REVIEW ARTICLE Sports Moo .

1997 f eb; 23 (2); 10/>-129

0112-1642/97/00J2.QI 06/ S12.CXJ/O

© AdisInternational Umited . Allrig htsreserved

Resistance Exercise Overtraining

and Overreaching
Neuroendocrine Responses
Andrew C. Fryl and William J. Kraemer?
1 Exercise and Sport Science Laboratories, Department of Human Movement Sciences and
Education, The University of Memphis, Memphis, Ten nessee, USA
2 Center for Sports Medicine, The Pennsylvania State University, Hershey, Pennsylvania, USA

Contents
Summary . 106
1. Definitions and Types of Overtraining . 107
2. The Role of Training Volume and Tra ining Intensity . 109
2.1 Increased Training Volume . 109
2.2 Increased Training Intensity . . . . . . . . . . 109
3. Considerations for Neuroendocrine Responsesto Exerc ise . 110
3.1 Steroid Hormonal Adaptations . . . . . . . 110
3.2 Sympathetic Ac tivity Adaptations . . . . . 110
3.3 Acute Responses vs Chronic Adaptations . 110
3.4 Factors Contributing to Circulating levels . 111
3.5 Effects of Different Resistance Training Protocols . 111
3.6 Diurnal Endocrine Variations . 111
4. Testosterone . . . . . . . . 111
5. Luteinising Hormone (LH) . . . . . . 113
6. Cortisol . 114
7. Ad renocorticotropic Hormone (ACTH) 116
8. Testosterone / Cortisol Ratio 116
9. Growth Hormone . 117
10. Adrenaline (Epineph rine) . 118
11. Noradrenaline (Norepinephrine) . 120
12. Peptide F . 121
13. Ad d itiona l Ind icato rsof Overtraining 121
13.1 Creatine Kinase 121
13.2 La c tate . . 122
13.3 Ammon ia 122
14. Conclusions . . . 122

Summary Overtraining is defined as an increase in training volume and/or intensity of

exerci se resulting in performance decrements. Recovery from this condition often
require s many weeks or months. A shorter or less severe variation of overtraining
is referred to as overreaching, which is easily recovered from in just a few days.
Many structured training programmes utilise phases of overreaching to provide
variety of the training stimulus. Much of the scientific literature on overtraining
Resistance Exercise Overtraining 107

is based on aerobic activities, despite the fact that resistance exercise is a large
component of many exercise programmes. Chronic resistance exercise can result
in differential responses to overtraining depending on whether either training
volume or training intensity is excessive. The neuroendocrine system is a complex
physiological entity that can influence many other systems. Neuroendocrine re-
sponses to high volume resistance exercise overtraining appear to be somewhat
similar to overtraining for aerobic activities . On the other hand, excessive resis-
tance training intensity produces a distinctly different neuroendocrine profile. As
a result, some of the neuroendocrine characteri stics often suggested as markers
of overtraining may not be applicable to some overtraining scenarios. Further
research will permit elucidation of the interaction s between the neuroendocrine
system and other physiological systems in the aetiology of performance decre-
ments from overtraining .

The development of optimal human perform-
ance is a primary objective of exercise training.
Proper training prescriptions are required to facil-
itate maximal performances. A fine line exi sts,
however, between optimal performance and im-
paired performances associated with overtraining.
The unde sirable condition of overtraining occurs
when phy sical performance decreases despite con-
tinued training. Whether this effect requires many
weeks or months for recovery, or whether it is al-
leviated in a matter of days, the physiological re-
sponses to variou s types of overtraining must be
understood in order to determine proper training
strategies for optimal performance. Many physio-
logical variable s have been implicated as indica-
tors of overtraining because of their responsiveness
Table I. Suggested endocrine and blood-borne variable responses
to an overtraining syndromewith endurance activities
Symptom
Decreasedtotal testosterone levels
Decreased total testosterone/cortisol ratio
Decreased free testosterone/cortisol ratio
Decreased total testosterone/SHBG ratio
Alteredcortisol levels
Decreased sympathetic tone 9.11 .12
(decreased nocturnaland resting catecholamines)
Increased sympathetic stress response 4 sity of exercise training resulting in long term (e.g.
