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Overtraining in Athletes
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ance in 5J:
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SpOTtSModicine 12 (I): 32-65. !991
01 12-1642J9 1/0007-0032/$ 17.00JO
C! Adis International Limited. All rights ~..rved.
SPOI 28
Overtraining in Athletes
An Update
Rod W. Fry, Alan R. Morton and David Keast
Departmcnt of Human Movcment and RecrcationStudies,The University of WesternAustralia, Pcrth,
Wcstcrn Auslralia, and Dcpartment of Microbiology, Qucen Elizabelh II Mcdical Centre,Pcrlh, Weslern
Australia. Australia
r
Contents
Summary
I. Overtraining
2. Terminology
3. The BasicTheory of Athletic Improvement-Ovl:rload Training
4. Consequencesof Failing Adaptation -Symptoms of Overtraining
5. Who is Susceptible?
6. Recognition of Overtraining
7. The Parasympatheticvs Sympathl:ticSystems
8. The NeuroendocrineSystem
9. Immunity
9.1 Regulation of Immunity
9.2 Catecbolaminesand Immunl: Regulationin Overtraining
9.3 Glucocorticoids and Immune Regulationin Overtraining
10. Psychology
II. Biochemistry{physiology
12. Muscular Damage
13. Practical Approachto the Preventionof Overtraining
13.1The Structureof the Training Programme
14. Which Tests ShDu1dBe Included in the Test Battery?
15. Conclusions and Directions for the Future
r
Summary
I!
Overtraining appearsto be causedby too much high intensity training and/or too little regeneration (recovery)time often combined with other training and nontrainingstrcssors.There
are a multitude of symptomsof overtraining, the expressionof which vary dependingupon too
athlete's physical and physiologicalmakeup,type of cxcrciseundertakcnand other factors. The
aetiology of overtraining may therefore bediffercnt in different peoplesuggestingthc need to be
aware of a wide varicty of parametersas markers of overtraining. At presentthere is no one
single diagnostic tcst that can define overtraining. The rccognition of overtraining requiresthe
identification of stressindicators which do not return to baselinefollowing a period of regeneration. Possibleindi~tors include an imbalanceof the neuroendocrinesystem.suppressionof the
immune system, indicators of muscledamage,depressedmuscleglycogenreserves,deteriorating
aerobic, ventilatory and cardiacefficiency,a depressedpsychologi~1profile, and poor perform-
1. Overtraining
The literature revealsexte:
dence linking excessiveexerc
ological conditions and Chl:QD
capacity which exists within t
to time (reviewed by Keast et
Keizer 1988).Examplesofhigl
have been forced to withdra\
events as a result of acute an
havealso beendocumented(Fi
athleteshave failed to meetpe
that they have achieved in pr
maintaining their high level tl
These athle~s
have often 1'1
chronic lethargy cbaracterise
general fatigue, inability to
weeksof training and inability
races' (Smith et aI. 1988).Atbl
shown to experienceovertrail1
their careers (Morgan et aj.
1990). The 'staleness'associ:
creasesin performanceresult
training load to which the att
It is obligatory that trainin
the athlete in order to provid
aptation to the stressesencol
petition (Bompa 1983).Expo~
els of exercisestressslightly t
which be/shehas previouslyeI
training
programme, has bel
training (Kuipers & Keizer 19
anism by which the stimuli I
plied. In order for the athlete
training, adequate rest must I
the training programmeand
_..~
-~..
Ovel1rainingin Athlctcs
~~"".\\!""~'~~.,t-"."'~1
~.::;i:::::;:';';::'~~i~'..}~
..
[.;
::: :~-~~-~-
'~
33
,;",; ;::'.:::':~"..,.:.'~;.:
ance in sport specifictests. c.g. timc trials. Screeningfor changesin parametersindicat~veof
ovcrtraining needsto be a routine component of the training programmcand mu;8tbe Incorporated into thc programmein such a way that the short term fatigue associatedwIth overload
training is not oonfusedwith the cltronic fatiguecharactcristicof ovcrtraining. An in-depthkn~w'
ledgeof periodisationof tmining theory may be necessaryto promote optimal perfo~ance Improvemcnts. prcvent overtraining. alKi develop a system for incorporating a screeningsystem
into the training programme. Scfceningfor ovcrtraining and performanceimprovementsmust
occur at the culmination of fcgenerationperiods.
-
1. Overtraining
Western Australia, Perth.
Centre. Perth, Western
Ring
L
r
~ing
.training
and/or
too
strcssors.
little
re-
There
--iary depending upon the
ken and other factors.The
..-uggesting the needto be
present there is no one
vertraining requires the
:Jwinga period of regenersystem,suppressionof the
reserves,deteriorating
lIe, and poor perform-
crementsin training avoided (Bompa 1983).If inadequate rest and/or too great an increment in
training load has been imposed, the athlete may
The literature revealsextensiveanecdotalevientera stateof failing adaptationor overreaching,
dence linking cxcessiveexerciscstresswith pathcharacterisedby fatigue and nonrecovery from
ological conditions and chronically reducedwork
training sessions(Kuipers & Keizer 1988). If a
capacity which exists within the athlete from time
heavytraining load is continued while the athlete
to time (reviewedby Keastet al. 1988;Kuipers&
is overreaching,chronic fatigue and stalenessmay
Keizer 1988).Examplesof high Calibreathleteswho
lead to deterioration in perfonnance and the athhave been forced to withdraw from major world
lete will become more susceptible to minor illevents as a result of acute and chronic infections
have alsobeendocumented(Fitzgerald1988).Other
neSSe5
and chronic inf~ctions.
Currently no model cited in the literature preathleteshave failed to meetperformancestandards
that they have achievedin previous yearsdespite sentsa reliable method for monitoring the training
maintaining their high level training programmes. regimenin sucha way that the overloading training stimulus is optimised, thus preventing overThese athletes have often reporte,depisodcs of
reaching.The developmentof valid, reliable and
chronic lethargy characterisedby 'symptoms of
general fatigue, inability to perform consistent objective methods for the early detection of overreachingwould allow a reduction in training load
weeksof training and inability to recoverafterhard
races' (Smith et 31.1988).Athleteshaveoften been prior to the more serioussymptoms of overtrainshownto experienceovertraining at somestagein
ing bccomingapparcnt.Symptoms ofovertraining
their careers (Morgan et at. 1987a,b,1988;Silva
have beenwell documented(reviewed by Hackney
et al. 1990;Kuipers & Keizer 1988)[see table I].
1990). The 'staleness'associatedwith these decreasesin performanceresults from an excessive The table prescntsa selectedlist of symptoms which
have beendescribedin the Jiterature as being the
training load to which the athlete fails to adapt.
It is obligatory that training programmesstress consequenceof overtraining and illustrates the
the athlete in order to provide the stimuli for adoverwhelming complcxity of the overtraining
problem. An understanding of this complexity is
aptation to the stressesencounteredduring comnecessaryto gain insight into the scope of the
petition (Bompa 1983).Exposingthe athleteto levovertraining problem. Recognition ofa state of faels of exerciscstressslightly greaterthan thoseto
tigue which renders the athlete susceptible to
whichhe/shehas previouslyencounteredwithin the
overtraining prior to the overt symptoms becomtraining programme, has been termed overload
training (Kuipers & Keizer 1988)and is the mech- ing apparent would be of obvious benefit to thc
anism by which the stimuli for adaptation is apathlete and coach.
plied. In order for the athleteto adaptto overload
Overtraining associatedin studies which have
carefullycontrolled the training stressimposed on
training, adequaterest must be incorporatedinto
the training programmeand large immediate inathletesarescarce.The works of Costill et al. (1988),
SportsMedicine 12 (I) 1991
34
t.bt.,.
Themajor symptoms of overtrGlnlngas Indicatedby their prevalenceIn the literature
Ph VII 01ogl CIII pertOrm8 nce
P,yehologle81/lnfonn8t1on
Feelings of depression
Decre~sed performance
InabilIty to meet pr4)vlously attained
prolJe"lng
General apathy
Decreased self-esleem/worsenlng
performance standarde/crlt9rla
feelings of self
Decreased muscular strength
Emotional Instability
Dlffloolty 'n ooneentratlng at work and training
SeJlsltive to environmental and emotional stre8s
Decreased maximum work capacity
Fear of competition
Loss of coordination
Decreased efflci4)ncy/decreased
Changes In personality
Decressed ability to narrow concentration
R9COV&ryprolonged
Reduced toleration of loading
amplitude of movement
Increased Internal and external distractability
Decreased capacity to deal with large amounts of Information
Reeppearanoe of mistakes alreecly corTected
Reduced capacity of cllfferentlatlon
and correcting
technical faults
Increased difference betNeen lying and standing heart rate
Gives up when the going gets tough
Abnormal T wave pattern In ECG
'fTlfTI"nologlc81
Heart discomfort on slight exertion
Changes In blood pressure
Increased susceptibility to and severity of
Changes In fleart rate at rest, exercIse and recovery
InCteaaed../requencyof respiration
Perfuse respIration
Decreased body fat
Increa8&d oxygen consumption at submaxlmal workloads
ITlCrea8&d ventilatIon and heart rate at submaxlmal
workloads
Overtraining results from
IIlnessfcold8/allergies
Flu-like Illnesses
Unconfirmed glandular fever
Minor scratches heal slowly
tween performance demand an,
ity (Arnold 1960; Mellerowicz &
Swelling of lymph glands
One-day colds
Oacre3sed functional activity of neutrophll8
Oecrtaeed totallymphocyl$
Decreased evening poStworkout
Reduced re8ponse to m\lOgons
IncreasOO blood eoe'nophll count
Elevated basal metabolic rate
Chronic fatigue
Insomnle with and without night sweats
Feels thIrstY
Anor&xla "en/osa
count8
08creased proportion of null (non- T, non-S Iymphocyt&s)
Bac1eriellnfecllon
Reactivation of herpes viral Infection
Significant variations In CD4 : CDS lymphocytes
LOBS of appetite
Bulimia
\~enorrh08a/ollgomanorrh08a
Hsadaches
Icreased achas and pslns
aatrolnlestlnal
BIochemical
Negative nitrogen balance
Hypothalamic dysfunction
Flat glucose tolerance curves
Neusea
cllsturbances
uscJa soreness/tenderness
Tendlnosllc complaints
PeriOsteal complaints
Depressed muscle glycogen concentration
DeCfeased bone mineraI content
Delayed menarche
Dacreased haemoglobin
Decreased serum Iron
Jscle damage
Decreased serum ferritin
Iveted C'r&actlve protein
Lowered TIBC
Ahabdomyolysls
Kirwin et al. (1988), Morgan et
phy ct al. (1990) are exception!
carefully controlled trnining s1
monitoring of that stress using
indices arc required before sc
thorough insight into ovcrtraini
prescribe trnining to optimise
avoid overtraining. Studies inv(
regulation and the effect of hc
tion in response to controlled
may be thc key to the developrr
monitoring training to prevent
2. Terminology
Shift of the lactate curve towards tile x axis
weight
Overtraining in Athlctcs
Minerai depletion (In, Co. AI, Mn, 5e, Cu, etc.)
