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Overtraining
D. Keast and A. R. Morton, Departments of Microbiology and Human Movement Research, The
University of Western Australia.
Modern athletic training requires two approaches: training to refine skills and
training to maximize cardiorespiratory endurance energy systems and the physical and
physiological capacities for the particular sport. To achieve any sustained improvement
or long term benefit athletes must enter into long-term training programs which may
require several years of macro- and micro-training cycles. These training cycles are not
successful unless the athlete undergoes not only physical but physiological and
biochemical stress. It is these stresses that provide the stimuli for the adaptation
necessary to ensure improved performance (8). However as adaptation occurs
increasing workloads are required to induce maximal and enduring increases in the
capacity to perform, which has been termed overload training.
It is slowly being recognized that the physiological and biochemical adaptations
that are occurring following exercise are not taking place over the training period but in
the period between two training bouts. It is also in this period that the natural fatigue of
training is felt. Therefore if inadequate rest or too great an exercise stress is applied over
the training period then an athlete may reach a state of failing adaptation which in the
first instance may be experienced as serious fatigue and non recovery from the training
sessions within the expected times. Should athletes or coaches superimpose new large
and unscheduled increases in workload into training programs then the chances of
moving rapidly into serious overtraining is greatly increased. If the athlete who is
seriously fatigued for whatever reason continues to train at heavy workloads then there is
an increasing chance that a more serious stage of fatigue will develop where several
days or weeks of reduced training will be required before full recovery can be achieved.
If early warning signs of chronic fatigue are ignored then performance times will
deteriorate and injury and infections are almost certain to follow. If the progression
through overtraining is ignored then the athlete can develop what is now being
recognized as a serious chronic clinical condition known as the overtraining syndrome
(7,8).
Unfortunately the transitions through the above states are through ill-defined
zones where some characteristics of two stages of overtraining can be present at the
same time [Table: 1, (8)].
Overtraining and the overtraining syndrome are not confined to elite athletes and
can occur at all levels of sports endeavor. It is more likely to be experienced in its most
severe form by highly motivated athletes who may choose to ignore early warning
symptoms of being overtrained. Probably the only reliable indicators, at the present time,
of the approach of severe overtraining are the failure to meet previously established
training criteria accompanied by chronic fatigue or recurring or chronic infections.
However there are documented cases of elite athletes apparently developing severe
overtraining symptoms with no prior warning. Evidence is accumulating which suggests
that once an athlete has experienced the overtraining syndrome for more than a few
months he/she may never again be able to return to their former top levels of
performance and in the worse cases may remain severely ill for up to and exceeding two
years. Currently there are no proven cures for the severe overtraining syndrome. It is
therefore imperative that the processes leading to overtraining are understood in order to
develop training programs that minimize the likelihood of overtraining and prevent the
loss of athletes to their chosen sports.
PHYSIOLOGY/BIOCHEMISTRY
An important function of the training process is to increase the athlete's ability to
tolerate and adapt to training stress both of which are functions of the intensity, the
duration and the frequency of the stressors routinely applied throughout the training
program (1). As a result of the training the body integrates the increased stress levels
into its normal homeostatic mechanisms thus allowing the athlete to do more work for an
equivalent homeostatic displacement above this new base line. This integration has been
called supercompensation and is considered to occur mainly over the rest periods and is
naturally accompanied by a "fatigue valley" from which the athlete has to recover before
the next level of stress is applied. The best example of fatigue-induced
supercompensation is that of the storage of glycogen but it has been shown to occur in
many enzyme pathways and in aerobic power. Supercompensation can take several
days after exercise and occurs in times of reduced training in running, swimming, and in
arm strength and power sports. In all instances the changes are reflected in both physical
and emotional homeostatic mechanisms. We also believe that the onset of overtraining is
more likely to occur in aerobically trained endurance athletes when they, for whatever
reason, superimpose severe anaerobic stress into their training programs.
Recent developments have suggested that the homeostatic mechanisms of the immune
system can also be displaced adversely in overtraining and may be responsible for the
increased susceptibility of some athletes to opportunistic infections (9) .
