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Psycho-biological monitoring of health
and performance among endurance
athletes
Luana Chandra Justice Main
Bachelor of Science (Honours)
School of Sport Science, Exercise & Health
The University of Western Australia
This thesis is presented in fulfilment of the
requirements for the degree of Doctor of Philosophy
2009
Page | II
Overview
To date, research has endeavoured to identify reliable early-warning markers to prevent
the onset of overtraining (OT). While numerous physiological and biochemical
symptoms have been proposed as potential indicators of OT, they have not been useful
in preventing it. Therefore, there is a need for long-term monitoring studies to determine
how to prevent overtraining. This research needed to consider a range of psychological,
physiological, and immunological parameters, as they are all thought to be interrelated
in this psycho-biological phenomenon. For this research to be directly applicable for
coaches and their athletes, it was necessary to observe the athletes training, without
intervention, across an entire training and competitive year.
Central to OT is the notion of a stress and recovery imbalance (chronic exposure to
stressors). Therefore, Study 1 explored the effect of stressors (training and non-training)
experienced by triathletes, on common self-report measures of training overload (mood
disturbance and physical symptoms of training overload), athlete burnout, and the
incidence of injury and illness across an entire training and competitive year. Study 2
investigated the possible association between perceived stress and the
psychoneuroendocrine response to training overload in elite rowers. In light of the
findings of Study 1, a simple self-report training distress measure was created in Study
3; incorporating the assessment of mood disturbance, perceived stress and training-
related symptoms. Finally, Study 4 explored the possibility of a cytokine hypothesis of
overtraining. Using the training distress measure created in Study 3, the possible
association between these components of training overload and selected indices of the
inflammatory response following a period of intense and prolonged endurance training
was assessed.
Page | III
Statement of Candidate Contribution
The work involved in designing and conducting the studies described in this thesis has
been completed primarily by Luana Main (the candidate). The thesis outline and design
of the studies were developed and planned in consultation with Professor Brian
Dawson, Professor Bob Grove, and Dr Grant Landers (the candidates supervisors). The
candidate was responsible for participant recruitment, along with organisation of all
testing sessions and data collection. All blood samples were collected by the candidate.
All assay preparation for Studies 2 and 4 were completed by the candidate under the
supervision of Ms Rosanna Soares Mendes from BD Diagnostics and Dr Kathy Heel
from the Biomedical Imaging and Analysis Facility (The University of Western
Australia). Dr Kathy Heel also assisted with the FLOW cytometry analysis for both of
these studies. Mr Kevin Murray provided statistical advice in regards to the Linear
Mixed Modelling analysis method employed in Studies 1 & 4. However, all analyses
and interpretations of these results were performed by the candidate. Finally, all
research manuscripts presented here were prepared by the candidate, with the
supervisors assisting in editing the manuscripts prior to submission.
Signed:
Page | IV
Table of Contents
Overview.
Statement of Candidate Contribution.
Table of Contents
Acknowledgements.
List of Publications.
List of Tables..
List of Figures.
List of Abbreviations..
II
III
IV
VI
VII
VIII
IX
X
Chapter 1: General Introduction
1.1 Background.....
1.2 The research problem......
1.3 Objectives of the research...
1.4 Significance of the research....
1.5 References...
Chapter 2: Literature Review..
Part 1: Introduction to overtraining...
1.1 Terms and definitions......
1.2 The prevalence of overtraining
1.3 Predisposing risk factors.
1.4 The overtraining continuum....
Part 2: Signs, symptoms and measures of overtraining
2.1 Hormonal measures.
2.2 Immunological measures.
2.3 Psychological measures...
Part 3: Previously proposed mechanisms of overtraining.....
3.1 Alterations to the endocrine axis......
3.2 Metabolic hypotheses..
Part 4: Cytokines in overtraining..
4.1 The sickness response..
4.2 Exercise induced cytokine release...
1
2
3
3
5
6
7
8
8
14
16
18
20
20
24
27
34
35
36
40
40
41
Page | V
4.3 Cytokines and depression.....
4.4 The tissue trauma hypothesis of overtraining..
4.5 The Interleukin-6 hypothesis of overtraining...
Part 5: Conclusion.....
References.
Chapter 3: Study One...
Paper 1: Training patterns and negative health outcomes in triathlon:
longitudinal observations across a full competitive season......
Chapter 4: Study Two.....
Paper 2: Impact of training on changes in perceived stress and cytokine
production
Chapter 5: Study Three
Paper 3: A multi-component assessment model for monitoring training distress
among athletes.....
Chapter 6: Study Four.
Paper 4: Relationship between inflammatory cytokines and self-report
measures of training overload.
Chapter 7: Thesis Summary and Future Research Directions....
7.1 Thesis Summary..
7.2 Practical Implications......
7.3 Future Research Directions.....
7.4 References...
Appendices.
Appendix A: Study One
Appendix B: Study Two
Appendix C: Study Three..
Appendix D: Study Four...
42
44
46
47
49
65
66
93
94
111
112
135
136
156
157
161
162
167
168
169
185
191
193
Page | VI
Acknowledgements
I would like to take this opportunity to thank and acknowledge the support of the many
individuals who have shared this journey with me.
Firstly, I would like to acknowledge my husband Tim Chambers. Many a time you
rescued me when I lost my way with my research, and you always held my hand until I
found my way again. Thank you for your unconditional support, love and rational
thinking over the years.
To my supervisors Professor Brian Dawson, Professor Bob Grove and Dr Grant
Landers, thank you for challenging me to grow. Daws, thank you for helping keep it
together over the years as coordinating supervisor, and for always telling me to just
keep at it. Grant, thank you for always being there for a chat, be it PhD, coaching, or
triathlon related. A big thank you also, for helping me to convince myself to race at the
Triathlon World Champs in Canada whilst still trying to finish. It was the opportunity
and experience of a lifetime, and Im glad I didnt let it pass by. To Bob, thank you for
being there on this journey since my honours, it was such a huge relief when our MTDS
paper was accepted. Thank you for teaching me how to respond to reviewers comments
thoughtfully and integrate new material and perspectives, where relevant.
To Dr Carmel Goodman, thank you for inspiring me to venture into the area of
overtraining all those years ago in that 3rd
year undergraduate rehab lecture; who would
have thought this was where it would end up. Thank you also for your support at the
commencement of my candidature, and input on my work since. I would also like to
acknowledge the invaluable support I received from Dr Kathy Heel and Mr Kevin
Murray. I am indebted to you for taking the time to help me find the answers in my
data.
To my family, Mum, Dad, Adelle and Alden, you never doubted my ability to complete
this work and have supported me throughout it. Your belief and confidence in me were
a constant source of encouragement. To my all my friends, and my fellow PhD crew,
thank you for all the laughs over the years, the many discussions and distractions that
you provided. To Sarah, Julie and Aditi, thank you for helping me get across that finish
line. And now, finally, I am finished, it is done!
Page | VII
List of Publications
Journal Articles
Main, L.C., Landers, G., Grove, J.R., Dawson, B., & Goodman, C. (2009). Training
patterns and negative health outcomes in triathlon: longitudinal observations
across a full competitive season. Journal of Sports Medicine & Physical Fitness
(Paper submitted for publication).
Main, L.C., Dawson, B., Grove, J.R., Landers, G., & Goodman, C. (2009). Monitoring
training distress: changes in perceived stress and inflammatory cytokines.
Research in Sports Medicine, 17, 121-132.
Main, L.C., & Grove, J.R. (2009). A multi-component assessment model for monitoring
training distress among athletes. European Journal of Sport Science, 9, 191-198.
Main, L.C., Dawson, B., Heel, K., Grove, J.R., Landers, G., & Goodman, C. (2010).
Relationship between inflammatory cytokines and self-report measures of
training overload. Research in Sports Medicine, 18, 1-13.
Conference Proceedings
Main, L.C., Dawson, B., Grove, J.R., & Landers, G. (2009). Cytokines and self-report
measures of well-being in rowing. Presented at the 12th International Society of
Sport Psychology World Congress, Marrakesh, Morocco.
Main, L.C., Dawson, B., Grove, J.R., & Landers, G. (2009). Training patterns and
injury in triathlon. Presented at the 12th International Society of Sport
Psychology World Congress, Marrakesh, Morocco.
Main, L.C., Dawson, B., Grove, J.R., & Landers, G. (2007). Monitoring training
distress: changes in perceived stress and inflammatory cytokines. Presented at
the14th Australian Congress of Sports Medicine, Adelaide, Australia.
Main, L.C., Dawson, B., Grove, J.R., & Landers, G. (2007). Longitudinal monitoring of
training distress in well-trained triathletes. Presented at the 12th European
Congress of Sport Psychology, Halkidiki, Greece.