Increased urea concentrations
Elevated cortisol levels
Elevated ketosterolds In urine
Low free testosterone
Increased serum hormone binding globulin
Oecrea8ed ratio of free te8tosterone to cortisol of
more than 30%
Increased uric acid produ~on
crtraining is defined principal
pcrfonnancc capacity (Kinderrr
& Keizer J988; Noakes 1989; R(
Gundersen ct al. J986), despite
tenance of training load. Kindc!
ifies this with the statement t
formance occurs in thc abscnc(
Kindermann's statement docs
correct, however, as evidcncc P
view suggests that the immune
prcsscd in overtraining, leadin,
ease accompanying overtrainin;
Historically no uniform ten
used to dcfine ovcrtraining (Co
Kuipers & Keizcr 1988). 5tal
must be encouraged in the inte
and the state of the art paper pr
and Kcizcr (1988) provides a s{
Scveral aspccts of that tcrmino
further in this paper. Kuipers
stale that confusion arises bet
gators do not discriminate bet\
overload training (stimulus for;
outcome, which may be overre
overtrdining), overtraining sync
ertraining) or muscular overstl
fatigue resulting from placing 1
specific muscle groups. Morga!
35
~
Sports Medicine 12 (1) 1991
r/OC...lng
9nlng 18811ng901 88\1
at work and training
I and emotional
stress
...;oncentratlon
ternal dlatraclabllity
0' "11th large amounts of Information
8 tough
Kirwin ct at. (1988), Morgan et al. (1988) and Murphy et ai, (1990) are exceptions. More studies with
carefully controlled training stress and systematic
'monitoring of that stress using a variety of stress
indices are required before scicntisls can gain a
thorough insight into overtraining and confidently
prescribc tr"dining to optimisc pcrformancc and
avoid overtraining. Studies investigating hormonal
l"cgulation and the cffcct of hormonal misrcgulation in response to controlled training situations
may be the kcy to the development of a system for
monitoring training to prevent overtraining.
2. Terminology
and severity of
..
'IV
of neutrophils
Ie oounw
Igens
Junt
(non.T, non-B lymphocytes)
II Infection
, .CD8
lymphocytes
co
:oooonlr8110n
OA\8n1
AI. Mn. Se, Cu, etc.)
fine
,ding globulin
"-
~rone
to cortl$Ol of
~Ion
i
"""-'--
Overtraining results from a discrepancy betwccn pcrformancc demand and functional capacity (Arnold 1960; Mellerowicz & Barron 191I). Ovcrtraining is defined principally as a decrcascd
performance capacity (Kindermann 1986; Kuipcrs
& Keizer 1988; Noakes 1989; Reidman 1950; StrayGundersen et al. 1986),despitc increased or maintenance of training load. Kindernlann (1986) qualifies this with thc statcmcnt that depressed performance occurs in the absence of.i>rganic illness.
Kindermann's statement does not appear to be
correct, however, as evidence presented in this reo
view suggests that the immune system can bc dcpressed in overtraining, leading to infectious disease accompanying overtraining.
Historically no uniform tcrminology has been
used 10 define ovortraining (Callister et al. 1990;
Kuipcrs & Kcizcr 1988). Standard terminology
must be encouraged in the international literature
and the state of the art paper presented by Kuipers
and Keizer (1988) provides a sound slarting point.
Several aspects of that tcrminolugy are dcveloped
further in this paper. Kuipcrs and Keizer (1988)
state that con fils ion arises because most investigators do not discriminate between the process of
overload training (stimulus for adaptation) and the
outcome, which may be ovcrreaching (short term
overtraining). overtraining syndromc (chronic ovel1raining) or muscular ovorstrain, which is loca!
fatigue resulting from placing too much strain on
specific musclo groups. Morgan et al. (1981) used
the term 'overtraining' to mcan ovcrload training,
and statedthat overtraining is approachedas a deliberatelyplannedand appropriatefeature of training microcycles.Coachesand sport scientistsin the
United States(Griffith 1926;Morehouse& Rasch
1958;Morgan 1985b;Wolf 1961)have historically
labelleda state of failing adaptationas 'staleness',
whereasEuropeanworkers have tendedto usethc
term 'overtraining'(Bompa 1983;Harre 1982;Kcrezty 1971;Mellerowicz & Barron 1971).The terms
'overfatigue'and 'overstrain' have also bccn used
synonymously with overtraining and staleness
(Czajkowski 1982),while 'chronic fatigue'has been
uscd to mean ovcrtraining (Kere-Lty1971; Wolf
1961).
The term which has emerged in tbc scicntific
literaturesinceFalsetti's (1983)and Brown's (1983)
statementsabout short term overtraining is 'overreaching'. Falsetti (1983) states that overreaching
is usedby somecoachesas a form of training using
a large stimulusfor adaptationto promote a fitness
peak prior to a major competition. This rcsults in
decreasedperformancefor a short period of time
but following an extended rccovcry period results
in supercompcnsationand increasedperformance
capacity(Fleck 1988; Kuipers & Keizer 1988).Overreacbingis, however,the first stageof overtraining which if disregardeddevelops into the more
severeovertraining syndrome.Complete recovery
from overtraining may require weeks or months
(Kuipers & Keizer 1988),
It now appearsthat some redcfinition of terms
is warranted:
I, The processof stressingan individual to provide a s1imulusfor adaptationand supercompensation is overloadtraining.
2. Training fatigue/stressis the normal fatigue
that is experiencedfollowing sevcraldays of heavy
training associatedwith an overload training stimulus. Tbis fatigue is reversed and supercompensation occurs by the last few days of a period of
reducedtraining load (regenerationI:t\icrocycle).
3. Overtrainingis the generaltcrm which indi.
catesthat the individual has beenstrcsscdby training and extraneousstressorsto the extent that hej
shecan not perform at an optimum levcl following
~
Sports Medicine 12 (I) 1991
36
an appropriate regenerationperiod. A drop in performance ,is necessaryfor overtraining diagnosis.
4. Overreachingfollows the intentional or unintentional induction of short term overtraining.
The symptoms of overreachingcan be revcrsedby
a longer than normal regenerationperiod.
S. The overtraining syndrome is the state of
chronicallydepressedperformanceaccompaniedby
one or more of the more serious symptoms.Overtraining syndrome and stalenesswill be considered synonymous, as discussed by Kuipers and
Keizer(1988). Recoveryfrom the overtrainingsyndrome requiresa significantly longertime than that
required in overreaching.
Overstrainfollows acute tissuedamagcinduced
by isolated intensive training sessionswhich exceedthe muscular stresstolerance. This generally
occurs after single or repeated bouts of excessive
exercisewhich result in damage to muscle fibres.
Muscular overstrain mayor may not accompany
overreaching or overtraining syndrome (Kuipers
and Keizer 1988).
Training stressorsare those resulting from the
physical.physiological,and psychologicalstressin.
duced by the training workloads administeredduring overloadtraining. Extraneousstressorsarethose
resulting from activities and psychologicalforces
related to lifestyle. Supercompensationis a stateof
heightenedwo,rk capacity,above that of which the
athlete has recently been capable. This has been
characterisedas a state of balanced homeostasis
with homeostaticmarkers reflecting eitherbaseline
values or improvements, depcnding upon the nature of the variable.
J. The Basic Theory of Athle/ic
Improt'ement-Overload Training
CelestUllrich states'Wheneverthe homeostatic
balanceof the body is upset, the human organism
attempts to adjust in such a way that the balance
is restored. Untit the balance is restored,a state of
stressexists' (Counsilman 1968).Improvements in
an athlete's ability to tolerate the demandsof competition and training are achieved through adaptation to the stressorsapplied in the training pro-
~
~
~
r
gramme (Bompa 1983, 1989; Counsilman 1968;
Harre 1982;Kukusbkin 1983;Matveyev 1981;Selye 1957).Thus the aim of the training processis
to apply a seriesof stimuli which will displacethe
homeostasisof the individual's functional systems
and thereforeprovide the stimulus for adaptation
(Matveyev 1981).
