Abstract
The aim of the present thesis was to experimentally test hypotheses originally forwarded by
Burnley and Jones (2007): that the VO2 kinetics interact with an individual’s capacity for
substrate-level phosphorylation and maximal oxygen uptake to determine the power-duration
relationship. Experiments were designed to manipulate the VO2 kinetics, the “anaerobic capacity,”
and/or the maximal oxygen uptake, and determine the effect of these manipulations on the powerduration relationship. Prior high-intensity exercise was used to investigate the classic priming
effect during subsequent high-intensity exercise. Both heavy- and severe-intensity exercise
‘primed’ the VO2 kinetics (i.e., increased primary amplitude, reduced the slow component
trajectory and amplitude). Following 10 min recovery, prior heavy-intensity exercise increased
exercise tolerance as a result of an increase in W (C: 16.0  4.8 vs. PHE: 18.7  4.8 kJ; 95% CI,
0.3, 5.2 kJ). In contrast, following the same recovery period, no difference was seen in performance
or the power-duration relationship after prior severe-intensity exercise. It was considered that the
accumulation of H+ ions (thereby reducing pH) during high-intensity exercise may be implicated in
the fatigue process. Sodium bicarbonate ingestion was used to increase the buffering capacity of
the blood. This intervention had no effect on the VO2 kinetics or VO2max , but increased CO2
production, VCO2max , and blood [lactate] at exhaustion. Despite these results, no overall difference
was seen in exercise tolerance between conditions; however, CP was reduced (Pl: 303 ± 48 vs. Na:
296 ± 53 W; 95% CI, 0,14 W) and W increased (Pl: 19.5 ± 8.6 vs. Na: 22.4 ± 9.2 kJ; 95% CI, -5.2,
-0.7 kJ), following alkalosis. The final two studies were designed to reduce muscle O 2 availability
by lowering the O2 carrying capacity of the blood (Blood donation), or through a reduction in
perfusion pressure (Supine exercise). Each of these interventions has similar effects on the VO2
kinetics: a reduction in the primary amplitude (and a longer time constant; supine only); no change
in the slow component trajectory; and a reduction in its amplitude and VO2max . Blood donation
reduced exercise tolerance, and supine exercise was performed at the same relative intensity, so no
difference was seen in time to exhaustion. Each of these interventions reduced CP for blood
donation and supine exercise (C: 259 ± 54; vs. BD: 246 ± 42 W; 95% CI: 2, 26W) and (UP: 275 ±
36 vs. SUP: 216 ± 13 W; 95% CI, 40, 78 W), while W was unchanged following each
intervention. The experiments conducted in the current programme of research demonstrate that
manipulating the VO2 kinetics, VO2max , or the parameters of the power-duration relationship have
predictable effects on exercise tolerance. Hence, these data support the notion that the interaction
between the VO2 kinetics, the maximal oxygen uptake, and substrate-level phosphorylation
determines exercise tolerance and therefore shapes the power-duration relationship.