Page | VIII
List of Tables
Chapter 2
Table 2.1. Reported symptoms of OT (adapted from Rowbottom et al., 1998b)
Table 2.2. Changes in hormonal markers associated with OTS
Table 2.3. The effect of normal and chronic training on immune function
(adapted from Mackinnon 2000a, 2000b)
Table 2.4. A summary of proposed metabolic hypotheses
Table 2.5. The metabolism alteration process proposed by Petibois et al. (2009)
21
23
25
38
39
Chapter 3
Table 1. The longitudinal effect (F-values) of potential sources of stress on
negative health outcomes
Table 2. Significant longitudinal model parameter estimates for each negative
health outcome
Table 3. Descriptive data (mean SD) for training factors averaged for each
training phase
79
80
81
Chapter 4
Table 1. Mean ( SD) values for the inflammatory cytokines and perceived
stress across the 8 week training period
104
Chapter 5
Table 1. Factor loadings, inter-factor correlations, and internal consistency
values for the six training distress factors
Table 2. Means ( SD) values for low, moderate, and high burnout risk
groups on each training distress factor
122
123
Chapter 6
Table 1. Participant characteristics
Table 2. Mean ( SD) values for the inflammatory cytokines and training
distress scores (TDS)
Table 3. Significant estimates of measures of inflammatory cytokines on the
prediction of factors associated with training overload
141
144
146
Page | IX
List of Figures
Chapter 2
Figure 2.1. Schematic representation of the relationship between training load
and performance (adapted from Lehmann et al., 1999)
Figure 2.2. Selected mechanisms underlying the genesis of OTS in endurance
sport (Lehmann et al., 1999)
19
35
Page | X
List of Abbreviations
ABQ
ACTH
ANS
BCAA
CNS
DALDA
ECSS
FSH
GAS
GH
HPA-axis
HPG-axis
HR
Ig
IL-1
IL-1ra
IL-6
IL-8
IL-10
IL-12p70
LH
mM
MAPSS
OR
OT
OTS
POMS
PSS
REST-Q
SAS
T:C
TDS
TNF-
UPS
URTIs
L
Athlete Burnout Questionnaire
Adrenocorticotropic hormone
Autonomic Nervous System
Branch Chain Amino Acids
Central Nervous System
Daily Analysis of Life Demands
European Congress of Sport Science
Follicular Stimulating Hormone
General Adaptation Syndrome
Growth Hormone
Hypothalamic-pituitary-adrenal axis
Hypothalamic-pituitary-gonadal axis
Heart Rate
Immunoglobulin
Interleukin-1
Interleukin-1 receptor antagonist
Interleukin-6
Interleukin-8
Interleukin-10
Interleukin-12p70
Luteinising Hormone
Millimolar
Mental and Physical States Scale
Overreaching
Overtraining
Overtraining Syndrome
Profile of Mood States
Perceived Stress Scale
Recovery Stress Questionnaire
Signs and Symptoms
Testosterone and Cortisol ratio
Training Distress Scale
Tumor Necrosis Factor-
Under Performance Syndrome
Upper Respiratory Tract Infections
Micro Litres
Chapter 1: General Introduction
Chapter 1 General Introduction
Page | 2
1.1 Background
Historically, stress has been defined by a series of physiological changes, including
activation of the hypothalamic-pituitary-adrenal (HPA) axis, as well as changes in the
autonomic nervous system (ANS). The neurobiological regulation of responding to
stressful events is a well-studied, and yet poorly understood, physiological
phenomenon. This confusion is due in part to the different definitions of stress that
exist, but also to individual variability in responding to a stressor. Often what is
perceived as a threat and evokes a physiological stress response in one person may not
be stressful (perceptually or physically) to another; and yet chronic exposure to stress
has a significant impact on virtually every system in the body. To date,
psychobiological investigations conducted in sport and exercise have combined
assessments of mood states and stress hormones to examine the beneficial effects of
exercise, with evidence of significant relationships being reported. However, optimising
athletic performance represents the primary aim of the majority of sport science
research, and as athletes engage in prolonged periods of heavy training, they increase
their risk of suffering from a range of negative health outcomes. Therefore, a
psychobiological approach has been considered to explain the impact of overtraining
(OT).
Exposure to a variety of stressors triggers the immune system, which in many ways
operates as a sensory organ for the brain. This feedback loop, allows the activation of
the immune cells to produce the physiological, behavioural, affective and cognitive
changes that are collectively called sickness (Maier & Watkins, 1998, p.83). Many of
the signs and symptoms commonly associated with OT may clearly be initiated by the
action of inflammatory cytokines. Two specific hypotheses have been presented
implicating cytokines in the aetiology of OT, namely Smiths (2000; 2004) tissue
Chapter 1 General Introduction
Page | 3
trauma hypothesis, and Robsons (2003) Interleukin-6 hypothesis. However, data on
training of competitive athletes and the cytokine mediated inflammatory response is
limited and further research is required.
1.2 The research problem
It is well supported that OT occurs when there is an imbalance between the stressors
imposed upon an athlete, and the athletes ability to adapt to or cope with these
stressors. The most notable sign of OT is a decrement in performance, despite continued
or increased training, together with symptoms of chronic fatigue which may persist
despite a brief recovery period of a few days. However, it is possible that other signs
and symptoms typically associated with OT are evident before deterioration in
performance. To date, no single factor or group of factors (biochemical, psychological,
physiological or other) has been shown to differentiate between effective intense
training and OT. Similarly, no factor has been confirmed as useful for the monitoring of
training, prevention of Overtraining Syndrome (OTS), or elucidation of the mechanisms
behind OT.
A variety of hypotheses have been proposed to explain the OTS, and while a number of
these remain viable, others have failed to gain support. It has been suggested that many
hypotheses represent pertinent aspects of the OTS, yet individually fail to account for
all observed changes. Furthermore, prediction and interpretation of performance
changes is often confusing as not all aspects of performance are affected simultaneously
nor are they impacted to the same degree.
1.3 Objectives of the research
The primary aim of this thesis was to investigate the relationship between prolonged
exposure to stressors (both training and life stressors) and the experience of associated
Chapter 1 General Introduction
Page | 4
negative health outcomes in endurance athletes. In addition to OT, other negative health
outcomes which have also been associated with an inability to adapt or cope with
imposed stressors include athlete burnout, injury and illness. Interrelationships between
these possible outcomes of the chronic exposure to stress and OT require further
research. Specifically, the role of training factors and general life stressors on the
development or occurrence of each of these states has yet to be examined. The second
key objective of this research project was to explore the possible association between
measures of perceived stress, mood disturbance and symptoms of OT, with selected
indices of the inflammatory response following periods of intense and prolonged
endurance training. Specifically, the aims of this thesis were to:
Identify whether exposure to stressors (either training factors or global life
stressors) had a significant effect on the experience of, or risk of suffering from
various negative health outcomes in the sport of triathlon, including the risk of
injury and illness, OT and athlete burnout.
Explore the possible association between perceived stress and selected indices of
the inflammatory response following a period of intense and prolonged
endurance training.
Create a simple self-report training distress measure that: (1) included an
assessment of mood disturbance, perceived stress and training-related
symptoms; (2) reflected both the frequency and intensity of these distress
dimensions; and (3) discriminated between groups of athletes with higher or
lower risk of developing problems as a result of training overload.
Explore the possible association between perceived stress, measures of mood
disturbance, symptoms of training overload (as measured by the inventory
Chapter 1 General Introduction
Page | 5
created in Study 3), and selected indices of the inflammatory response following
a period of intense and prolonged endurance training.
1.4 Significance of the research
Theoretically, the associated signs and symptoms of OT may be explained from a
psycho-immuno-biological standpoint, with all major systems of the body being
affected by, or involved in the development of symptoms. Two specific hypotheses
have been presented implicating cytokines in the aetiology of OT; however, data on the
training of competitive athletes and the inflammatory response is limited. Therefore,
examination of the role of inflammatory cytokines and exposure to stressors warrants
investigation with the long-term objective to both provide an explanation for the
aetiology of OT, as well as identify a marker, or series of markers to monitor training
responses.
This combined approach appeared to be the logical progression in the research process
and will help provide a better understanding of the interaction between physiological
and psychological components of OT. In addition, psychological monitoring to date has
generally focused on single measures, so the proposed multi-component approach is
unique. Potentially, the results of the research will be useful for coaches, athletes and
medical personnel who are responsible for preventing and managing OTS.
Chapter 1 General Introduction
Page | 6
1.5 References
Maier, S. F., & Watkins, L. R. (1998). Cytokines for psychologists: implications of
bidirectional immune-to-brain communication for understanding behaviour,
mood, and cognition. Psychological Review, 105, 83-107.
