Zhang et al., 2019). Zhang and colleagues (2019) found that jerk could be used
reliably as an indirect measure of fatigue in construction workers and jerk profiles accurately
reflected workers’ skill level and that the use of IMU’s was easy to use in a real-life environment.

Study Objectives

26
 To investigate the effects of fatigue on efficiency in dance, this study replicates the high
intensity, interval nature typically seen in performance and uses wearable devices to capture
kinematic and physiological data in vivo. This is the first study to attempt model V̇ O2 and HR kinetics
and assess the relationship between both kinematic and physiological parameters during fatiguing
dance activity.

Therefore, the first aim is to model the kinetics parameterising the separate phases of the V̇ O2
and HR responses when plotted as a function of time. This study focuses specifically on the phase-III
component and uses the model to extrapolate the magnitude of the V̇ O2sc (ΔV̇ O2sc) and HRsc (ΔHRsc) in
each trial.

The second aim of this study is to analyse the effect of high intensity dance exercise on the
quality of movement and within bouts by assessing the change in jerk (ΔARM, ΔLEG, and ΔCOM) during
four, four-minute bouts of high intensity dance.

The third and final aim of this study is to correlate the ΔARM, ΔLEG, and ΔCOM with both ΔV̇ O2sc and
ΔHRsc in each trial and compare the strength of the correlational relationships.

Experimental Hypotheses

a) Due to the high intensity of the choreography, there will be significant differences between
jerk values at the beginning and end of each trial.
b) The magnitude of the V̇ O2sc (ΔV̇ O2sc) will positively correlate with the magnitude of the rate of
change in all jerk measurements in each trial.
c) The magnitude of the HRsc will positively correlate with the rate of change in all jerk
measurements in each trial.
d) Due to the relationship between the V̇ O2sc and peripheral fatigue, the correlations between
ΔV̇ O2sc and of ΔARM, ΔLEG, and ΔCOM will be of greater statistical significance than the
relationships between ΔHRsc and ΔARM, ΔLEG, and ΔCOM.

Null Hypotheses

a) There will be no significant differences between jerk values in each trial

b) There will be no significant correlation between the V̇ O2sc and the change in jerk in each trial
c) There will be no significant correlation between the HR sc and the change in jerk in each trial

Chapter 2: Methods

Participants

27
Participants were full-time dance students from the same year of the same vocational dance school
recruited via poster (Appendix 1) and email (Appendix 2). Eight participants, two male, six female
mean age: 21.25 ±1.04 years old, Height: 161.63 ±4.69 cm, Mass: 59.83 ±6.44 kg, Years Dancing: 9.75
±2.49 were recruited. To homogenise the participants and strengthen inter-subject comparisons,
undergraduates were selected from the same year group (2 nd year) and the same dance
conservatoire. A Medical PAR-Q (Appendix 3), consent form (Appendix 4), and information sheet
(Appendix 5) were completed to assess their eligibility and obtain their consent for the study.

Exclusion Criteria

Applicants were also excluded if they:

 Had previously completed the DAFT test.

 Had an injury that is affecting their normal movement strategy
 Were over the age of 40 years old.
 Had tested positive for COVID-19 at any time.

Preparation and Pilot Phases

Preparation

The preparation and piloting phase of this study coincided with the second UK national
lockdown (5th November 2020 – 8th March 2021) due to the SARS-CoV-2 pandemic. The restrictions
that were in place at Trinity Laban meant that while the laboratories space and equipment were
accessible, space was limited to single person use. This meant that all piloting undertaken prior to
March 8th, 2021, was conducted by the lead researcher alone.

The original choreography was adapted and initially piloted by the lead researcher. During
March 2021, after COVID-19 restrictions had been eased, the adapted choreography was piloted on
three students from the same dance conservatoire. It produced an end mean V̇ O2 of 92.8% between
VT1 and V̇ O2peak.

Pilot

The nature of the ADAFT choreography is representative of contemporary dance where lines
and limb trajectories are clear and smooth. Therefore, trajectories of the limbs were better recorded
by placing the IMU’s on the distal aspects of the limb rather than close to the centre of mass. Placing
the IMU’s closer to the centre of mass would result in recording limb movements that would relate
with intralimb coordination patterns rather than the intended pathways of the task (Latash &
Zatsiorsky, 2016). The midpoint between the bony landmarks on the limbs minimized unnecessary
noise from movements of the hand or foot while capturing data representative of the limb
trajectories.

28
 The wide range accelerometer was selected for this study rather than the low noise
accelerometer due to its large signal range. The low noise accelerometer has a ±2g range and the
wide range has up to ±16g. It was found during piloting that any sensor under ±8g would cap the
data and not register true maximum values during some of the high velocity movements of the
ADAFT such as, jumps.

Sampling frequencies in the Shimmer IMU’s range from 1-2000hz. It was decided that
201.3hz was the optimal frequency to minimise packet losses (average of 99.9% packets kept per
trial) while recording ample information each second.

Methods of gas analysis have improved from capturing expired gas in Douglas bags to
telemetric, wearable units (Koga et al., 2005). While these portable devices are extremely practical,
their use is predominantly activities such as running and cycling. It was found that positioning the
gas analyser on the back of the participant was the least restrictive for the dynamic dance
movements in the ADAFT the holding pack of the gas analyser was less restrictive when placed on
the back of the participants.

Testing Protocols

Adapted DAFT (ADAFT)

The ADAFT uses the original stage three from the DAFT test but includes steps that require
more technique from the participants. The original choreography was designed to be simple so the
fitness test could be used by dancers with differing skill levels and minimize the effect of movement
economy (Wyon et al., 2003). It has been shown to have an end, mean V̇ O2 value of 63.7-89.9% of
postgraduate and undergraduate students’ LT (Beck et al., 2018). The current study adapted the
choreography to require more technicality from the participants and include more high intensity
movements. The ADAFT choreography produced a mean, end trial V̇ O2 value of 128.87% of pilot
participants’ VT1 calculated from the treadmill protocol with a visible and progressive rise in oxygen
uptake throughout the trial confirming its appropriateness for use in the experiment. A video link
can be found in Appendix 6.

Treadmill Test

The protocol followed recommendations specifically for treadmill testing in dance

populations to ‘minimize trauma to the subject’ (Wyon, 2006b). Participants warmed up on the
treadmill for five minutes at a self-selected speed of 6-9 km.h -1. Once the test had begun the speed
was increased every minute by 1 km∙h-1 and was at a constant incline of 1%. The test was either
stopped by voluntary cessation or until two of the following criteria were met: heart rate within 10
beats∙min of age-predicted maximum, respiratory exchange ratio (RER) above 1.15, V̇ O2 plateau
despite increase in speed, or inability to match the treadmill speed. Throughout the test,
participants wore a telemetric gas analyser and a heart rate monitor and were given verbal
encouragement. On completion, participants cooled down by walking at a speed of 5-6 km∙h -1 for a
further 5 minutes or until a heart rate value of less than 100 beats∙min -1 was achieved.

29
Experimental Design

Within two weeks after completing the treadmill test participants completed two studio
sessions where they performed an adapted stage three of the DAFT (ADAFT. Participants performed
the four-minute stage, four times in each session with an equal work to rest ratio of 1:1 (Figure 2. 1),
recording trial RPE with the original Borg scale (Borg et al., 1987) directly after each trial. Following
Brogden and colleagues’ (2018) considerations for unit placement during dance activity, jerk was
collected by IMU’s (Shimmer3, Shimmer, Ireland) placed in three specific locations: above the
sacrum at L5 on the vertebral column, at the midpoint between the humeral lateral epicondyle and
the lateral styloid process on the right arm, and the midpoint between head of the fibula and the
lateral malleolus on the right leg. During each trial raw data on kinematics, pulmonary kinetics and
heart rate were collected using the IMU’s accelerometers, a telemetric gas analyser (Metamax, 3B,
Cortex Biophysik GmbH, Germany) and a heart rate monitor (Polar, Polar Electro, Finland),
respectively. A representation of what participants wore can be found in Figure 2. 2. In the
preparation of the kinematic analysis, each trial was separated into time points; time point one and
time point two (TP1 and TP2) (Figure 2.3). An outline of the jerk measurements taken in the session
can be found in Table 2. 2. Accelerometer data was used to calculate the root mean square of triaxial
jerk (jrms) corresponding to the left and right sides of the ADAFT which aligned with the time points.
Oxygen and heart rate kinetics were modelled for analysis.

Figure 2. 1. Representation of work and rest intervals one session.

30
Figure 2. 2. Illustration of the placement of the gas analyser and mask, heart rate monitor and
IMU’s.

31
Figure 2. 3. Representation of time periods (dotted line) for the jerk time point one (TP1) and time
point two (TP2) measurements during ADAFT trial one.

Table 2. 1. Outline of jerk TP1 and TP2 measurements in a whole session

Trial Time Point 1 Time Point 2

(s) (s)
1 138.5-175.4 323.1-360
2 618.5-655.4 803.1-840
3 1098.5-1135.4 1283.1-1320
4 1578.5-1615.4 1763.1-1800

Pre-test

Familiarisation Session

Participants were required to come to the laboratory prior to the studio testing for a
familiarisation session. This session consisted of fitting the participants with all the equipment to

32
ensure they felt comfortable to move and were wearing the appropriate size of face mask.
Participants completed the graded treadmill test in the same session.

Calibration

An outline of the IMU, Metamax and Polar Heart Monitor calibration procedures can be
found in appendix 7, 8 and 9, respectively.

Control Parameters and Procedures

Metabolic

Following McGregor and colleagues' (2009) protocol, participants were instructed to refrain
from eating and drinking caffeinated beverages two hours before each testing session to minimise
the effect of digestion and caffeine on heart rate and metabolic parameters.

Due to the COVID-19 crisis, the participants vocational training in the months leading up to
the experiment was largely remote learning. Data collection happened over a three-week period,
during the Easter break which was after a three-week period of a return to full time training. The
participants may have been involved in varying levels of supplementary training and a return to full
time training would somewhat re-familiarise them with studio-based classes and homogenise their
training schedule. Participants were instructed to not partake in any progressive training program
during the days of their first to their last ADAFT sessions. This was to control for potential changes in
the variables being due to a change in their physical condition. To control for the negative impact of
fatigue on performance (McGregor et al., 2009) or metabolic parameters (Compher et al., 2006),
participants were informed to not partake in strenuous exercise eight hours before any testing
session.

Participants completed the same warm up outlined in appendix 10 and had exactly four
minutes of static recovery in between trials. Sessions were organised at least 12 hours apart and no
more than 72 hours apart and all participants completed their ADAFT sessions at a similar time of
day.

ADAFT Choreography

The first testing session was the first time that the participants observed and learnt the
choreography. Participants were taught the choreography by the lead researcher. Participants were
given at least ten but no more than 20 minutes to learn the material and were allowed to mark it as
many times as they wanted, with or without the music. Participants were asked if they were
confident in performing the material by themselves before proceeding to the next phase of the
experiment.

33
 Based on the criteria from the handbook provided with the DAFT test (Wyon et al., 2003)
and from research that explored the effect of movement quality on heart rate (Tiemens et al., 2018),
a list of performance criteria was prepared (Appendix 11). All participants were reminded of these
criteria at the beginning of each testing session and were verbally encouraged throughout each trial.

Inertial Measurement Units

To standardize IMU placement, the midpoint between each bony landmark/muscle was
measured and marked at the beginning of each session by the same person. The locations were also
chosen to minimize the risk of impact with other sections of the body during the test. Participants
were also given prior instructions about what to wear (Appendix 5) to minimize the effect the
unnecessary movement of the IMU’s due to the clothing material.

Data Collection

All ADAFT testing and data collection took place in the same studio at Trinity Laban, London,
UK and a camera was used to record the session. All testing equipment was prepared and calibrated
in advance by the lead researcher prior to each testing bout. Participants completed the warmup
and were given an additional 3 minutes to complete any additional warm up they needed. Following
this, participants’ IMU placement was measured and marked with a non-permanent marker then
participants learnt the choreography with the lead researcher. Participants were then fitted with the
IMU straps and the mask and pack of the telemetric gas analyser. Participants were then instructed
to stand quietly in the starting position and breathe as normally as possible for four minutes. This
period was to allow the data from the gas analyser to normalise and reach a baseline and where the
data for the IMU zeroing algorithm was captured. Before starting the trials, participants were
reminded of the list of performance criteria and the experimental procedures and instructed not to
talk, cough, adjust any of the sensors or move unnecessarily throughout the choreography or
between trials. They were also reminded that they could stop at any time for any reason.
Participants were given a ten second cue before starting the first trial.

Ethical Considerations

Ethical procedures are outlined in appendix 12.

Data analysis

There was a participant dropout rate of 42.9% due to illness or inability to complete all trials
during the experiment. Participant five appeared to struggle with the technicality of the phrase and
had a mean heart rate of 98.4% HR peak in the first trial with the O2 response appearing to be in the
extreme domain. Participant six had a pre-existing condition which meant that working at high
intensities could cause them to vomit. This participant had experienced this at the end of the

34
treadmill test and precautions were taken during studio testing to be prepared for such an event.
They were unable to complete all trials due to the high intensity of the choreography provoking the
same response. Participant seven was excluded from the study as they had not followed the
instructions regarding caffeine and food consumption prior to testing. Participant eight stopped the
experiment as they had difficulty breathing during the trial with the gas analysis equipment and the
overall intensity of the ADAFT.