i
Table of Contents
Page
Abstract
Table of contents
List of tables
List of figures
Symbols, abbreviations and definitions
Declaration and statements
Communications and publications
Acknowledgements
i
ii
vi
vi
vii
xi
xii
xiii
Introduction and review of literature
Chapter 1
Introduction
Endurance performance is a question of speed and time
Energy, oxygen and muscular work
Chapter 2
2
3
Review of literature
2.1 - Parameters of the physiological response to exercise
Maximum oxygen uptake
Lactate threshold / gas exchange threshold
Exercise economy / efficiency
Anaerobic capacity
2.2 - Oxygen uptake response to exercise
Oxygen uptake response at exercise onset - the oxygen deficit
Technological advances and the development of more complex oxygen uptake models
Phase I - the 'cardiodynamic' component
Phase II - the 'primary' component
Control of cellular respiration at exercise onset
Pulmonary vs. muscle oxygen uptake
Phase III - the 'steady-state' or the 'slow component'
Mechanisms for the oxygen uptake slow component
Muscle temperature, acid-base status and blood [lactate]
Motor unit recruitment and muscle fibre energetics
Characteristics of the oxygen uptake response across the exercise intensity spectrum
Exercise below the lactate/gas exchange threshold
The moderate intensity domain
Exercise above the lactate/gas exchange threshold - 'high' intensity exercise
The heavy intensity domain
The severe intensity domain
Exercise above the maximum oxygen uptake
The 'extreme' intensity domain
7
7
8
9
10
12
12
14
15
16
17
19
20
21
23
23
25
25
25
26
26
26
27
27
ii
2.3 - The power duration relationship
Historical perspectives
Mathematical modelling of the power-duration relationship
Two-parameter models
Key assumptions and considerations of modelling the power-duration relationship
Three-parameter models
Model selection considerations
Protocol design and implementation considerations
Determination of time to exhaustion and the influence of practice
Duration of trials
Number of trials and recovery time between trials
Cadence
The physiological response to exercise above and below critical power
Physiological determinants of W'
2.4 - Mechanisms of fatigue
Determinants of endurance performance - traditional perspectives
Determinants of endurance performance - a contemporary viewpoint
Interaction between the oxygen uptake kinetics and the power-duration relationship
2.5 - Intervention to test the link between the oxygen uptake kinetics and the
power-duration relationship
3.3
29
31
31
32
33
35
36
36
37
38
39
40
41
46
46
47
48
50
Muscle metabolism
High-energy phosphate stores
Metabolite accumulation
Acid-base status
Muscle oxygen availability
Inspired oxygen fraction
Oxygen transport in the blood
Perfusion pressure
Conclusion
50
50
51
52
53
54
54
56
57
Aims and hypotheses
58
Chapter 3
3.1
3.2
29
General Methods
Health and safety
Participant recruitment, preparation and care
Familiarisation, feedback and test termination procedures
Measurement procedures
Descriptive data
Cycle ergometers
Pulmonary gas exchange
Incremental test to determine the gas exchange threshold and the
maximal oxygen uptake
Pulmonary gas exchange during square-wave exercise
Determination of the power-duration relationship
Heart rate
60
60
61
62
62
62
62
63
64
65
66
iii
3.4
Haematology
General preparation
Determination of whole blood haematology
Determination of acid-base status
Determination of blood [lactate]
Statistical analysis
66
66
67
67
68
68
Experimental chapters
Chapter 4
4.1
4.2
4.3
4.4
Introduction
Aims and Hypothesis
Methods
Experimental design and protocols
Results
Incremental exercise and the 'control' condition power-duration relationship
Heavy priming
Severe Priming
Discussion
Heavy priming
Severe priming
Recovery duration
The oxygen uptake slow component and exercise tolerance
Limitations
Conclusion
Chapter 5
5.1
5.2
5.3
5.4
70
72
72
72
73
73
73
74
78
78
79
80
80
81
82
Sodium bicarbonate and the power-duration relationship
Introduction
Aims and Hypothesis
Methods
Experimental design and protocols
Results
Incremental exercise
Acid-base status
Oxygen uptake kinetics
Carbon dioxide kinetics
Blood [lactate] and heart rate
Exercise tolerance and the power-duration relationship
Discussion
Acid base status
Oxygen uptake kinetics
Exercise tolerance
Power-duration relationship
Conclusion
Chapter 6
6.1