Robson, P. J. (2003). Elucidating the unexplained underperformance syndrome in
endurance athletes: the interleukin-6 hypothesis. Sports Medicine, 33, 771-781.
Smith, L. L. (2000) Cytokine hypothesis of overtraining: a physiological adaptation to
excessive stress? Medicine & Science in Sport & Exercise, 32, 317-331.
Smith, L. L. (2004). Tissue trauma: The underlying cause of overtraining syndrome?
Journal of Strength & Conditioning Research, 18, 185193.
Chapter 2: Literature Review
Chapter 2 Literature Review
Page | 8
Part 1: Introduction to overtraining
1.1 Terms and definitions
Due to the nature of the overtraining (OT) phenomenon, research in this area has been
plagued by a number of uncertainties and shortcomings. One of the greatest problems
has been the number of different definitions that exist. This, coupled with inconsistent
terminology usage has hindered the comparison of results from previous research
studies. Perhaps because of the complexity of the overtraining syndrome (OTS),
considerable variation exists in the terms used to describe this phenomenon.
Overreaching (OR), OT, OTS, staleness, overload, underperformance, under-recovery,
short- and long-term OT, and more recently, the under-performance syndrome (UPS;
Budgett et al., 2000) have all been used by different researchers to describe, define and
discuss what appears to be aspects of the same phenomenon.
Historically, OTS was referred to as staleness by researchers in the United States
(Hackney, Pearmann, & Nowacki, 1990), while researchers in Europe tended to use the
term OT to describe the same phenomenon (Kuipers & Keizer, 1988). Further
complications arose due to a lack of differentiation by researchers between the process
and outcome. Morgan, Brown, Raglin, OConnor and Ellickson (1987a) regarded
staleness as the outcome of periods of unsuccessful overload training, while Silva
(1990) suggested that the phenomenon should be differentiated into stages from
staleness to OT and finally, burnout.
1.1.1 Overreaching & Overtraining
When discussing OT, it is important to differentiate it from OR, which is a transient
period of reduced athletic performance. Indeed, OR can be a deliberate process resulting
from periods of specific overload training, with the purpose of eliciting performance
Chapter 2 Literature Review
Page | 9
gains (Steinacker & Lehmann, 2002). With a brief recovery period of a few days,
performance capacity can generally be fully restored. Many recent papers have referred
to, and adopted the definitions presented by Kreider, Fry and OToole (1998a). As such,
OR has been defined as:
An accumulation of training and/or non-training stress resulting in a short-term
decrement in performance capacity with or without related physiological and
psychological signs and symptoms of OT, in which restoration of performance
capacity may take several days to several weeks. (p. viii)
In contrast, OT has been defined as:
An accumulation of training and/or non-training stress resulting in a long-term
decrement in performance capacity with or without related physiological and
psychological signs and symptoms of OT, in which restoration of performance
capacity may take several weeks or months. (p. viii)
It should be noted that the critical factor in both these definitions is the duration of the
decrease in performance capacity, with the difference being the time taken to restore
optimum performance. While these definitions are not entirely satisfactory, they have
provided the most accurate description of the conditions to date and are frequently cited
in the literature (Halson & Jeukendrup, 2004). However, these definitions suggest that
the difference between OR and OT is the amount of time required for recovery, not the
type or duration of training stress experienced (Budgett et al., 2000; Lehmann, Foster,
Gastmann, Keizer, & Steinacker, 1999). These definitions also imply that it is possible
to experience these two states without the presence of psychological disturbances and
physiological signs and symptoms.
Chapter 2 Literature Review
Page | 10
Meeusen and colleagues (2006) suggested that there are actually two forms of OR, one
that is functional (as discussed above) and the other that is non-functional. Periods of
intensified training, in the context of training periodisation, or during a training camp
for example, are commonly included in athletes training programs to induce a super-
compensation effect. This successfully occurs when appropriate periods of recovery are
observed and the athlete exhibits an enhanced performance compared to baseline levels
(Steinacker, Lormes, Reissnecker, & Liu, 2004). In this situation, the physiological
responses compensate the training-related stress, and may be referred to as short-term
OT or functional-OR.
In comparison, Meeusen and colleagues (2006) suggested that non-functional OR
represents the point where the first signs of prolonged training distress and hormonal
disturbances occur. At this point it was suggested that several confounding factors such
as inadequate nutrition, illness, psychosocial stressors and sleep disorders may be
present. Therefore, differentiation between OR and OTS at this stage would be very
difficult and would depend on the results of clinical diagnosis. Given these difficulties,
Meeusen and colleagues (2006) felt that diagnosis of OTS could only be made
retrospectively when the time course for recovery can be overseen. As such, it was
suggested that OTS may be best considered as the prolonged maladaptation of several
biological, metabolic, neurochemical and hormonal regulation mechanisms (Meeusen et
al., 2006; Petibois, Cazorla, Poortmans, & Deleris, 2003b).
1.1.2 Under Performance Syndrome
Due to the inherent confusion surrounding the OT phenomenon, a round table
discussion was held in 1999 to discuss the diagnostic criteria to be used in the future.
Budgett and colleagues (2000) felt that the term OTS was inappropriate as it implied
that excessive exercise was the sole causative factor, whereas its aetiology appears
Chapter 2 Literature Review
Page | 11
multi-factorial. Concern has been raised that assuming OTS is solely caused by
excessive exercise could limit further investigations into the aetiology of the syndrome
(Robson, 2003). As such, the OTS was redefined as the UPS, or more specifically a
persistent, unexplained performance deficit (recognised and agreed by coach and
athlete) despite two weeks of relative rest (Budgett et al., 2000, p. 67). It should be
noted that the critical factor in describing UPS is still a decrease in performance
capacity, although this definition recognises that the cause of the underperformance and
chronic fatigue is not necessarily solely related to the training load.
1.1.3 Athlete Burnout
Originally coined by clinical psychologist Herbert Freudenberger in 1974, burnout was
used to describe stress responses among staff members of clinical institutions. The
original burnout literature was from the human services domain, where there was social
interaction between a provider and a recipient. Referring to the processes surrounding
stress overload, burnout is grounded in a psychosocial framework, where excessive
physical stressors are possible but not requisite antecedents. Most burnout research has
been based on Maslach and Jacksons (1981) definition of burnout as a stress reaction
syndrome comprised of three dimensions: emotional exhaustion, depersonalisation, and
associated feelings of low personal accomplishment. Currently, burnout is proposed to
be the result of chronic psychosocial stress, and has been associated with attentional
difficulties (Van Der Linden, Keijsers, Eling, & Schaijk, 2005).
Sport scientists have suggested that the negative, unmotivated and exhausted states
sometimes described by athletes are a sport-related manifestation of the burnout
syndrome (Gould, Tuffey, Udry, & Loehr, 1997). While burnout is a commonly used
term within the sporting community, there is much debate as to the definition and
Chapter 2 Literature Review
Page | 12
measurement of athlete burnout (Raedeke & Smith, 2001). To date, three main
operational definitions of athlete burnout have been presented.
The first, Smiths (1986) cognitive-affective model of athlete burnout, is conceptually
grounded in social exchange theory (Thibaut & Kelley, 1959). This description of
athlete burnout emphasizes imbalances between demands and resources, and the
cognitive appraisal of the perceived imbalance. In comparison, Silva (1990) presented
athlete burnout as the endpoint of excessive physical training. Silva proposed that the
negative responses to overload training lie on a continuum from staleness to OT, and
finally to burnout. Therefore, it is an initial failure of the bodys adaptive mechanisms
in responding to psycho-physiological stress created by training stimuli (Silva, 1990,
p.10) that is the entry point to the continuum. Burnout in this definition is the ultimate
consequence of the chronic experience of OT; with Silva suggesting that withdrawal
from sport involvement is an inevitable consequence of burnout.
Coakley (1992) described athletic burnout as a physical withdrawal from sport
following an intense investment of effort and high achievement. This conceptualisation
focuses upon burnout as something particular to those whose achievements are
exceptional in some way. It also views psychosocial stress as a consequence of the
process leading to sport withdrawal (i.e., burnout in Coakleys terms), rather than a
cause of sport burnout as described in other commentaries (e.g. Raedeke, 1997; Smith,
1986). This difference of opinion may explain partly why researchers investigating
athlete burnout have often confounded the antecedents, characteristics, and
consequences of the burnout syndrome (Cresswell & Eklund, 2006). Researchers are
currently investigating a motivational approach to the study of burnout in elite athletes
(Cresswell & Eklund, 2007; Lemyre, Treasure, & Roberts, 2006; Lemyre, Roberts, &
Stray-Gundersen, 2007). For example, Lemyre,et al. (2007) suggested that self-
Chapter 2 Literature Review
Page | 13
determined motivation and symptoms of overtraining were both independently linked to
signs of burnout in elite athletes. Although no moderating effect was found, pairing self-
determined motivation with symptoms of overtraining at the start of the winter sport
season increased the prediction of burnout in elite athletes at the end of the season.