Increased creatinekinase
Decreased exercise-induced lactate
Abbreviation: SHBG = sex-hormone binding globulin.
to an overtraining stimulus. A list of these variables
can be found in table I. Several comprehensive re-
view s have pre sented these overtraining factors in
detaiUI 5.1 8.1 9]
It has been sugges ted that endurance trained
and strength trained individuals respond differ-
ently to severe training stre sses PO] In a survey of
overtrained athletes, it was found that 77 % were
involved in sports requiring high levels of
strength, speed or co-ordination.Uf This implies
that athletes performing these types of activities
may be more susceptible to overtraining, although
the exact aetiologies of these overtrained condi-
tions are not clear. Of the activities requiring high
levels of strength, speed, or co-ordination, resis-
tance exercise is the most studied anaerobic activ-
ity in the overtraining literature.f6.16.21 -27] Although
the focus of thi s review is on resistance exercise,
comparisons will be made with the aerobic-based
overtraining literature.
References
1-5
1. Definitions and Types of Overtraining
2,5
6.7 The literature on overtraining is confusing be-
2 cause of a lack of universal terrninology.f6.1 6.1 8.28-301
2.5.8-10
For the purposes of this review, overtraining will
be defined as any increase in volume and/or inten-
9,13,14 several week s or months, or longer) performance
9.12.13,15-17 decrements. Overtraining results in fatigue[16.29.3 1]
due , in part, to a lack of proper rest and recovery[16.1 8]

© Adi s lnte rno tio no l Lim ited . All righ ts reserved. Sports Med. 1997 Fe b ; 23 (2)
108
Acute fatigue
(positive
adaptation
to training)
Fig. 1. Overtraining continuum as modified from Fry et al.l181to illustrate the progression to overtraining .
and coincides with the General Adaptation Syn-
drome (GAS) proposed by Han s Selye.l 6.32] The
GAS may be applied to a number of settings, not
just phy sical performance or phy siological sys-
tem s. It is initiated with a disruption (stress) of the
homeostatic nature of a sys tem, foll owed by an
adaptive phase. If the adaptation is not adequate,
an exhaustion phase results, and eventuall y death
of the involved sys tem. When an exercise stress
produce s an overtraining sy ndro me, a healthy
physiol ogical sys tem will attempt to return to
homeostasis as part of the adaptation strateg y.[l8]
As a result, a marker of an overtraining syn drome
will be operationally defined as the change of a
physical, physiological , or psychol ogical charac-
teristic assoc iated with the overtraining stimulus
that precedes or accompanies the appearance of the
actual overtraining syndrome. Although markers
that do not precede the onset of an overtraining
syndro me cannot assist in the avoid ance of this
condition, they can help verify its pre sence .
Overtraining includes the stimulus ,116,29,3 1]
con sisting of an increase in training volume and/
or intensity, II ,25,33] and the re sulting decrease in
performance. If Alternative term s have been sug-
gested for overtraining, including chro nic over-
work,16] physical over strain,11 6] overtraining syn-
drome,116,25,29,34j burn-out,18,1 6,29] stale ness,11 8]
overfatigue,11 6,1 8] chronic fati gue syndrome,[8J and
fa ilure to adapt. 135] The en suing collecti on of
sy mpto ms and malad aptation s ca use d by over-
training is referred to as an overtraining syn-
drome. The se term s should be different iated from
mu scul ar over strain, which has been used to define
© Adis international Umited. Allrightsreserved.
Fry & Kraemer
Overreaching
(positive
adaptationif
used correctly)
the short term acute fatigue that occurs immedi-
ately post exercise.l' vl
Overtraining should be differentiated from
overreaching, which occurs on a short term basis
of several day s.16,8,16,1 8,22,25] Thi s condition is eas-
ily recovered from within a few days. Overreaching
is often a pl anned phase of man y tra ining pro-
grammes since it is believed to contribute to sub-
sequent improve d performances.Isl It has been pro-
posed that overreac hing is actually an early stage
of overtraining. If left unchecked, overreaching
develops into overtraining and the accompanying
performance decrements, which is itself the final
stage of a train ing continuum.I'U An ove rtraini ng
continuum has been modified from Fry et al.[1 8] to
illu str ate this progression to overtraining (fig, I ).