Followingoverloadit hasbeenshownthat there
is a period where metabolism fe-establishes
homeostasis,
the lengthof this perioddependsupon
the degreeto which homeostasishas been disrupted (Bompa 1983;Harre 1982).In addition to
regaininghomeostasis,
the organismadaptsto the
stressorsuch that, if the same stressorwere im~
posed again,the homeostaticmechanismswould
not be displacedto the sameextent(Bompa 1983;
Harre 1982iKukushkin1983;Selye1957).Follow~
ing this adaptationan individual has been shown
to becapableof doing morework for an equivalent
homeostaticdisplacement
For this adaptationand supercompensation
to
be of benefit, a period where no further homeostatic displacementoccurs is necessaryto providc
adaptationslprocesses
time to becomereorg&nised
(Harre 1982). For this reason,rest has been re.
garded as an organic componentof the training
process(Counsilman1968;Harre 1982;Matveyev
1981).Howeverifno secondaryadaptationalstirn.
ulus is applied during the phaseof supercomp~n.
sationit has beenshownthat involution in the degreeof adaptationoccursand the training effect is
lost (Bompa 1983, 1989; Harre 1982; Matveyev
1981).
The degreeof supercompensation
achieveddependsupontbe size of stimulusfor adaptationand.
therefore.the degreeof imbalancein homeostasis
induced. For this reason,a seriesof fatigue inducing stimuli maybe applied in orderto creatca 'valley of fatigue' (Counsilman1968).This fatigue valley occurs becausefull recoveryis not permitted
betweentraining sessions,
creatinga progressively
greaterimbalancein homeostaticmechanismsand,
consequently,a more powerfulstimulus for regeneration and supercompensation.
In general,physiologicaland biochemical researchhave supportedthe concept of fatigu~in-
Ovcrtraining in Athletes
duced supercompensatior.
compensation has beende
of glycogen(Astrand & R.
J97Ia,b), the concentratiol
bit metabolic pathway (Sc
acrobic power (Adams 19.
In each of these studies:
demonstrated 2 or 3 day
stimulus. Other studies ha
compensation during a pc
following intensive trainir
ance (Adams 1966),swim!
till et al. 1988)and arm stl1
eta!. 1985).
4'. Consequencesof F,
Symptoms of Overtttj
There is no evidenceil
vides clear guidelinesfor
from thc symptoms of the
Thcrc is a continuum oftl
symptoms (see fig. I). th
those that reflect the im
Symptoms associ!
Acute
fatigue
as a resu1t
of Ihe
training
session in
isolation
Fig.1. A continuum of ovcrtr:
[
SpOrlg Medicine 11 (I) 1991
38
with the definition of overtraining may be separating the normal fatigue which results from a series of high intens.itytnlining sessionsand is necessary to promote a training effect from the
underlying fatigue associatedwith overtraining.The
problem arisesb~use we do not yet have a clear
definition for the point at which training fatigue
finishes and overtraining begins, in addition the
symptoms of training fatigue will be superimposed
on those of overtraining, further complicating the
picture. The key to separatingovertnlining from
the normal training responsemay lie in the struc.
ture of the training programme through the defi.
nition of the time point in each block of training
when full regenerationshould be complete. Poor
performanceor indicators of an imbalancein homo
eostatic mechanisms at this stagewould indicate
that residual fatiguc is still presentand that subsequentheavy training should not be initiated.
It is likely that everyonerespondsto stress in
different ways and, therefore,the large variety of
symptoms presentedin table I representsindividual variation in the expressionof overtraining
symptoms. In addition, different types of activity
(e.g. predominantly anaerobic vs predominantly
aerobic) may result in different symptoms.
At the outset of overtraining, increasedfatigue
and decreasedperformancemaybe the only symptoms, but with accumulation of fatigue other objectiveand subjective symptomshave be"enshown
to appear progrcssively(Kuipers & Keizer 19&&).
Falsetti (1983) states that there is a cOnstellation
of symptoms. However, short and long tcrm overtraining may differ only in the Icngth of time that
the symptoms have existed and the time it takes
for rccovery' (Henschen 1986;Nideffer 1988).
More recently it has beensuggestedthat somc
of the symptoms associatedwith the ovcrtraining
syndrome may be associatedwith excessiveproduction ofcytokines (Lloyd et al. 1989;McDonald
et a1. 1987; Wakefield & Lloyd 1987)due to an
unbalancedimmune system.The role of stressproteins in perpetuatingthe symptomsof overtraining
syndrome is also worthy of research(Burdon 1987;
Khansariet al. 1990;Lazlo 1988;Lindquist& Cnlig
1988;Locke et al1990; Polla 1988;Polla & Young
l
1989;Schlesinger1986;Welch 1987;Young & Elliot 1989). It is probable that continued training
while under the stressof overreachingstimulates
the transcription, translation, and subsequent
expressionof stre$sproteins resulting in their associatedsymptoms.
5. Who is Susceptible'!
Athletes at all levelsof performanceare at risk
of overtraining,but it is the most highly motivated
athleteswho are most prone (Costill 1986; Kar.
povitch 1965;O'Brien 1988;Town 1985).This is
probably regardlessof the athlete's level of performance(Town 1985;Stray-Gundersen
ct al. 1986)
and it may be overtraini!lg that prevents many
sportspeople from becomingelite.
Emulating the training of elite performers may
be a particular problemfor the inexperienced(Falsetti 1983).Lessexperienced
athletesand thosewho
train themselvesmay be particularly prone to overtrainingdueto inexperienceat recognisingsymp.
toms and naivity with regardsto the relative roles
of overload and regenerationin the training process (Falsetti 1983;Noakes 1989; O'Brien 1988).
Theseathletesare more likely to bc subjectedto
amateurcoachingtechniqucs.
Wolf, in 1961,studied 95 athletes(aged 15 to
34)who had exhibited symptomsof overtraining.
He found that 73 out of the 95 casesoccurred in
sportswherestrength,speedand coordination were
essential.Athletes who are going through a bad
patch,or attemptingto 'break a plateau', may be.
gin to train incessantlyand, insteadof improving,
performancesbecomeworse (Karpovitch 1965).
This may lead to overtraining becoming an epidemic in a whole squad if it is experiencinga particularly difficult period of training and competition (Wolf 1961).Fmally, those;tthleteswho have
beenabsentfrom a SQuad
can not rejoin at the same
level of intensity of training as when they left, as
they will have lost condition and prepan.'dness
to
train (O'Brien 1988).
The most outstanding training.related factor
leadingto ovcrtraining is reportedto be the failure
to include enoughregenerationunits in the train~
Overtminins in Athletes
ing programme(Bompa 1
erick 1983;O'Brien 1988;'
are many other training~,
factorsaswell as nontrainir
shown to contribute to 0'
Keizer 1988).
6. Recognitionof Dye,
It can be seen from this r
will be represented by VI
homeostatic balance,while
be recognised by enhanced
formance on test criteria c
vious levels. Ideally, subseql
take place until supercomJ
(Bompa 1983; Harre 1982;.1
The athlete's own previ.
to population or group norr
her own standard (Bompa 1
1983; Colwin 197Gb; Czl\i~
del et al. 1988a). Relating]
lation ranges may not be s(
tify the subtle changes ths
the onset of overtraining. R(
markedly before they ma
clinically significant in ten
lation; howevcr, the degrec
to the athlcte's own scores I
at the onset of overtmining.
staleness may occur well bI
move out of the normal
merely characterises athlete
does not indicate a directic
abIes (Van Handel et al. }4
data can be used to defin'
data must be generated ~
normally trained state (Bro
Van Handel et al. 1988a).
To date there has been
that can show overtrainin
tionships between variable
ated with overtraining or 4
able that there will ne
parameter diagnostic of til
cause overtraining will aft
Sports Medicine 12 (1) 1991
86; Welch 1987;Young & Elbable that continued training
:ssof overreachingstimulates
translation, and subsequent
proteins resulting in their as-
'ets of performanceare at risk
it is the most highly motivated
ost prone (Costill 1986; Karen 1988;Town 1985).This is
of the athlete's level of per.,5; Stray-Gundersen
et al. 1986)
rtrainipg that prevents many
~ '>ecomingelite.
lining of elite performers may
.!em for the inexperienced(Falmencedathletesand thosewho
r 'f be particularly prone to ovL ;perienccat recognisingsympith regardsto the relative roles
.'~neration in the training pro'loakes 1989; O'Brien 1988).
_-orelikely to be subjectedto
:chniques.
.died 95 athletes(aged 15 to
d symptomsof overtraining.
,utof the 95 casesoccurred in
b,speedand coordinationwere
L 1Dare going through a bad
:0 'break a plateau', may be1tly and,insteadof improving,
r
worse
~rtraining
(Karpovitch
becoming
1965).
an
epi-
..Id if it is experiencinga par~riod of training and competiV'ftlly, thoseathleteswho have
.ad cannot rejoin at the same
[uaining as when they left, as
condition and preparednessto
Ii
ta ling training-related factor
lingis reportedto be the failure
rerseneration
units in the trajn~
~
1\
ing programme(Bompa 1983;Brown 1983; Frederick 1983;O'Brien 1988;Vermaet al. 1978).There
are many other training- and competition-related
factorsas well asnontrainingfactorsthat have been
shown to contribute to overtraining (Kuipers &
Keizer 1988).
6. Rtcognition of Ol'ertraining
~ptibk?
39
Overtraining in Athlctcs
It can be seenfrom this reviewthat overtraining
will be representedby variablcs not achieving
homeostaticbalance,while supercompensation
will
be recognisedby enhanced,or at leastequal,performance on test criteria comparedwith the previous levels.Ideally,subsequent
training shouldnot
take place until supercompensation
has occurred
(Bompa1983;Harre 1982;Kuipers& Keizer 1988).