The confusion surrounding burnout and OT is understandable as both terms are
independently shrouded in some confusion, and clear, universally-accepted definitions
have not been determined. Of most concern is the assumption that burnout is the
ultimate outcome of the OT process, with withdrawal from sport as the inevitable
endpoint (Silva, 1990). This assumption should be viewed with caution. While the
burnout concept has indeed been successfully integrated into sport research (Smith,
1986; Cresswell & Eklund, 2007), it is at this point inappropriate to use the terms
burnout and OT interchangeably. For this reason, Smiths (1986) definition of burnout
will be adopted for the current discussion, with withdrawal from sport as one of the
many possible consequences.
1.1.4 Conclusions regarding terminology
Given the confusion in the literature to date, and the numerous attempts that have been
made for uniformity of terms, deciding the terms and definitions to be used for the
current research program becomes somewhat difficult. Overload training will be used as
a noun, to describe the type of intensified training; while the term OR will be
considered synonymous with Meusen and colleagues (2006) short-term functional OR.
As such, it will refer to an accumulation of training and/or non-training stress resulting
in a desired short-term decrement in performance capacity with improved performance
following a rest period. Related physiological and psychological signs and symptoms of
OT may or may not be present, and restoration of performance capacity may take up to
14 days.
Chapter 2 Literature Review
Page | 14
Overtraining will be used as an adjective to describe both the process and the
accumulation of training and/or non-training stress beyond overreaching. Training
distress will be employed in reference to the psychological and behavioural response to
(or outcome of) OT.
Overtraining syndrome (OTS) will be considered the ultimate outcome of the OT
process, at which point the athlete is forced to withdraw from training and competition,
until they are physically able to resume participation. Specifically, it will be defined as a
chronic accumulation of training and non-training stressors, resulting in a decrement of
performance capacity with prolonged maladaptation of several biological,
neurochemical, hormonal and metabolic regulation mechanisms. This will commonly
result in physiological and psychological signs and symptoms of OT in which
restoration of performance capacity may take several months. It is hoped that this use of
terminology will be viewed as consistent with Kreider and colleagues (1998b), while
also agreeing with Meeusen and colleagues (2006) position statement made on behalf of
the European Congress of Sport Science.
1.2 The prevalence of overtraining
The prevalence of OTS in different sports has not yet been clearly established. This may
partly be due to the number of different definitions of OT that exist, coupled with
inconsistent terminology usage which has hindered the ability to compare the results of
previous research studies. However, it has been estimated that 65% of all long-distance
runners will be affected by OTS at some time during their competitive career
(McKenzie, 1999). These findings are consistent with the earlier work of Morgan and
colleagues with elite distance runners which reported that reported that 64% of males
(Morgan, OConnor, Ellickson, & Bradley, 1988b) and 60% of females (Morgan,
Chapter 2 Literature Review
Page | 15
OConnor, Sparling, & Pate, 1987b) indicated they had experienced OT at some point
during their careers.
Over a shorter timeframe, Gould et al. (1999) reported that 28% of the 296 strong
United States Atlanta Summer Olympic team, and 10% of their 83 member Nagano
Winter Olympic team reported that they were overtrained in the 90 days prior to the
Olympics. Yet a clear definition of OT was not provided to the athletes prior to
responding to the statement I overtrained in preparation for the Olympics (p. 181);
and given the frequent colloquial use of the term OT, these prevalence statistics should
be interpreted with caution.
Raglin, Sawamura, Alexiou, Hassmn, and Kentt (2000) reported that from a sample
spanning across four countries an average of 35% of young swimmers reported
experiencing performance decrements for at least two weeks during their swimming
careers, which was not a result of injury or illness, but rather due to training (20% from
Sweden, 24% from USA, 34% from Japan, and 45% from Greece). While the accuracy
of the recall ability of these young swimmers may be questioned, these figures are
similar to those reported by Hooper and colleagues (1995), who indicated that
approximately 21% of swimmers were identified as overtrained following the
Australian National swim titles. Thus, it is clear that while exact prevalence figures are
not yet available, OT will affect a significant number of athletes at some point during
their athletic career. Further research to explore pre-disposing risk factors, early
warning signs and methods for monitoring training overload is therefore certainly
warranted.
Chapter 2 Literature Review
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1.3 Predisposing risk factors
Numerous researchers, including Armstrong and Van Heest (2002) have noted that the
border between optimal performance and performance impairment due to OT is subtle
(p. 341). Consequently, many researchers have explored a number of risk factors which
may contribute to, or prolong the experience of OT. Factors which have been identified
may be loosely grouped into one of three possible categories: 1) training issues; 2)
situational and environmental stressors; and 3) athlete issues. Athlete issues may be
separated into two further sub categories: a) physical issues and b) beliefs, behaviours
and attitudes (Richardson, 2006). While an in-depth analysis of the literature regarding
each predisposing risk factor identified is beyond the scope of this review, a brief
discussion of key factors within each category will be presented.
Training issues are probably the most commonly cited risk factors in terms of the
development of OT. Of particular note is high volume or high intensity training, which
has received a great deal of attention (e.g. Budgett, 1990; Kentt & Hassmn, 2002;
Kuipers, 1996; Uusitalo, 2001). For example, Lehmann and colleagues (1992) explored
the influence of an increase in training volume versus an increase in training intensity
on running performance. Two studies were carried out with eight and nine experienced
middle-or long distance runners, with experimental training periods lasting for three
weeks. Results indicated that an increase in training intensity produced an improvement
in running velocity at 4 mM lactate concentration and in total running distance in the
incremental test. In comparison, the increase in training volume study protocol resulted
in stagnation of running velocity at 4 mM lactate concentration and a decrease in total
running distance in the incremental test. It was suggested that the associated changes in
metabolism and catecholamine measures may have indicated an exhaustion syndrome
Chapter 2 Literature Review
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(OR) in the athletes from the increased training volume study; however, this hypothesis
requires further research (Lehmann et al., 1992).
Other possible training risk factors that have been proposed include training monotony,
lack of periodisation, and/or a failure to include adequate recovery into the training
program (Kreider et al., 1998b). Sudden increases in training load or volume,
specifically during transition periods within a training year, may also predispose
athletes to OT (Budgett, 1990; Hawley & Schoene, 2003; Uusitalo, 2001). One
significant risk factor is a lack of monitoring for signs and symptoms of OT (Hooper &
Mackinnon, 1995). If athletes and coaches are aware of the early warning signs, then
preventative measures can be taken and any increased risk of OT may be reduced.
Therefore, it is clear that the type of training greatly influences the performance
outcome. At the same time, training factors alone are not the only contributors to the
development of OT. Situational and environmental stressors may also have a significant
impact on an athletes ability to respond to training stimuli. For example, poor nutrition
(Costill et al., 1988), travel (especially across time zones) and jet lag can have a
significant impact on athletic performance (Rushall, 1990), particularly combined with
changes in training environment, altitude, temperature and or humidity (Hug, Mullis,
Vogt, Ventura, & Hoppeler, 2003). Conflicts with coaches, team-mates, friends or
parents within an athletes sporting involvement may also contribute to the development
of a training stress state (e.g. Hollander & Meyers, 1995; Kentt & Hassmn, 2002;
Kuipers & Keizer, 1988). In addition to these stressors, athletes may also be subjected
to stressors external to their sport environment. For example, work, study or relationship
stressors may also affect an athletes ability to train and respond to the training stressors
(Rushall, 1990).
Chapter 2 Literature Review
Page | 18
Finally, issues suffered by the athlete may also increase their risk of OT. For example, it
has been suggested that premature return from injury (Budgett, 1990); poor or
inadequate sleep (Kentt & Hassmn, 2002; Uusitalo, 2001); and poor or inadequate
nutrition (Berning, 1998) (e.g. caloric restriction, insufficient carbohydrate intake, iron
deficiency); may all impact on an athletes ability to cope with and positively adapt to
imposed training loads. While these factors are possible additional stressors, there is
insufficient support for most of these as potential triggers initiating an OT response.
Furthermore, identifying these possible pre-disposing risk factors, sometimes referred to
as initiating events, has not revealed the mechanisms of OTS (Kreider, Fry, & OToole,
1998a).