Performance decr ement s due to a lack of variation
in the training stimulus, or monotony, can occ ur
despite no alte rations in the training volume or in-
tensity.F'l Thi s type of overtraining will not be of
concern to the present review,
Overtraining ca n involve alterations to a num-
ber of phy siological systems.l6, 8,16,18,28] Two dis-
tinct type s of overtraining syndromes ha ve been
proposed, sympathetic (i.e. Basedowian ) and
parasympathetic (i.e. Addisonoid) syndromes.f36]
Th ese overtraining syndro mes have pre viou sly
been de scribed in severa l comprehensive re-
views ,16,8.11 ,15,16,18] The sympathetic syndrome in-
cludes increase d sympathetic acti vity at rest, while
the parasymp athetic syndrome includes decreased
sympathetic activity with parasympathetic act ivity
predominating at rest and with exercise. Both are
form s of ove rtraining . Para sympathetic overtrain-
ing is uniqu ely characterised by low resting heart
SportsMed. 1997 Feb; 23(2)
Resistance Exercise Overtraining
rates, rapid heart rate recovery post exercise, hypo-
glycaemia during exercise, decreased maximal
plasma lactate during exercise, and decreased cate-
cholamine level s.!16] It is believed the sympathetic
syndro me develops before the parasympathetic
syndrome, and is predominant in younger individ-
ual s who train for speed and/or power.! 6,1 8] All
overtraining may eventually result in the para sym-
pathetic syndrome. Changes in autonomic nervous
system function could account for numerous
phy siological responses to an overtraining stress,
including modifications to the neuroendocrine
system.
2. The Role of Training Volume
and Training Intensity
The effect of increased training volume (e.g.
distance for runners, number of sets or training
sess ions for weightlifters) and/or intensit y [i.e.
percentage maximum oxygen uptake (Y0 2max) or
percentage of maximal voluntary contraction] on
human performance and physiological mecha-
nism s has been investigated in a number of studies .
Increased training volume has been investigated
in activities that primarily emphasise aero-
bic[2.9.11 .3o.37-43] or anaerobicI 23,24,26,291exercise ac-
tivities. The effect of increasing both training vol-
ume and intensity of aerobic exercise activity has
recei ved little attention,l9,I0,44] while virtually no
studies of this type have been performed with an-
aerobic training, Likewise, few investigations
have monitored the effects of increased training
intensity alone for aerobic activities ,lI5,45] and only
I series of studies has addressed this topic with
resistance exercise.! 1.25,46-48]
2,1 Increased Training Volume
The effects of dramatic increases in mode-
specific training volume have been monitored in
di stance runners.l'':I I J swimmers,' 13,49] judo ath-
lete s l29] and weightlifters.!22-24.26] In each instance,
training intensity was not altered . Increased
training volume ha s re sulted in mode-specific
decreases in strength l29] or runninglf performance.
Other studies of increased training volume, how-
© Adis Inte rna tio na l Umite d . All rig hts rese rved .
109
ever, have not documented any performance
changes.1 13.22-24.26,49] It appears that there may be a
threshold of training volume necessary before
physical performance is affected, with onl y a few
scientific investigations actually using the required
exercise volume needed for performance decre-
ments. Future studies of volume overtraining must
provide an adequate training volume stimulus in
order to properly study this type of overtraining.
It is interesting to note that, in some instances
with resi stance exercise, return to a normal volume
of training result s in enhanced performances be-
yond those measured before the volume in-
crease,l22.24] This is evidence of a carefully planned
increase in training volume that does not always
impair performances, but does contribute to sub-
sequent improved physical performance. Thi s
phenomenon is also known as a 'rebound effect'.
Therefore, simply increasing training volume doe s
not nece ssarily result in an overtraining syndrome.
It is critical, however, for the coach and athlete to
know when to decrease training volume to avoid
overtraining.