The athlete's own previous results(as opposed
to population or group norms)mustbe usedashis!
her own standard(Bompa.983; Brown 1983;Burke
1983;Colwin 1970b;Czajkowski1982;Van Handel et al. 1988a).Relatingresultsto normal population rangesmay not be sensitiveenoughto identify the subtle changesthat may be indicative of
the onsetof overtraining.Resultsmayhaveto move
markedly before they may be consideredto be
clinically significant in terms of the normal population; however,the degreeof movementrelative
to the athlete'sown scoresmaybe relatively minor
at the onsetof overtraining.Grossovertrainingand
stalenessmay occur well before anathlete'sresults
move out of the normal range. One-off testing
merelycharacterises
athletesrelativeto a groupand
doesnot indicate a directionof movementin variables (Van Handel et ai, 1988a).Therefore,before
data can be used to define overtraining,baseline
data must be generatedwhen the athlete is in a
normally trained state(Brown 1983;Nideffer 1988;
Van Handel et al. 1988a).
To date there has beenno singledefinitive test
that can showovertraining. Due to the interrelationships betweenvariables which may be associated with overtraining or overreaching,it is probable that there will never be one definitive
parameterdiagnosticof the overtrained statc,becauseovertraining will affect different bodily sys-
tems in different waysdependingupon the nature
of the sport. The approachto be recommended,
therefore,is the developmentof an integrated set
of tests based on severalparametersknown to be
associatedwith unbalancedhomeostasis.The ideal
screeningtest battery would be designedto be incorporated within the periodised training programme and include componentsuseful for moni.
toring improvement, establishing training
workloads,and screeningfor overtraining.
The time required for the restorationof homeostasiswill vary dependingupon the functional sys.
tems beingstressed.As a consequence
the decision
of which teststo include in a test battery must be
basedupon the identification of parameterswhich
reflect the homeostaticsystemsidentified in the literatureas those most likely to be disrupted as ovcrtraining develops. A discussionof such systems
and parametersfollows.
7. TheParasympatheticvs Sympathetic
Systems
Israel (1976)identified 2 types of overtraining
one as the result of a sympadteticnervous system
dominance (basedowoid)and the other characterised by parasympatheticnervous system dominance (addisonoid). The discussionof the differentiation betweenthe 2 types of overtraining is
carried further in the works of severalother authors (Bompa 1983;Kere2ty1971;Kinderroann1986;
Kuipers & Keizer 1988).Kindermann (1986) lists
symptoms of sympathetic overtraining as increasedpulserate at rest,decreasedbody mass,disturbed sleep,decreasedpu.se recoveryafter load,
decreasedappetite, emotional instability. Bompa
(1983)addssweatingto this list and goesinto more
detail with regards to psychologicalsymptoms.
Kerezty (1971)statesthat elevatedbasalmetabolic
rate, negative nitrogen balanceand ECO abnormalities are also symptoms of sympathetic overtraining.
Symptoms of parasympatheticovertraining are
reported by Bompa (1983)to include progressive
anaemia,low blood pressureand digestivedistur~
ances.Kerezty (1971)states that parasympathetic
.
Overtraining in Athletes
40
dominance may be characteriscdby a diminished
countcrregulatorycapacity againsthypogiycaemia.
The existenceof sucha diminished capacityis supportcd by the researchfindings of Barron et al.
(1985) and Kuipers and Keizer (1988), although
these may also be evident in sympathetic ovcrtraining as Barron et al; (1985)reported elevated
basal cortisol levels in their study. Kuipers and
Keizer (1988)add early fatigue, low resting pulse,
a fast return of heart rate to basallevels following
exerciseas other important factorsassociatedwith
parasympathetic ovcrtraining. The authors also
state that parasympatheticovertraining may be.
more difficult to define as the symptoms are less
alarming and, in the initial stages,are more likc
the effectsof training jmprovcments.
Symptoms in table I generallyreflcct a predominancc of the sympathctic form of overtraining in
the literature, and this is supported by statemcnts
citcd in Kerezty (1971) and Kuipers and Kcizer
(1'988).An outstanding factor for the diagnosisof
ovcrtraining is that both types will be reflectedby
a decreasedwork capacity(Kerczty 1971).It is clcar
that overtraining rcprescntsa perturbation ofnervous regulation (Bompa 1983; Michael 1961).
It has beenproposcd that the parasympathetic
form of overtraining may be a fcflection of an advancedstateof overtrain ing closclyassociatcdwith
exhaustionof the ncuroendocrinesystem,while the
sympathetictype may reflecta prolongedstressresponsepreceding cxhaustion (Kindermann 1986;
Kuipers & Keizer 1988).This fits nicely into the
gencraladaptation modelproposedby Selye(1957).
Altcrnatively, sympathetic overtraining may predominantly affcct spccd and power athlctes,while
enduranceathletes are more prone to parasympathctic symptoms(Bompa 1983;Kerezty 1971;Kindcrmann 1986). Nilson et al. (1981) propose that
young athletes may suffer more from sympathetic
signs and older athletes more from parasympathetic signs of overtraining. Individual differences
in the nervous systemwill also predisposeto either
sympatheticor parasympatheticovertl"dining(Harrc
1982).
The existcnceof both types of overtraining in.
dicates that the physiologist must be alerl to both
down-regulation and up-regulation of the neuroendocrine homeostasis when attempting to screen
for and diagnose ovcrtraining in athlctes. It is apparent that the differences in the ncurocndocrine
response may be due to either a progression through
different stagesof thc overtraining response: individual variation or differences in the stress imposed by the sport undertaken. Certainly, however,
there are many reports of sympathetic symptoms
in endurance athletes.
8. TheNellroendocrineSystem
Training maybc ablc to facilitate an adaptation
to stressbecausegraduallyincreasingtraining loads
have beenshownto increascstability of the pitui.
tary-adrenocorticalsystem as indicated by lower
basal levels of stresshormoneslike prolactin and
adrenocorticotrophichormone (Ac.'TH) [Keizer ct
al. 1987a,b; Viru 1985a,b).Howcver, cxcessive
stressleadingto imbalancesin the neurocndocrine
axis may alsocontributc to the symptoms of ovcrtraining (Israel 1976).Rcpeatedexcrcise when
hormonal balanceis derangedmay further stress
thc hormonalsystem,thus compromisingrecovery
(Kuipers & Keizer 1988).
Barron et al. (1985)presentedevidencc for adrenocorticalinsufficiencyin athletessufferingfrom
overtraining, as suggestedby prcvious authors
(Kerezty 1971;Mellerowicz & Barron 1971; Prokop 1963).The authorsfound that the hypothalamus was lesssensitiveto the stress of bypoglycaemia in overtrainedsubjcctsand attributed this
to hypothalamicexhaustion.The data revealedimpuired growth hormone,ACTH, cortisol and prolactinresponsesto insulin-inducedhypoglycaemia.
The samplegroup(n = 4)usedin the Barron etat.
(1985) studyis small and it would be of benefitto
overtraining researchto havc the study repeated
with a largernumberof subjects,althoughthe difficulties of such a task are appreciated.The hypothalamusis known to bc the coordinativc centre
betweenthe hormonal system,autonomous nervous systemand behaviour (Selye 1957). Insulininduced bypoglycaemiaacts by alt~ring the the se.
cretion of hypothalamic factors which have been
shown to stimulate the r
hormone and prolactin fro
(Barron et al. 1985).Baril
pituitary dysfunctionas a '
suggestedthat the dysfun
They do state that pituita
sibility. but that this caul
their study due to the tar
The conceptof alteredhon
been supported by the fir
levels were elevated(Barr
ability to regulateblood Sl
duced in overtraining (Bar
& Keizer 1988). HypothaJ
tion has the potentialto in,
symptoms reported in ove
Further supportfor hyp.
function in overtrainedathl
female athletes who have,
amenon-hoeathrough exert
Dale et al. 1979;De Souza
1978: Frisch et al. 1980;L
et al. 1980;Ruffin et al. 19'
1980).Impaired ovarian fL
be related to diminished pi
tion (Feicht et al. 1978)dl
hypothalamic control of ,
(McArthur et al. 1980).Exe
tive changesappearsimila
severe illness, major weig
stress,environmentalstress
(Prior 1982,1987).The com
pothesisedto be the hypotl
lation of reproductive-and Sl
(Prior 1987). The hypothal:
sensingand -producing regi<
gan stimulates the pituitary
to produce luteinising horm
stimUlating hormone (FSH:
responsiblefor the regulatio
in this context, much of 1
induced amenorrhoeamay
(Prior 1987). Other mar
changes,and hence overtr~
include changesin the puts
FSH release,luteal phase i
.sportsMf!dicine /2 (1) 199/
j up-regulation of thc neurosis when attempting to screen
ertraining in athlctes. It is ap:renccs in the ncuroendocrine
10cither a progression through
\e ovcrtraining responsc," indidilTcrences in the strcss imndertaken. Certainly, however,
)rts of sympathetic symptoms
~s.
docrine Spstem
, able to facilitate an adaptation
dually increasing training loads
.\ increase stability of the pituisystem as indicated by lower
, s hormones like prolactin and
c hormone (ACTH) [Keizer et
I 985a,b). However, cxcessive
'alances in the neurocndocrinc
ribute to the symptoms of ov.
-976). Repeated exercise whcn
, I deranged may further stress
L I, thus compromising recovery
1988).
~5) presented evidence for adency in athletes suffering from
'-68estcd by previous authors
llerowicz & Barron 1971; Pror"jors found that the ilypothal! livc to the strcss of hypogly.ed subjects and attributed this
haustion. The data revealcd imIne, ACfH, conisol and prosulin-induced hypoglycacmia.
:n D 4) used in the Barron et al.
~II and it would be of bcncfit to
l to have the study repeated
of subjects, although the diftask are appreciated. The hy[ to be the coordinative centre
II system, autonomous nervviour (Selye 1957), InsuJinemiR acts by altering the the scLic
factors which have been
Overtraining in Athletes
shown to stimulate the releaseof ACTH, growth
hormone and prolactin from the anterior pituitary
(Barron et al. 1985).Barron et al. (1985)excluded
pituitary dysfunctionasa causeof overtrainingand
suggestedthat the dysfunctionwas hypothalamic.