1.4 The overtraining continuum
Endurance exercise induces a variety of physiological and metabolic adaptations in
skeletal muscle that function to minimise cellular disturbances during subsequent
training sessions (Hawley, 2002). In order to optimise performance and ensure the
desired physiological adaptations are achieved, it is necessary to determine the
appropriate stimulus required. The key components of a training program are the
volume/duration, frequency and intensity of training sessions. Taken collectively, these
components are the training stimulus, the manipulation of which will alter the ultimate
performance outcome/response.
It is evident that underestimation or overestimation of training load and performance
level, together with insufficient recovery, will lead to inappropriate training responses
of the athlete (Steinacker et al., 2000). Optimal training is achieved when an athlete
progressively overloads, and positive physical adaptation occurs through a gradual
development of the capacities required to tolerate the stimulus. While it is apparent that
repeated bouts of exercise are essential to achieve the cumulative stress necessary to
Chapter 2 Literature Review
Page | 19
induce the metabolic and morphological adaptations in skeletal muscle, training that is
of an intensity greater than the body can cope with will achieve the reverse effect, as is
evidenced in Figure 2.1.
Figure 2.1: Schematic representation of the relationship between training load and
performance (adapted from Lehmann et al., 1999)
Steinacker and colleagues (2000) demonstrated that clear signs of OR were found after
18 days of intense training. Specifically, high training loads of approximately 3.2 hours
per day were sustained for 18 days prior to the 1995 Rowing World Championships in
10 junior elite rowers and reserves, with decreases in performance, gonadal and
hypothalamic steroid hormones. Also noted was a deterioration of recovery as measured
by the Recovery-Stress-Questionnaire for Athletes (REST-Q Sport; Kellmann & Kallus,
2000). Following a recovery period of two to three weeks, maximum performance and
endurance were improved, and all hormone measures improved. Steinacker and
colleagues concluded that the data from this study confirms that the critical borderline
to acute OT/OTS in adapted endurance athletes may be around three weeks of
intensified or prolonged training lasting three hours per day.
Chapter 2 Literature Review
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Part 2: Signs, symptoms and measures of overtraining
It is interesting to note that research discussing possible markers of OT can be
objectively examined, while much of the literature on the symptoms of OT is
predominantly based on anecdotal reports. In addition, much of the research regarding
OT involves studies that have examined athletes in a state of OR, or acute-short term
OT, as it is unethical to intentionally induce a state of full OT (i.e. OTS/UPS). The
question remains as to whether the signs and symptoms that are observed during these
intervention studies are indeed the same as those associated with anecdotal reports of
athletes who are experiencing OTS (Halson & Jeukendrup, 2004). Fry, Morton and
Keast (1991) presented a comprehensive table of the major symptoms of OT, as
indicated by their prevalence in the literature. Rowbottom, Keast and Morton (1998b)
later presented a very similar list of symptoms (Table 2.1) with greater distinction
between sub-categories, illustrating the increased involvement of researchers from
different disciplines investigating the area of OT. Although these observed
physiological measures have been effective in confirming the OTS, they have not been
useful in preventing it. This is partly due to uncertainty about whether the symptoms
noted precede OT or are merely manifestations of the OTS (Fry et al., 1991).
2.1 Hormonal measures
For several years it has been hypothesized that a hormone-mediated central deregulation
occurs during the pathogenesis of the OTS. Numerous hormonal indices have been
proposed as possible markers for monitoring OT and have been extensively examined
(e.g. Lac & Maso, 2004). In particular, cortisol and testosterone have been identified as
reliable markers of training stress (e.g. Filaire, Bernain, Sangol, & Lac, 2001; Kraemer
et al., 2004; Maso, Lac, Filaire, Michaux, & Robert, 2004; Mackinnon & Hooper, 1991;
Page | 21
Table 2.1: Reported symptoms of OT (adapted from Rowbottom et al., 1998b)
Performance/physiological:
Decreased performance in competition
Decreased performance in training
Reduced tolerance of training load
Increased fatigue during exercise
Prolonged fatigue
Decreased muscular strength
Decreased maximum work capacity
Chronic fatigue
Decreased muscle glycogen
Decreased maximal lactate
Elevated basal metabolic rate
Sensorimotor performance:
Loss of coordination
Decreased mechanical efficiency
Loss of muscle tone
Poor muscular control and balance
Slow sensory motor performance
Lengthened decision/reaction times
General clumsiness
Nutritional disorders:
Loss of appetite
Gastrointestinal and digestive disorders
Feelings of thirst
Increased fluid intake
Mineral and vitamin deficiencies
Cardiorespiratory function:
Increased heart rate
Higher heart rate at standard work load
Decreased maximum heart rate
Abnormal t-wave pattern in ECG
Elevated blood pressure
Shortness of breath
Increased frequency of respiration
Haematology:
Decreased haemoglobin
Decreased serum iron
Decreased serum ferritin
Decreased red blood cell count
Decreased hematocrit
Biochemistry:
Elevated plasma creatine kinase
Elevated plasma urea
Elevated plasma 3-methylhistidine
Increased uric acid production
Depressed plasma glutamine
Hormones:
Hypothalamic dysfunction
Elevated plasma catecholamines
Elevated serum cortisol
Depressed serum testosterone
Immunology:
Increased susceptibility to and severity of
infections/ colds/ allergies
Frequent persistent cold/flu-like
symptoms
Sore throats
Glandular fever
Minor scratches heal slowly
Swelling of lymph glands
Decreased serum immunoglobulin
Decreased salivary immunoglobulin a
Decreased white blood cell count
Decreased lymphocyte count
Reduced mitogen responses
Physical complaints:
Cold hands and feet
Headaches
Nausea
Backaches
Decreased body fat
Sleep problems:
Insomnia
Sleep disturbances
Problems falling asleep
Night sweats
Musculoskeletal complaints:
Increased incidence of injury
Muscle pain
Muscle soreness/ stiffness
Stress fractures
Joint pain
Muscle damage
Psychological symptoms:
Feelings of depression
Anxiety
General apathy
Increased anxiety
Increased perceived effort
Decreased self esteem
Lethargy
Decreased energy/ vigour
Loss of enthusiasm
Lack of interest in competition and
training
Difficulty in concentrating at training
Loss of libido
Page | 22
Mackinnon, 1996; Rowbottom et al., 1997; Urhausen et al., 1998a). Application of the
urinary cortisol/cortisone ratio has also received attention for its use in monitoring
swimmers (Atlaoui et al., 2004). Plasma catecholamines have also been presented as a
possible marker, with Hooper and colleagues (1995) suggesting that adrenaline and
noradrenaline may provide an objective means of diagnosing the OTS when considered
in conjunction with the athlete's self-assessment of well-being. A brief summary of
research findings is presented in Table 2.2.
Results from research in this area are far from clear. One reason for this is differences in
measuring methods, and/or detection limits of the analytical equipment used. While
hormones provide interesting diagnostic information, they remain unsuitable for
practical application, as results require clinical analyses that are not readily available to
all athletic bodies (Hug et al., 2003). These inconsistent findings and the inability to
distinguish acute fatigue resulting from intensified training from OT do not support the
use of the majority of biochemical markers as diagnostic tools. Uusitalo (2001)
commented that:
Hormonal changes have not proven to be sensitive or specific indicators of the
OT state... reliable measures of hormone levels during maximal exercise require
appropriate lab conditions, which are not always possible. For results to be
meaningful, identical collection, transportation, storage, and protocols of
analysis must be observed. (p.9)
Thus, it remains difficult to draw conclusions about possible changes in hormone
concentrations. It is hoped that future developments in technology, improvements in
testing conditions and controlled training programs, will allow further growth of
understanding in this area.