The effect of priming exercise on the power-duration relationship
83
84
85
85
86
86
86
86
87
90
91
92
92
93
95
97
99
Blood donation and the power-duration relationship
Introduction
Aims and Hypothesis
100
100
iv
6.2
6.3
6.4
Methods
Experimental design and protocols
Results
Incremental exercise
Oxygen uptake kinetics
Blood [lactate] and heart rate
Exercise tolerance and the power-duration relationship
Discussion
Haematology
Oxygen uptake kinetics
Exercise tolerance and the power-duration relationship
Conclusion
Chapter 7
7.1
7.2
7.3
7.4
101
101
102
102
102
103
103
105
105
106
108
109
Supine exercise and the power-duration relationship
Introduction
Aims and Hypothesis
Methods
Experimental design and protocols
Results
Incremental exercise
Oxygen uptake kinetics
Blood [lactate] and heart rate
Exercise tolerance and the power-duration relationship
Discussion
Incremental exercise
Justification for using relative exercise intensities
Oxygen uptake kinetics
Power-duration relationship
Conclusion
111
112
113
113
114
114
114
115
118
118
119
119
120
122
123
General discussion
Chapter 8
General discussion
Summary of the main themes investigated in this thesis
Summary of the oxygen uptake response to severe-intensity exercise
Summary of the power-duration relationship
Limitations of this thesis - methodological considerations
Summary of the main experimental observations
Study 1 - Priming exercise and the power-duration relationship
Study 2 - Sodium bicarbonate and the power-duration relationship
Study 3 - Blood donation and the power-duration relationship
Study 4 - Supine exercise and the power-duration relationship
Main research findings
Determinants of the capacity to perform work above CP
Future directions
Final conclusions
References
125
126
126
127
129
129
130
130
131
131
132
134
135
137
v
List of Tables
Page
4.1
4.2
5.1
5.2
5.3
6.1
6.2
7.1
7.2
Power-duration relationship following priming exercise
Oxygen uptake kinetics and exercise tolerance following priming exercise
Oxygen uptake kinetics following sodium bicarbonate ingestion
Carbon dioxide kinetics following sodium bicarbonate ingestion
Blood [lactate], heart rate and time to exhaustion following sodium
bicarbonate ingestion
Haematological parameters following blood donation
Oxygen uptake kinetics following blood donation
Oxygen uptake kinetics during supine exercise
Blood [lactate], heart rate and time to exhaustion during supine exercise
75
76
87
88
90
102
104
116
117
List of Figures
Page
1.1 The relationship between average speed and finishing time during
World record efforts in running and swimming
3.1 Determination of the gas exchange threshold
4.1 Oxygen uptake responses and power-duration relationships following
priming exercise
5.1 Pulmonary gas exchange response following sodium bicarbonate ingestion
5.2 Power-duration relationship following sodium bicarbonate ingestion
6.1 Power-duration relationship
7.1 Oxygen uptake responses following supine exercise
3
64
77
89
91
105
118
vi
Symbols, Abbreviations and Definitions
[]
concentration (mM)
31
P
phosphorus
31
P-MRS
31
A
P nuclear magnetic resonance spectroscopy
asymptotic amplitude of a mathematically modelled response
for example, of the increase in VO 2 above baseline
a-vO2 diff
arteriovenous oxygen difference (mLO2∙100mL-1 of whole blood)
a measure of O2 extraction from the blood
ADP
adenosine 5' -diphosphate
APVE
acute plasma volume expansion
ATP
adenosine 5' -triphosphate
ATPase
enzyme that catalyses the decomposition of ATP into ADP
BD
blood donation
BL
baseline
Ca
2+
calcium
C6H10O5
microcrystaline cellulose
C
control
Cr
creatine
CK
creatine kinase
CO2
carbon dioxide
CP
critical power (W)
asymptote of the hyperbolic relationship between power output and time to exhaustion
CV
critical velocity (m·min-1)
determined from the hyperbolic relationship between velocity and time to exhaustion
CWR
constant work rate
∆
delta; a difference or a change in value
%Δ
percentage delta
the difference between the VO 2 at the GET and VO2max
e
exponential term (2.71828)
ECG
electrocardiogram
EDTA
ethylenediaminetetraacetate
EMG
electromyogram (mV)
GET
gas exchange threshold
G
change in VO2 per unit change in external work (i.e.  VO 2 /ΔWR; mL∙min-1∙W-1)
H+
hydrogen ion
Hb
haemoglobin (g∙dl-1)
HbO2
oxyhaemoglobin
Hct
haematocrit (%)
HCO3-
bicarbonate
HHb
deoxyhaemoglobin
vii
HR
heart rate (b·min-1)