They do state that pituitary insensitivity is a possibility, but that this could not be determined in
their study due to the largedose of insulin used.
The conceptof alteredhormonalregulationhasalso
been supported by the finding that basal cortisol
levels were elevated(Barron et al. 1985)and the
ability to regulateblood sugarlevelshave beenreduced in overtraining (Barron et al. 1985;Kuipers
& Keizer 1988). Hypothalamic..pituitarydysfunc.tion hasthe potentialto inducea largerangeof the
symptoms reportedin overtmining (seefig. 2).
Further supportfor hypothalamic-pituitarydysfunction in overtrainedathletesis providedthrough
female athleteswho have been shownto develop
amenorrhoeathrough exercise(Cohenet al. 1982;
Dale et al. 1979;De Souzaet al. 1990;Feicht et al
1978; Frisch ct at. 1980;Loucks 1990; MCArthur
et al 1980;Ruffin et al. 1990;Ryan '1983;Warren
1980).Impaired ovarian function was thoughtto
be related to diminished pituitary b.ormonesecre-tion (Feicht et al. 1978)due to alteration in the
hypothalamic control of gonadotrophin release
(McArtbur et al. 1980).Exercise-relatedreproductive changesappear similar to those induced by
severe illness, major weight loss, psychological
stress,environmentalstressand energymisbalance
(Prior 1982,1987).The common link has beenhypothesiSedto be the bypothalamic.-pituitaryregulation of reproductive-and stress-related
hormones
(Prior 1987).The hypothalamusis the emotionsensingand -producing regionof the body; the organ stimulates the pituitary in a pulsatile fashion
to produceluteinising honnone (LH) and folliclestimulating hormone (FSH)and other hormones
responsiblefor the regulationof homeostasis.Seen
in this context, much of the work on exerciseinduced amenorrhoeamay relate to overtraining
(prior 1987). Other markers of reproductive
changes,and henceovertraining, may eventually
include changesin the pulsatile nature of LH and
FSH release,luteal phaseshortening,changesin
41
gonadalsteroid concentrations (estradiol, progesterone or testosterone),low TJ levels, lack of appropriate thyroid-stimulating hormone (TSH) responseto thyrotropin-releasing hormone (TRH),
decreasein neurotransmitters, increased endorphins, increasedcirculating dopamine,changesin
the catecholamineresponseto exercise,decreased
quantity of menstrual flow and anovulation (see
reviewsof Prior 1987and Cumming et al. 1989).
Cumming et al. (1985)demonstrateda diminished
LH pulsatility and pulse amplitude in regularly
menstruatingrunners at rest, suggestingthat even
in eumenorrhoeicrunners, there is some degreeof
central .inhibition of the hypothalamic-pituitarygonadalaxis.
Although the incidence of menstrual disorders
appearsto be high in runners and baltet dancers
(Loucks & Horvath 1985),swimmers,rowers,fencers,volleyballers,tennis players,skiers,gymnasts,
cyclists,field athletesand aerobicdanceinstructors
are susceptible(Sbangold 1985). Sbangold states
that menstrualdysfunction is most likely to occur
in sportswhere loss of body fat is combined with
excessivelevels of exercise;these are mainly endurance activities by nature. Other studies have
supportedthis statement(Frisch et al. 1980;Lutter
& Cushman1982;Schuarts1981;S~angold& Lev~
ine 1982;Speroff& Redwine 1980)and have suggestedthat amenorrhoeicathleteslosemore weight
in training thancyclic athletes. Frisch et al. (1980)
found tbatathleteswho begantraining beforemenarche experiencedtheir first period at an average
ageof 15 years,whereasthose who begantraining
post.menarcheexperiencedtheirs at an averageage
of' 12.7 years, which was similar to the general
population. Warren (1980) found that there was a
prompt onsetof menarche in ballet dancersduring
injury- or vacation-relatedsuspensiol)sof exercise
of at least2 months. Lutter and Cushman (1982)
and Sanbornet al. (1982)demonstratedabnormal
luteal functions and loss of LH surge and found
that thesedisturbancescon-elatedwith the distance
run by athleteseachweek, but othershave found
no correlation betweenreproductive function and
training load. The consequencesof disturbed hormonal regulation associated with chronic repro-
42
.\'p(}rl.~ Ml'dicil/l'
/2 (I)
J99J
Fig. 2. The hypotilaJamic-pituilary axis and ovenraining. Stress gencrates many of lite symptoms of overtraining through
thc respon5cofthc hypothalamic-pituitary axis. Notc thallhis figun: docs Ilot attempt to portray the complexity of hormonal
regulation but ratJIer pori ray the effects tltat misregulatioll may have on scvcral bodily systcms.
ductive dysfunction may include endometrial hyperplasia, adenocarcinoma, atopic endometrial
hyperplasia (Coutam et at. 1983),vaginitis, urethritis, low bone density, osteopenia(Dalsky 1990;
Drinkwater 1984; Lindberg et at. 1984;Marcus et
I
at. 1985)and a higherincidenceof stressfractures
than cyclic athlctcs (Lindberg et al. 1984;Marcus
et at. 1985).Reproductivedysfunction in malesis
lessobviousand the most overt symptomsmaybe
a decreasedlibido and spermcount. Similar nor-
Overtraining in Athletes
monal mecharosmsare
amic-pituitary dysfunctiol
to be the mediating mect.
1989).
Severely overtrained
Europeancountries who CI
months and possiblyyear!
develop Addison's disease
explains the causeof Addi!
ure of the adrenal gland t<J
monal concentrations,in p
Changes in circulatory
tions have beenshownto aii
and the duration of the reo
ercise(Hickson et al. 1990;I<
A neuroendocrinestressrest
the recovery phase may ha'
tions, becauseKuoppasalmiI
state that a changedbalance
anabolic hormones may affe
Intense physical exerciseha~
to increased cortisol, decrea
and an increased sex horml
(SHBG) which contributes t(
terone levels by increasingthf
capacity of serum(Aldercreu1
been shown that the down-r
production is of prime impon
anabolic processes(Kelly et al.
& Aldercreutz 1985; Kurows~
& Viru 1982)as is the eleval
Decreasedtestosteronelevels l
direct inhibition of testicular
through elevated cortisol leve
stad 1985; Cumming et al. 19
anisms (Cumming et al. 1989)
be slow to retum to normal lev
exercise(Cumming et al. 1989;
Griffith et al. 1990; Hakkinen
et al. 1986: Kuoppasalmi et al
1984)and may take severalda
1989).Testosteronemay beele"
term exercise (for reviews see
ming et at. 1989);however,Aldj
have suggested
that a decreaseil
free testosteroneto cortisone
--" "~
--'
,
Sports MLOdicine 12 (I)
/99/
I~.y...m;
c.
~&\I&idls~se
)\etlB/illfectJon
-v'
"
"
d;'~I'b8:I~nce
JO1'lfji.rst'
¥llon:,~
, I
"
","""
., ..
fII~~bo}~
il~1j;,;,
"-"'I;,.;;;:":,
.".
,..
':".
"' '. ...:
.
.".,
.~
..
WJdi~~~~ "~'.._'I
e symptoms of overtraining through
r-ortray the complexity of hormonal
Lstems.
j1-' incidenceof stressfractures
I .indberget at. 1984; Marcus
uuCtivedysfunction in malesis
Lemostovert symptoms may be
I i spermcount. Similar hor-
Ovcnraining in Athletes
monal mechanismsare involved and hypothalamic-pituitary dysfunction has beenhypothesised
to be the me<liatingmechanism(Cumming et ai,
1989).
Severely ovenrained athletes from Eastern
Europeancountries who continueto overtrain for
months and possibly yearshave beenreponed to
developAddison's disease(Noakes1989).Noakes
explains the causeof Addison'sdiseaseasthe failure of the adrenal gland to properly regulatehor,.
monal concentrations,in particular conisol
Changes in circulatory hormonal concentra.
tions have beenshownto affectthe rateof recovery
and the duration of the recoveryphase after exercise(Hickson et al 1990;Kuipers& Keizer1988).
A neuroendocrinestressresponsewhichpersistsin
the recoveryphase may have imponant implications, becauseKuoppasalmiand Aldercreutz(1985)
state that a changedbalancebetweencatabolicand
anabolic hormones may affect recoveryprocesses,
Intense physicalexercisehas beenshown to lead
to increasedcortisol, decreasedfree testosterone.
and an increased sex hormone-binding globulin
(SHBG) which contributes to the low free testosteronelevels by increasingthe testosteronebinding
capacity of serum (Aldercreutzet al. 1986).It has
been shown that the down-regulationof conisol
productionis of prime importancefor the onsetof
anabolicprocesses(Kellyet al. 1986;Kuoppasalmi
& Aldercreutz 1985; Kurowski et al. 1984;Seene
& Vim 1982)as is the elevationof testosterone.
Decreasedtestosteronelevelshave beencausedby
direct inhibition of testicular secretion,possibly
through elevated conisol levels (Aakvaag & Opstad 1985; Cumming et al. 1989)or other mechanisms (Cumming et al. 1989).Testosteronemay
be slowto return to normal levelsfollowing severe
exercise(Cumming et al. 1989;Dufauzet al. 1919;
Griffith et al. 1990;Hakkinen et al. 1981;Jansson
et at 1986; Kuoppasalmi et al. 1980;Webb et al.
1984)and may take severaldays(Cumming et al.
1989).Testosteronemay beelevatedfollowing short
term exercise (for reviews see Bunt 1986; Cumminget aI. 1989);however,Aldercreutzetal. (1986)
havesuggested
that a decrease
in theratio ofplasma
free testosteroneto cortisone of more than 30%,
43
combined with a high levelofSHBG capacity,may
be a useful indicator of overtraining.
