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A Practical Approach to the

Overtraining Syndrome
P.Z. Pearce, MD

The Rockwood Clinic, 14408 East Sprague Street,
Spokane, WA 99216, USA.
Current Sports Medicine Reports 2002, 1:179183
Current Science Inc. ISSN 1537-890x
Copyright 2002 by Current Science Inc.

The overtraining syndrome is a chronic fatiguing illness that

affects highly motivated endurance athletes. It is
characterized by declining performance when maintaining a
normal training program. The cause seems to be failure of
adaptation within the neuroendocrine system, due to
inadequate periods of rest. The onset is insidious and
unfortunately, once it manifests, the only treatment is rest.
This article discusses the known pathophysiology of
overtraining, along with practical aspects of evaluation
and treatment.

Scott Tinley is a professional triathlete and friend, who
came to me with a training problem. He had always
been active in athletics, running track, swimming, and
sailing. When the sport of triathlon began, arguably in
1976 [1], it was a perfect test of his physical ability.
During the late 70s and early 80s he was a member of a
small group of athletes who dominated the sport.
Through years of training and racing, he had developed
a routine that was reliable and effective. Then, after a
tough race at Ironman Canada (2.4 mile swim, 112 mile
bike, 26.2 mile run), which included a lengthy sprint-tothe finish with Japans Shingo Tanji, something
changed. He was physically fatigued, and no longer able
to train or race at his previous level of competition. It
was hard for him to sleep, and he started to experience
upper respiratory infections. It ultimately impacted
every facet of his life and family. He began searching for
a solution, undergoing numerous physiologic and
blood tests, stool analysis, and multivitamin therapy
without success. Ultimately he has retired, but remains
active, with a different perspective on training and
racing. I believe that he suffered classic symptoms
of the overtraining syndrome, and his experience
highlights many of the principles discussed in the
following paragraphs.

The overtraining syndrome is a collection of symptoms
that imply maladaptation to the training response. An
athlete is no longer able to perform at a previously
demonstrated level of proficiency, despite maintaining or
increasing his or her usual training program. The
prevalence is not known, but it is usually reported among
endurance athletes, such as cyclists, distance runners, and
triathletes. It is not nearly as common in women as men
[2]. The diagnosis is elusive and often made in retrospect,
once the athlete is hopelessly mired in its symptoms.
Unfortunately the only known treatment is rest (sometimes prolonged), which obviously impacts an athletes
career. In a group whose self image is inextricably
intertwined with physical performance, there may be
significant psychologic morbidity, as well. The onset is
insidious, with signs and symptoms only subtly different
from those experienced during normal training. An
athletes susceptibility depends upon the sport, training
volume (intensity, duration, and frequency), and individual variables, such as physical conditioning, response to
stress, and outside influence (family, job, concurrent
illness or injury). There is no single test that can determine
when an athlete is exceeding his or her limit, and therefore
at risk of developing the overtraining syndrome. Consequently, the best treatment is prevention, which requires a
working knowledge of exercise physiology and the human
response to training stress. There is a wealth of basic
science in the literature concerning this complex phenomenon, and I will highlight a few illustrative studies, while
concentrating on the practical aspects of management.

The training response is a basic principle of exercise
physiology that simply states when a system is stressed,
then allowed adequate time to rest and recover, it will
adapt to tolerate greater stress in the future [3]. This is also
known as overload training [4], not to be confused with
the overtraining syndrome, which occurs when the two
independent variables of stress and rest are not balanced.
Stress, therefore, could be defined as that which causes the
system to adapt, and is either internal or external. In
addition to the load of training, physiologic stress includes
growth in young athletes, and the bodys response to
illness or injury. Many athletes also face external pressures