2,2 Increased Training Intensity
The effects of increased training intensity have
received little attention. Why this is the case is dif-
ficult to understand since training inten sity is one
of the acute training variables that must be con sid-
ered for any exercise programme.Pv' Swimmingl-f
and weight training ll,25,46-48] studies have utili sed
marked increases in relative intensity compared
with what is normal for their activities, while using
very low training volumes. Improved swimming
velocity has resulted for swimmers using abnor-
mally high training intensities (i.e. near maximal
swim velocitiesj.l'P'
Unsuccessful research attempts to induce resis-
tance exercise overtraining have resulted in
decrements for isokinetic leg extension strength
( 1.05 rad/sec ) when training with ver y high intens-
ity [i.e. 90 to 95 % of I repetition maximum (RM)]
resistance exercise, although lRM strength on a
leg squat machine was unaffected.Pf Increasing
the relative training intensity to 100% I RM (i.e. 2
Sports Me d . 1997 Feb: 23 (2)
110
weeks duration; 6 days/wk; 10 x I at 100% IRM),
however, has produced definite decreases in
training-specific strength and a variety of physio-
logical responses. 11,46-481These results of such short
term maximal relative intensity resistance exercise
overtraining will be discussed in detail later.
Although the above studies increased exercise
volume or intensity, overtraining and the concom-
itant performance decrements did not develop in
many cases . It then becomes evident that studies
of overtraining must utilise adequate changes in
exercise volume or intensity in order to elicit the
desired overtraining response. Furthermore, the
rest and recovery characteristics of the training
programme must be carefully considered when
attempting to elicit an overtraining response. Al-
though much of the literature cited in this paper
does not deal with actual decreases in performance,
the physiological responses to increases in training
volume or training intensity can provide insight on
what may occur physiologically in the early stages
of a developing overtraining syndrome. Also, care-
ful use of such variation in training (i.e. increased
volume or intensity) is often a desirable training
goal that may eventually lead to optimal perfor-
mances .tf
3. Considerations forNeuroendocrine
Responses to Exercise
Different types of exercise (e.g. aerobic or an-
aerobic) may result in different neuroendocrine re-
sponses.f5 1-56j Much of the literature on exercise
and neuroendocrine responses has dealt primarily
with aerobic training, but the response of each hor-
mone or compound can differ when comparing aer-
obic with anaerobic exercise responses. Therefore,
the demands of the exercise stimulus must be con-
sidered when interpreting neuroendocrine re-
sponses to different metabolic and mechanical re-
quirements.
3.1 Steroid Hormonal Adaptations
A single session of prolonged aerobic exercise
results in decreased exercise-induced (i.e. acute)
levels of total testosterone and free testosterone.l"
© Adis Intemational Limited. All rights reserved .
Fry & Kraemer
while chronic aerobic training may result in either
increased'V' or decreasedf" testosterone levels.
In addition, resting testosterone levels have been
shown to decrease from a mean level of 29.5
nmol/L to 23.5 nmol/L with chronic aerobic train-
ing.[57] This is in contrast to heavy resistance exer-
cise, which has consistently demonstrated elevated
acute testosterone levels,[22-24,47,58-6Ij and augmented
resting levels after training programmes of at least
several months duration,l2°,22,53,54,6o,62,63] These
changes in resting testosterone levels may result
in a diminished capacity for cortisol to interact
with skeletal muscle tissue, perhaps contributing to
the anabolic-catabolic state of an individualp,55]
Changes in circulating testosterone levels also re-
sult in altered interactions with the neural sys-
tem,[64,651 which may further contribute to the re-
sulting physiological profiles of various athletes.