Many authorshave reportedelevatedblood cortisol following exercise(Bunt 1986;Dessypriset al.
1976;Kuoppasalmiet 31.1980;Kuoppasalmi & AIdercreutz 1985),while others have reported decrements following prolonged exercise(Bunt 1986;
Viru 1985b).Maron etal. (1977)have reported that
cortisol returns to pre-exerciselevels within 2 to 3
hours of exercisecessation.However, with longlastingintense exercise,cortisoland catecholamine
levels may decreasebelowpre-exerciselevels for
several days (Viru 1985a). Ryan (1983) has reported that there is great individual variability in
levels of hormones after exercise,which makes
generalisationdifficult.
Since the testosterone/conisolratio has implications for the switching on of anabolic processes
in recovery,and as this may require more than I
day to occur, the ratio may be associatedwith the
reported catabolic state reponed in overtraining
(Kuipers & Keizer1988).Increasedbinding of cortisol in muscle tissue,combined with the high levels of plasma cortisol, may lead to greater protein
catabolismthan anabolisminside the muscle cells.
This would explain the increasedureaand loss of.
body mass in overtrained athletes (Kindermann
1986).Kindermann (1986)has suggesteda control
value of 8.3 mmol/L urea in serumshould riot be
exceededduring training. Monitoring urea levels
during the regenerationphasemay thus be useful
in indicating the return to baselineof the nitrogen
balance,and as this is hormonally driven, may be
representativeof resto..ationin hormonal mechanisms;
It is assumedthat the strong activation of the
pituitary-adrenocortical system is related to the
sympathetic type of ovenraining while strong inhibition or exhaustionof the sympatheticnervous
systemrelatesto the parasympathetictype of overtraining. Stressfractures may be causedby a reduction in capacityof the body to recoverand repair tissueand may be related to changesin levels
of hormones in the body (Frederick 1983). Alterations in caloric intake may reflect neurophysiological changes,since it has been shown that the
thcmsclvesas beingmo
pcriods of heavy train
gcmld 1988; Koch 1981
Salo 1989; Schouten et
the immune system m.
human performance (F
letes have indicated thl
to be cnhanced with rr
(Anderson 1989;Koch I
havc dcmonstratedthat
programmesare capabl,
(Good & Ferrandcs198
There is now a pletl
cating that immunity ca:
poor training programn
(1987) rcport that elite a
training through illness
runncrs. When physicall)
monitored over a 9,wee~
to have more frequent ~
tory tract infections than
& Hansen 1978). In a I-:
orienteers,it was noted ;
as colds causcdmore abs
did injurics(JohanssonI~
studiesofclite sportswoml
skiers (Anderson1989; R(
al. 1982)and an epidemil
and Bateman(1983),whel
parcd with 15.3%of con1
piratory infections in the;
athon run. They also dem
highly trained runners sur
of infection with almost h
expcricncing symptoms. I
crcascdsusceptibilityto SPI
recorded regularly over tI
has beenassociatedwith 1
rcactivation of latent her!:
colt-Glaser & Glaser 198:
borsky et al. 1976). Foil.
herpes virus, individuals
fected for life (Kiecolt-Gla
hepatitis outbreakat the Ii
United States (Fox 1985;
Morse et al. 1972) cause
changesassociatedwith training may be a tuning
of the immune systemand not overtraining responses.Keast et al. (1988)and Cameron (1988)
have reviewedthe acuteresponsesof the immune
systemto exercise.The responseof natural killer
cells,immunoglobulinsand the leucocytosisof exercisehavealso beenreviewed(Mackinnon 1989;
McCarthy & Dale 1988).
Thereis no doubt that exercisehasa major impact on componentsof the immune system, but
whetherthe immunomodulation which occurs in
associationwith acuteexerciseis clinically significant or not has yet to be determined.There is no
evidence,anccdotal,epidemiologicalor otherwise
that is able to associateincreasedincidence of infection directly with acuteexercise.There is, however, considerableevidenceto suggestthat acute
exercisecanexacerbatecurrentinfection. Evidence
suggesting.that
exercisetraining,as opposedto one.
One of the most serious consequences
of over.
ofTintensive exercise,canlead to an immunosup.
training may bea suppressionof immune function
pressiondoesexist.
such that the athlete becomes subjectto shon or
According to Surkina (1982)the immune syslong term reduced perfonnance due to the coli.
tem plays an essentialrole in maintaining the
traction of infectious disease.It is known that parbody'shealthand hQmeostaticstate.Surkina states
ticipation in exerciseduring the incubation period
that, during participation in sports,the immune
of a viral illne~ can induce more serious sympsystemis subjectedto the training effectsof phystoms and cause death from complications (Ames
1989).The first documented associationbetween ical and emotional loads which expand its functionallimits. Ivanovaand Talko (1981)have shown
overtraining and increasedincidence of infection
that acute intensive exerciseinducesa disruption
was recognised in 1928 following the St Moritz
Winter Olympics (Heis 1971). Since then, a sub-- of immunologicalhomeostasisand that this provides a stimulus for immunological compensation
stantial body of evidence has accumulatedwhich
and supercompensation
following a regeneration
supports such an a~ociation. The athlete may be.
period. Their studydemonstratedthat training imcome progressivelymore susceptibleto infectionas
proved baselinevaluesof a number of immuno~
training progressesat an intensive level throughthe
courseof the season(Asgeirsson& Bellanti 1987; logical parameters,T-lymphocyte blast transformation in responseto mitogens was significantly
Jokl 1984; 8alo 1989; Tomasi et al. 1982).The
training processhas also been shown to be asso- higher than values prior to the training period.
However, Surkina (1982)has shown that when
ciated with considerablepsychologicalstress,parworkloads were excessive,the immune system
ticularly during periodsof competitionand this may
be an important contributor to immune suppres- homeostasiswas displacedto the extent that the
athletesbecameincreasinglysusceptibleto opporsion and increased morbidity in athletes under
tunistic infection. This may result from extremely
stressful training and competition conditions
sharpstress(2 marathonsover 2 days)or from the
(Khansari et al. 1990; Morgan et al. 1987).
accumulationof trainingand competitionstressdue
It is essential,however, to separatethe acute
to insufficient or no recoverytime (chronic stress).
immune responsesto exerciseand responsesdue
Thereare manyreportsof athleteswho perceive
to failing adaptation. Some of the immunological
hypothalamus is important in regulating food in.
take (Keesey& Powley 1986).
Since honnone levels may be altered in statcs
of physicalfatigue (Aakvaag & Opstad 1985; Viru
198Sa)monitoring hormones maybe usefulfor the
indication of overtmining. Measurement of the
ACTH and cortisol response to insulin-induced
hypoglycaemiacould be a usefuldiagnostic testfor
overtraining in athletesand for monitoring recovery. Details of methods are describedin Barron et
al. (1985). Regulationof blood glucoselevels may
be inadequateresulting in thc depressionof blood
glucose following a standard exercise protocol,
measurementof pre- and postexerciseglucoselev.
els may be an indication.
-*!--
...,
'
45
Nith training may be a tuning
tern and not overtraining reo
I. (1988)and Cameron (1988)
iCuteresponsesof the immune
The responseof natural killer
tins and the leucocytosisof ex:n reviewed (Mackinnon 1989;
988).
It that exercisehas a major imIS of the immune system, but
lomodulation which occurs in
Jteexerciseis clinically signifi.
to be determined.There is no
I, epidemiologicalor otherwise
~iateincreasedincidence of in1acuteexercise.There is, howevidenceto suggestthat acute
)ate currentinfection. Evidence
::isetraining, as opposedto one~, can lead to an immunosupIrkina (1982)the immune sysntial role in maintaining the
)meostaticstate.Sui'kinastates
!)ation in sports, the immune
to the training effectsof physI loads which expand its func.
1and Talko (1981)have shown
-exercise induces a disruption
homeostasisand that this proimmunological compensation
tion following a regeneration
, demonstratedthat training imIlues of a number of immuno, r -lymphocyte blast transforto mitogens was significantly
8 prior to the training period.
,(1982) has shown that when
: essive, the immune system
l )Iaoedto the extent that the
lCfeasingiy
susceptibleto opporTl.is may result from extremely
ri Ions over 2 days)or from the
I ngand competitionstressdue
0 recoverytime (chronic stress).
j IOrtsof athleteswho perceive
thcmsclvcs as bcing morc pronc to infcction during
pcriods of hcavy training (Andcrson 1989; Fitzgerald 1988: Koch 1988; Reilly & Rothwell 1987;
5alo 1989: Schoutcn et al. 1988), suggesting that
the immune system may be a limiting factor for
human performance (Fitzgerald 1988). Some athletes have indicated that their immunity appears
to be enhanced with moderate levels of training
(Anderson 1989; Koch 1988). Exl>eriments in micc
have demonstratcd that carefully designed training
programmcs arc capablc of cnhancing immunity
(Good & Fcrrandes 1981; Liu & Wang 1987).