HRmax
maximum heart rate (b·min-1)
H2O
water
iEMG
intergrated electromyogram (mV∙s-1)
Intensity
work rate characterised by a distinct gas exchange response profile
IU
international units
kt
rate constant
K
+
potassium
L-Name
L-nitro arginine methyl ester (inhibits nitric oxide synthase)
LBF
leg blood flow
LT
lactate threshold
exercise intensity which elicits a sustained increase in blood [lactate] above resting values
Mb
myoglobin
mVO2
muscle oxygen utilisation (L∙min-1; mL∙min-1)
rate at which mitochondria consume oxygen in aerobic ATP resynthesis
MAOD
maximal accumulated oxygen deficit (L)
MBF
muscle blood flow
MCV
mean cell volume (µm3)
MLSS
maximal lactate steady state
the highest VO 2 at which blood lactate can be stabilised
MSS
maximal steady state
highest exercise intensity that elicits stable VO 2 , blood lactate, pH etc over time
MRS
magnetic resonance spectroscopy
MRT
mean response time (s)
time taken to reach 63% of the VO 2 response, thereby estimating the overall 'speed' of
the VO 2 kinetics
MSS
maximal steady state
n
number (e.g. of participants)
Na
+
sodium
NaCl
sodium chloride (salt)
NaHCO3
sodium bicarbonate
NIRS
near infra-red spectroscopy
NO
nitric oxide
O2
oxygen
O2 deficit
difference between energy requirement of a work rate and that supplied through
oxidative metabolism
pH
a logarithmic scale used to express the acidity or alkalinity of a solution
pVO2
P
pulmonary oxygen uptake (L∙min-1; mL∙min-1)
PCr
phosphocreatine
power output (W)
viii
PCO2
partial pressure of carbon dioxide (mmHg)
PFK
phosphofructokinase
PHE
prior heavy exercise
Pl
placebo
PSE
prior severe exercise
Pi
inorganic phosphate
PO2
partial pressure of oxygen (mmHg)
Phase I
phase I of the VO2 kinetics
the 'cardiodynamic' component of the VO 2 kinetics following a step change in work-rate
Phase II
phase II of the VO2 kinetics
the 'primary' phase of the VO 2 kinetics, the exponential increase in VO 2 following a step
change in work-rate
Phase III
phase III of the VO2 kinetics
the attainment of a steady-state in VO 2 following a step-increase in work-rate
P-t
power-time relationship
Q
cardiac output (L∙min-1)
product of HR and stroke volume per unit of time
rpm
revolutions per min
used to define pedal cadence during cycle ergometry
RhEPO
recombinant human erythropoietin
RBC
red blood cell count (106·mm3)
RDW
red cell distribution width
(subscript) 'p'
signifies 'primary', for example the primary VO2 response
(subscript) 's'
signifies 'slow', for example the slow component of the VO2 response
SD
standard deviation
SEE
standard error of estimate
SLP
substrate level phosphorylation
ATP re-synthesis via non-O2-dependent pathways
SUP
supine exercise
SV
stroke volume
t
time (s)
t1/2
half-time
time point at with 50% of the change in VO 2 from baseline to the end of exercise occurs
TD
time delay
Tlim
time to exhaustion (s)
Tau (τ)
phase II VO2 time constant (s)
time taken to achieve 63% of the asymptotic amplitude in an exponential function
UP
upright exercise
ix
VCO2
carbon dioxide output (L∙min-1; mL∙min-1)
volume of carbon dioxide expired per unit of time
VE
expired minute ventilation (L∙min-1)
volume of air expired in one minute
VE / VCO2
ventilatory equivalent for CO2
VE / VO2
ventilatory equivalent for O2
VCO2max
maximal carbon dioxide output (L∙min-1; mL∙min-1)
maximal carbon oxygen output per unit of time
VO 2
pulmonary oxygen uptake (L∙min-1; mL∙min-1)
volume of oxygen extracted and utilised from the inspired gas per unit of time
VO2max
maximal oxygen uptake (L∙min-1; mL∙min-1)
maximal oxygen uptake per unit of time
VO2peak
peak oxygen uptake (L∙min-1; mL∙min-1)
peak oxygen uptake per unit of time
VO 2 SC
oxygen uptake 'slow-component'
the increase in VO 2 above phase II of the VO 2 response seen during exercise above the
LT/GET - with an amplitude (mL.min-1) and a trajectory towards VO2max (L.min-2)
VO 2 /WR
oxygen uptake to work rate relationship (mL∙min-1∙W-1)
typically used to describe exercise economy
VT
ventilatory threshold
W
watts
unit of power, i.e., work done per unit time
W'
curvature constant of the power-duration relationship (J; kJ)
WR
work rate (W)
WRpeak
work rate peak (W)
W-t
work-time relationship
x
Declaration and statements
Declaration
This work has not previously been accepted in substance for any degree and is not concurrently
submitted in candidature for any degree.