The recorded symptoms of overtraining are numerous (Table 2, (7)) and indicate
that a simple diagnosis is likely to be impossible while at the same time the observations
suggest that individual "weak-links" may initiate the clinical presentation of overtraining
(7,8).
It can be seen from Table 2 that the appearance of overtraining is closely related to
symptoms of reduced ability to perform, loss of skills, fatigue, and failure to recover from
exercise stress. These factors can also be associated with cardiovascular changes,
eating and gastric disturbances, loss of weight, nausea, headaches, insomnia and night
sweats. All of these symptoms suggest that gross long-term physiological disturbance
has occurred which in turn can lead to further physical damage such as tendonitis,
periostitis and joint dislocations and bone fractures. There is also a strong psychological
component (Table 2) to severe overtraining and currently there is debate as to whether
this is an initial contributor to overtraining or results from the general debilitation which
has caused the reduced performance.
Profound biochemical changes occur and are sustained as an integral part of the
homeostatic mechanisms of athletic training. Many of the biochemical changes are
geared to the stores of energy and the enzymes associated with the provision of energy.
However at the onset of overtraining there appear to be significant changes in the
accumulation of metabolic end products such as urea and uric acid accompanied by
negative nitrogen balance and loss of body weight. Energy stores such as glycogen
become deplenished and mineral depletion also can occur. There may also be depletion
of important oxygen carrying capacity of the blood due to lowered hemoglobin, iron
stores and ferritin. However many of the biochemical changes reported have occurred
following the imposition of an acute bout of exercise on the athlete and may not be a true
reflection of any underlying overtraining.
Neuroendocrine/Hormones
A natural response to increased workload is increased levels of stress hormones. These
hormones may be adrenaline ( epinephrine ), noradrenalin (norepinephrine),
vasopressin, glucagon, growth hormone, adrenocorticotrophic hormone (ACTH), cortisol,
and thyroid stimulating hormone (TSH). However it has been suggested that an
adaptation of the pituitary-adrenocortical system occurs with long term training stress and
it is only with overtraining that hormonal variations from newly established levels might be
expected to occur. Several hormones can also function as neurotransmitters which could
lead to significant changes in the function of the nervous system.
Two types of overtraining have been proposed to result from significant changes
within the nervous system. Either the sympathetic or the parasympathetic nervous
system may dominate. It has been suggested that if the sympathetic overtraining
dominates it will lead to increased resting pulse rate and decreased pulse recovery after
exercise, decreased body mass and loss of appetite, disturbed sleep, emotional
instability and sweating. Elevated basal metabolism, ECG abnormalities and negative
nitrogen balance may also result from sympathetic overtraining.
Symptoms of parasympathetic overtraining appear to be directed towards more
subtle changes initially which mimic the effects of training improvements. These factors
may include early fatigue, low basic pulse rate, rapid return of heart rate to basal levels
with low blood pressure, hypoglycemia and progressive anemia and digestive
disturbances. Overall sympathetic and parasympathetic overtraining are both functionally
represented by significant decreases in work capacity. It has also been argued that
speed and power athletes may be more prone to sympathetic overtraining while
endurance athletes may be more prone to parasympathetic overtraining. Furthermore
young athletes may be more susceptible to sympathetic problems while older athletes
may exhibit the symptoms of parasympathetic overtraining.
The existence of both types of overtraining indicates that down- and up-regulation
of neuroendocrine pathways can occur in overtraining. In close association with the
above changes are changes in other hormones such as insulin, corticosteroids, ACTH
and in female athletes major changes in hormones regulating the menstrual cycle such
as estradiol, progesterone or testosterone along with luteinizing hormone and follicle
stimulating hormone. Table 3 illustrates that there is little doubt that many of the
symptoms resulting from the hormonal modifications associated with overtraining can be
influenced by the hypothalamic-pituitary axis (7).