There is now a plethora of information indicating that immunity can be adversely affected by
poor training programmcs. Rcilly and Rothwell
(1987) rcport that elite athlctes had more days off
training through illness than club or rccreational
runncrs. Whcn physically conditioned rowcrs wcrc
monitorcd ovcr a 9-weck period, thcy wore found
to have morc frequent and scvcre upper rcspiratory tract infections than control subjects (Douglas
& Hansen 1978). In a I-year prospective study of
orienteers, it was noted that minor diseases such
as colds caused more absences from training than
did injuries (Johansson 1986). Thisis supported in
studies of elite sportswomen, marathon runners and
skiers (Anderson 1989; Rcid ct al. 1989; Tomasi et
al. 1982)and an cpidemiological survey by Pcters
and Bateman (1983), where 33.3%of runners compared with 15.3% of controls suffered upper respiratory infections in the 2 weeks following a maratbon run. They also demons1ra1cd that the more
highly trained runners sufTcrcd a grcatcr incidcncc
of infection with almOS1half of thc faster runncrs
experiencing symptoms. Furthcr cvidencc of incrcased susceptibility to specific infections has bcen
rccordcd rcgularly over the past 20 years. Stress
has been associated with the dcvelopment of and
reactivation of latent herpes virus infection (Kiecolt-Glaser & Glaser 1987; KosI et al. 1979; Luborsky et al. 1976). Following infection with a
herpes virus, individuals will rcmain latently infected for lifc (Kiccolt-Glaser & Glascr 1988). In a
hepatitis outbreak at the Holy Cross Collcge in thc
United States (Fox 1985; Friedman et al. 1985;
Morse et al. 1972) caused by polluted drinking
wAter,90 out of 97 members of a college football
team wereaffcctcd. No othcr studcnts or employces who were using thc same facilitics contracted
the virus. In a polio outbreak all of thc 9 people
affected (aged between 12 and 18 years)were actively participating in strenuous sport (Weinstein
1973).The incidenceof asepticmeningitiswastwice
as high and symptoms were more severeamong
members of a football team than other students
(Barron ct al. 1982). 43 of the 61 membersof the
team were affectcd; echovirus 16 was isolatcd as
beingthe aetiologicalagent.The authorsconcluded
that the severity of enterovirus infection may be
greaterin groups engaging in strenuous physical
exercise.
Surkina (1982)found that, following a 4-month
pcriod of tightly packcd competitions, Soviet top
level athletes suffered a significant drop in the
numberand function ofT .cellscomparcdwith just
prior to the competition period. Threc,athletesbecame sick. The following season,the competitive
period was shortened,the immunological reactivity of the athletes remained adequatelyhigh and
there were no casesof illness. In a third experiment, seasonalfluctuations in immunity were assessedand were found not to be significant when
compared to the fluctuations observed due to
training and competition in a ski team. However,
an athletefrom the ski team who showed'the greatest changes in T-cell proliferative ability in responseto mitogensuffered6 recurringillnesseswith
different aetiologiesand localisations over the 5
subsequentmonths. In another study, Surkina
(1982)found that the most promising athlete in n
tcamof middle and long distancerunncrs who pre.
paredhard for competition with high intensityloads
had the lowest indices of immune function; one
and a half months later he becameill. Surkina
(1982)found that training loads exert a transient
depressiveinfluence upon 'T-cell immunity' which
recoveredafter lighter training and hc placcd considerableemphasis on the need for training programmcs to maintain adequate levels of immu.
nological rcactivity as well as increased
performance.Matvienko (1981)found thatathletes
who becamestagnantin their training programmes
,I
Svortt Ml'dicint' 12 (I) /99J
46
t
f;
f:
I.:
t,
t'
"
I:
r'
i~t
f'.
.
.i:
ti
I
I
L:.
tr,
-
had low leucocytecountsand that thesecounts became lower as training progreSsed.On the other
hand,a characteristicof promisingathleteshasbeen
found to be a high comparative leucocyte count
which persists throughout their career.Matvienko
encountered cases that resembled leucocytosis;
howevcr, the athletes displayed good performances.He statesthat care must be takcn in the assessmentofhaematologicaldatasinceathlctescould
be wrongly excludcd from a team when they have
high luecocytecounts as these may be indicative
of infection in some athletes.Thc importance of
comparing an athlete's own data with his/her own
previous baselinedata is highlighted by such cx.
amples. Umarova (1982) has shown that special
care must be taken whcn administering heavy
training loads to childrcn as greaterdepressionsof
immunological parameters occur following training in children than with adults.
Sl<insepsisand other bactcrial infections may
bemore frequent in athletes(Asgeirsson& Bellanti
1987). Although it has oflcn beendifficult to differentiate betweenphysical exertion and physical
factors, such as trauma or crowding, as the cause
of clinical symptoms, skin infections are commonly caused by staphylococci, strcptococci or
herpessimplex virus, and there is evidcnceto suggest that thcsc occur predominantly through skin
to skin contact(Dorman 1981;Ludlum & Cookson
]986; Sclling & Kibrick 1964;Wheeler& Cabaniss
1965;White & Grant-Kels 1984). Other common
skin infections among athletesare groin infection
and athlete's foot (Asgeirsson& Bellanti 1987).
What is not yet clearis the relativc importance
of training-induced immune suppressionand the
close proximity of athletes in many of the above
situationsas the predominantaetiologicalfactor for
the abnormally high incidenCeof infection.
9.1 Regulationof Immunity
The regulationof the immune responseis very
complcxand involves a numbcr of functional body
systcms,complex feedbackmechanisms,an cnor.
mous range of messengermoleculesand an as yet
undetermined rangc of leucocytepopulations and
I
I
subpopulatiolJs. Morc dctailed discussions of factors involved in immunoregulation can be found
in the immunology literature (Khansari ct al. 1990;
Malc et al. 1981; Roitt et al. 1989) [seefig. 3J.There
are as a consequence a largc number of po5sible
mcchanisms by which ovcrtraining may affect the
immune responsc.
It is now becoming apparent that the immune
system relies exclusively on glutamine for cell replication (Ardawi & Newsholme 1985). Muscle may
be the main source of this glutamine as cells of the
immune system cannot synthcsise these glutamine
requirements de no.,(). The rate of glutamine utilisation of quiesccnt and dividing lymphocytes has
been shown to be high (Newsholme 1990)and these
cells cannot replicatc in its absence (Griffiths &
Keast 1990; Szondy & Newsholme 1989). Because
glutamine synthesis and/or release across the
muscle cell membrane appears to bc thc flux-generating step for other cells of the body such as cclls
of the immune system (Newsholme 1990; Newsholme & Leach 1983), under normal physiological
conditions thc dynamics of this system may be
critical to the supply of glutamine to thcsc tissues.
Because of this, Newsho!me states that the muscular systcm is part of the immune system and failure of the muscle to relcasc sufficient glutamine
may result in an impairment of immunc function
(Newsholmc 1990). The author proposes that psychological, environmental and/or exercisc Slress
may reduce the glutamine outflux fi'om the muscle.
Decreased motor unit recruitment and increased
levels of fatigued muscle fibrcs at rest in thc overtrained state may therefore result in depressed
immune function due to a decreasedavailability of
glutamine for glutaminolysis within otherwise immunocompetent cclls (Newsholmc 1990). Recently
Parry- Billings ct 31. (1990) havc extended thcsc
concepts to involve ccntral fatigue and thc overtraining syndrome.
9.2 Catccholamines and Immune Regulation
in Overtraining
Catecbolamincs stimulate adenyl cyclase which,
in turn, modifics endogenous Icvcls of cyclic adcn.
osine monophosphate (cAMP). It is known that the
Overtraining
in AthIe!
..
/14
.I
I'
~'
,,
~,\.
c
'
-:..1
Fig. 3. Ncuroendocrinc interact
(Roil! el al. 1989). The diagra
tential connections between thl
munc systcms. Opcn lines indic:
lines indicate hormonal intcrac
cate postulated connections for
have not been established.
intracellular levelsof cAN
in regulating immune fut1
man 1979). Both enhancet
immunological function I
catecholaminesin in vitro s
et al. 1988). Cateeholamit
act on lymphocytes by ir
activity, leading to an i
cAMP (Strom et al. 1977).
Sp(lrt.f Medicine
J2 (I)
199/
re detailed discussions of facmunoregulation can bc found
iterature (Khansari cl al. \ 990;
it! et al. 1989) [seefig. 3}, Thcre
~e a largc number of possible
ch overtraining may affect the
ing apparent that the immune
ively on glutamine for cell rep\/ewsholme 1985). Muscle may
of this glutamine as cells of the
mot synthesist these glutamine
va, The rate of glutamine utiland dividing lymphocytes has
sit (Newsholmc 1990) and these
,te in its absence (Griffiths &
, & Newsholme 1989). Because
s and/or release across the
.me appears 10 be the flux-gen!r cells of the body such as cclls
rem (Newsholme 1990; NewshLI), undcr normal physiological
amics of this system may be
y of glutaminc to thesc tissucs,
~ wsholme states that the mugI )fthe immune system and failto release sufficient glutamine
l\\>8irment of immunc function
rhe author proposes that psylental and/or exercisc stress
amine outflux from the muscle.
'~it recruitment and increased
lscle fibres at rest in 1hc ov) therefore result in depressed
.ueto a decreased availability of
.nOIYSiSwithin otherwisc im-
~
(Ncwsholme 1990). Recently
1990) have extended these
.e central fatigue and thc over-
'iL
and Immune Regulation
r rlulateadenylcyclasewhich,
IQugenous
levcls of cyclic aden.
\te(cAMP). It is known that the
r
Fig. 3. Ncurocndocrinc intcractions with thc immunc systcm
(Roitt Cl al. J989). The dillgranl indicates somc of thc polcmial oonncclions betwcen the endocrine. nervous and immune systcms.O~n lines illdicalc ncrvOIiSconn«tions, black
lints indicatc hormonal intcrnclions. and brokcn liucs indicatc poslulatcd conncctiol1Sfor which thc cffcctor molcculc$
have not becn established.
intracellular levels of cAMP are important signals
in regulating immune nmction (Burchiel & Melman 1979).Both cnhanccmcntand suppressionof
immunological function havc bcen attributed to
catecholaminesin in vitro and in vivostudics(Keast
et al. 1988).Catecholamineshave been shownto
act on lymphocytes by increasingadenyl cyclase
activity,
leading to an increase in intracellular
cAMP (Strom et al. 1977).This has beenfound to
decreasetheir responseto T and B cell mitogens
(Estcs et al. 1971; Watson 1986),although a mitogenic effect of low conccntrationsof exogenous
cAMP on lymphocytes in culture has also been
demonstrated(Watson 1986).