The remaining sample (n=4) was four females with a mean age: 21.25 ±1.26 (years), Height:
163.5 ±4.51 (cm), mass: 62.85 ±7.43 (kg) and years dancing: 10.21 ±2.14. Due to the size of the
sample and highly individualised nature of the response to the ADAFT, the following analysis
comprises both individual and group data. For the group analysis, physiological and kinematic data
from both sessions were combined and statistical tests were run on group means to test the
experimental hypotheses. Individual analysis using the physiological data is presented and
observationally discussed.

Oxygen Data Smoothing and Modelling

Treadmill Test

Raw oxygen data from the treadmill test was smoothed using a five-breath moving average
and outliers within 10 points from the mean removed. Due to the weight bearing nature of both
modalities (dancing and running) all data points were reported as relative V̇ O2 (ml∙kg-1∙sec-1). None of
the participants met the previously outlined criteria for a true V̇ O2max so V̇ O2peak values were recorded
from the final 30 seconds of exercise. VT1 was taken as the point where the ventilatory equivalent
(VE/V̇ O2) increased without a concomitant rise in VE/V̇ CO2 and VT2 was taken as the point where
V̇ CO2 increased relative to VE/V̇ O2 and RER = 1 (Wasserman et al., 2012).

ADAFT Test

The raw data from the ADAFT trials were smoothed by interpolating the values to one
second then a moving median over a box of seven data points was applied. Previous research which
has measured oxygen uptake in contemporary dance have usually applied a moving average (Beck et
al., 2018; Wyon et al., 2003). However, it was discovered that using this method with this distorted
the O2 amplitude in relation to time creating an early bias of the onset and termination of exercise
across all trials. The method of this study required the data to be as accurate as possible due analysis
of discrete time points therefore, limiting the distortion of the plots in relation to time was
important.

Oxygen data from the ADAFT were separated into individual trials to model the three stages
of the kinetics using a double exponential function (Ӧzyener et al., 2001):

( )+H(t- TD ( )
t- TD p t- TD sc
- -
V̇ O2(t) = τp τ sc
V̇ O2baseline +H(t- TD p ) A P 1- e sc ) Asc 1- e

35
Where:

{
H ( t ) = 0,t<0
1,t≥0

However, despite the design of the choreography mimicking a steady state and appeared to
be largely in the heavy/severe intensity domains, only 56.25% of trial data was able to be
successfully modelled by the double exponential function due to varying responses to the repeated
bouts within and between participants.

Therefore, to model the phase-III component of the V̇ O2 data, linear regression models were
applied to each trial using the data analysis pack in Excel (Microsoft 365, version 2105). An outline of
the discrete time points selected for TP1 and TP2 can be seen in Figure 2. 4 and both correspond
with the end of the jerk measurements in each trial.

Figure 2. 4. Representation of V̇ O2 and HR time point one (TP1) and time point one (TP2)
measurements (dotted lines) during the ADAFT trial one.

36
Table 2. 2. Time points (seconds) corresponding to the O2 and HR measurements in each trial

Trial Time Point 1 Time Point 2

(s) (s)
1 175.4 360
2 655.4 840
3 1135.4 1320
4 1615.4 1800

While this method will not give as rich data as the bi-exponential model and is far less
accurate due to the linearity of the regression line, it allows for the detection of a change in
pulmonary uptake that could be representative of the magnitude V̇ O2 slow component.

Individual O2 trial regression equations used the format, Y = A + BX, where the slope of the
line is B, and A is the intercept. The values corresponding to time points 1 (TP1), time points 2 (TP2)
(Table 2. 1.) were calculated using the regression equations and used in the group analysis. The rate
of change in oxygen consumption between the two time points was calculated where: ΔV̇ O2 = TP2 –
TP1.

Heart Rate Data Smoothing and Modelling

37
Treadmill Test

Heart rate peak value was taken from the final 30 seconds of the treadmill test.

ADAFT Test

To allow for direct comparison of the HR and jerk correlation results with the O 2 data, the
same method of analysis was used. Therefore, to model the phase three component of the beat-by-
beat HR data, linear regression models were applied to the HR data of each trial at the time points
(TP1 and TP2) for each trial outlined in Table 2.1. However, raw HR data from ADAFT trials were used
for the modelling of the data as beat by beat recordings usually exhibit spontaneous fluctuations
which may have biological significance (Zakynthinaki, 2015). Accordingly, smoothing of the heart
rate data was not carried out. For the group analysis, values corresponding to time points 1 (TP1),
time points 2 (TP2) (Table 2.0) were calculated using the regression equation. Using these discrete
values, the rate of change in heart rate between the two time points was calculated where: ΔHR =
TP2 – TP1.

RPE
Mesan RPE scores were calculated for each trial.

Accelerometer Data Smoothing and Jerk Calculation

Each accelerometer recorded linear X, Y, Z acceleration components at a frequency of

201.3Hz. Event markers corresponding to the two 48 count phrases prior to TP1 and TP2 and the
section for the zeroing algorithm were applied to the data and synced across devices in the Shimmer
software. The raw data was exported to MATLAB and filtered with a third order, low pass
Butterworth filter with optimal cut off frequency of 14Hz determined by following the protocol of
Winter (2009, p.89). The data was then scaled to g’s (g) by dividing each X, Y, Z component by 9.8.

The MATLAB script applied the zeroing algorithm to the data prior to filtering. Ideally,
calibrated accelerometers should read ±9.8 (m/s) in one axis and zero in the remaining two when
stationary on a flat, horizontal surface. This value should be offset to by subtracting ±9.8 in the axis
that is perpendicular to the horizontal surface therefore, all accelerations measured thereafter will
have the same origin. In this experiment, the origin was the starting position of the dancer before
they began each session. This meant there were offsets in all axes, subject to individual variability
between participants due to differences in stance, postural sway, and individual morphology. This
offset value was taken from the IMU’s when each participant was in a quiet stance at the start of the
first trial. The first 0.5 seconds of the X,Y,Z components were averaged out and subsequently
subtracted so that each component started from the same origin of zero.

The MATLAB script also measured the overall packet losses to manually determine the
quality of each recorded trial, if the packet losses were over 10% then the trial would be discarded.
However, all trials recorded ≥99.9% of successful recordings.

38
 The smoothed data was then used to calculate the jerk (j) at each interval. This was
calculated as the difference between two neighbouring acceleration magnitudes (a (n+1) – a(n)) divided
by the time interval. Finally, the root mean square of jerk values was calculated to give the j rms in
g∙sec-1:

ⅆa (t)
j( t)=
ⅆt

√
jrms= ( ∑ j 2n )
N
(Where n=1,2,…N)

The time periods for the jrms calculations of each trial are outlined in Table 2.1.

For the final analysis, jrms values for the Arm, Leg and COM (centre of mass) corresponding to
TP1 and TP2 from both sessions were combined by averaging the values. The rate of change (Δ) was
calculated by jTP2 – jTP1 and reported with the group data.

Group Statistical Analysis

As the bi-exponential models could not be applied across all results to allow for direct
comparisons, the linear fitting of the phase-III components of HR and V̇ O2 data meant that discrete
values could be extrapolated using the regression equations. Thus, analysing the significance of the
change in V̇ O2 and HR between timepoints in each trial increase will implicate the existence of a slow
component. Equally, this method also allowed for the calculation of ΔHR and ΔV̇ O2 and these values
can subsequently be used in the correlational analysis.

The accepted p-value for significance was set at p < 0.05 for all statistical analyses. All
variable combinations were checked for normal distribution using the Shapiro-Wilk statistic. SPSS
(IBM, version 27) was used for all statistical analysis. Paired samples t-tests were run on TP1 and TP2
V̇ O2, HR, jARM, jLEG, and jCOM values to analyse differences within trials. Pearson’s product correlation
tests were run on the ΔO2 and ΔHR corresponding to ΔARM, ΔLEG, and ΔCOM in the same trial.

39
 Chapter 3: Group Results

Participants Cardiorespiratory Profile

Table 3. 1. Columns one to three displays participants’ mean ventilatory threshold 1 (VT 1),
ventilatory threshold 2 (VT2) and V̇ O2peak results from treadmill test. All units displayed are in
(ml∙kg-1∙min-1). Column four displays mean HRpeak results from the test. Units displayed are in
(beats∙min-1).

VT1 VT2 V̇ O2peak HRpeak

34.74 42.75 46.25 195.25

T-tests

Table 3. 2. Paired t-test results on V̇ O2 (ml∙kg-1∙sec-1) means and standard deviations of TP1 and TP2
for each trial. * Indicates significant result where p < .05 (two-tailed).

Mean
change Lower Upper
TP1- p Confidence Confidence
V̇ O2TP1 V̇ O2TP2 TP2 value t value Interval Interval η2
38.93 43.63
Trial 1 ±5.48 ±5.94 -4.7 0.001* -10.71 -6.10 -3.31 0.97
40.73 42.52
Trial 2 ±5.05 ±4.71 -1.78 0.01* -6.73 -2.62 -0.94 0.94
40.43 41.85
Trial 3 ±4.19 ±6 -1.41 0.35 -1.11 -5.46 2.63 0.29
39.13 41.06
Trial 4 ±3.95 ±5.01 -1.93 0.13 2.12 -4.83 0.97 0.60

40
Figure 3. 1. Combined V̇ O2 values at TP1 and TP2 from both sessions. Increases in all trials with trial
1 and trial 2 reaching significance. * Indicates significant result where p < .05 (two-tailed).

45
*
44
*
43

42
VO2 (ml∙kg-1∙min-1)

41

40

39

38

37

36
Trial 1 Trial 2 Trial 3 Trial 4

TP1 TP2

Table 3. 3. Paired t-test results on HR (beats∙min -1) means and standard deviations of TP1 and TP2
for each trial. * Indicates significant result where p < .05 (two-tailed).

Mean
change Lower Upper
  HRTP1 HRTP2 TP1-TP2 p value t value CI CI η2
179.48 188.69
Trial 1 ±9.09 ±8.36 -9.21 0.01* -15.22 -11.13 -7.28 0.99
185.27 192.65
Trial 2 ±8.94 ±10.02 -7.39 0.01* -5.48 -11.68 -3.10 0.91
184.82 194.75
Trial 3 ±4.68 ±8.52 -9.93 0.01* -5.15 -16.06 -3.79 0.90
186.92 194.73
Trial 4 ±10.17 ±9.28 -7.82 0.01* -5.12 -12.68 -2.95 0.90

41
Figure 3. 2. Combined HR values at TP1 and TP2 from both sessions. Increases in all trials were
significant. * Indicates significant result where p < .05 (two-tailed).

200
* *
*
195

*
190
HR (beats∙min-1)

185

180

175

170
Trial 1 Trial 2 Trial 3 Trial 4

TP1 TP2

Table 3. 4. Mean rating of perceived exertion (RPE) for all trials displaying a gradual increase.
Means and standard deviations (SD) are combined from both sessions.

 Trial RPE SD
1 12.75 ±1.3
2 12.875 ±1.5
3 13.375 ±0.8
4 13.75 ±0.6

Table 3. 5. Paired t-test results on jARM (g∙sec-1) means and standard deviations of TP1 and TP2 for
each trial. * Indicates significant result where p < .05 (two-tailed).

Mean
change Lower Upper
  jARMTP1 jARMTP2 TP1-TP2 p value t value CI CI η2
0.0573 0.0614
Trial 1 ± 0.007 ±0.012 -0.004 0.43 -0.919 -0.0180 0.0099 0.22
0.0558 0.0592
Trial 2 ± 0.007 ± 0.003 -0.0034 0.26 -1.375 -0.0112 0.0044 0.39
0.0531 0.0572
Trial 3 ± 0.006 ± 0.005 -0.004 0.003* -9.052 -0.0055 -0.0026 0.96
0.0547 0.0566
Trial 4 ± 0.005 ±0.004 -0.002 0.24 -1.471 -0.0063 0.0023 0.42

42
Figure 3. 3. Combined jARM values at TP1 and TP2 from both sessions. Increases in all trials with only
trial three achieving significance. * Indicates significant result where p < .05 (two-tailed).

0.064

0.062

0.06

0.058 *
Jerk (g∙sec-1)

0.056

0.054

0.052

0.05

0.048
Trial 1 Trial 2 Trial 3 Trial 4

TP1 TP2

Table 3. 6. Paired t-test results on jLEG (g∙sec-1) means and standard deviations of TP1 and TP2 for
each trial. * Indicates significant result where p < .05 (two-tailed).

Mean
change Lower Upper
  jLEGTP1 jLEGTP2 TP1-TP2 p value t value CI CI η2
0.1307 0.1436
Trial 1 ± 0.03 ± 0.031 -0.0129 0.016* -4.903 -0.0213 -0.0045 0.89
0.1323 0.1382
Trial 2 ± 0.024 ±0.024 -0.006 0.205 -1.612 -0.0177 0.0058 0.46
0.128 ± 0.1363
Trial 3 0.027 ± 0.027 -0.0083 0.088 -2.496 -0.0189 0.0023 0.68
0.1284 0.1354
Trial 4 ±0.021 ± 0.021 -0.007 0.066 -2.828 -0.0149 0.0009 0.73

43
Figure 3. 4. Combined jLEG values at TP1 and TP2 from both sessions. Increases in all trials with only
trial one achieving significance. * Indicates significant result where p < .05 (two-tailed).