IMMUNITY
Often athletes appear to be more susceptible to infection than untrained
individuals. However it has also been proposed that moderate training can reduce the
risk of infection. The outcome has been the development of a "J-shaped " model relating
relative risk of infection, in particular to respiratory infections, and amount of exercise
undertaken by athletes(4). Care has to be exercised in the interpretation of many of the
published results as athletes often compete in environments where the numbers of
pathogenic organisms can be high, where abrasions occur and open up the possibility for
increased incidence of infection, and they can be brought together at major sports
events, from all over the world, in close proximity in both their living areas and
competitive venues. All of these circumstances are conducive to high risks of cross
infection and exposure to microorganisms against which there is likely to be overall low
immunity. In these circumstances there is no need to invoke any exercise/stress related
lowering of immunity for the higher incidence of infection that may be experienced by the
athletes. Various micro-organisms such as staphlococci, herpes simplex, tinea pedis,
hepatitis A, B & C, the common cold viruses, influenza viruses and Epstein Barr virus are
classical examples of agents linked with the above situations.
In addition to these types of infection, which represent the events of classical herd
immunity and infectious processes, studies have been carried out in attempts to relate
the intensity and duration of exercise with increased susceptibility to infection. In the case
of the longer endurance track athletes, marathon runners and triathletes there is a
relationship between the distance run in training and susceptibility to upper respiratory
tract infection. This may also be the case where intensity of training is dramatically
increased during a training program and more particularly if the increase is rapid and
unscheduled. It is variously proposed that the increase in susceptibility to infection
experienced by these athletes is due to loss of mucosal and hence IgA protection of the
nasopharyneal areas as a result of increased respiration or a true increase in
susceptibility to infection as a direct result of exercise induced immune suppression (9).
These largely epidemiological observations have led to a plethora of results on
changes in cells of the immune system with exercise. Many of these studies have
documented acute changes that occur following a single bout of exercise; whether these
are any reflection of true susceptibility to infection or not is still controversial and remains
to be resolved. However there is some evidence that cell numbers, in circulation are
reduced over a training period and hormones, such as cortisol, are increased with
training. Cortisol can function as an immune suppressant at elevated levels.
One thing is clear, however, and that is that continued high level training during
the course of an infection can be extremely detrimental. All training programs should be
reduced or suspended during the period of an infectious episode and probably should be
extended into convalescence. This approach may be of particular importance in the case
of viral infections.
Animal studies have shown clearly that moderate training enhances resistance to
infection from both bacterial and viral pathogens while serious overtraining leads to
increased susceptibility to infection.
At the present time much of the evidence for involvement of the immune system in the
apparent increased susceptibility to infection of the seriously overtrained athlete comes
from the dynamic changes registered by the immune system post exercise. There are
suggestions that much of these changes result from increased circulatory flushing
resulting from the oxygen demands of exercised muscles aided by epinephrine induced
mobilization of immune cells to the peripheral circulation. Many of the in vitro results
which have suggested an immune suppression in these cells can be explained by
subpopulation changes which indicate that mitogen responsive T-lymphocytes have been
replaced by mitogen unresponsive Natural Killer(NK) cells. However there is some
evidence that some of the cytokines, in particular Interleukins 1,2 and 6 may become
variable, thus providing the potential for the induction of abnormal metabolism within the
immune system, while reductions in circulating interferons, potential NK cell activators,
can also occur and hence provide the environment for abnormal immune responses(3,8).
Historically cells of the immune system have been considered to be resting cells
exhibiting an extended Go phase awaiting antigenic stimulation to be activated both
immunologically and metabolically. Early biochemical studies on the cells of the immune
system indicated that there was nothing unusual in their biochemical pathways. Interest
in the cells remained low until recently when it was discovered that they appeared to
have an absolute requirement for an external supply of the amino acid glutamine.
Glutamine was shown to function both as an energy source and precursor for nucleotide
synthesis for both DNA and RNA. However it has now been shown that cells of the
immune system are extremely metabolically active in the resting state and that their
ability to respond to both T- and B- cell mitogens, their ability to produce both interleukin1 and interleukin-2, their ability to phagocytose both unopsonised and opsonised antigen
and their ability to produce antibody is proportional to the availability of glutamine. Linked
closely with these observations has been a recognition that muscle is a major producer of
glutamine and it has been strongly argued that it is this glutamine that functions as the
major source of this amino acid for the immune system. Immune function appears to be
compromised before the levels of circulating glutamine approach that of the Michaelis
constant (Km) for glutaminase, the first crucial enzyme in glutamine metabolism.