Table 1. Clinical presentation

Overuse injury
Decreased strength
Decreased efficiency
Increased recruitment
Decreased economy of motion
Increased basal metabolic rate
Negative nitrogen balance
Decreased maximal lactate production
Increased heart rate at submaximal loads
Decrease maximum heart rate/VO2
Decrease muscle glycogen stores
Frequent infection
Poor healing of wounds
Delayed menarche
Decreased libido (males only)
Decreased sperm count
Depressed mood
Disordered sleep
Poor concentration

imposed by their family, job, and interpersonal relationships. Although impossible to quantify, stresses are additive, and define the amount of rest needed to adapt [5].
The physiologic adaptation to stress involves a complex
neuroendocrine response. As discussed in The Stress of Life
by Hans Selye [6], the hypothalamus and pituitary, along
with endocrine glands under their control, allow an organism to respond to changes in its environment. Training
causes release of cortisol, epinephrine, growth hormone,
and prolactin, the stress hormones. Usually cortisol levels
fall to normal and free-testosterone rises within a few
hours after an intense exercise session [7]. It is believed
that this signals the anabolic process, in which muscles
hypertrophy, expand their capillary vascular bed, increase
the density of mitochondria per cell, and store more glycogen. These are the cellular effects that correlate with
increased power and endurance in the athlete. It seems that
the critical step in this process is a downregulation of
cortisol, linked with an increase in free-testosterone [8].
Unfortunately, intense training without adequate rest
elicits a maladaptive hormonal response, as defined by

Selye [6]. Cortisol levels remain elevated for several days,

and do not recover before more training stress is added.
That causes direct suppression of the testes [9], and an
increase in the level of sex hormone-binding globulin
(SHBG), further compromising the effect of testosterone
[10]. This may explain the different presentation of
overtraining between the two sexes. Although the ovaries
do produce some testosterone, women are not as
dependent upon that hormone, and therefore demonstrate
menstrual irregularity when the pituitary-ovarian axis is
disturbed. Circulating cortisol also binds to muscle, and
induces catabolism, with negative nitrogen balance and
production of urea [11]. Sensing muscle breakdown, the
immune system releases monocytes, which respond by
producing proinflammatory cytokines, IL- , IL-6, and
tumor necrosis factor-. The resulting systemic inflammation induces a central nervous system (CNS) response
termed sickness behavior, which produces malaise, fatigue,
and ultimately reduction in training [12].

Because there is no test battery that is pathognomonic for
overtraining syndrome, the diagnosis is clinical. That
requires a familiarity with the population at risk, some
predisposing training errors, and features of the clinical
presentation. Most affected individuals are highly
motivated, but not necessarily the most successful.
Recreational athletes, without an adequate knowledge of
training principles, often accelerate their program too
rapidly, and dont include enough rest. That may also be
the fate of team-sport athletes who return after extended
absence from illness or injury, and respond to peer
pressure. Elite amateurs emulate the training regimen of
professionals, but must also balance the stress of a fulltime job, usually without the supervision of a coach.
Although unsubstantiated (except by personal experience),
I believe professionals succumb to years of pushing the
envelope, and simply fatigue the stress response. Finally,
highly motivated individuals may misinterpret the cause of
their declining performance, and feeling inadequately
prepared, respond with increased training.
When reviewing the clinical presentation by system, it
really resembles any other fatiguing illnesses, as seen in
Table 1 [13]. Musculoskeletal symptoms are obvious,
and reflect the nature of excessive physical activity. The
immune system is intimately linked to contractile tissue
through glutamine, necessary for lymphocyte proliferation
and function, but unavailable from any other source [14].
Overtrained muscles cannot devote the metabolic machinery to keep up with glutamine demand, which leads to
impaired immune function, and leaves the athlete
susceptible to opportunistic infection [15]. Neuroendocrine manifestations underscore the fact that overtraining
is a central phenomenon, and I believe illustrate the
pathophysiologic model discussed earlier. Women may

A Practical Approach to the Overtraining Syndrome Pearce

experience delayed menarche then oligo- or amenorrhea,

whereas men suffer from decreased libido. Israel [16]
suggested that signs and symptoms could be divided by
autonomic classification. These were further elucidated by
subsequent investigators [11,17], and form the basis for
Table 2. As the sympathetic symptoms seem to be the first
to manifest, I believe they represent a prolonged stress
response, whereas those of a parasympathetic nature seem
to imply neuroendocrine failure. Finally, as further
evidence of a central origin, there is a depressed psychologic profile, with disordered sleep, poor concentration,
and impaired memory.
Although much is made of laboratory abnormalities,
from Table 3 it should be obvious that the testing is either
prohibitively complex, or the results so nonspecific, that they
are not very useful in predicting when an athlete is beginning
to overtrain. There is so much individual variation in physiologic response that it is more predictive for an individual to
collect baseline data, then perform interval sampling over
time. Although race results may be the best performance
indicator of fitness and preparation, there are too many
independent variables to make them useful clinically. Timetrials or other tests of submaximal exertion are much more
controlled and reproducible. These include measurement of
isokinetic strength, and time to fatigue at near-maximal
(anaerobic) exercise intensities [17].