3,2 Sympathetic Activity Adaptations
Adrenal medullary responsiveness is increased
with aerobic training. This is evident in both max-
imal adrenaline (epinephrine) secretion rates as
well as decreased adrenaline levels at the same ab-
solute exercise intensity,f52,66] Noradrenaline levels
with chronic endurance exercise do not change at
rest or at similar relative exercise intensitiesJ44 ,67]
Similar absolute exercise loads, on the other hand,
will result in decreased noradrenaline levels with
endurance training.l 44,67] Preliminary data sug -
gests that long term heavy resistance exercise will
result in similar exercise-induced sympathetic
responses.[68]
3,3 Acute Responses vs
Chronic Adaptations
Investigations that monitor neuroendocrine
responses and adaptations to resistance exercise
have utilised both resting (i.e. chronic) and exercise-
induced (i.e. acute) levels . It is essential to note
that these 2 levels are not the same,[23,24,27,63,69]
and may be controlled by different regulatory
mechnisms.U'" This difference has important
physiological implications. Changes in the resting
hormonal environment due to chronic adaptations
Sports Med. 1997 Feb: 23 (2)
Resistance Exercise Overtraining
represent a physiological regulatory mechanism to
which the involved tissues are constantly exposed.
On the other hand, changes in the exercise-induced
hormonal responses represent the systemic re-
sponse to an applied exercise stress, and the sys-
tem's ability to cope with the immediate demands
of this exercise stress. These differences must be
considered when comparing resting and exercise-
induced hormonal levels with each other. The ma-
jority of overtraining investigations have focused
primarily on resting neuroendocrine levels.
3.4 Factors Contributing to Circulating levels
A complete understanding of the chronic or
exercise-induced responses to exercise include
accounting for each of the listed concentrating
mechanisms. Most investigations are not able to
determine which of these mechanisms is most re-
sponsible for the resulting neuroendocrine
responses to a particular exercise activity. These
various possibilities provide many questions for
future research on resistance exercise over-
training.
3.5 Effects of Different Resistance
Training Protocols
An often overlooked aspect of resistance
exercise is that different resistance exercise proto-
cols will produce dramatically different neuro-
endocrine profiles. Each resistance exercise train-
ing session is developed around 5 acute training
variables, including choice of exercise, order of
exercise, number of sets, rest intervals, and load
(i.e . RM loadingj.P'" Alterations of I or several of
these variables can greatly changes the exercise-
induced neuroendocrine responses. For example,
decreasing the rest intervals from 3 minutes to I
minute, and changing the RM loading from 5 to 10
RM results in dramatic increases in the exercise-
induced growth hormone response.f54,58,59) In ad-
dition, simply increasing the volume of resistance
training can produce decreased exercise-induced
responses of testosterone, cortisol , and lactate.!23,24]
Thus, to properly understand the neuroendocrine
physiology of resistance exercise, each of the acute
e AdisInternationalUmited. All rightsreserved.
111
training variables must be carefully controlled or
quantified.
3,6 Diurnal Endocrine Variations
The diurnal variations of many hormones must
be considered when interpreting endocrine data.
Chronic and exercise-induced hormonal responses
may be greatly affected by the time of day blood
samples are collected.l27,70] The time frames of
blood sample collection must be carefully regu-
lated to account for diurnal variations as much as
possible or, as has recently been determined, non -
exercise control days must be included.Fv' In addi-
tion, stressful activity, both physical and psycho-
logical, must be carefully controlled prior to the
blood collection to permit a clear determination of
the physiological effects of the exercise stress
alone.
4. Testosterone
Testosterone is a sex-related steroid hormone,
responsible for many anabolic and androgenic
(sex characteristics) properties.f53,71 1 Men possess
greater circulating levels than women, due primar-
ily to secretion of testosterone from the Leydig
cells of the testes.In] Women also exhibit low lev-
els in the circulation, due primarily to secretion
from the ovaries and the adrenal cortex. 153,73] Many
sexual characteristics depend on proper timing of
testosterone release during developmental phases,
as well as throughout life .(41) Testosterone has been
associated with development of male sex charac-
teristics such as hair growth, deepening voice, and
muscular development.P''l Testosterone exerts
most of its actions via interaction with a cytosolic
receptor in the target tissue. The ligand-receptor
complex moves to the nucleus where it regulates
DNA transcription.F'!
Regulation of testosterone levels is primarily
controlled by the hypothalamic-pituitary axis .