Chapter 2 Literature Review
Page | 23
Table 2.2: Changes in hormone markers associated with OTS
Variable
After intense training
not causing OT/OR
After intense training causing
OT/OR
ACTH
Increase Rietjens et al. (2005)
Decrease Barron et al. (1985)
Urhausen et al. (1998a)
Meeusen et al. (2004)
Catecholamines
Decrease Atlaoui et al. (2006)
Mujika et al. (1996)
Increase Fry et al. (1994a)
Atlaoui et al. (2006)
Urhausen et al. (1998a)
Decrease Uusitalo (1998)
Cortisol
Increase Atlaoui et al. (2004)
Filarie et al. (2001)
Suzuki et al, (2000)
Tyndall et al. (1996) () Decrease Tyndall et al. (1996) () No change Filarie et al. (2004)
Mujika et al. (1996)
Rowbottom et al. (1997)
Increase Coutts et al. (2007)
Urhausen et al. (1998a)
Decrease Atlaoui et al. (2004)
Fry et al. (1992a)
Meeusen et al. (2004)
Rietjens et al. (2005)
Steinacker et al. (2000)
GH
Increase Suzuki et al. (2000) Increase Rietjens et al. (2005)
Decrease Barron et al. (1985)
Meeusen et al. (2004)
Urhausen et al. (1998)
Prolactin
Increase Suzuki et al. (2000)
Decrease Barron et al. (1985)
Steinacker et al. (2000)
Meeusen et al. (2004)
FSH
Decrease Steinacker et al. (2000)
No change Fry et al. (1992a)
Urhausen et al. (1998)
LH
No change Mujika et al. (1996)
Decrease Steinacker et al. (2000)
No change Fry et al. (1992a)
Urhausen et al. (1998)
T:C ratio
Decrease Filarie et al. (2001)
No change Hug et al. (2003)
Filarie et al. (2004)
Rowbottom et al. (1997)
Decrease Coutts et al. (2007)
No change Fry et al. (1992)
Testosterone
Decrease Filarie et al. (2001)
Tyndall et al. (1996)
No change Filarie et al. (2004)
Mujika et al. (1996)
Rowbottom et al. (1997)
Increase Urhausen et al. (1998)
Decrease Coutts et al. (2007)
Steinacker et al. (2000)
No change Fry et al. (1992)
Note: Hormone abbreviations, ACTH: adrenocorticotropic hormone; GH: Growth hormone;
FSH: follicular stimulating hormone; LH: luteinising hormone; T:C ratio: testosterone and
cortisol ratio.
Chapter 2 Literature Review
Page | 24
2.2 Immunological measures
Anecdotal reports have linked periods of heavy training, sometimes associated with
prolonged fatigue and underperformance, with susceptibility to infections. In two
independent review papers, both MacKinnon (2000a) and Nieman (1998) concluded
that while overtrained athletes are not immune deficient by clinical standards, they are
susceptible or at an increased risk of suffering from upper respiratory tract infections
(URTIs) during periods of heavy training, and the 1-2 weeks following prolonged
intense aerobic exercise training. To date, research investigating the role of the immune
system in OTS has focused on one of three primary issues:
1. The association between OR/OT and an increased incidence of infection
2. Monitoring of leukocytes and other immune factors during periods of OT
3. The possibility that disease and infections may increase the risk of OTS.
Yet despite the variety of measures examined, there is still uncertainty about the effect
of exercise and training on immune function, which may depend on the pre-existing
state of the athlete and the type of exercise. Mackinnon (2000a, 2000b) presented two
very comprehensive review tables summarising available research on the effects of OT
on immunity and performance. A compilation of these two review tables is presented in
Table 2.3 as a summary of the research findings in this area. For further explanation on
any of the markers presented, the reader is referred to the studies referenced in Table 2.3
as it is beyond the scope of this review. Therefore, while immune markers do not appear
to be reliable markers of impending OT, recurrent infections and immunodepression are
common among overtrained athletes. It has been purported that cytokines may play a
role in the aetiology of OT, which would explain a number of the findings to date;
however, this will be discussed in greater detail in Part 4.
Page | 25
Table 2.3: The effect of normal and chronic training on immune function (adapted from Mackinnon 2000a, 2000b)
Immune parameter Resting values in athletes After normal or moderate training After intense training not causing
OT/OR
After intense training causing
OT/OR
Leukocyte number Normal
Hooper et al. (1995)
Gleeson et al. (1995)
Nieman (1994)
No change
Baum et al. (1994)
Nehlsen-Cannarella et al. (1991)
No change
Gleeson et al. (1995)
Hooper et al. (1995)
Or decrease
Hack et al. (1997)
Lehman et al. (1996)
No change
Mackinnon et al. (1997)
Or decrease
Lehman et al. (1996)
Granulocyte number Normal
Pyne et al. (1995)
Nieman et al. (1995a)
No change
Baum et al. (1994)
Mitchel et al. (1996)
Nehlsen-Cannarella et al. (1991)
No change or slight increase
Bury et al. (1998)
Hooper et al. (1995)
Pyne et al. (1995)
Increase
Hooper et al. (1995)
Lymphocyte number Normal
Mackinnon et al. (1997)
Gleeson et al. (1995)
Nieman et al. (1995a)
Nieman et al. (1995b)
No change
Nehlsen-Cannarella et al. (1991)
Baum et al. (1994)
No change
Fry et al. (1992b)
Gleeson et al. (1995)
Mackinnon et al. (1997)
Or decrease
Hack et al. (1997)
No change
Fry et al. (1992b)
Or transitory decrease
Mackinnon et al. (1997)
Natural killer cell number Normal
Nieman et al. (1995a)
Nieman et al. (1995b)
Or increase
Gleeson et al. (1995)
Rhind et al. (1994)
No change
Nieman et al. (1990)
Tvede et al. (1991)
No change
Baj et al. (1994)
Or decrease
Fry et al. (1994)
Gedge et al. (1997)
Gleeson et al. (1995)
Decrease
Fry et al. (1992)
Leukocyte adhesion molecule
expression
Increase
Baum et al. (1994)
Increase
Baum et al. (1994)
Increase
Baum et al. (1994)
-
Neutrophil function
Lower
Bury & Pirnay (1995)
Pyne et al. (1995)
Smith et al. (1990)
No change
Hack et al. (1994)
Decrease
Bury et al. (1998)
Hack et al. (1994)
Pyne et al. (1995)
Smith et al. (1990)
No current data available
Page | 26
Table 2.3 (cont.): The effect of normal and chronic training on immune function
Lymphocyte activation or
proliferation
Normal
Gedge & Mackinnon (1998)
Gleeson et al. (1995)
Nieman et al. (1995)
Or increase
Rhind et al. (1994)
No change
Lehman et al. (1996)
Mitchell et al. (1996)
Nieman et al. (1995b)
Or decrease
Bury et al. (1998)
Nieman et al. (1990)
Increase
Baj et al. (1994)
Baum et al. (1994)
Fry et al. (1992b)
Hack et al. (1997)
Increase
Immune parameter Resting values in athletes After normal or moderate training After intense training not causing
OT/OR
After intense training causing
OT/OR
Natural killer cytotoxic action Normal
Nieman et al. (1995a)
Or increase
Nieman et al. (1995b)
Pedersen et al. (1989)
Increase
Nieman et al. (1990)
Or no change
Bury et al. (1998)
Decrease
Gedge et al. (1997)
No current data available
Serum Ig concentration In the lowest 10% clinical norms
Gleeson et al. (1995)
No change
Mitchell et al. (1996)
Nehlsen-Cannarella et al. (1991)
No change
Gleeson et al. (1995)
No current data available
Serum specific antibody Normal
Bruunsgaard et al. (1997)
Mackinnon et al. (1989)
No effect on ability to mount
specific antibody response
Gleeson et al. (1996)
(elderly female subjects)
No current data available
Mucosal Ig-A concentration Normal
Gleeson et al. (1995)
Mackinnon et al. (1989)
Or low Tomasi et al. (1982)
Gleeson et al. (1999)
Mackinnon & Hooper (1994)
No change
McDowell et al. (1992)
No change
Mackinnon et al. (1994)
Or decrease as intensity increased
Gleeson et al. (1995)
Tharp & Barnes (1990)
No change
Mackinnon & Hooper (1994)
Plasma glutamine concentration Clinically normal
Keast et al. (1995)
Lehman et al. (1996)
But lower in overtrained athletes
Mackinnon &Hooper (1996)
Rowbottom et al. (1995)
No change
Lehman et al. (1996)
Mackinnon & Hooper (1996)
Or decrease
Hack et al. (1997)
Keast et al. (1995)
Decrease
Keast et al. (1995)
Or no change
Lehman et al. (1996)
Mackinnon & Hooper (1996)
Key: Ig - immunoglobulin; Ig-A = Immunoglobulin-A
Chapter 2 Literature Review
Page | 27
2.3 Psychological measures
While numerous physiological and biochemical symptoms have been proposed as
potential indicators of OT, few have proven to be consistent across different studies
involving different athletic groups. As such there is no single parameter available to
predict or diagnose OT (Hartmann & Mester, 2000). Conversely, stronger and more
consistent relationships have been observed with self-report measures. Indeed, there is
general agreement that OT is characterised by a marked increase in negative affective
states, such as anxiety and depression (Morgan, 1985; Morgan et al., 1987a;
Tenenbaum, Jones, Kitsantas, Sacks, & Berwick, 2003a, 2003b; Veale, 1991). Self-
report measures exhibit reliable dose-response relationships with training load, and
appear to be sensitive to the symptoms of both short-term and long-term training
distress across a range of different sports (Morgan et al., 1987a; Raglin & Morgan,
1994; Raglin & Wilson, 2000).