It should follow from the preceding paragraphs that
prevention is clearly the best approach. Unfortunately one
must therefore be able to balance a desire for maximal
performance, with the limits of physiologic adaptation.
That obviously requires an understanding of fundamental
training principles. The ancient Greek Olympians were first
to realize the value of varying workout intensity over weeks
and months throughout the season [19]. This concept of
periodization is a perfect framework for scheduling rest
intervals between sessions of active training [5]. Typically
the year is divided into four macrocycles of varying length,
each with specific focus. During the preparation phase, the
athlete works on flexibility, strength training, and
establishing an aerobic base. This is followed by a precompetitive cycle, which emphasizes intervals, speed work, and
other sport-specific tasks. During the competitive season,
some flexibility and strength training are maintained, but
the emphasis is on performance. The final phase is postcompetition, in which the athlete rests, and engages in
low-intensity cross training, or recreational activities. Each
week is termed a microcycle, during which it is customary
to alternate training between hard and easy (or rest) days.
In addition to rest, Costill [20] recommends an adequate
high-carbohydrate diet to facilitate recovery and adaptation. Most investigators would agree with a composition of
60% to 70% carbohydrate (at least 50% complex), 20% to
30% protein, and 10% to 20% fat.


Table 2. Neurophysiologic expression



Increased resting pulse

Prolonged pulse recovery
Disordered sleep
Increased sweating
Emotional instability

Decreased resting pulse

Rapid pulse recovery
Poor digestion
Decreased blood pressure
Early fatigue

Table 3. Laboratory abnormalities

Decreased iron and ferritin with normal hematocrit
Increased CPK/myoglobin/3-methylhistadine
Increased resting cortisol
Elevated sex hormone-binding globulin
Decreased ratio of plasma free-testosterone to cortisol
Increased serum urea/uric acid
Decreased cortisol response to insulin-induced
Decreased pulsatile FSH/LH secretion
Exercise-induced hypoglycemia
Increased hypoxanthine (oxypurine) response to exercise
Decreased CD3, CD4, CD8, natural killer cells
Decreased salivary IgE
Depressed Profile of Mood States
CPKcreatine phosphokinase; FSHfollicle-stimulating hormone;
LHluteinizing hormone.

Recognizing overload so you can intervene before it

becomes pathologic, requires an understanding of the
signs and symptoms in Table 1, but also the cumulative
nature of stress. Obviously an athlete should not increase
training load when other major life events are occurring. In
that respect, it is helpful to have an independent way of
monitoring training stress and response. Although the
luxury of a coach is not available to most, certainly an exercise log is essential. Use it to record training volume (both
attempted and completed), in terms of intensity (heart
rate), and duration. Include some sense of perceived exertion, and general sense of well-being. As above, make some
notation about diet (caloric intake), and quality of sleep.
Finally, it is helpful to define some personal stress indicators that can be monitored from day to day throughout
the season, to detect a decrement in performance. The key
is to establish a baseline from which to make individual
comparison, because variability within the population
makes normative data unreliable. With due respect to all
the preceding information, most is really not useful for the
average athlete. I believe a very simple and practical
approach is best (Table 4). If sophisticated testing
equipment is available, I would still favor measurements of
performance including submaximal VO2 and lactate
profiling, which have an established track record. One
provocative lab test that I have found useful is the free
testosterone to cortisol ratio. If SHBG is concomitantly
elevated, a change in ratio of greater than 30% implies
catabolism, and therefore overtraining. In the future we



may be able to use FT-infrared spectroscopy to detect

changes in metabolic response during exercise [21]. Once
overload is recognized, however, it is imperative to react
appropriately. The athlete must listen to his or her body,
believe his or her coach (or data), and resist the temptation
to increase training in the face of decreased performance.