Circulating levels are detected by the hypothal-
amus, resulting in a release of gonadotropin-
releasing hormone to the portal veins of the ante-
rior pituitary.P''l This in tum signals release of
LH from gonadotrophs in the anterior pituitary.l"
Sports Med. 1997 Feb: 23(2)
112
which in turn regulates testicular secretion in
men.F" Neural innervation of the teste s is also
responsible in part for testosterone secretion, al-
though the exact extent has not been determined.Uf
A number of physiological factors contribute to
both resting and exercise-induced testo sterone
levels in resistance trained individuals. It has been
suggested that adaptation of the steroid synthesis
or secretory capacities of the cell s of Leydig in
the testes may be an important cau se of increased
testosterone following resistance exercise for
men.l 58] Long term resi stance exercise training can
result in lower levels of sex-hormone binding
globulin (SHBG))261 Since it is the free, or un-
bound, fraction of testosterone that is biologically
active, changes in the unbound pool of testosterone
can markedly affect the bioavailability of this
hormone. In this manner, total testosterone may
not alway s change, but testosterone turno ver (ki-
netics) and receptor activity level s may change
con siderably.[6Z1
Acute bouts of heavy resistance exercise result in
greater levels of total testosterone.l22-Z4,Z7,47.59.60,79] In
young weightlifters (aged 15 to 20 years), the mag-
nitude of these respon ses depends on the relati ve
inten sity of the exercise, but is not related to the
absolute strength level of the individuals.l'v l Reg-
ulation of exercise-induced testosterone doe s not
appear to be mediated by concurrent cortisol level s
and is not alway s under adrenergic control. P?' In
some instances, adaptation of the testo sterone pro-
ducing and/or secreting capacities of the testes
may be responsible for exercise-induced testoster-
one responses.[58] Additionally, afternoon exercise-
induced testosterone levels are sometimes greater
than morning values,l81] indicative of the diurnal
nature of testosterone levels.
It appears that resting testosterone level s are af-
fected by chronic resi stance exercise before other
endocrine variables.[22-z4.27,63] Short term weight
training programmes of approximately I-week
duration have resulted in decreased resting testos-
terone levelsp 6,Z71while longer programmes of I
or more years ' duration produce no change and no
increase in levels.lz6,6Z,63] The exact mechanisms
© Ad is Intern a tion a l Umited . All rights re se rved .
Fry & Kraemer
responsible for the se adaptations have not been
elucidated. It appears that increased resting and
exercise-induced testo sterone level s develop
within 4 week s of initiating a resi stance training
programme. P" Similar patterns of increased levels
have been shown for free testosterone.F' P-' Rest-
ing testosterone level s reflect changes in the train -
ing stresses, being negatively related to increases
in training volume.l z4,z6,Z7]
Chronic resistance exercise of 2 year s or more
can result in greater post-exercise testosterone lev-
els for young weightlifters (aged 15 to 20 years),
although strength levels are not always associated
with these changes.I'P' Hormonal levels can be al-
tered with long term resistance exercise although
these changes are often very subtle.l zo,zz.z6.63,791 Al-
though total testosterone level s may not always
significantly change, hormonal turnover and re-
ceptor activity level s may vary.[6Z] The endocrine
adaptations that do occur, such as increased free
testosterone, free testo sterone/cortisol and total
testosterone/cortisol have demon strated significant
relation ship s with strength increases)26.6Z] Al-
though endurance overtraining using high volumes
of training has been associated with imp aired
hypothalamic-pituitary control of peripheral hor-
mones,[J 5,83] no studies have examined the role of
trophic hormones (i.e. LH , follicle stimulating
hormone) on testosterone level s in the periphery
with normal resistance exercise.