In the well trained individual the blood levels of glutamine appear to rise after an
acute exercise. However in overtrained individuals the blood levels of glutamine are
significantly reduced from normal, and remain so for extended periods of time. In our own
experience this reduction of glutamine can be present when a large range of standard
blood biochemical tests and immunological and hematological parameters all remain
within normal ranges. It has been suggested that a low blood glutamine level may be a
good predictor of serious exercise fatigue and by implication may be associated with low
responsiveness of the immune system in the overtrained athlete. This is and area
deserving intensive study at the present time.
The Overtraining Syndrome
While overtraining occurs from time to time in top athletes there has been
acceptance recently that a most serious clinical form of overtraining exists and leads to
long-term debilitation(2,8). The overtraining syndrome may first appear as chronic
tiredness with an inability to meet performance criteria by the athlete. The athlete is likely
to be strongly motivated and from the elite ranks, although this is not always the case.
The chronic fatigue has to be sufficient to be debilitating to the athlete and must have
persisted for longer than two weeks in the absence of any other identifiable illness.
However there are cases where the onset has been rapid with subjects developing the
syndrome within a few hours or following overnight rest.
The athlete almost always exhibits severe stress and depression, however
whether this is the initiator or follows from the onset of the syndrome is unclear at the
present time. The depression seems to have a central origin and often requires
psychiatric treatment. The syndrome often is associated with an increased susceptibility
to infection, recurrent infections or chronic infection. Once established the syndrome
does not resolve itself by reduction in, or suspension of, training and the athlete can be
so debilitated as to be bedridden. There appears to be a major breakdown in normal
physiological and emotional processes which can be further aggravated by dietary
problems, physical injuries and failure of normal healing processes accompanied by
infections(2). Simple exercise, especially if anaerobic in nature, can reactivate the full
extent of the syndrome at short notice and the subjects metabolic response to light acute
exercise will be abnormal usually accompanied by decreased maximal lactate production
during exercise. However in our experience most if not all of the normal biochemical and
immunological screening tests fall within the normal ranges for unstressed individuals
except that in some instances there has been evidence of unusual interleukin activity and
reduced plasma glutamine concentrations. Several of the properties of the overtraining
syndrome are similar to those of the post viral syndrome and the chronic fatigue
syndrome(4,5). These are two chronic debilitating conditions which are known to occur
often in non sports people who are under considerable stress as a result of their
lifestyles.
Treatment/Prevention
Early overtraining is usually cured by allowing longer regeneration times between
exercise bouts and in the more severe cases by restriction of training schedules until
physical well-being returns to the athlete. These rest periods can be days or weeks with a
graded return to full training being essential if more than a few days of rest are required
for recovery. There is no known cure for the overtraining syndrome and various strategies
for management of the subject have been proposed. Extended rest periods in excess of
several weeks are required. However, light exercise is to be encouraged. It is often
difficult to persuade elite athletes that light exercise may mean simply walking short
distances with a slow build up over as many as three to four months to a regular light
training program. However if the athlete attempts to return to full training too soon then a
full relapse is almost certain to occur. There is no guarantee that an athlete may not
suffer one or more relapses many months after an apparent recovery. Because there is a
strong psychological element associated with the overtraining syndrome then return to
regular cardiovascular fitness training should be based on therapeutic aspects rather
than through a return to competition ranks (2).
Because overtraining in any form can progress to the chronic overtraining
syndrome which is likely to terminate an athletes career at competitive level and may
seriously compromise all aspects of life, it becomes essential to develop and enter into
long-term training programs. In these programs the maximum care needs to be taken to
reduce the chances of overtraining while maximizing athletic development. Currently
there is much emphasis placed on the development of training programs where macroand micro- training cycles form the overall plan but into which adequate regeneration
times are built (1,6). It is only slowly being accepted that the major part of the adaptation
process is occurring in the rest period between exercise bouts.
References
1. Bompa, T. O. Theory and methodology of training. Pub: Kendall/Hunt, Dubuque, IO
1983.
2. Budgett, R. Overtraining syndrome Br. J. Sp. Med. 24:231-236, 1990.
3. Friman, G. and Ilback, N-G. Exercise and infection- interaction, risks and benefits.
Scand. J. med. Sci. Sports. 2:177-189 1992.