0.145 *

0.14

0.135
Jerk (g∙sec-1)

0.13

0.125

0.12
Trial 1 Trial 2 Trial3 Trial 4

TP1 TP2

Table 3. 7. Paired t-test results on jCOM (g∙sec-1) means and standard deviations of TP1 and TP2 for
each trial. * Indicates significant result where p < .05 (two-tailed).

Mean
change Lower Upper
  jCOMTP1 jCOMTP2 TP1-TP2 p value t value CI CI η2
0.0478 0.051
Trial 1 ± 0.007 ± 0.009 -0.0032 0.127 -2.1 -0.0081 0.0017 0.6
0.05 ± 0.0519
Trial 2 0.008 ± 0.009 -0.0019 0.205 -1.616 -0.0055 0.0018 0.47
0.0497 0.0518
Trial 3 ± 0.009 ± 0.008 -0.0022 0.110 -2.245 -0.0053 0.0009 0.63
0.0502 0.0526
Trial 4 ± 0.009 ± 0.009 -0.0024 0.302 -1.244 -0.0085 0.0037 0.34

44
Figure 3. 5. Combined jCOM values at TP1 and TP2 from both sessions. Increases in all trials with no
significant differences. * Indicates significant result where p < .05 (two-tailed).

0.054

0.053

0.052

0.051
Jerk (g∙sec-1)

0.05

0.049

0.048

0.047

0.046

0.045
Trial 1 Trial 2 Trial 3 Trial 4

TP1 TP2

Correlations

Table 3. 8. Pearson’s product-moment correlation coefficient between ΔΟ2 and ΔARM in the same
trial. There were non-significant effects for all trial combinations with both a positive correlation
in trial one and negative correlations present in trials two, three and four. * Indicates significant
result where p < .05 (two-tailed).

ΔΟ2 Trial ΔΟ2 Τrial ΔΟ2 Τrial ΔΟ2 Τrial

  1 2 3 4
0.856
ΔARM Trial 1 p = .144      
-0.518
ΔARM Trial 2   p = .482    
-0.618
ΔARM Trial 3     p = .706  
-0.148
ΔARM Trial 4       p = .562

45
Table 3. 9. Pearson’s product-moment correlation coefficient between ΔΟ2 and ΔLEG in the same
trial. There were non-significant effects for all trial combinations with a negative correlation in
trial one and positive correlations in trials two, three and four. * Indicates significant result where
p < .05 (two-tailed).

ΔΟ2Trial ΔΟ2 Τrial ΔΟ2Τrial ΔΟ2Τrial

  1 2 3 4
-0.415
ΔLEG Trial 1 p = .585      
0.572
ΔLEG Trial 2   p = .428    
0.465
ΔLEG Trial 3     p = .535  
0.22
ΔLEG Trial 4       p = .780

Table 3. 10. Pearson’s product-moment correlation coefficient between ΔΟ2 and ΔCOM in the same
trial. There were non-significant effects for all trial combinations with trials one and two displaying
a positive relationship and trials three and four negative correlations. * Indicates significant result
where p < .05 (two-tailed).

ΔΟ2Trial ΔΟ2 Τrial ΔΟ2Τrial ΔΟ2Τrial

  1 2 3 4
0.55
ΔCOM Trial 1 p = .450      
0.262
ΔCOM Trial 2   p = .738    
-0.366
ΔCOM Trial 3     p = .632  
-0.515
ΔCOM Trial 4       p = .485

46
Table 3. 11. Pearson’s product-moment correlation coefficient between ΔHR and ΔARM in the same
trial. There were non-significant effects for all trial combinations with positive correlations in trials
three and four and negative correlations in trials one and two. * Indicates significant result where
p < .05 (two-tailed).

ΔHR Trial ΔHR Trial ΔHR Τrial ΔHR Τrial

  1 2 3 4
-.167
ΔARM Trial 1 p = .833
-.122
ΔARM Trial 2 p = .878
.813
ΔARM Trial 3 p = .187
.420
ΔARM Trial 4 p = .580

Table 3. 12. Pearson’s product-moment correlation coefficient between ΔHR and ΔLEG in the same
trial. There were non-significant effects for all trial combinations with negative correlations in
trials one, three and four. Trial two displayed a positive correlation. * Indicates significant result
where p < .05 (two-tailed).

ΔHR Trial ΔHR Τrial ΔHR Τrial ΔHR Τrial

  1 2 3 4
-.385
ΔLEG Trial 1 p = .615
.640
ΔLEG Trial 2 p = .360
-.079
ΔLEG Trial 3 p = .921
-.284
ΔLEG Trial 4 p = .716

Table 3. 13. Pearson’s product-moment correlation coefficient between ΔHR and ΔCOM in the same
trial. There were non-significant effects for all trial combinations with a negative correlation in
trial one and positive in trials two, three and four. * Indicates significant result where p < .05 (two-
tailed).

ΔHR Trial ΔHR Τrial ΔHR Τrial ΔHR Τrial

  1 2 3 4
-.206
ΔCOM Trial 1 p = .794
.100
ΔCOM Trial 2 p = .900
.650
ΔCOM Trial 3 p = .350
.053
ΔCOM Trial 4 p = .947

47
 Chapter 4: Individual Physiological Results

Due to the small sample size and therefore lack of statistical power further examination of
the data is needed. However, the lack of correlation between the biomechanical and physiological
variables and the seemingly erratic presentation of the jerk data only the cardiopulmonary and self-
reported data of participants one and two will be presented.

Participant one’s data demonstrate the variability that affected the mean trial RPE values as
it contrasted with the general trend of all other participants. Yet, participants one and two displayed
similar V̇ O2 trends over both sessions, but the underlying mechanisms may differ. Hence, only P01
and P02 will be presented and discussed. Participants three and four can be found in Appendix 13
and 14, respectively. They will be referenced in conjunction in the individual discussion, but their
scores are closer to the mean of the group data.

For the individual presentation, participants V̇ O2 and HR TP1 and TP2 values are reported as
well as the ΔΗR and ΔV̇ O2. HR and V̇ O2 baseline values are also included. To determine the baseline
corresponding to the beginning of each trial, 60 seconds of data prior to the onset of exercise of
each trial were averaged and reported. An outline of the start time of each trial is outlined in Table
4.1.

Using the V̇ O2 and HR regression lines (Appendix 15) from each trial, predicted times to
V̇ O2peak and HRpeak were calculated and either time spent at (positive value) or time to (negative value)
V̇ O2 or HR peaks displayed. R2 values for each regression line were reported. To indicate the energy
systems used in each trial mean and peak respiratory exchange ratio (RER) between TP1 and TP2
were also calculated and reported with trial RPE.

Table 4. 1. Time periods corresponding to the mean HR and V̇ O2 baseline calculations

Trial Baseline Time Calculation

(s)
1 60-120
2 540-600
3 1020-1080
4 1500-1560

Participant One

Table 4. 2. P01 anaerobic thresholds and V̇ O2 peak.

VT1 VT2 V̇ O2peak

33 45 47

48
Table 4. 3. P01 session one V̇ O2 linear regression calculations with peak and mean respiratory
exchange ratio.

Time
Time to Spent at
Baseline Δ (TP2 – V̇ O2 V̇ O2 Peak RER
2
O2 TP1 TP2 TP1) Peak Peak R Value (mean)
Trial 1 6.09 42.84 50.70 7.86 272.85 87.15 0.59 1.1(1.05)
Trial 2 12.20 45.76 46.50 0.74 898.60 -58.60 0.02 1.02(0.98)
Trial 3 11.24 44.71 45.58 0.87 1622.55 -302.55 0.01 1.02(0.99)
Trial 4 10.13 43.22 44.63 1.41 2111.84 -311.84 0.04 1.05(0.97)

Table 4. 4. P01 session one RPE scores.

Trial RPE
1 16
2 16
3 15
4 14

Figure 4. 1. P01 Session one V̇ O2 with anaerobic thresholds and V̇ O2 peak.

60

50
VO2 (ml∙kg∙miin-1)

40

30

20

10

0
2 86 170 254 338 422 506 590 674 758 842 926 1010109411781262134614301514159816821766
Time (s)

vo2 VT1 VT2 V02 Peak

Table 4. 5. P01 Heart rate peak value from treadmill test.

Heart Rate Peak

193

49
Table 4. 6. P01 Session one heart rate linear regression calculations.

Time
Spent
Baseline Δ (TP2 – Time to at HR
HR TP1 TP2 TP1) HR Peak Peak R2 Value
Trial 1 119.87 180.99 187.96 6.97 493.63 -133.60 0.90
Trial 2 127.14 183.27 191.24 7.97 880.74 -40.74 0.81
Trial 3 134.85 183.59 192.65 9.07 1313.74 6.26 0.77
Trial 4 138.85 182.54 192.73 10.19 1804.88 -4.88 0.77

Figure 4. 2. P01 Session one heart rate with heart rate peak

250
Heart Rate (beats∙min-1)

200

150

100

50

0
0 200 400 600 800 1000 1200 1400 1600 1800
Time (s)

Heart Rate Peak HR

Table 4. 7. P01 session two V̇ O2 linear regression calculations with peak and mean respiratory
exchange ratio.

Time
Time to Spent at
Baseline Δ (TP2 – V̇ O2 V̇ O2 Peak RER
2
O2 TP1 TP2 TP1) Peak Peak R Value (mean)
Trial 1 6.44 43.04 47.22 4.18 350.27 9.73 0.22 1.07(1.03)
Trial 2 11.59 43.44 46.72 3.27 855.93 -15.93 0.24 1.02(0.96)
Trial 3 10.32 42.92 45.29 2.37 1453.83 -133.83 0.10 1(0.96)
Trial 4 9.97 38.67 45.72 7.05 1833.67 -33.67 0.62 1.03(0.98)

50
Table 4. 8. P01 session two RPE scores.

Trial RPE
1 13
2 13
3 13
4 12

Figure 4. 3. P01 Session two V̇ O2 with anaerobic thresholds and V̇ O2 peak.

60

50
VO2 (ml∙kg∙min-1)

40

30

20

10

0
3 60 117 174 231 288 345 402 459 516 573 630 687 744 801 858 915 972 1029108611431200
Time (s)

vo2 VT1 VT2 V02 Max/Peak

Table 4. 9. P01 Session two heart rate linear regression calculations.

Time
Spent
Baseline Δ (TP2 – Time to at HR
HR TP1 TP2 TP1) HR Peak Peak R2 Value
Trial 1 113.38 176.86 187.29 10.43 461.17 -101.17 0.78
Trial 2 121.25 182.51 193.53 11.03 831.04 8.96 0.87
Trial 3 127.38 184.73 194.32 9.58 1294.59 25.41 0.80
Trial 4 134.60 181.78 195.52 13.75 1766.07 33.93 0.86

51
Figure 4. 4. P01 Session two heart rate with heart rate peak

250

200
Heart Rate (beats∙min-1)

150

100

50

0
0 200 400 600 800 1000 1200 1400 1600 1800
Time (s)

Heart Rate HR Peak

Participant Two

Table 4. 10. P02 anaerobic thresholds and V̇ O2 peak.

VT1 VT2 V̇ O2peak

36 42 46

Table 4. 11. P02 session one V̇ O2 linear regression calculations with peak and mean respiratory
exchange ratio

Time
Time to Spent at
Baseline Δ (TP2 – V̇ O2 V̇ O2 Peak RER
O2 TP1 TP2 TP1) Peak Peak R2 Value (mean)
Trial 1 8.84 37.56 40.84 3.27 651.58 -291.58 0.24 1.03(0.96)
Trial 2 9.52 40.20 41.61 1.41 1417.89 -577.89 0.03 1.06(0.97)
Trial 3 11.40 38.95 35.86 -3.09 n/a n/a 0.17 1(0.95)
Trial 4 9.61 33.26 31.59 -1.67 n/a n/a 0.06 1.04(0.95)

Table 4. 12. P02 session one RPE scores.

Trial RPE
1 12
2 13
3 13
4 14

52
Figure 4. 5. P02 Session one V̇ O2 with anaerobic thresholds and V̇ O2 peak.

50
45
40
35
VO2 (ml∙kg∙min-1)

30
25
20
15
10
5
0
2 86 170 254 338 422 506 590 674 758 842 926 1010109411781262134614301514159816821766
Time (s)

vo2 VT1 VT2 V02 Peak

Table 4. 13. P02 Heart rate peak value from treadmill test.

Heart Rate Peak

202

Table 4. 14. P02 Session one heart rate linear regression calculations.