4.1 Resistance Exercise Overtraining
Compared with peptide hormones or other
steroid hormones, total testosterone adapt s most
readily to a resistance exercise overtraining stimu-
lus, exhibiting decreased levels with increased
training volumes.lzz-Z4,Z6] Re sting testosterone
levels generall y decrease with greater training
volume,[16,z3.z6] although increases have been ob-
served.P'l Although overtraining was not apparent,
resting level s of free testo sterone also decrease
when training volume or intensity are 10-
creased)26,811
Thi s unbound component appears to be af-
fected by changing training volume more than total
Sports Med. 1997 Fe b; 23 (2)
Resistance Exercise Overtraining
testosterone.U!' thus reflecting decreased bioavaila-
bility. Exercise-induced changes in testosterone
will also decrease with increased resistance train-
ing volumes,[23·24.26] or when high intensity endur-
ance training is combined with high intensity
resistance exercise.l 551 No changes in resting tes-
tosterone have been observed when resistance
training intensity is increased.F'l Previous training
experience may affect these responses, since an in-
creased exercise-induced testosterone response
has been observed after I year of weightlifting
training.I-ll
Actual decrements in muscular strength result-
ing from a short term maximal relative intensity
resistance exercise overtraining programmel!' have
resulted in no changes in resting testosterone lev-
els, although slight increases in exercise-induced
levels were evident after 2 weeks of overtrain-
ing.l 47] Such a hormonal response suggests that
high intensity resistance exercise produces a dif-
ferent hormonal response when compared with in-
creased resistance exercise training volume or
overtraining with highly aerobic activities.
Although not identical to heavy resi stance
exercise overtraining, preliminary data on wrestlers
during a competitive tournament (5 matches over
2 days) indicates that acute testosterone levels sig-
nificantly decreased from matches I to 5.l84] De-
spite the large anaerobic component and muscular
force requirements of wrestling, the physiological
stresses encountered are still of relatively large
volume, thus a testosterone response similar to
high-volume resistance exercise overtraining. It
has also been demonstrated with a nonresistance
exercise modality, that testosterone levels may
not have returned to pre-exercise levels 24 hours
after a stressful exercise session.l 85] Such a recov-
ery pattern could contribute to exhaustion of the
hypothalamic-pituitary-gonadal axis with an over-
training protocol.
The unbound component of circulating testos-
terone, free testosterone, exhibits a similar re-
sponse pattern to total testosterone in responses to
maximal intensity resistance exercise overtrain-
ing.l 47] The net result is that the percentage of un-
© Adi s Internaftonal Umited. All right s reserved .
113
bound testosterone does not change at rest or after
exercise during this type of resistance exercise
overtraining. Thi s suggests that the role of SHBG,
and other testosterone binding proteins, does
not change with intensity dependent resistance
exercise overtraining. It has been suggested that
changes in the percentage of unbound testo sterone
can counter decreases in circulating total
testosterone.Ul but this does not appear to be nec-
essary when testosterone levels are not compro-
mised.
Testosterone has been reported to increase ex-
citability of central nervous system neurons .l'<l
Androgens will also increase acetylcholine recep-
tor density and size of motor endplates of certain
peripheral muscles,186] as well as help maintain
dopaminergic neurons in the central nervous sys-
tem .[87] In addition, the enzyme Sa-reductase,
which is responsible for the conversion of testos-
terone to dihydrotestosterone, has been found in
neural myelin.l 64] This suggests that testosterone
may serve to modify neural function in some man-
ner. The net result of decreased testosterone levels
with resistance exercise volume overtraining may
impact not only contractile proteins, but also nu-
merous other physiological systems. Strength po-
tential may be compromised because of both de-
creased protein synthesis in skeletal muscle tissue,
and modification in some manner of neural regu-
lation of skeletal muscle activity. Evidence also
exists that skeletal muscle androgen receptor
binding capacity may be modified by resistance
exercise in a muscle-specific manner.l 88] How this
phenomenon may contribute to resistance exercise
overtraining remains to be elucidated.