Existing approaches to the monitoring of training state via self-report can be placed into
three categories based on the primary psychological parameter examined. The classic
approach has been monitoring of mood disturbances with the Profile of Mood States
(POMS; McNair, Lorr, & Dropplemann, 1971). A second approach has been to focus on
the magnitude of training-specific symptoms (Fry et al., 1994; Morgan, Costill, Flynn,
Raglin, & O'Connor, 1988a), while the third approach has been to examine changes in
perceived stress (Kellmann & Kallus, 2001; Rushall, 1990). These self-report measures
have the added advantages of being efficient, inexpensive, non-invasive, and can easily
be administered by coaching staff or team personnel to monitor athletes progress
throughout a training and competitive year.
Chapter 2 Literature Review
Page | 28
2.3.1 Mood disturbance
To date there has been substantial research undertaken on mood fluctuations in
connection with changes in training volume. Indeed, the single most consistent finding
reported in the OT literature is that increases in training load are associated with shifts
towards negative mood states, while reductions in training loads are associated with
improvements in mood (Hooper, MacKinnon, & Hanrahan, 1997; Hooper et al., 1995).
Based on the findings of this research, monitoring of mood fluctuations has been
frequently proposed as a useful tool for reducing the incidence of athletes suffering
from OT (Hooper et al., 1997; Morgan et al., 1987a, 1988a, 1988b; Raglin, 2001).
The most well-documented and widely-used approach focuses on mood disturbance as
assessed by the POMS (McNair et al., 1971). This 65-item adjective checklist was
developed as a measure of typical and persistent mood reactions to current life
situations and provides a global or total mood disturbance score based on measures of
specific mood states. Specifically, the total mood disturbance score is calculated by
summing scores for the negative mood states of tension, depression, anger, fatigue and
confusion and then subtracting the score for vigour. Designed to assist with the
assessment of progress in psychotherapy and counselling in outpatients, McNair and
colleagues (1971) indicated that a secondary application could be in research settings
with normal populations (+18 years, with some high school education).
In a classic series of studies, Morgan and colleagues (1987a, 1988b) demonstrated that
increases in training load among swimmers were reliably associated with increases in
POMS mood disturbance scores, while decreases in training load were associated with
decreases in mood disturbance scores. These studies were conducted over a 10-year
time-frame and involved 400 competitive collegiate swimmers (200 female and 200
male). Results revealed that a dose response relationship existed between training load
Chapter 2 Literature Review
Page | 29
and mood state, such that significant increases in training load were associated with
increases in mood disturbance. The earliest psychological changes noted on the POMS
occurring with OR were increases in fatigue and decreases in vigour. Changes in
tension, depression and anger appeared to follow with chronic OT. From their research,
five to 10% (20 to 40) of swimmers were diagnosed as suffering from training distress,
and 80% (16 to 32) of swimmers from this subgroup exhibited clinical depression.
Based on these findings, Morgan and colleagues (1987a, 1988b) concluded that the
interpretation of individual mood profiles may successfully predict the performance
decrements associated with OT. Thus, the POMS was accepted as an effective method
of monitoring the consequences of OT.
Subsequent studies have replicated these findings for swimmers and documented
similar responses to heavy training for many other sport activities including running,
cycling, canoeing, and basketball (e.g., Berglund & Sfstrm, 1994; Flynn et al., 1994;
Martin, Andersen, & Gates, 2000; Raglin, Eksten, & Garl, 1995; Rietjens et al., 2005).
Raglin and Morgan (1994) have also identified a subset of POMS items that they
believe are particularly sensitive to the effects of high intensity training. However, while
the majority of research to date has found mood disturbances to be consistently higher
in athletes showing signs of OR or OT (O'Connor, 1997), some exceptions have been
noted.
Hooper and colleagues (1997) suggested that based on previous research, OR athletes
may present with similar levels of tension, depression, anger, vigour, fatigue and
confusion as athletes who are intensely trained but not suffering from training distress.
Fourteen swimmers were subsequently monitored over a six-month training period. Of
this group, three swimmers were classified as suffering from training distress. The
researchers concluded that while the POMS appears to be useful for monitoring those
Chapter 2 Literature Review
Page | 30
athletes predisposed to OR, it does not differentiate between athletes experiencing
training distress as opposed to those simply exhibiting the signs and symptoms
associated with intense training.
Furthermore, while the POMS has been the most frequently used psychological
inventory in OT research, some authors have disputed its validity. One common
criticism has been that the POMS is essentially a clinical screening instrument and was
not designed for athlete use, particularly not for diagnostic purposes. Therefore, it is
possible that a sport-specific mood instrument, such as the Training Distress Scale
(TDS) developed by Raglin and Morgan (1994) from the POMS scale items may be
more appropriate. In addition, the POMS restricts its focus to mood states. Depression
and other negative mood states such as tension can occur for reasons unrelated to OT,
and an exclusive focus on mood disturbance could therefore be problematic for accurate
diagnosis of athletes at risk of OT (Raglin & Wilson, 2000). Self-report measures that
supplement measures of mood disturbance with measures of other physiological states
might reduce this type of measurement error.
2.3.2 Behavioural Changes
A second approach to the monitoring of training distress via self-report involves the use
of behavioural symptom checklists. A variety of such checklists have been used, based
on observations of muscle soreness, general lethargy, insomnia, loss of appetite, and/or
susceptibility to minor illness during periods of high-intensity training (e.g., Fry et al.,
1994b; OConnor, 1997; Raglin & Wilson, 2000). Morgan and colleagues (1988) were
among the first to systematically monitor such parameters. While the primary focus of
their research was on mood disturbance following increased training, they also took a
number of physical symptom measures. Muscle soreness was measured with a seven
point categorical scale on a daily basis prior to training. An overall rating of muscle
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soreness was obtained as well as ratings for the calf, thigh, forearm and shoulder.
Results revealed a significant increase in perceptions of muscle soreness within each
muscle group as well as an increase in overall muscle soreness.
Hooper and colleagues (1995) investigated a wide range of parameters during a 6-month
swimming study. The purpose was to determine which parameters could be used to
monitor OT and recovery. In addition to a range of biochemical markers, a battery of
well-being questions were included in a daily training log. Questions included quality of
sleep, fatigue, stress and muscle soreness and subjective ratings were measured on a
scale of 1-7. Body mass, early-morning HR, occurrence of illness, menstruation and
causes of stress were also recorded. Regression analysis revealed a battery of well-being
ratings which predicted OT scores, accounting for 76% of the variance. It was
concluded that self-reported ratings of well being may provide an efficient means of
monitoring both OT and recovery.
Similarly, the use of training-specific symptoms as a means of monitoring OR was
further investigated by Fry and colleagues (1992a, 1994b). Symptoms identified
included behavioural, psychological, and physical complaints. Fry and colleagues
(1994b) found that OT was accompanied by severe fatigue, immune system deficits,
mood disturbance, physical complaints, sleep difficulties, and reduced appetite. Mood
states moved toward baseline during recovery, but feelings of fatigue and immune
system deficits persisted throughout the study. It must be acknowledged that it is
entirely possible that these enduring feelings of fatigue are a consequence of factors
outside of an athletes sport participation.
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2.3.3 Perceived Stress
Athletes who train with adequate rest and recovery periods still have other sources of
stress to cope with. In addition to the physiological responses to excessive overload
training, failure to cope with everyday, sport-specific, social and other environmental
stressors also contribute to the OT process (Tenenbaum et al., 2003b). It is entirely
possible for OTS to develop when a normally tolerable volume and intensity of training
is undertaken, but other stressors from the environment, such as work and private (i.e.
family) circumstances are present (Cohen, Kamarck, & Mermelstein, 1983; Kellmann,
2002; Rowbottom et al., 1998b). During periods of high extraneous stress (e.g.
educational, environmental, occupational, or social stress), training volumes and
intensities may need to be modified and scaled down; as together, the combination of
stressors may exceed the individuals capacity to adapt.
Indeed, high self-reported stress levels have been shown to be associated with both OT
(Hooper et al., 1995) and OR (Mackinnon et al., 1997). As such, a third approach to the
monitoring of training distress via self-report has focused on measures of perceived
stress. Rushall (1990) as well as Myers and Whelan (1998), argued that training-specific
stressors often combine with various sources of stress outside of sport to influence an
athletes mental and physical readiness to perform. Rushall (1990) further suggested
that it was particularly important to monitor perceived stress during periods of heavy
training, because of the potential for perceived stress to increase fatigue levels and, in
turn, decrease performance capabilities.