Time
Spent
Baselin Δ (TP2 – Time to at HR
e HR TP1 TP2 TP1) HR Peak Peak R2 Value
Trial 1 122.17 195.63 202.54 6.92 265.24 94.76 0.87
Trial 2 125.29 200.20 208.70 8.49 628.76 211.24 0.85
Trial 3 139.04 183.79 208.00 24.21 1207.65 112.35 0.58
Trial 4 140.68 202.51 208.00 5.49 1517.96 282.04 0.71

53
Figure 4. 6. P02 Session one heart rate with heart rate peak

250
Heart Rate (beats∙min-1)

200

150

100

50

0
0 200 400 600 800 1000 1200 1400 1600 1800

Time (s)

Heart Rate HR Peak

Table 4. 15. P02 session two V̇ O2 linear regression calculations with peak and mean respiratory
exchange ratio

Time
Time to Spent at
Baseline Δ (TP2 – V̇ O2 V̇ O2 Peak RER
O2 TP1 TP2 TP1) Peak Peak R2 Value (mean)
Trial 1 5.98 36.51 41.75 5.24 510.32 -150.32 0.30 1.03(0.96)
Trial 2 9.85 38.48 40.29 1.81 1422.86 -582.86 0.06 1.03(0.96)
Trial 3 9.85 39.44 39.59 0.15 9336.25 -8016.3 0.00 1(0.93)
Trial 4 9.99 39.38 40.59 1.20 2632.77 -832.77 0.03 1.02(0.96)

Table 4. 16. P02 session two RPE scores.

Trial RPE
1 13
2 13
3 13
4 13

54
Figure 4. 7. P02 Session two V̇ O2 with anaerobic thresholds and V̇ O2 peak.

50
45
40
35
VO2 (ml∙kg∙min-1)

30
25
20
15
10
5
0
2 86 170 254 338 422 506 590 674 758 842 926 1010109411781262134614301514159816821766
Time (s)

vo2 VT1 VT2 V02 Peak

Table 4. 17. P02 Session two heart rate linear regression calculations.

Time
Spent
Baselin Δ (TP2 – Time to at HR
e HR TP1 TP2 TP1) HR Peak Peak R2 Value
Trial 1 109.73 189.39 198.88 9.49 420.86 -60.86 0.91
Trial 2 113.83 196.73 204.88 8.16 774.60 65.40 0.87
Trial 3 120.63 199.46 206.32 6.86 1203.50 116.50 0.77
Trial 4 130.48 201.24 208.00 6.76 1632.49 167.51 0.89

Figure 4. 8. P02 Session two heart rate with heart rate peak

250
Heart Rate (beats∙min-1)

200

150

100

50

0
0 200 400 600 800 1000 1200 1400 1600 1800
Time (s)

Heart Rate HR Peak

55
 Chapter 5: Discussion

Group Discussion

Participants’ mean V̇ O2peak scores (46.25 ml∙kg-1∙min-1) in this study are in the upper range
between previously tested student (39.2 ml∙kg-1∙min-1) and professional (49.1 ml∙kg-1∙min-1) female
contemporary dancers’ scores (Angioi et al., 2009). Participants in this study had a mean VT 1 of 34.74
ml∙kg-1∙min-1 which was 75.1% of their V̇ O2peak scores. Participants’ VT2 scores were 92.4% of V̇ O2peak
and resembled that of other contemporary dance undergraduates’ anaerobic thresholds measured
in a recent study at 95.48% of V̇ O2peak (Needham-Beck et al., 2019). Beck and colleagues (2018) also
found female undergraduates to have a LT at 86.29% of their V̇ O2peak scores (42.44 ml∙kg-1∙min-1). It
should be noted that the methods for threshold determination between those studies and the
present one differ as the LT and VT1 are different measurements (Pettitt et al., 2013). However, the
V̇ O2peak scores seen in Beck’s 2018 study are lower than found in the current study. This could be
attributed to the fitness training participants in the current study anecdotally shared they had been
doing in their own time as a response to lockdown and the increased focus from dance schools to
maintain physical activity during lockdown (Bruyneel et al., 2020).

The mean, TP1 and TP2 V̇ O2 of all ADAFT trials was 38.8 and 42.3 ml∙kg-1∙min-1, respectively
which was 86.1 and 91.4% of V̇ O2peak and 114.6% and 121.8% of VT1. The original stage three was
shown to be ~63.4% of undergraduates V̇ O2peak scores and 73% of participants’ LT. This places the
relative intensity of the ADAFT similar to aerobic responses seen in stage four and five of the DAFT
(Wyon et al., 2003) while also demonstrating the intensity changes that occurred due to the addition
of some technical steps. Mean TP1 and TP2 HR responses were 95.1% and 99.4% of participants
HRpeak, confirming its similarity to dance performance intensity and to the later stages of the DAFT
(Tiemens et al., 2018; Wyon, 2009).

Due to the small sample size, statistical analysis of the data was limited, and only within-trial
data was statistically analysed. Therefore, discussion of the changes occurring over the sessions are
observational only. However overall, the findings warrant further discussion in relation to the
hypotheses of this study.

Primary Aim

The first aim, to model the kinetics of the V̇ O2 and HR responses, was hindered by the
fluctuations that were observed in the individual data meaning they could not be fitted by the
model. This is likely explained by the intermittent nature of dance which meant that the fluctuations
in intensity between the movements affected the linearity of the phase-III component. Alternatively,
though participants were instructed to perform as if they were on stage and to keep work rate at a
constant, the high-intensity, interval nature of the sessions may have meant participants
implemented a pacing strategy during trials in response to the initial bout affecting their work rate
(Seiler & Hetlelid, 2005). This could explain the fluctuations seen in HR and V̇ O2 kinetics after the first
trial.

Thus, accurately categorising the intensity domain of the ADAFT is difficult. Trials one (T1)
and two (T2) had significant increases in the V̇ O2 values and produced end values at 94.3% and 91.9%

56
of V̇ O2peak, respectively. However, trials three (T3) and four (T4) did not reach significance but end
V̇ O2 continued to descend finishing at 90.5% and 88.8% of V̇ O2peak, respectively. TP1 V̇ O2 values
however did not follow a linear pattern increasing from 84.2% to 88.1% of V̇ O2peak from T1 to T2,
respectively. This increase is consistent with the ‘priming’ effect of prior heavy exercise leading to a
faster phase-II response and a subsequently decreased phase-III amplitude (Burnley et al., 2006).
Still, from T2 onwards further decreases in TP1 V̇ O2 values were observed from 87.4% to 84.6% of
V̇ O2peak, respectively. As each trial lasted four minutes and V̇ O2peak values were obtained for all
participants, their true time to exhaustion is unknown and classifying the ADAFT as heavy or severe
exercise is not possible. However, the decreases in significance seen in the mean change in V̇ O2 from
T1 to T4 (Table 3.2) indicate a change in the intensity of the trials themselves but also suggest that
there was a V̇ O2sc present in all trials. Billat and colleagues (1998) showed the difference in the
magnitude of the V̇ O2sc between exercise modes at ~90% V̇ O2max. Their findings showed running to
have a significantly smaller V̇ O2sc in comparison to cycling; 21 ml/min and 269 ml/min, respectively.
While the time to exhaustion in their study was ~10 minutes, the magnitude of change in this study
for each trial was 295 ml/min, 113 ml/min, 89 ml/min and 121 ml/min, respectively. This may place
the intensity of the ADAFT in the upper range of heavy exercise or possibly severe or extreme
domain although this cannot be confirmed. The results of this study, suggest a greater V̇ O2sc during
dance activity in comparison with running and cycling. This may be to the larger ranges of motion
and significant eccentric component seen in dance comparatively inducing a greater load on the
neuromuscular system and requiring more mechanical efficiency (Paschalis et al., 2012). However,
this was not consistent throughout the trials and the slope of the V̇ O2sc is reduced from the priming
effect high intensity exercise has on muscle recruitment in subsequent bouts (Burnley et al., 2002).
Equally, changes in the relative intensity could be representative of a learning effect that increases
the participants movement economy (Sparrow et al., 1999). The methods of analysis in this study
have questionable validity so caution must be taken in when interpreting the comparisons made.
Nevertheless, the movement economy in trained endurance athletes performing steady-state
activity is sure to be better than the participants in the current study performing a dance sequence
they had only just learnt. This is certainly true when comparing movement economy in shuttle runs
with changes of direction to steady-state running (Dolci et al., 2021). Billat (1998) posits that through
utilisation of the stretch-shortening-cycle (SSC) in running it is more mechanically efficient than the
predominantly concentric work done during cycling. Therefore, the contraction regimen is possibly
responsible for the reduced V̇ O2sc seen in a whole-body activity such as running. As an activity, dance
is much closer to running than cycling, due to its weight bearing nature (Wyon, 2006). However,
dancers are required to learn and rehearse new material to increase the efficiency of movement and
perform new choreography on a regular basis (Kimmerle & Cote, 2007). Dance utilises many SSC
movements and with practice, skilled movements become more economical and decreases in energy
expenditure can be observed (Deighan, 2005; Sparrow & Newell, 1998). This may offer an alternative
explanation to the changes in the TP2 O 2 cost through the session, but are likely more closely related
to pacing and fatigue as self-optimising mechanisms are usually present over much longer time
courses (Sparrow & Newell, 1998).

The significant changes in HR values in each trial indicate the high intensity participants were
working at during the ADAFT. The TP1 HR values across the four trials were 91.9%, 94.9%, 94.7% and
95.7% of HRpeak, and trial TP2 values were 96.6%, 98.7%, 99.7% and 99.7%, respectively. The end
values exceed those seen in the high intensity dance performance fitness test designed by Redding
and colleagues (2009). However, in their study mean HR values from each minute-long trial were
reported and therefore peak values may be closer to the end HR responses seen in this study. The
high values in this study could partially be due to the high resting HR values seen in participants prior

57
to the first bout (see Individual Data). An elevated HR is a known somatic symptom of performance
anxiety (Walker & Nordin-Bates, 2010) which many participants in this study expressed around the
idea of being ‘tested’.

In the case of this study, dancers were not marked on a specific movement criterion. But, HR
has been shown to be sensitive to changes in the aesthetic movement quality during the DAFT
(Tiemens et al., 2018). Before each trial, verbal instructions based on Wyon and colleagues’ (2003)
and Tiemens and colleagues’ (2018) findings were read, and participants were verbally encouraged
throughout the test. However, the lack of data regarding the quality of the performance means that
the lack of control over this variable may explain the variations seen in the physiological data.

Furthermore, the significant increases in HR within all trials suggest that the relative
amplitude of the HRsc is more pronounced than the V̇ O2sc during the high-intensity, intermittent
dance choreography used as is seen in high-intensity steady-state exercise (Zuccarelli et al., 2018).
This has important implications for tolerance to dance activity, especially when working at
performance intensities and in performance conditions. For example, dancers can be required to
wear costumes in performance which may contribute to an increased HR and core temperature
(Örer & Doğu, 2017). In the current study, it is likely that by the end of T3 and T4 that participants
were working at or near to HRmax, possibly contributing to a decrease in aerobic power (Wingo et al.,
2012). During high-intensity interval running the HR sc has been shown with HR peak values increasing
in subsequent trials (Seiler & Hetlelid, 2005). The trained distance athletes in that study showed
lower relative HR values while working at a similar % of V̇ O2max (94-95%) to the present study. These
differences are probably explained by the training status of the sample they used in conjunction with
the steady-state exercise mode (Buchheit & Laursen, 2013).

The average group RPE increase over the four trials in this study was small and equal to 1
(Table 3.4). Interestingly, the scores were lower than expected for the intensity of the sequence (T1=
12.75, T2= 12.875, T3=13.375 and T4=13.75). The low scores in this study are in contrast with
previous findings that work >GET is associated with RPE scores >14 (Cochrane et al., 2015). The low
net increase in RPE scores was due to the large individual variation, especially in the first trial, which
can be seen in the individual analysis. The gradual increase in RPE scores throughout bouts however
is similar to findings in high-intensity interval activities (Laursen & Bucheit, 2019). However, the lack
of relationship between the group RPE scores and the relative intensity of the ADAFT is unclear. On
the one hand, the original choreography was designed to be simple, and the modifications made for
the present study may not have significantly increased the difficulty of the sequence. This could have
resulted in the dancers reporting the perceived choreographic complexity rather than perceived
intensity. On the other hand, this may be representative of a dissociative tendency towards exertion
seen in dancers (Thomson et al., 2011). During high-intensity work, perceptions of ventilation, heart
rate and metabolite build-up contribute to the sensation of exertion (Borg et al., 1987; S. Gandevia
et al., 2002). The results of this study are in agreement with Tiemens et al (2018) suggesting that RPE
responses are not representative of the overall intensity of individual trials and must be taken in
conjunction with other internal measurements such as HR. However, RPE may still be representative
of session load over an entire contemporary class or rehearsal (Jeffries et al., 2017). Finally, the
group means are only partially representative of participants’ perceptual responses. Gillach and
colleagues (1989) highlighted the importance in analysing individual RPE responses which will be
presented in the following chapter.

58
Secondary Aim

The secondary aim of this study was to analyse the effect fatigue had on jerk in specific
locations on the body. Results showed consistent, though largely non-significant increases j ARM, jLEG
and jCOM within all trials. For jARM, an increase of 7.2%, 6.1%, 7.5% and 3.5% was observed for T1, T2,
T3, and T4, and jLEG showed increases of 9.9%, 4.5%, 6.4% and 5.4% for each trial, respectively. Lastly,
jCOM showed increases of 6.7%, 3.8%, 4.2% and 4.8% for T1, T2, T3, and T4, respectively. However,
small but significant increases were observed for two of the twelve results. These occurred in j ARM in
T3 and jLEG in T1. Therefore, no consistent, significant pattern or whole-body effect was observed for
any one trial. This may be explained by the capped length of trials meaning the extent to which
fatigue was present in individual participants differed, affecting the significance. Therefore, neither
the null hypothesis nor hypothesis can be fully accepted.