When prevention fails, an athlete has no choice but to rest.
The length of time can vary from 6 to 12 weeks (or longer),
and depends upon the type of sport, level of competition,
and individual variables mentioned earlier. In the evaluation, I recommend a thorough history and physical to
exclude other causes of fatiguing illness. Explore recent
changes in training load, and previous episodes of overtraining, then metabolic abnormalities including decreased body
weight, irregular menses, or change in libido. The psychologic profile will be depressed, reflecting the central nature of
this disorder. Athletes usually manifest the classic symptoms
of anhedonia, sleep disturbance, and difficulty with concentration or memory, possibly even history of a recent increase
in life stress. A routine physical should be performed to
screen for thyroid disorder, exercise-induced asthma, heart
murmurs, and abdominal masses. Evaluate the lymph nodes
for enlargement, indicating possible infection or malignancy.
The basic lab screen I use is included in Table 5.
The key to successful treatment is developing a trust
relationship with the athlete. Their competitive nature is
tremendous, and to most rest is a four-letter word. I have
found, from personal experience, that empathy is more
effective when one participates in the sport oneself. Anticipate rebellion, and all five stages of a typical grief reaction.
With patience one will be rewarded an opportunity to
discuss physiology, the biochemical basis of behavior, and a
rational approach to training. Compromise will be necessary,
including sensible testing, and maintenance of some physical activity. It is unreasonable to expect highly motivated
individuals to simply stop exercising. Finally, I have found
the selective serotonin reuptake inhibitor (SSRI) class of
antidepressants useful in restoring normal neuroendocrine
function, similar to their effect in clinical depression. They
can be taken once daily, have rapid onset, and minimal
adverse reactions. I usually favor sertraline or fluoxetine, due
to their neutral or slightly stimulating side effects. They are
prescribed at the usual dosage and continued for at least 3
months, but never stopped in the winter, when production
of serotonin in the CNS is at its lowest level. The tricyclic antidepressant medications amitriptyline, and trazadone (25 mg
at bedtime) have been shown to re-establish restorative sleep
patterns, and may also be useful for the first 3 to 6 weeks.

The overtraining syndrome is a form of chronic fatigue that
occurs when an athlete does not allow enough time for rest,

Table 4. Personal stress indicators

Monitor daily
Resting pulse*
Pulse recovery after training
Monitor periodically
Sport-specific time trials
Isokinetic strength
Time to fatigue at near-maximal exertion
*Measure for 1 full minute after waking up but before getting up.
Consider a rest cycle if pulse increases 5 beats/min on 2
consecutive days.
At end of rest cycle/before increasing load/every 46 weeks.

Table 5. Exclude systemic illness


T3/T4/TSH/Hgb A1C
Screen for types AE

*With overtraining, hematocrit will be normal or increased.

ANAantinuclear antibody; CMVcytomegalovirus; CRPCreactive protein; ESRerythrocyte sedimentation rate; Hct
hematocrit; Hgbhemoglobin; HLAhuman leukocyte antigen; RA
rheumatoid arthritis; TSHthyroid-stimulating hormone.

recovery, and adaptation to training stress. It is characterized

by declining performance, despite maintenance of an
adequate training program. The actual incidence is
unknown, but it is usually seen in highly motivated, male,
endurance athletes (running, cycling, triathlon, Nordic
skiing). The diagnosis is difficult because there is no single
test that can determine when an athlete may be overstressing
the system. Because recovery is prolonged once the
syndrome occurs, prevention is the best treatment. The
coach and athlete must understand basic principles of
training, such as periodization, and should develop a set of
personal stress indicators to determine when training is
exceeding the capacity to adapt. Although many tests have
been proposed in the basic science literature, most of them
are either too nonspecific or technically complex to be of
much value clinically. I favor simple measurements of adaptation (resting pulse, and pulse recovery after exercise) or
performance (isokinetic strength, time to fatigue at or near
VO2 max, and sport-specific submaximal time trials). Once
the diagnosis is made the only treatment is rest, which is difficult for highly motivated athletes to accept. It requires an
empathetic and trusting relationship with his or her physician, for support during recovery. SSRI antidepressants may
be helpful, as the pathophysiology seems to be a central
neuroendocrine failure, similar to clinical depression.
Certainly more research needs to be done in the recognition
of stress indicators, which may help predict the onset of
overtraining, and the use of techniques to speed recovery.