With the understanding that the cumulative nature of stress has the potential to be
detrimental to performance, Rushall (1990) developed a self-report inventory for
measuring stress tolerance in elite athletes called the Daily Analysis of Life Demands
(DALDA). Rushall recognised that athlete stressors originated from outside, as well as
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within the sporting environment. As such, to understand an athletes response to the
specific stress of training, Rushall perceived that it was necessary to measure all sources
of stress. The DALDA identifies 12 areas of life stressors and 42 symptoms of stress
(Rushall, 1990). The inventory is divided into two parts and results are kept in a log
book. Halson et al. (2002) documented predictable workload-related increases in
perceived stress among cyclists during a two-week period of high intensity training and
proposed that the DALDA questionnaire may be an effective and practical tool to
determine whether a reduction in performance is the result of the fatigue response to
acute training or from OR/ OT.
Kellmann and others (Kentt & Hassmn, 1998; Kellmann, 2002) have added
consideration of recovery processes to this approach and have conducted a number of
studies examining stress-recovery states (Kellmann, 2002). Kellmann and Gnther
(2000), for example, found significant changes in stress-recovery profiles of German
rowers during high-intensity training periods prior to the 1996 Olympics. Similar
findings were obtained for junior rowers preparing for the 1995 and 1998 World
Championships (Kellmann, Altenburg, Lormes, & Steinacker, 2001; Steinacker et al.,
2000). In order to assist with the identification of an athletes physical and mental
stress, as well as the extent of current recovery activities, Kellmann and Kallus (2001)
developed the Recovery-Stress Questionnaire for Athletes (RESTQ-Sport). The
Recovery-Cue (Kellmann, Botterill, & Wilson, 1999) was subsequently developed in
addition to the RESTQ Sport to provide feedback regarding current stress and recovery
states, but also to increase an athletes knowledge and awareness of their stress and
recovery. Both of these measures have been shown to be practical and effective in the
assessment and monitoring of training stress and recovery (Kellman, Patrick, Botterill,
& Wilson, 2002; Steinacker et al., 2000).
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Part 3: Proposed Mechanisms of Overtraining
Although many of the symptoms of OT are similar to the resistance and exhaustion
stages of the Hans Seyles 1956 general adaptation syndrome (GAS), this model does
not clarify the exact mechanism of OTS. Attempts to understand the causes of OT have
approached the phenomenon from a number of different perspectives. These range from
initiating events and biological markers or indices of fatigue as discussed above;
nutritional imbalances and bodily responses to stressors; to hormonal perturbations,
changes in immune response and disturbances of mood state. While several theories
now exist, scientists acknowledge that the mechanisms of OT remain unknown.
However, there is consensus that it is most likely to result from a combination of: a)
inadequate recovery between training sessions, b) excessive amounts of high intensity
training, c) sudden increases in training loads, and d) additional training and non-
training stressors (Fry et al., 1991; Halson & Jeukendrup, 2004).
Lehmann, Foster, Dickhuth and Gastmann (1998) presented a figure that outlined
potential mechanisms underlying the genesis of OTS in endurance sport. The original
figure was revised and has been presented below as Figure 2.2 (Lehmann et al., 1999).
Based on the premise that OT develops as the result of a stress-recovery imbalance, the
diagram implies that performance decrements are the result of altered immune function,
peripheral fatigue, altered mood state and central fatigue. Altered reproductive function
is also believed to be involved. However, these outcomes of a stress-recovery imbalance
are only hypothesised to cause a performance decrement. Further research is needed to
confirm this model.
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3.1 Alterations to the endocrine axis
Although many hormonal indicators of OR and OT have been proposed, appreciation of
the exact mechanism behind the aetiology of OT has been difficult (Smith & Norris,
2000). It has been suggested that OT may result from a multitude of factors; including
an anabolic/catabolic imbalance (Aldercrentz et al., 1986), hormonal dysfunction of the
pituitary axis (Barron, Nokes, Levy, Smith, & Millar, 1985; Urhausen et al., 1998a), an
amino acid imbalance (Bailey, Davis, & Ahlborn, 1993; Newsholme, Parry-Billings,
McAndrew, & Budgett, 1991) or autonomic dysfunction (Lehmann et al., 1998). One
proposal was that overreaching is probably associated with insufficient metabolic
recovery, resulting in a decline in ATP levels, while acute OT or OTS may be
attributed to failure of the hypothalamus to cope with the total amount of stress
(Kuipers, 1998).
Figure 2.2: Selected mechanisms underlying the genesis of OTS in endurance sport
(Lehmann et al., 1999)
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Several investigators have focused on the role of the hypothalamus, activation of the
autonomic nervous system and the hypothalamic-pituitary-adrenal axis (HPA), as well
as the hypothalamic-pituitary-gonadal axis (HPG). Alteration of each of these endocrine
axes, may account for alterations in blood catecholamine, glucocorticoid, and
testosterone levels, which have been frequently associated with OTS. However, recent
developments suggest that activation of these pathways may be consequential rather
than causational. Further research is required to assess this proposal.
3.2 Metabolic hypothesis
Following periods of overload training, it has been shown that there is a period during
which homeostasis is restored through metabolic processes, enhancing the energetic
supply to skeletal muscles (Petibois, Cazorla, Poortmans, & Deleris, 2002). The length
of this period is dependent on the degree to which homeostasis was disrupted (Fry et al.,
1991).
Both physical activity and diet stimulate processes that, over time, alter the
morphologic composition and biochemical function of the bodyThe metabolic
stress of physical activity can be measured by substrate turnover and depletion,
cardiovascular response, hormonal perturbation, accumulation of metabolites, or
even the extent to which the synthesis and degradation of specific proteins are
altered, either acutely or by chronic excessive training. (Colye, 2000, p. 512S)
One popular view has been that OT is caused by alterations in the metabolic processes.
Seven main hypotheses involving metabolic processes or pathways have been presented
in relation to OT, with each one relating to a central parameter (i.e. carbohydrates,
branched-chain amino acids, glutamine, polyunsaturated fatty acids, leptin and
proteins). As with all other areas of OT research, there is mixed support for each of
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these hypotheses and, while there appear to be valid links, there is also supporting
evidence as to why each hypothesis is unlikely to be the primary cause of OT as
illustrated in Table 2.4. While this table is very simplistic and only offers a brief glance
at each of these proposed hypotheses and research areas, it provides a general
background to current research trends.
The ability to distinguish more clearly between previously proposed mechanisms may
be enhanced by recent advances in technology. Analytical equipment now exists that
provides researchers with a global, sensitive, and highly reproducible physiochemical
analytical technique that identifies structural moieties of bio-molecules on the basis of
their infra-red absorption (Petibois, Cazorla, & Deleris, 2000). Fourier-transform infra-
red (FT-IR) spectrometry provides researchers with the ability to analyse 50L capillary
blood samples and obtain a complete biochemical breakdown of the whole sample.
Using this technology, recent studies have shown that OT could result from successive
and cumulative alterations in metabolism that become chronic during prolonged periods
of endurance training (Petibois et al., 2002, 2003a, 2003b).
Petibois and colleagues (2000) described the process of OT as successive alterations in
exercise metabolism that shift from the main energetic stores of exercise (carbohydrates
and lipids) towards molecular pools (proteins) normally not used for the energetic
supply of skeletal muscles. These stepwise progressions are illustrated in Table 2.5. As
such, a general biochemical model of the OT process may soon be proposed which
includes most of the previously identified metabolic pathways.
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Table 2.4: A summary of proposed metabolic hypotheses
Hypothesis Presumptions However
Carbohydrate hypothesis
(Achten et al., 2003; Manetta et
al., 2002)
Fatigue may be induced by a slight transient hypoglycaemia, due to
hepatic and/or muscle glycogen store depletion, and/or failure in
glycogenolytic metabolic flux
It has been suggested that long-term glycogen depletion would lead to
an increased BCAA oxidation which is more likely to be responsible
for a central fatigue process and subsequent negative mood states
BCAA hypothesis
(Gastmann & Lehmann, 1998)
Increased free fatty acid transport to skeletal muscles induced a
higher utilisation of albumin transport capacities. This in turn leads to
increased release of free tryptophan. Increased cerebral tryptophan is
converted into serotonin. Instrumental in modulation of the body
Although an influx in serotonin does not appear to be a sufficient
inducer of central fatigue to lead to OT in endurance athletes, it may
increase athlete susceptibility. Results concerning this hypothesis are
inconclusive and require more controlled experimental research.
Glutamine hypothesis
(Boelens et al., 2001)
One of the most abundant amino acids in the body, it is metabolised
by immune cells. Proliferation depends on glutaminolysis, suggesting
that a decrease in blood glutamine concentration may be at least
partially responsible for immune function deficiency or impairment.
Immunosuppression has been observed in OT athletes without
decreases in glutamine concentrations and in the absence of URTIs.
Polyunsaturated fatty acid
hypothesis
(Calder & Newsholme, 1992)
Given the recurrent occurrence of immune suppression in overtrained
athletes, this alt