Still, the consistent increase in jerk suggests that this measure could provide a useful means
of assessing dancers in the field and warrants further research. Measurements of jerk are highly
task-specific and therefore cannot be directly compared with other research (Balasubramanian et
al., 2015) but this research design has multiple measurements of the same movement sequence
allowing for observational comparison of within-session data. Like the change within-trial V̇ O2
changes, ΔARM, ΔLEG and ΔCOM reduced in magnitude as the session progressed. Although the
longitudinal data is not statistically analysed, there are observable within-session trends which will
be discussed with the within-trials data.

What is unclear is whether the results in the current study are from a conscious change in
movement strategy from participants as a form of pacing, self-optimising mechanisms through
repeated practice of the sequence, or fatigue. All are likely to contribute to the changes in
movement kinematics over time and athletes are known to alter their movement strategies in a
fatigued state in a highly individualised manner (Salo & Scarborough, 2006).

Physiological tremor is associated with states of fatigue and its effects can extend to the
whole body after isolated fatiguing muscle work (Morrison et al., 2005). High-intensity exercise
induces greater changes in dynamic balance when compared to longer forms of exercise
(Nourbakhsh et al., 2011). Furthermore, a fatigued muscles ability to store and utilise elastic energy
diminishes, affecting the motor strategy (Zago et al., 2019). All phases of contraction see reductions
in force production and a steeper force-velocity curve during fatigue (Ruiter et al., 2000). Slower
crossbridge cycling and post-contraction muscle relaxation may reduce the ability to optimally
maintain the tempo of the ADAFT (Ruiter et al., 2000). As a result, the sustained, high intensity of
trials may be the main cause of the increased jerk in the limbs and COM.

Yet, accurately delineating the changes in movement patterns from the current data is
impossible and such analysis would require more complex measurement and analysis methods.
However, the degree of significance was generally greater in the limb measurements in comparison
to the COM. This suggests that the limb trajectories and peripheral motor control were more
affected by fatigue in comparison to the COM within trials. Contemporary dance, such as the
choreography used in this study, requires coordinated movement of the upper and lower body to
accurately negotiate the transitions between steps. Along with the reductions in force, changes in
motor variability and strategy are seen in fatigued states to compensate for postural instability
(Cortes et al., 2014; Nagano et al., 2014). Along with this decreases in intrinsic muscle stiffness and
altered proprioception force the system to work harder in order to perform the task (Paillard, 2012).
Furthermore, the ‘priority’ of ventilatory drive and importance of the trunk muscles in whole-body

59
stabilisation may lead to further degradation of limb motor performance during sustained, high-
intensity work (Gandevia et al., 2002). Therefore, the greater increases in jerk seen in j ARM and jLEG
may be due to their continuous and important function throughout the sequence.

Without sufficient recovery during the bouts, it appears that the sustained intensity
deteriorates the movement economy which in this case is represented by increased O 2 cost and jerk.
However, TP1 values across all devices appear to reset with the four-minute recovery period and j ARM
and jLEG have an opposite longitudinal trend to jCOM. Lower jerk is associated with smoother, fluid
movement which is related to precision and accuracy (Choi et al., 2014). TP1 jerk values decreased
by 4.5% and 1.8% from T1-T4 in jARM and jLEG, respectively while jCOM increased by 5% throughout the
session. The decreasing trend in the limbs is consistent with the notion that acquiring skilled
movement is accompanied with better mechanical efficiency and energy exchanges (Kadota et al.,
2009). However, systematic alterations to technique in response to fatigue cannot be ruled out
either. Runners are shown to decrease their stride length but maintain stride rate during long
distance events (Elliot & Ackland, 1981). However, decreases in COM control during high-intensity
running have not been detected (Möhler et al., 2019). The dynamic direction changes and relative
complexity of the sequence in comparison to running may therefore account for the increasing trend
in jCOM seen in the present study. Fatigue deteriorates the attainment of the task goal and the CNS
increases movement variability of the COM to facilitate consistent performance (Sedighi &
Nussbaum, 2017). Consistent with this notion, dancers have been shown to use a greater trunk and
hip strategy in landings in response to fatigue to possibly compensate for undesirable forces in the
lower limbs (Jarvis & Abergel, 2019). Attributing the changes in jerk to peripheral or central
mechanisms of fatigue is not possible with this data and the longitudinal changes are small. Still, the
increase seen in the jCOM could be representative of the central fatigue mechanisms and the
progressive degradation of motor output as the session progresses (Paillard, 2012). However, with
the low sample size, high signal-noise ratio typical of IMU measurements and lack of statistical
analysis, this speculation would require experimental confirmation.

Tertiary Aim

The third aim was to assess the correlations between Δj with ΔV̇ O2 and Δj with ΔHR. No
significant correlations were detected in any of the comparisons and in some unexpected instances
negative correlations were measured. This is explained by the highly variable response where in
some participants, Δj was a negative value producing non-significant, negative correlations in the
group calculations. Neither ΔV̇ O2 or ΔHR had a clearly observable stronger relationship with ΔjARM, Δj-
LEG or ΔjCOM. The lack of connection means the null hypotheses was accepted in this case. Heart rate is

more related to central mechanisms, so the lack of correlation is understandable (Dampney et al.,
2002). However, jerk relates to the spatial-temporal aspect of the movements and V̇ O2 relates to the
cost. Without adequate recovery at high intensities, the decline in neuromuscular efficiency affects
the economy of the movement (Garnacho-Castaño et al., 2018). Efficiency largely refers to the
process of energy transformation from biological substrates (mostly lipids and glycogen) in oxidative
processes during mechanical work in muscles, but it can also represent the function of single or
multiple systems and organisms (Ferretti, 2015). Therefore, movement economy is negatively
affected by the development of the V̇ O2sc (Garnacho-Castaño et al., 2018). Jerk represents a
qualitative property of the movement outcome rather than allowing for analysis of specific
kinematic adaptations. This may represent a clear limitation in the measurement of jerk which does

60
not provide such rich kinematic data about the spatial and mechanical aspects of the overall
movement pattern which may explain the lack of correlation found. However, it still highlights the
importance of monitoring both physiological and biomechanical variables during dance research.
Given their relationship to fatigue it is likely that both contribute to the V̇ O2sc (Borrani & Candau,
2003). However, the results of this study suggest jerk not correlated the V̇ O2sc.

Individual Data Discussion

Sessions one and two are separated for the individual analysis as they further illuminate the
group findings by individually discussing the interactions between perceptual and internal bodily
responses. As seen in Figures 4.3, 4.4, 4.7 and 4.8 and Tables 4.8 and 4.16, for P01 and P02 the
second session displays a possible learning effect that stabilised the responses in comparison to the
first possibly because participants had prior experience of the intensity of the entire session. This
was present across all participants but the overall trend of responses between trials one to four was
similar across both sessions. However, the following discussion will unpick aspects from the
physiological and self-reported responses of P01 and P02.

The baseline calculation before each trial allowed for analysis of cardiopulmonary recovery.
In all participants the HR did not fully recover after each trial and continued to rise due to the HR sc as
demonstrated in the group data. Similar to the mean V̇ O2 TP1 measurements, all participants
displayed an elevated V̇ O2 baseline after the first trial which has been shown to be linked with the
‘priming’ effect previously discussed (Burnley et al., 2006). The initial bout of the ADAFT produced a
mean RER of ~1.02 across the trial and by the final trial indicated ~0.95. RER values >1 usually
indicate the accumulation of lactate which may act as a proxy variable for the priming effect which
can affect the V̇ O2 baseline and the V̇ O2 kinetics up to 20 and 60 minutes after the end of the bout,
respectively (Burnley et al., 2006). The priming effect is related to improved endurance performance
which can be characterised by the speeding of the primary amplitude and an increase in the W’
(Burnley et al., 2011). However, this does not seem to have a noticeable impact on participants’ jerk
which may be more sensitive to fatigue rather than short term motor learning. Further dance-
specific research would be needed to understand the impact, if any, of priming on dance
performance.

P01 appears to mitigate the time at HR peak by trial four (Table 4.6 and Figure 4.2) which
corresponds with a decrease in RPE from 16 to 14 (Table 4.4). The effect of this was carried into the
second session as RPE declines further from 13 to 12 (Table 4.8). However, the same pattern is not
seen in the HRsc which is marginally higher in the second session (Table 4.9). Additionally, the oxygen
cost, relative to V̇ O2peak, decreased throughout both sessions with TP1 trial one starting at 91.15% in
session one and finishing at 82.27% by trial four, session two. TP2 followed a similar pattern starting
at 107.87% and finishing at 97.27%. Considering the priming effect that prior high intensity (>GET)
exercise has on the phase-II oxygen kinetics (Burnley et al., 2006), there is a clear decrease in energy
expenditure seen in this participant throughout the trials and the sessions. This may relate to self-
optimising mechanisms that occur as the participant moves from a cognitive to a more autonomous
state when executing the sequence (Sparrow et al., 1999; Wulf & Lewthwaite, 2016). This transition
refers to motor learning that develops through practice. As the participant repeats the steps, the
mechanical efficiency improves as the motor program becomes more refined, which in turn has an
effect on the metabolic cost of the movement itself (Sparrow & Newell, 1998).

61
 P02 displayed some similar trends in V̇ O2 and HR responses to P01. However, perceptual
responses were opposing suggesting a difference in the underlying mechanisms. This participant
exceeded the HRpeak measured in the treadmill test by the end of the first trial and thus time at HR peak
is increased as the session continues, and a clearer plateau of HR is apparent indicating they were
working at HRmax (Table 4.14). Both participants demonstrate that measurements from treadmill
tests are not fully representative of dancers’ true cardiopulmonary capacities. This may be due to
the larger muscle mass used during changes of direction in comparison to in-line running (Dolci et
al., 2021) and/or dancers’ notorious inability to perform maximally on non-dance-specific exercise
tests meaning they are prepared to push themselves harder during dance-specific activity (Redding
et al., 2009). The %V̇ O2peak/%HRpeak ratio also differed between P01 and P02. P01 displayed a higher
%HRpeak response in comparison to %V̇ O2peak and P02 had the opposite relationship. P01 had a ratio of
~100%/97.4% while P02 had a ratio of ~88.8%/100% if adjusting the values taken from the ADAFT to
be the true V̇ O2max and HRmax. The exact cause of this finding remains elusive but the V̇ O2/HR
relationship during team sport activity such as basketball and football has been shown to be
79%/92% and 52%/72%. The results seen in this study may be due to different modality used for
ascertaining V̇ O2peak and HRpeak and thus affecting the accuracy of the relative measures. However, the
greater HRsc in relation to the V̇ O2sc in this study is possibly due to the greater neuromuscular demand
from the larger muscle mass and non-linear contraction regime used in dance when compared to
high-intensity steady-state activity (Zuccarelli et al., 2018).

During session one, the HRsc of P02 appears to influence oxygen uptake and aerobic power is
lost (Figure 4.5). As discussed in the literature review the V̇ O2 max is dependent on oxygen transport
to, and utilisation within, the working muscle. The V̇ O2 max has been shown to decrease
proportionately to the rising HRsc when maximal cardiac capacity is obtained (Wingo et al., 2012).
Wingo and colleagues (2012), describe how this decrement in aerobic capacity potentially increases
the overall relative metabolic intensity of the activity in relation to the V̇ O2 max. Furthermore, the
decrease in oxygen cost during session one appears to inversely correspond with the increasing RPE
values from 12 to 14 (Table 4.12) which is the more typical perceptual response to interval training
using high intensity bouts (Laursen & Buchheit, 2019) and is seen in the RPE scores of P03 (Appendix
13) and P04 (Appendix 14). However, for P02 in session two, the deleterious effect on
cardiopulmonary function was not seen and V̇ O2 and RPE responses are more stable with a lower HR
than session one (Figure 4.7 and Tables 4.16 and 4.17) indicating a potential pacing strategy and
learning effect as seen in the other participants.

Impact for Dance and Future Research

The process of refining of dance choreography is something that requires further research as
it is of great importance for the dancer. The best dancers are often the best learners and can
efficiently self-regulate, adapting to the environment in a fast and efficient manner (Kimmerle &
Cote, 2007). In this study, strategies that reduced the internal bodily responses of participants may
have related to pacing strategies in response to fatigue. Indeed, the HR sc has been shown to be highly
sensitive to pacing strategy and inversely correlated with marathon performance in elite runners
(Billat et al., 2020). Equally, it could have related to the fact that dancers will usually strive to
improve and perfect movement that caused the decreases in the energy demand (Kimmerle & Cote,
2007). In the words of Laban & Lawrence (1974., p. 13) “The contentment accompanying the beauty

62
of well-rhythmised and therefore skilled movements plays a great role in the economy of human
effort”. Whether the aesthetic of the ADAFT performance was significantly affected is unknown as it
was not directly measured but by reducing their physical effort and thereby intensity, the HR sc and
V̇ O2sc would be attenuated, delaying fatigue. It is still unknown whether these changes were due to
deliberate changes in the movement quality, a pacing strategy or improved movement economy.
Future research should explore the distinction between the self-optimising mechanisms and pacing
strategies that dancers implement when learning new choreography in further detail.