4. Fry, R. W., A.R. Morton And D. Keast. Overtraining syndrome and the chronic fatigue
syndrome Part 1. New Zealand J. Sports Med. 19:48-52, 992.
5. Fry, R. D., A. R. Morton and D. Keast. Overtraining syndrome and the chronic fatigue
syndrome Part 2. New Zealand J. Sports Med. 19: 76-77,1992.
6. Fry, R. W., A. R. Morton and D. Keast. Periodization of training stress- A Review.
Canad. J. Spt. Sci. 17:234-240, 1992.
7. Fry, R. D., A. R. Morton And D. Keast. Overtraining in athletes an Update. Sports
Med. 12:32-65, 1991.
8. Keast, D. And A.R. Morton. Long-term exercise and immune functions. In Exercise and
disease. Eds R. R. Watson and M. Eisinger Pub: CRC
Press. pp 89-120.
9. Nieman, D. C. and Nehlsen-Cannarella S. L. Exercise and infection. In Exercise and
disease. Eds: R. R. Watson and M. Eisinger Pub: CRC Press. pp 121-148, 1992.
_________________________________________________________
Table 2: The Major Symptoms Of Overtraining As Suggested By The Literature.7
_________________________________________________________
PHYSIOLOGICAL/PERFORMANCE
PSYCHOLOGICAL/INFORMATION
PROCESSING
Feelings of depression
General apathy
Decreased self esteem/Worsening feelings
of self
Emotional instability
Difficulty in concentration at work/training
Sensitive to work and environmental
stress
Fear of competition
Not eating well
Changes in personality
Decreased ability to narrow concentration
Increased internal and external
distractibility
Decreased capacity to deal with large
amounts of information
Gives up when going gets tough
Decreased performance
Inability to meet previously attained
performance standards
Recovery prolonged
Reduced toleration of loading
Decreased muscular strength
Decreased maximum work capacity
Loss of co-ordination
Decreased efficiency/amplitude of
movement
Reappearance of previously corrected
mistakes
Inconsistency in rhythmical movements
Reduced capacity of differentiation
and correction technical faults
Increased difference between lying
and standing heart rates
Abnormal T wave pattern in ECG.
Heart discomfort on slight exertion
IMMUNOLOGICAL
Changes in blood pressure
Increased susceptibility to and severity
Changes in heart rate at rest,
of illness/colds/allergies
exercise and recovery
Flu-like illnesses
Increased frequency of respiration
Unconfirmed glandular fever
Decreased body fat
Minor scratches heal slowly
Increased oxygen consumption at
Swelling of lymph glands
submaximal workloads
One day colds
Increased ventilation at submaximal
Decreased functional activity of neutrophils
workloads
Decreased total lymphocyte counts
Increased heart rate at submaximal
Reduced mitogen response
workloads
Increased eosinophil count
Shift of lactate curve towards the
Decreased proportion of null ( non-T
X axis
non B lymphocytes)
Decreased evening post workout
Bacterial infection
weight
Reactivation of Herpes viral infection
Chronic fatigue/feelings of heaviness
Insomnia
BIOCHEMICAL
Night sweats
Negative nitrogen balance
Thirst
Elevated basal metabolic rate
Anorexia nervosa
Hypothalamic dysfunction
Loss of appetite
Flat glucose tolerance curve
Bulimia
Depressed muscle glycogen concentration
Amenorrhea/oligomenorrhea
Decreased bone mineral content
Delayed menarche
Decreased hemoglobin/serum iron ferritin
Headaches and nausea
Mineral depletion: Zn, Co, Al, Se, Cu, etc.
Increased aches and pains
Increased urea concentrations
Muscle soreness and tenderness
Elevated cortisol levels/low testosterone
Gastrointestinal disturbances
Increased serum hormone binding globulin
Muscle damage/tendinositis
Testosterone to cortisol ratio less than 30%
Elevated C-reactive protein
Increased uric acid production
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Table 3: The Involvement Of The Hypothalamic/Pituitary Axis In The
Stress Induced By Overtraining