A Practical Approach to the Overtraining Syndrome Pearce

References and Recommended Reading

Papers of particular interest, published recently, have been
highlighted as:

Of importance
Of major importance

Plant M: Iron Will. Chicago: Contemporary Books; 1987.

Counsilman JE: The Science of Swimming. Englewood Cliffs, NJ:
Prentice Hall; 1968.
3. Shephard RJ: Exercise and training in women, Part I:
Influence of gender on exercise and training response.
Can J Appl Physiol 2000, 25:1934.
4. Kuipers H, Keizer HA: Overtraining in elite athletes: review
and directions for the future. Sports Med 1988, 6:7992.
5. Harre D: [Principles of Sport Training: Introduction to the Theory
and Methods of Training]. Berlin: Sportverlag; 1982.
6. Selye H: The Stress of Life. London: Longmans Green; 1957.
This classical work explores the neuroendocrine response to stress,
establishing the pathophysiology of clinical depression,
and overtraining.
7. Viru A: Hormones in muscular activity; adaptive effect of hormones
in exercise. Boca Raton, FL: CRC Press; 1985.
8. Kelly FJ, McGrath JA, Goldspink DF, Cullen JM: A morphological/biochemical study on the actions of corticosteroids on
rat skeletal muscle. Muscle Nerve 1986, 9:110.
This is the biochemical result of overtraining. Prolonged elevation of
serum cortisol suppresses testosterone, and elicits a catabolic response
in skeletal muscle.
9. Aakvaag A, Opstad PK: Hormonal response to prolonged
physical strain, effect of caloric deficiency and sleep deprivation. In Exercise Endocrinology. Edited by Fotherby, Pal. Berlin:
de Grugler; 1985:2564.



Adlercreutz H, Harkonen M, Kouppasalmi K, et al.: Effect of

training on plasma anabolic and catabolic steroid hormones
and their response during physical exercise. Int J Sports Med
1986, 7(Suppl 1):2728.
11. Kindermann W: [Overtraining an expression of faulty
regulated development]. Deutsche Zeitschrift fur Sportmedizin
1986, 37:238245.
12. Smith LL: Cytokine hypothesis of overtraining: a physiological adaptation to excessive stress? Med Sci Sports Exerc
2000, 32:317331.
This article discusses the immune response, and biochemical basis of
sickness behavior, seen in illness and overtraining.
13. Fry RW, Morton AR, Keast D: et al.: Overtraining in athletes.
Sports Med
1991, 12:3265.
The best review of overtraining I have seen. It includes seven pages of
basic science references!
14. Ardawi MS, Newsholme EA: Metabolism in lymphocytes and
its importance in the immune response. Essays Biochem
1985, 21:143.
15. Nieman DC: Exercise and resistance to infection. Can J Physiol
Pharmacol 1998, 76:573580.
16. Israel S: Zur problematic des Ubertrainings aus internistischer und leistungsphysiolgisher Sicht. Med Sport 1976, 16:51.
17. Barron JL, Noakes TD, Levy W, et al.: Hypothalamic dysfunction in overtrained athletes. J Clin Endocrin Metab 1985,
18. McKenzie DC: Markers of excessive exercise. Can J Appl Physiol
1999, 24:6673.
19. Bompa TO: Theory and Methodology of Training. Dubuque, Iowa:
Kendall/Hunt Publishing Company; 1983.
20. Costill DL: Inside Running: Basics of Sports Physiology.
Indianapolis: Benchmark Press; 1986.
21. Petibois C, Cazorla G, Deleris G: et al.: FT-IR spectroscopy
utilization to sportsmen fatigability evaluation and control.
Med Sci Sports Exerc 2000, 32:18031808.