Jerk as a measurement requires further dance-specific study as using IMU’s to quantify

session training load in dance has become more popular in recent research (Jeffries et al., 2017;
Shaw et al., 2020) and machine learning algorithms that recognise dance activity have been
proposed as a method to measure training volume (Hendry et al., 2020). However, implementation
of qualitative measures such as jerk has received less research in dance (Park, 2016). Jerk could be
useful in monitoring fatigue and the development of skill throughout a dancers training or career.
The IMU’s provide a non-invasive tool that could be regularly utilised by coaches in dancer profiling.
The jerk calculation in this study produced a lot of variability indicating that finding optimal methods
of reducing the noise from sensors during dance activity may increase the efficacy of jerk as a
measure. Then, before in-field utilisation is possible, research should aim to validate the best
method of jerk calculation and correlate it with subjective measures of aesthetic competence in
contemporary dance (Krasnow & Chatfield, 2009; Park, 2016). Research could investigate more
complex algorithms and possibly sensor fusion to create dance-specific load metrics such as
PlayerLoad™ (Gómez-Carmona et al., 2020). Due to the complex, non-linear nature of dance activity
and the varying individual responses it induces, quantifying and monitoring training load with
multiple measurements is more accurate than any measure alone (Jeffries et al., 2017). If proved
valid, jerk could be used in conjunction with other measures to assess a qualitative aspect of the
dancers’ movement and provide a richer picture of dancer’s condition and form. Team sports often
assess athletes readiness to play which informs team selection (Burgess, 2017). Wearable
technology may provide key insights into a dancer’s physical condition which could serve as a
valuable monitoring tool informing training load management and casting. This may subsequently
reduce injury risk as qualitative aspects of a dancer’s movement could be used as a marker of
fatigue.

Performance is arguably the most important aspect of a dancer’s career. While this study
emulates intensities typically seen in dance performance it acknowledges that in reality dance
performance produces a broad range of intensities. Contemporary dance performances have been
documented to last for a mean time of 36.45±30.32 (mins) and have a mean work percentage time
of 59.37±13.81% (range 35-86%) (Wyon, 2009). The time spent dancing in this study totalled 16
minutes with a 50% work percentage time and while it is not representative of real dance
performance, it demonstrates the acute effects fatigue can have on biomechanical and metabolic
efficiency. Dancers will often perform at high intensities for short periods and spend time resting
actively and passively. Further study assessing the longitudinal effects of fatigue would be beneficial
as it is common for professional dancers to maintain class and rehearsals during a performance
period where often new work is being created and similarly student dancers’ load is often increased
around performances (Grove et al., 2013). Consequently, lack of recovery in dancers may result in
residual fatigue having detrimental ramifications for neuromuscular performance as well as skill
acquisition and retention (Bompa & Buzzichelli, 2019; Branscheidt et al., 2019).

Fitter dancers will have better recovery after high intensity exercise, and be able to perform
exercise at a lower relative intensity, therefore delaying fatigue (Wyon, 2005). It is still a topic of

63
debate as to how fit dancers should be but it is important to supplement the deficit between class
and performance to ensure dancers are better prepared to cope with their workloads (Redding,
2019). Furthermore, dancers’ movement economy will improve with their skill level resulting in a de-
training effect in dance-specific movements practiced in class (Beck et al., 2018; Guidetti et al., 2008;
Wyon, 2009). While this may produce dancers that are specifically biomechanically efficient, training
with a dance only approach is likely to be ineffective in maintaining their condition due to lack of
overload and monotony (Rafferty et al., 2009). The goal of training should be to produce an athlete
with an efficient and robust neurosignature that can withstand high levels of emotional stress,
cognitive challenge and varied, high levels of external demand (Liebenson, 2014). It seems logical
then that a dancers training should aim to optimise both biomechanical and metabolic efficiency.

There is now a significant amount of research on the benefits of supplemental training for
dancers and circuit training has been shown to increase anaerobic power and the V̇ O2max (Angioi yet
al., 2009; Koutedakis et al., 2007; Rafferty, 2010; Ramel et al., 2007). However, specific
cardiorespiratory training has received less attention throughout the literature. This may be as
cardiorespiratory indices have not been shown to correlate with performance competence in
dancers (Angioi et al., 2009; Needham-Beck et al., 2019). Yet, dancers are still exposed to high
training loads (Jeffries et al., 2017; Kozai et al., 2020) and periodisation is often difficult to
incorporate into dancers’ training (Rafferty & Stanton, 2017). Investigating optimal methods of
specific cardiorespiratory training for dancers would improve the efficacy of supplemental and pre-
season training. Further to this, research should assess the impact cardiorespiratory training has on
injury incidence in dancers. It is possible that reductions in energy expenditure, improved endurance
and enhanced recovery could have more immediate benefits for the wellbeing of a dancer than an
obvious impact on the aesthetic of dance performance.

Wyon (2005), recommends development of the aerobic and glycolytic systems through
cardiorespiratory training at %V̇ O2max or %HRmax, ideally using the modality of dance. However, as
seen in the results of the present study, this poses a challenge for coaches as exercise prescription at
specific intensities is difficult to define in dance. Using velocities corresponding to percentage of
HRmax or V̇ O2max on a treadmill or cycle ergometer makes prescription in cyclical modalities more
straightforward. Prescribing dance exercise at a constant workload is technically not possible due to
the non-steady-state nature of the activity which is further complicated by varying individual
responses and the V̇ O2sc and HRsc at seen higher intensities. Consequently, the overall training effect
may be sub-optimal if the training is not monitored and individualised.

Interval training is the most effective and specific way of increasing dancers’ aerobic power
(Wyon, 2005). High intensity interval training (HIIT) refers to work rates above the CP and
encapsulates large range of work and recovery intensities (Laursen & Buchheit, 2019). Long interval
HIIT (LIHIIT) consists of intervals of 2-5 minutes in length at or near the V̇ O2max (≥90% V̇ O2max) (Laursen
& Buchheit, 2019). If implemented correctly, this type of training will develop both aerobic and
anaerobic systems (Laursen & Buchheit, 2019). The format of sessions in this study resembled a
LIHIIT session with a w:r ratio of 1:1 but produced different intensity responses with some
participants reaching exhaustion (P05 and P08) before the end of the trial whereas for others, (P03
and P04) the intensity appeared closer to the heavy/severe domains. Even in steady-state activity
there are large amounts of individual variation in the V̇ O2 kinetic response that is sensitive to age,
gender, sex, training status and exercise modality (Laursen & Buchheit, 2019). Furthermore, the low
R2 values seen in the individual V̇ O2 data, demonstrate the difficulty of accurately modelling the on-
kinetics during dance activity, complicating the picture further. Estimating the energy cost and

64
energy sources using the off-kinetics may serve as a more suitable method for analysing the
bioenergetics of dance activity for future studies to consider (Guidetti et al., 2007).

To optimise training, developing dance-specific strategies that can adapt training to the
individual responses may be a useful area of investigation. Laursen and Buchheit (2019), propose the
manipulation of variables such as w:r ratios and intensities to elicit more controlled responses. In the
case of dance, a steady-state is not assumed and it is possibly more comparable to game based HIIT
due to the changes of direction, accelerations and decelerations (Buchheit & Laursen, 2013).
Consequently, intensity cannot be accurately prescribed as a function of measured physiological
entities such as the CP or V̇ O2max. Thus, to alter the intensity the rules and conditions of the games
are manipulated to provoke different responses (Laursen & Buchheit, 2019). This could be adapted
to a dance-specific context and variables such as choreography, improvisational task, tempo,
recovery periods and effort levels could be controlled to alter the intensity and would be interesting
avenues for future research to investigate. Furthermore, sequences should have the flexibility to
progress and regress accordingly to each dancer to alter the intensity. Finally, sessions could be
structured in a way that could possibly facilitate individual w:r ratios within a group setting.
Theoretically, working with dancers that have an improved cardiorespiratory capacity would give
choreographers more potential in their choreographic works as fatigue would be a less limiting
factor. Not only may this increase the potential for dancers to work at higher intensities for longer,
but it may also decrease the extent of fatigue experienced by dancers.

For coaches, monitoring training load in dancers is especially important when applying the
principles of periodisation (Shaw et al., 2020). However, the methods and equipment used in this
study would be highly impractical to implement regularly with a large group of dancers. This poses a
further challenge to coaches as accurately quantifying HIIT bouts with measures of HR or RPE alone
could be prone to errors in exercise prescription if aiming to achieve specific cardiorespiratory
adaptations (Buchheit & Laursen, 2013). Additionally, if prescribing exercise corresponding to a fixed
%HRmax caution must be taken as a reduction in metabolic intensity, proportionate to the HR sc
hinders the overall adaptation effect (Zuccarelli et al., 2018). Future research should determine
accurate methods of load quantification that can accurately be used for individual exercises or
bouts.

A possible limitation to HIIT training in a non-steady-state modality is that cardiac

adaptations are hindered by the fluctuations in SV which is thought to be more important than
maintaining a high HR in causing long term adaptation (Buchheit & Laursen, 2013). As suggested by
the data the V̇ O2/HR ratio may affect the ability to maintain a high intensity meaning longer HIIT
using dance may not be optimal when attempting to improve cardiac function. Furthermore,
maintaining a high intensity can reduce the aerobic power due to the HR sc (Wingo et al., 2012) and
maximising time spent near or at V̇ O2max is key in signalling adaptations during HIIT activity (Buchheit
& Laursen, 2013). At present, optimal sub-maximal and supra-maximal HIIT methods for dancers are
not researched and may be a key area of investigation for dance science. However, the length of
bouts will be limited by the amount of time the individual can spend above the CP and also the size
of their anaerobic power reserve (Laursen & Buchheit, 2019). This is further evidence that the
individualisation of dance-specific cardiorespiratory training may be required if the training is to be
optimised.

Accurate and reliable methods of quantifying individual trial load in non-steady state activity
would be useful for dance teachers and coaches as this would increase the efficacy of exercise
prescription. Therefore, future studies should compare dance-specific of HIIT with other modalities

65
to evaluate the efficacy of dance-specific cardiorespiratory training. Moreover, investigating non-
invasive wearable devices and methods of load monitoring for in field use would enable more
accurate exercise prescription.

Limitations

The study was the first of its kind to conflate biomechanical and physiological variables
during dance activity, however due to the nature of the dance activity it presented some limitations.

The sample size was small meaning the statistical power was low so conclusions drawn from
the analysis are limited. Also, the study coincided with the SARS-CoV-2 virus pandemic which may
have affected the measurements as participants’ dance training and levels of daily activity were
significantly altered. Hence, comparison of their physiological profiles and responses with other
research was approached with caution.

Modelling of the kinetics with validated methods used in other research proved difficult and
the methods employed showed low accuracy across the data. The use of a linear model in this type
of transient data portrays a limited picture of the kinetics and the analysis of the physiological data
should be viewed with caution. Furthermore, for the sake of continuity, the discrete time points
used for the V̇ O2, and HR data analysis were dictated by the length of the ADAFT sequences. TP1 was
taken ~55.4 seconds after the onset of exercise. This may be unrepresentative of the primary
response as it does not account for the individual phase-I components usually seen in response to
exercise further affecting the validity of the observations made.

Lastly, despite the sequence being taught each time by the lead researcher and the intent
and intensity controlled for through verbal cues, there was not a specific attempt to control the way
in which participants learnt and performed the phrase. This meant some participants had more
practice than others or performed the movements with a different range of motion or movement
strategy. This may have affected the results as participants were essentially free to change their
motor strategy as they wanted. Furthermore, kinematic measurements were taken unilaterally and a
whole-body effect technically cannot be assumed.

Conclusion

This study highlights the varied physiological and biomechanical responses that dancers can
have to the same choreographic stimulus and demonstrates the acute effect of fatigue and practice
on the cost of performance. It shows that without sufficiently reducing the intensity or allowing for
full recovery, performance becomes harder, and the energy and effort required to produce the same
outcome increases. However, when analysed individually, it demonstrates that a learning effect and
pacing strategy can also alter the dancers physiological and perceptual responses. The exact
mechanisms behind these changes remain unclear and warrant further study. The varied responses
pose a challenge for accurate load quantification which in turn makes optimal and accurate exercise
prescription difficult. More in-depth research combining physiological and biomechanical responses
may elucidate methods that could lead to more objective measures of load quantification. This could
in turn lead to a better understanding of ‘optimisation’ in dance performance and inform dancers’
training and casting in ways that are sensitive to the individual.

66
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 Appendices
Appendix 1
Sample Recruitment poster

85
Appendix 2
Sample Recruitment Email

To whom it may concern,

86
My name is Michael Doolan and I am currently studying an Msc (Master of Science) in dance science
at Trinity Laban, London. I am currently planning a research that will explore the difference between
movement economy profiles in dance based on different levels of experience. The title of the study
is ‘Does experience affect movement economy in dancers?’. Participants will complete two small
sections of an aerobic and a high intensity dance fitness tests while wearing portable technology
that will collect data on oxygen kinetics and biomechanical markers. More information is available
on request. Available applicants will be entitled to a familiarisation session where all procedures and
protocols will be demonstrated and any questions or issues that may arise will be answered in as
much detail as possible.

Groups are defined as such:

Pre-professional Group

 Dancers must have not completed a full-time vocational dance education.