Signed…………………………………… (candidate)
Date………………………………………
Statement 1
This thesis is the result of my own investigations, except where otherwise stated. Where correction
services have been used, the extent and nature of the corrections is clearly marked in the
footnote(s).
Other sources are acknowledged by footnotes giving explicit references.
A bibliography is appended.
Signed…………………………………… (candidate)
Date………………………………………
Statement 2
I hereby give consent for my thesis, if accepted, to be available for photocopying and for interlibrary loan, and for the title and summary to be made available to outside organisations.
Signed…………………………………… (candidate)
Date………………………………………
xi
Communications and publications
The following communications and publications are a direct consequence of this work:
Communications:
Baker, J.R., Davison, G. and Burnley, M. (2008). Oxygen uptake kinetics as a determinant of
severe-intensity exercise tolerance. BASES, Bedfordshire.
Baker, J.R., Davison, G. and Burnley, M. (2010). The effect of blood donation on the VO2 and the
power-duration relationship. BASES, Glasgow.
Publications:
Burnley, M., Davison, G. and Baker, J.R. (2011). Effects of heavy and severe priming exercise on
VO2 kinetics and the power-duration relationship. Medicine and Science in Sports and Exercise,
43, 2171-2179.
xii
Acknowledgements
This work was supported by a full-time research scholarship from department of Sport and
Exercise Science at the University of Wales, Aberystwyth. As such, I am grateful to the University
and both the staff and students of department for supporting my studies over the past seven years –
it has been quite a journey! Professor Jo Doust provided my first glimpse into the wonders of
academia, he taught me the value of logical thinking and his teachings gave the confidence to
question the available evidence and to formulate my own conclusions, for this I am very grateful. I
would also like to thank Professor John Barrett for providing the opportunity to pursue my
postgraduate research, and to Professor David Lavallee and Dr Joanne Thatcher for their continued
support throughout this period.
I have had the privilege to work under an exceptional supervisor in Dr Mark Burnley. He truly is a
leader in the field of oxygen uptake kinetics and his tutorage has been fundamental in my
understanding of this complex topic – furthermore, providing the freedom to find my own path has
pivotal to my development as an independent researcher. I am similarly grateful to Dr Glen
Davison for his time and attention, for providing the alternative viewpoint, and highlighting the
bigger picture where required.
I have had the pleasure to work alongside some fantastic postgraduate students, the experiences I
have had over the past four years are something that I will never forget. Special thanks go to Dr
Simon Payne and Stuart Flint for providing humour and hindrance in equal measure – without you
guys I would have completed some time ago, but I wouldn’t have had so much fun. Of course, I am
also indebted to the poor individuals who agreed to take part in my studies, and especially to those
who came back time and again – who in their right mind would want to put themselves through so
much suffering?
I am forever indebted to both my friends and family for providing continued support throughout
my life, without you all I would not be where I am today. And finally, to Rosamund, thank you for
your understanding, patience and most of all, for your encouragement over the past two years.
Jonathan Baker
th
17 September 2011
xiii