While Hadden et al. (1970) demonstrated that
cpinephrine (adrenaline)did not inhibit in vitro
phytohacmagglu1inin
(PHA)-stimulated thymidine
uptake of Icucocytcculturcs whcn added at physiological concentrations,Crary et al. (1983) found
that the in vitro responscto PHA, concanavalin A
and PQkeweedmitogen wassuppressedif subjccts
had received an epinephrine injection prior to the
blood sample being taken. Inhibition of tritiated
thymidine uptake by PHA-stimulated T lymphocytes in culture has bccndcmonslra1edwith physiological concentra1ionsof isoprcnalinc(isoproter~
enol), a nonselectivc {3-adrenoceptor agonist
(GoQdwin et al. 1980; Haddcn ct al. 1970).However, human B lymphocytescu!turcd in thc prcsence of isoprenaline and no mitogens,exhibitcd
cnhanced Ig synthesis(Shermanet al. 1983).
Proliferation of human lymphocytesstimulated
with PHA has been shown to both increase (Hadden et al. 1970, 1971)and decrease(Goodwin e1
al. 1980)ifnorepincphrinc (noradrenalinc)is added
tQ cultures in physiologicalconcentrations.
Thcse studies shed little light on whether immunocnhanccmcntor immunosuppressionresults
from the incrcascd catccholamineconcentrations
presentduri:1g cxercisc (Bunt 1986;Galbo 1983).
Clearly there is further work neededto d(}finc thc
relationship of catecholaminesand immune function during exercise.
9.3 Glucocorticoidsand Immune Regulation
in Ovcrtraining
Cortisol is releasedfrom thc adrcnal cortcx in
responseto adrenocorticotrophichormone sccrc*
tion from the anterior pituitary (Bunt 1986).
PHA-, concanavalinA- and pokeweedmitogen*in*
duced lymphocyte transformationhas beenshown
to bc deprcssedwhen cortisol is addedto cultures
(Gillis et al. 1979;Goodwin ct al. 1980;Gordon &
Noun 1981;Neifield & Tormey 1979;Nowell 196i;
~..
Smith et al. 1911; Webel & Ritts 1971). The in
vitro mixed lymphocYtereactionis also reducedby
cortisone (llfetd et aI. 1911;'Katz & Fauci 1979).
Cuppsand Fauci (1982) state that corticosteroids
have a generallyimmunosuppressiveeffect.Cooper
et al. (1981)have demonstrated,on the other hand,
enhancedIg synthesiswhen low levelsof cortiso~e
are added to pokeweed mitogen-stimulated
lymphocyte cultures.
In vivo administration of low dosesof corticosteroids has induced some suppressionof immune
functions while greaterthan physiologicalconcentrations have produced lethal modification to the
immune system(Keast 1968,1969).Administering
hydrocortisone,dexamethasoneand prednisolone
in vivohas been shownto significantly modify the
ability of lymphocytesto respond subsequentlyto
both mitogensand by immunoglobulin production
in vitro (Fauci 1916;Gillis et al. 1979;Saxonet al.
1978).
Circadian rhythm of the PHA-induced lymphocyte transfonnation has beenshownto coincidedirectly with changesin plasma cortisol, suggesting
a positive effectof cortisol on lymphocyte function
at physiological levels (Tavadia et al. 1915). Increasedcortisol levels may, at least partly, account
for the immunomodulation as~ociatedwith acute
exercise.Changesin the hypothalamic-pituitaryaxis
reported during overtraining may also be manifest
in immunomodulation mediated by altered cortisol levels. Much work is required to determinethe
effectsof exercise-inducedhormonalmodifications
on the immune 5ystem.
Exercise-inducedchangesin the concentrations
of immunological cytokines such as the interleukins, interferons, prostaglandins or other differentiation, growth or communicationalfacton may
be respon5ible for exercise-inducedimmunomodulation. This representsa field of investigationyet
to be exploited.
10. Psychology
It may also be difficult to distinguishthe effect
of exercise on immune function in athletes from
that of the psychic stressof competition and train-
-.
,
-/--=-
Sports Medicine 12 (J) 1991
/mpic and high level sporting
~ more emotional and psychic
lemands on them to perform,
hletes (Asgeirsson & Bellanti
8; Simon 1984) and the com'sica! work and psychic unrest
.ive immunosuppressive effect
mmott 1984; Schouten et ai,
iblished that various types of
affect immune function (As.
1987; Bartrop et al. 1977; Bor0 1982; Fauman 1982; Gructt et al. 1983; Jemmott &
lsari etat. 1990; Kiecolt-Glaser
~1982; Locke et al. 1984; Rogjifer et al. 1983; Solomon et ai,
946), Psychological stress can
lajor factor contributing to the
(Nideffer 1988).
O'Brien
, ming
!,hatovertraining
results
from
, hlete either physically and/or
'qt promotes 'tiredness' in the
been shown to influence the
.tminingand contribute to perDUSregulation (Kerezty 1971;
I t990). Some emotional fac..
demandsof competition, der failure, setting unrealistically
1expectationsof coach or famIe t957).
, )8)demonstratedthat, followtraining volume, athletes expe,;~gsof fatigue, dep~ion and
t return to normal even after
r In someathletes.The chronic
)meis characterisedby negative
r ~chasanxiety, depression,fa1.. of self esteem(Feigiey 1984;
lorpn 1985;Morganetal. 1987;
lQQO).
~ ndocrine system has been
~./e to a variety of emotional
al. 1990)and thereis good evile nd neuroendocrinemodula-
Overtraining in Athletes
tion of immunity (Adner 1981; Cameron 1988;
Keast et aI, 1988),
The symptoms of overtrained athletesare rcmarkably similar to manyof those seenin primary
or endogenousdepressionand in the chronic fatigue syndrome(Askiskal& McKinney 1975;Fitzgemld 1988;Khansariet al. 1990;Manu et al. 1989;
Wessely 1990; Wessely & Powell 1989). These
symptoms include physiologicaland psychomotor
retardation, chronic fatigue, deprcssedappetite,
weight loss, insomnia, decreasedlibido, muscle
soreness,increaseddepressionand tension(Askiskal & McKinney 1975).
Chronic fatigue syndromeis a term which bas
been used to describea large number of clinical
conditions of divcrse aetiology and/or pathogenesis (Oin et a1. 1989;Uoyd et ai, 1989)and it is
proposedhere that overtmining syndromemay be
classifiedas a 'chronic fatiguesyndrome',Research
into the aetiologyof thesediseasesmay contribute
to our understandingof conditions that leadto overtmining.
The associatedsymptomsand conditions oftbe
chronic fatiguesyndromehave beenshownto me..
diate unexplainedmusclefatigue-lliIrticularly after
exercise(Holmes et al. 1988),sore throat, mild
fluctuating Iymphoadenopathy,neuropsychological disturbances-depression, insomnia, difficulties with concentration(Gin et al. 1989).Basedon
their study of lOOchronic fatigue syndrome sufferers,Lloyd etal. (1989)reportedthat patientswith
chronic fatiguesyndromeappearedto have an impaired immune response.Immunological events
identified include atypical lymphocytosis,or lymphopeniain peripheralblood,isolatedselectiveIgG
subclassdeficiency(lg3Gand Ig[O), impaired cell.
mediated immunity based on decreasedlymphocyte responseto mitogen, impaired response$to
delayedtype hypersensitivityin skin tests,and decreasedabsolutenumbers of T (CO2), T helper/
inducer (CD4)and T cytotoxic/suppressor(CDS)
lymphocytes. These observationswere based on
comparison with agt}-and sex-matchedhealthy
controls (Gin et ai, 1989).Other laboratory findings which have beenassociatedwith chronic fa~
tigue syndromchave included an increasedoutput
49
of creatine (Albrecht et al. 1964)and excessivcinterferona production (Lever et al. 1988).Lloyd et
al. (1989)have also argued that excessiveproduction of cytokines may account for some of the
symptomsassociatedwith the chronic fatigue syndrome although the point is made that these are
difficult to measureduct();shorthalf-livesand their
binding with soluble receptors. The advent of
cDNA probes for levels of mRNA to thesecytokines may overcome current detectionproblems.
11. Biochemistry/Physiology
Causesof decreasedefficiency of muscularper~
formancesdue to overtraining are not fully understood (Costill 1986)but could be attributed to incomplete restoration of cellular homeostasis
resulting in early fatigue of the motor units normally involved in movements. Additional and
therefore less efficient motot units must be reo
cruited resultingin increasedoxygencost,heartrate
and ventilation at any given submaximalworkload
due to lesseffective summation of forces (Costill
1986; Kuipers et al. 1985; Kuipers & Keizer 1988;
Van Handel et al. I 988a).The lower the fractional
utilisation of oxyen at any time point, the greater
the rescrve capacityand it is the &actional utilisation that has been shown to determine the per~
ception of stressand the extent to which anaerobic
metabolismhascontributed to the total ~nergyde.
mand (Van Handel et al. 1988a).Metabolic effi.
ciency has beenshownto vary due to genotypeof
metabolic regulatory enzymes (Mitton & Grant
L984)and other factors which affect the function
of theseenzymes(Van Handel et al 1988a).Several
authors report higher heart rates at any given submaximal workload in overtrained subjects(Carlile
1964;Conconi et at. 1982; Costill L986;Van Han.
del et al. 1988b)[seefig. 4.).
Bouts of endurance(Costill 1986; Costin et al.
1988),sprint (Jacobset al. 1982)and weight-training (Jacobset a1.1982;Teschet al. 1986)have been
shown to cause significant reductions in musclc
glycogenstoreswhich may reduCethe capacityof
the athlete to perform short term, high intensity
work (Jacobset al. 1982; Pascoeet al. 1990)and