Student Group

 Dancers must be currently undertaking a full-time vocational dance training

Professional Group

 Has completed full time dance training

 Has been exclusively employed as a freelance dancer or dancer for at least one year

Elite Group

 Dancers must currently be employed full time by a company and have been for at least three
years

Participants must also fit these criteria:

 Between the age of 18-40

 Has no injury that is negatively affecting their movement
 Is comfortable learning and repeating a simple, short choreography

Please get in touch if you are interested or have any questions.

Hope to hear from you soon.

Michael Doolan

Email: michael.d19@edu.trinitylaban.ac.uk

Phone: 07880565668

Appendix 3
Modified Medical PAR-Q

Please read the following carefully and answer as accurately as possible

87
 1. Have you ever suffered from low blood pressure?

2. Have you ever been prescribed a long term course of steroids or anything in your blood?

3. Has your doctor ever said you have heart trouble?

4. Do you suffer frequently from chest pains?

5. Do you often feel faint or have dizzy spells?

6. Has a doctor ever said you have epilepsy?

7. Has a doctor ever said you have high blood pressure?

8. Has a doctor ever said you have diabetes?

9. Has a doctor ever said you have asthma?

10. Do you have a bone, joint or muscular problem which may be aggravated through exercise?

11. Do you have any form of injury?

12. Are you currently taking any prescription medications?

13. Have you suffered from a viral illness in the last two weeks?

14. Is there anything in your past medical history that you have not mentioned so far
(conditions, diseases)?

Adapted from Chisholm, D.M., Collins, M.I., Davenport, W., Gruber, N., & Kulack, L.L. (1975) PAR-Q validation report. British Colombia
Medical Journal, 17.

Have you eaten within the last hour?

Have you consumed alcohol within the last 24 hours?

Have you performed exhaustive exercise in the last 48 hours?

IF YOU HAVE ANSWERED YES TO ANY OF THESE, PLEASE INFORM THE RESEARCHER

Appendix 4
Informed consent form

88
Project: Analysing Differences and Correlations Between Economy Profiles and Jerk in Different
Groups of Dancers during an Adapted Stage Three of the Dance Aerobic Fitness Test.

Please read the following carefully. Please sign only when you have agreed with the statements
and when you have had any relevant questions answered.

By signing this I confirm that:

 I am willing to take part in the test

 The testing procedures have been explained to me. I am clear about what I will be involved
in and the purpose.
 I am aware that there may be possible risks involved and these risks have been explained to
me. I understand that every effort will be made to minimize these risks based on information
that I have provided and observations carried out by the researcher.
 I have/will inform the researcher about any medical condition I am currently suffering from
or have suffered from which may affect or be affected by the test.
 I am free to withdraw from the test at any time without necessarily giving a reason.

Your participation in this investigation and all data collected from the above testing procedures ill
remain strictly confidential. Only the researchers involved in this study will have access to your
information and the information will not be accessible to any other member of staff. In compliance
with the Data Protection Act (1998) and the Freedom of Information (2000). You will be able to
access all information collected upon completion of the study.

I have read the information sheet and consent form and I fully understand the testing procedures. I
consent to participate in these tests.

Participant Name (print):

Date:

Signature:

Researcher Name (print):

Date:

Signature:

Appendix 5
Participant Information Sheet

Title: Analysing Differences and Correlations Between Economy Profiles and Jerk in Different Groups
of Dancers during an Adapted Stage Three of the DAFT

89
Researcher: Michael Doolan

You are invited to partake in a thesis study for Trinity Laban that involves measuring oxygen kinetics
and triaxial accelerometery during an adapted stage three of the Dance Aerobic Fitness Test.

Objective: The primary aim of the study is to analyse dancers’ economy profiles across a range of
abilities (student to elite) and correlate the oxygen uptake with kinematic variables.

Equipment:

1. Telemetric Gas Analyser (Metamax, 3B, Cortex Biophysik GmbH, Germany) x 1

2. Heart Rate Monitor (Polar, Polar Electro, Finland) x 1
3. IMU- Inertial Measurement Units (Shimmer3, Shimmer, Ireland) x 3

Testing Procedures:

Firstly, participants will receive a familiarisation session where the equipment will be introduced to
you, fitted to you and your height and weight will be recorded. During this session, a V02 max
treadmill test will be performed which requires participants to run on a treadmill. The treadmill will
increase in speed every minute and the test is either stopped voluntarily by yourself or until two of
the following criteria are met: heart rate within 10 b/min of age-predicted maximum, respiratory
exchange ratio (RER) above 1.15, VO2 plateau despite increase in speed, or inability to match
treadmill speed. The results from the test will be used to calculate your individual anaerobic
threshold (or lactate threshold) and V02 max (your maximal aerobic power) which are indicative of
your cardiorespiratory fitness levels. This session should take no more than 30 minutes.

In the three ADAFT testing sessions, you will complete a short, cycling warm up (on an exercise bike)
and will then learn the choreography from a video and be able to mark it once on each side. The
choreography is a 24 count, one-sided phrase that continuously alternates sides for four minutes.
Once fitted with the equipment, you will perform the choreography three times with a 3-4 minute
break in between. This session will take no longer than 1 hour from start to finish and will be
completed three times. In the rest phases, you may be given feedback and corrections on the
phrase.

The ADAFT sessions will happen a minimum of two days and a maximum of 14 days after completing
the treadmill testing session. The three ADAFT sessions will happen at least 12 and no more than 48
hours apart.

All ADAFT sessions will be video recorded.

Participants should not discuss the nature of the testing sessions or the experiment with anyone
until the entire testing phase is finished on the 1 st of May 2021.

All sessions will happen either in the laboratory or the studio of Trinity Laban.

Possible Risks:
During the treadmill test, some participants may be working at maximal or supra-maximal
intensities. If this is unusual for some of the participants and may cause them some fatigue or
physical discomfort shortly after completion. During the treadmill test at least one researcher will be
present and safety precautions put in place to maximize your safety. You can terminate the test at
any time without explanation.

90
Participants may experience some discomfort wearing the mask and the pack of the telemetric gas
analyser. This will be reduced by fitting the correct size and adjusting the fixing straps to the
participants requirements. Also, the participant will be wearing four more sensors – two on the torso
and one on the right arm and right leg. These will also be adjusted to the participants requirements
and are designed to be subtle and comfortable.
The test itself (stage three of the DAFT) should be of no greater risk than those experiences when
participating in a dance class or performance. Participants will always have at least the researcher
present if assistance is needed. Participants also have the right to pull out at any time for any reason.
Exercise: Participants are instructed to not participate in any progressive training program for the
duration of your participation in the study (from your first treadmill session until your final ADAFT
session). A Progressive training program is one that has been designed specifically to cause
physiological adaptation (Increase in muscle strength or increase in cardiorespiratory parameters
etc). Participants may continue to participate in dance class, rehearsal and any light physical activity
they would normally participate in outside of the study (pilates/yoga etc).

Participants should also not participate in any strenuous physical activity in the eight hours prior to
each ADAFT testing session.

Clothing: Participants will be required to dance in socks, these should be socks that you are
comfortable with wearing to dance in the studios at Laban. The treadmill test will require running
shoes/trainers.

Comfortable dance clothing is required. The material should not be shiny or slippery (such as lycra)
as this will stop the sensors from staying in a fixed position. Sensors are being placed on the forearm,
torso and shin.

The heart rate monitor and one IMU sensor is required to be placed on the skin of the torso (just
below the chest). Participants can fit it and remove it themselves with relative ease so may want to
wear clothing that leaves this area relatively accessible.

Food and Drink: Participants should not consume food or caffeinated beverages for at least two
hours prior to each ADAFT session. Participants should not eat an hour before coming for the
familiarisation session.

Formality: Trinity Laban’s Ethics Committee has reviewed and approved this project. All data will
remain confidential and used for the purpose of this research only.

Confidentiality: Information received during testing will only be revealed to the participant and the
investigator. The participants identity will remain anonymous and will be destroyed after the study.
You will be given access to all data collected upon your request.

Voluntary Participation: Participation is completely voluntary. No negative consequences will occur

as a result of stopping.

COVID-19: All testing procedures will comply with Trinity Laban’s COVID-19 guidelines. Participants
should undergo COVID testing weekly to ensure compliance with Trinity Laban’s COVID regulations
and upon arrival to the building must complete a self-temperature check. Participants must strictly
follow the practices in place within the building involving social distancing, facial coverings and one
way systems.

Contact Information: For any questions, comments or additional information contact,

91
Michael Doolan: 07880565668

Email: michael.d19@edu.trinitylaban.ac.uk

For complaints or an aspect of this study that concerns or disturbs you please contact the project
supervisors Emma Redding and/or James Brouner:

e.redding@trinitylaban.ac.uk

james.brouner@kingston.ac.uk

Participant Authorization

I have read this document and the study has been fully explained to me. I have had all my queries
adequately answered. I volunteer to participate in this study. I declare that I have no known injuries
or cardiorespiratory problems, nor have I needed serious medical treatment within three months
prior to participation in this study.

Participants signature:

Date:

Researchers signature:

Date:

Appendix 6

https://youtu.be/sVHtncrbVas

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Appendix 7
IMU Unit calibration, placement & fixture

The IMU’s accelerometer was individually calibrated in the 9DoF Calibration App (version. 2.10,
Shimmer, Realtime Technologies Ltd) using the calibration stand. The wide range accelerometer with

93
±16g range was selected before individual axis calibration. The sampling frequency was set to 201.3
Hz in the Consensys Pro software (version. 1.60, Shimmer).

Appendix 8
Metamax

The telemetric gas analyser was calibrated using the Metasoft-Studio Toolbox software (ref). The
oxygen and carbon dioxide sensors were calibrated before each test in the space that they would be

94
used in for ambient conditions of barometric pressure and volume and gas content against precise
gas mixtures of 5.02% carbon dioxide and 15.07% oxygen. Disposable Turbines were used meaning
the flow calibration was not necessary.

Appendix 9
Polar Heart Rate Monitor

95
 The heart rate monitor was connected and for the data to be synchronised with the gas
analysis via the Metasoft studio software.

Appendix 10
Warm Up

Participants completed four warm up exercises in any order they chose:

1. Stick and Hop 2-1: 3 x 5

96
 2. Mountain climbers: 3 x 20
3. Leg Swings with dynamic arm: 3 x 10
4. Light Wattbike cycling for 5 minutes

Appendix 11
Script for participants

From DAFT handbook:

97
  Execute each stage as fully and accurately as possible.
 Maintain the integrity of the movement.
 Start each stage at relatively the same place in space.
 Pick up the movement as quickly as possible if they get lost.
 Not fiddle, fidget, stretch, or perform any extra movements.
 Imagine they are in a performance setting or on stage.

Added for the purpose of the test:

 To perform the movements as smoothly and efficiently as possible.

Criteria for assessing the movement quality of the steps from handbook:

 Sequencing
 Coordination
 Effort levels
 Traveling distance
 Pointed feet
 Consistent arm positions
 Lunge depth (Chest to thigh)
 Jump height
 Overall movement quality

Appendix 12
Ethical Considerations

98
 A full ethics application was submitted to and approved by Trinity Laban’s Research Ethics
Committee. Only upon receiving approval did participant recruitment and data collection
commence. Participants were provided with an information sheet (Appendix 5) detailing the purpose
of the study with terms of participation. Participants had the right to withdraw at any time
throughout the study and this was outlined in the consent form (Appendix 4) along with a medical
PARQ (Appendix 3) which was completed prior to any testing. All data or information collected from
the participants was securely stored, password protected, and destroyed in accordance with GDPR
2008 regulations. Identities were protected by coding any names or information that would reveal
the participants identity unless written consent was provided by the participant for their data to
become public. Files stored electronically were password protected and coded to nullify the risk of
participants’ identities being revealed. A risk assessment of all testing procedures will be conducted.
Testing complied with Trinity Laban’s Covid-19 guidelines and procedures at the time testing took
place. All participants were subject to weekly COVID testing and completed a temperature check as
soon as they arrived on site. All testing procedures were done with relevant PPE in place to enhance
the safety of both the researcher and the participants. A participant COVID pre-screening form
(Appendix 13) was completed by all participants to increase the safety of those working in the
building.

Appendix 13
Participant 03

Table 4.18. P03 anaerobic thresholds and VO2 peak.

99
 Ventilatory Threshold One Ventilatory Threshold Two VO2 Peak
(VT1) (VT2)
30 38 43

Table 4.19. P03 session one VO2 linear regression calculations with peak and mean respiratory
exchange ratio

Time
Time to Spent at
Baseline Δ (TP2 – VO2 VO2 Peak RER
O2 TP1 TP2 TP1) Peak Peak R2 Value (mean)
Trial 1 6.21 31.42 37.67 6.25 517.69 -157.69 0.38 1.09(1.03)
Trial 2 9.61 35.29 37.50 2.20 1302.52 -462.52 0.10 1.04(0.98)
Trial 3 10.11 34.90 37.43 2.53 1726.35 -406.35 0.15 1.03(0.96)
Trial 4 8.17 34.24 36.33 2.09 2390.53 -590.53 0.10 1.03(0.93)

Table 4.20. P03 session one RPE scores.

Trial RPE
1 13
2 14
3 15
4 15

Figure 4.9. P03 Session one VO2 plot with anaerobic thresholds and VO2 peak.
45

40

35
VO2 (ml∙kg∙min-1)

30

25

20

15

10

0
1 85 169 253 337 421 505 589 673 757 841 925 1009109311771261134514291513159716811765

Time (s)

vo2 VT1 VT2 V02 Peak

Table 4.21. P03 Heart rate peak value from treadmill test.

Heart Rate Peak

188

Table 4.22. P03 Session one heart rate linear regression calculations.

100
 Time
Spent
Baselin Δ (TP2 – Time to at HR
  e HR TP1 TP2 TP1) HR Peak Peak R2 Value
Trial 1 100.55 181.57 186.97 5.40 743.04 -383.04 0.71
Trial 2 110.42 184.52 191.83 7.31 395.21 444.79 0.80
Trial 3 125.37 185.52 192.20 6.68 1203.60 116.40 0.82
Trial 4 131.68 185.85 191.75 5.90 1682.45 117.55 0.80

Figure 4.10. P03 Session one heart rate with heart rate peak
200

180
Heart Rate (beats∙min-1)

160

140

120
100

80
60

40

20

0
0 200 400 600 800 1000 1200 1400 1600 1800
Time (s)

Heart Rate HR Peak

Table 4.23. P03 session two VO2 linear regression calculations with peak and mean respiratory
exchange ratio

Time
Time to Spent at
Baseline Δ (TP2 – VO2 VO2 Peak RER
O2 TP1 TP2 TP1) Peak Peak R2 Value (mean)
Trial 1 6.62 32.64 34.97 2.33 997.54 -637.54 0.07 1.03(0.99)
Trial 2 7.79 33.07 35.61 2.53 1379.49 -539.49 0.10 1.01(0.95)
Trial 3 8.22 35.19 34.30 -0.89 n/a n/a 0.01 1.01(0.97)
Trial 4 8.82 36.65 38.50 1.85 2250.00 -450.00 0.06 1(0.94)

Table 4.24. P03 session two RPE scores.

Trial RPE
1 12
2 13
3 13
4 14

Figure 4.11. P03 Session two VO2 plot with anaerobic thresholds and VO2 peak.

101
 45

40

35
VO2 (ml∙kg∙min-1)

30

25

20

15

10

0
2 86 170 254 338 422 506 590 674 758 842 926 1010109411781262134614301514159816821766
Time (s)

vo2 VT1 VT2 V02 Peak

Table 4.25. P03 Session two heart rate linear regression calculations.

Time
Spent
Baselin Δ (TP2 – Time to at HR
  e HR TP1 TP2 TP1) HR Peak Peak R2 Value
Trial 1 78.98 164.06 176.58 12.52 528.66 -168.66 0.66
Trial 2 83.05 173.45 182.71 9.27 945.51 -105.51 0.78
Trial 3 96.88 177.40 186.37 8.97 1353.61 -33.61 0.67
Trial 4 108.14 182.68 188.06 5.38 1797.94 2.06 0.65

Figure 4.12. P03 Session two heart rate with heart rate peak
200

180
Heart Rate (beats∙min-1)

160
140
120
100
80
60
40
20
0
0 200 400 600 800 1000 1200 1400 1600 1800
Time (s)

Heart Rate HR Peak

Appendix 14
Participant 04

Table 4.26. P04 anaerobic thresholds and VO2 peak.

Ventilatory Threshold One Ventilatory Threshold Two VO2 Peak

102
 40 46 49

Table 4.27. P04 session one VO2 linear regression calculations with peak and mean respiratory
exchange ratio

Time
Time to Spent Peak
2
Baselin Δ (TP2 VO2 at VO2 R RER(mean
  e O2 TP1 TP2 – TP1) Peak Peak Value )
Trial 1 6.83 44.76 48.59 3.83 379.9 -19.9 0.15 1.06(1.02)
Trial 2 9.57 44.8 45.08 0.28 3456 -2616 0.01 1.01(0.97)
1339.1
Trial 3 9.82 44.43 48.57 4.14 5 -19.15 0.21 1.03(0.98)
Trial 4 10.34 45.29 47.12 1.83 1989.7 -189.7 0.06 1.01(0.96)

Table 4.28. P04 session one RPE scores.

Trial RPE
1 11
2 11
3 13
4 14

Figure 4.13. P04 Session one VO2 plot with anaerobic thresholds and VO2 peak.
60

50
VO2 (ml∙kg∙min-1)

40

30

20

10

0
2 86 170 254 338 422 506 590 674 758 842 926 1010109411781262134614301514159816821766
Time (s)

vo2 VT1 VT2 V02 Peak

Table 4.29. P04 Heart rate peak value from treadmill test.

Heart Rate Peak

198

Table 4.30. P04 Session one heart rate linear regression calculations002E

103
 Time
Spent
Baseline Δ (TP2 – Time to at HR
  HR TP1 TP2 TP1) HR Peak Peak R2 Value
Trial 1 119.41 177.77 187.61 9.84 555.26 -195.26 0.74
Trial 2 124.20 184.6 185.58 0.98 3183.02 -2343 0.04
Trial 3 129.96 185.97 192.43 6.46 1479.66 -159.66 0.64
Trial 4 130.08 184.21 190.68 6.47 2009.14 -209.14 0.62

Figure 4.14. P04 Session one heart rate with heart rate peak
200
180
Heart Rate (beats∙min-1)

160
140

120
100
80
60
40
20
0
0 200 400 600 800 1000 1200 1400 1600 1800

Time (s)

Heart Rate Peak Heart Rate

Table 4.31. P04 session two VO2 linear regression calculations with peak and mean respiratory
exchange ratio

Time
Time to Spent Peak
Baselin Δ (TP2 – VO2 at VO2 R2 RER(mean
  e O2 TP1 TP2 TP1) Peak Peak Value )
Trial 1 6.79 42.64 47.30 4.66 427.50 -67.50 0.45 1.08(1.01)
Trial 2 8.46 44.83 46.83 2.00 1041.30 -201.30 0.06 1.01(0.96)
Trial 3 9.19 42.94 48.16 5.22 1349.75 -29.75 0.26 1.03(0.96)
Trial 4 8.94 42.36 44.03 1.67 2352.78 -552.78 0.03 1.02(0.94)

Table 4.32. P04 session two RPE scores.

Trial RPE
1 12
2 11
3 12
4 13

Figure 4.15. P04 Session two VO2 plot with anaerobic thresholds and VO2 peak.

104
 60

VO2 (ml∙kg∙min-1)
50

40

30

20

10

0
3 87 171 255 339 423 507 591 675 759 843 927 1011109511791263134714311515159916831767
Time (s)

vo2 VT1 VT2 V02 Peak

Table 4.33. P04 Session two heart rate linear regression calculations.

Time
Spent
Baseline Δ (TP2 – Time to at HR
  HR TP1 TP2 TP1) HR Peak Peak R2 Value
Trial 1 105.47 169.59 181.67 12.08 610.11 -250.11 0.81
Trial 2 121.10 176.85 182.73 5.88 1320.13 -480.13 0.49
Trial 3 125.06 178.11 185.71 7.60 1618.98 -298.98 0.63
Trial 4 121.95 174.53 184.33 9.81 2057.89 -257.89 0.68

Figure 4.16. P04 Session two heart rate with heart rate peak

200
Heart Rate (beats∙min-1)

180
160
140
120
100
80
60
40
20
0
0 200 400 600 800 1000 1200 1400 1600 1800

Time (s)
Heart Rate HR Peak

105
Appendix 15
P01 T1 O2
60

50
f(x) = 0.0425359429279305 x + 35.4044080219978
40

30

20

10

0
150 200 250 300 350 400
Time (s)

P01 T2 O2
52

50

48

46 f(x) = 0.00427072050735033 x + 43.1356307096945

44

42

40

38
600 650 700 750 800 850 900
Time (s)

P01 T3 O2
60

50
f(x) = 0.00470694078649549 x + 39.3742423630842
40

30

20

10

0
1100 1150 1200 1250 1300 1350
Time (s)

106
 P01 T4 O2
60

50

40 f(x) = 0.00756855853933941 x + 30.9497575751073

30

20

10

0
1600 1650 1700 1750 1800 1850
Time (s)

P01 T1 HR
190
188
f(x) = 0.0377443300557433 x + 174.390153494648
186
184
182
180
178
176
174
172
150 200 250 300 350 400
Time (s)

P01 T2 HR
195

190 f(x) = 0.0431426961463782 x + 155.037452360507

185

180

175

170
600 650 700 750 800 850 900
Time (s)

107
 P01 T3 HR
195
f(x) = 0.0495287534199166 x + 127.973048443652
190

185

180

175

170
1100 1150 1200 1250 1300 1350
Time (s)

P01 T4 HR
200

195

f(x) = 0.055084361910758 x + 93.5514834604774

190

185

180

175

170
1600 1650 1700 1750 1800 1850
Time (s)

P02 T1 O2
50
45
40
f(x) = 0.0177156306641316 x + 34.4670358424727
35
30
25
20
15
10
5
0
150 200 250 300 350 400
Time (s)

108
 P02 T2 O2
50
45
40 f(x) = 0.00756938929843419 x + 35.2238477539822
35
30
25
20
15
10
5
0
600 650 700 750 800 850 900
Time (s)

P02 T3 O2
45
40
f(x) = − 0.016675847314713 x + 57.9010774227523
35
30
25
20
15
10
5
0
1100 1150 1200 1250 1300 1350
Time (s)

P02 T4 O2
40
35
30 f(x) = − 0.00897690450824784 x + 47.7926990259362

25
20
15
10
5
0
1600 1650 1700 1750 1800 1850
Time (s)

109
 P02 T1 HR
204
202 f(x) = 0.0374110993715135 x + 189.079009904415
200
198
196
194
192
190
188
150 200 250 300 350 400
Time (s)

P02 T2 HR
210
208 f(x) = 0.0459289089086621 x + 170.144008971523
206
204
202
200
198
196
194
192
600 650 700 750 800 850 900
Time (s)

P02 T3 HR
250

f(x) = 0.209309121997114 x − 53.7607212871477

200

150

100

50

0
1000 1050 1100 1150 1200 1250 1300 1350
Time (s)

110
 P02 T4 HR
212
210
208 f(x) = 0.0362104978769892 x + 144.047817487429
206
204
202
200
198
196
194
192
1600 1650 1700 1750 1800 1850
Time (s)

P03 T1 O2
45
40
35 f(x) = 0.033793287146477 x + 25.5016603949137
30
25
20
15
10
5
0
150 200 250 300 350 400
Time (s)

P03 T2 O2
45
40
35 f(x) = 0.0119279917412483 x + 27.4997937954039
30
25
20
15
10
5
0
600 650 700 750 800 850 900
Time (s)

111
 P03 T3 O2
45
40
35 f(x) = 0.0137064746209716 x + 19.3487287180992
30
25
20
15
10
5
0
1100 1150 1200 1250 1300 1350
Time (s)

P03 T4 O2
45
40
35 f(x) = 0.0113059705028116 x + 15.987055538008
30
25
20
15
10
5
0
1600 1650 1700 1750 1800 1850
Time (s)

P03 T1 HR
188

186 f(x) = 0.0291718491791122 x + 176.462879026063

184

182

180

178

176

174
150 200 250 300 350 400
Time (s)

112
 P03 T2 HR
194
192
f(x) = 0.0395202146186984 x + 158.653911662811
190
188
186
184
182
180
178
176
174
600 650 700 750 800 850 900
Time (s)

P03 T3 HR
194
192
f(x) = 0.0361426323373391 x + 144.553961328777
190
188
186
184
182
180
178
1100 1150 1200 1250 1300 1350
Time (s)

P03 T4 HR
194
192
f(x) = 0.0319452446889578 x + 134.329396130327
190
188
186
184
182
180
178
176
1600 1650 1700 1750 1800 1850
Time (s)

113
 P04 T1 O2
60

50
f(x) = 0.0207184567124619 x + 41.135764498935
40

30

20

10

0
150 200 250 300 350 400
Time (s)

P04 T2 O2
60

50

f(x) = 0.00153664370133129 x + 43.8162096196032

40

30

20

10

0
600 650 700 750 800 850 900
Time (s)

P04 T3 O2
60

50
f(x) = 0.022384844831135 x + 19.0025378539458
40

30

20

10

0
1100 1150 1200 1250 1300 1350
Time (s)

114
 P04 T4 O2
60

50
f(x) = 0.00993169285512573 x + 29.3019743501437
40

30

20

10

0
1600 1650 1700 1750 1800 1850
Time (s)

P04 T1 HR
190

f(x) = 0.0531611059047581 x + 168.464378151341

185

180

175

170

165
150 200 250 300 350 400
Time (s)

P04 T2 HR
190

188

186
f(x) = 0.0052651557865999 x + 181.127532745045
184

182

180

178

176
600 650 700 750 800 850 900
Time (s)

115
 P04 T3 HR
194
192 f(x) = 0.034904054200972 x + 146.359333470801
190
188
186
184
182
180
178
1100 1150 1200 1250 1300 1350
Time (s)

P04 T4 HR
195

190 f(x) = 0.034955570744853 x + 127.676738192182

185

180

175

170
1600 1650 1700 1750 1800 1850
Time (s)

116