5. Luteinising Hormone (LH)
LH is a glycoprotein consisting of a (89 amino
acids) and ~ (115 amino acids) subunits.P'" Se-
creted from basophilic cells of the anterior pitu-
itary, LH is the primary regulator of testosterone
secretion from the Leydig cells of the testes .[53] The
androgenic regulating properties of LH are con-
tained entirely in the ~ subunit, while the a subunit
of LH is identical to that of other anterior pituitary
Sports Med. 1997 Feb; 23 (2)
 114
glycoproteins (i.e. follicle-stimulating hormone
and thyrotropin).189] High affinity binding of LH at
the Leydig cells of the testes activates a cyclic
adenosine monophosphate (cAMP) mechanism,
resulting in increased testosterone synthesis.F"l
This activation is dependent on the frequency and
amplitude of LH pulsatility,190] with pulses occur-
ring in the human at the rate of approximately 8 to
14 pulses/day in men.l 74)
Secretion of LH is principally regulated by LH
releasing hormone (LHRH) via portal circulation
from the hypothalamus.P'" High affinity binding of
LHRH in the anterior pituitary activates LH
secretion by a calcium-dependent rnechanism.l'"]
resulting in LH secretion in a pulsatile manner.l 90]
Negative feedback of testosterone acts to modulate
LHRH and LH secretion in the hypothalamic-
pituitary axis,!92)
LH levels are positively related to the volume
and intensity of the resistance exercise stress. 12I,26]
Long term (24-week) weight training programmes
do not necessarily alter resting LH levels with
recreationally trained men .F'" but 2 years of train-
ing have exhibited slight increases in both resting
LH and testosterone with elite weightlifters,163]
thu s contributing to a greater hypothalamic-
pituitary signal for testosterone secretion. Exercise-
induced increases in LH have not been observed
with resistance exercise,[27.47] indicating that exer-
cise-induced testosterone increases are due to
other regulatory mechanisms. Resting LH levels
will increase with greater resistance exercise train-
ing volumes (>45 x 103 kg/mo; sets x repetitions
x load[kg]),[21.26.81] and decrease with decreased
training volumes «30 x 103 kg/mo),12I,26] al-
though 1 week is not long enough to demonstrate
any changes.F" It has been proposed that LH levels
are regulated via cybernetic mechanisms by free
testosterone levels,121,26,81) although LH responses
to long term programmes have corresponded to
changes in testosterone.I'i'l It should be noted that
all of these investigations of LH responses to resis-
tance exercise have used temporal levels and have
not accounted for LH pulse magnitude or fre -
quency.
© Adis Internaftonal Umited . Ail right s reserved.
Fry & Kraemer
5.1 Resistance Exercise Overtraining
There are few data regarding anterior pituitary
responses to resistance exercise overtraining.
Overtraining with highly aerobic activities (e.g.
long distance running) has indicated that the
hypothalamic-pituitary axis activity is altered,[IS,83]
and it has been theorised that the pulsatility of
LHRH from the hypothalamus may be affected by
such endurance overtraining.Uf When overtrain-
ing has been induced via high relative intensity
resistance exercise.F'] resting LH did not change,
mirroring the responses of resting testosterone.
Slight decreases, however, were observed for exer-
cise-induced LH after 2 weeks of the overtraining
protocol, despite the slight increases observed for
acute testosterone levels . This suggests the possi-
bility that a non-LH dependent regulatory mecha-
nism(s) exists under these overtraining conditions
for the acute testosterone responses, as opposed to
resting levels. There is evidence of direct neural
communication between the hypothalamus and the
testes[76) as well as regulation by the sympathetic
nervous system. However these LH data are based
on temporal LH levels , and that altered LH pulsatil-
ity cannot be ruled out as a contributing regulatory
mechanism.
Although the exercise-induced responses of tes-
tosterone are not related to LH, resting levels of
testosterone are related. In this manner, pituitary
control of testicular activity, via LH, is present dur-
ing periods of non-exercise. Thus, the potential pi-
tuitary influence on testosterone levels is consider-
able despite the lack of an exercise-induced
relationship. Comparison of LH and testosterone
levels can provide information regarding the site(s)
of maladaptation with overtraining, the pituitary
and/or the testes.
6. Cortisol
Cortisol is a steroid hormone that originates
primarily from the zona fasciculata and zona
reticularis in the adrenal cortex.l 93) It functions as
a regulator of many physiological systems such
as the liver, skeletal muscle, adipose and skeletal
Sports Med. 1997 Feb: 23 (2)
Resistance Exercise Overtraining
among others. 194] Some of cortisol's principal ef-
fects involve energy substrate availability by in-
creasing gluconeogenic activity in the liver, de-
creasing glucose uptake and increasing glycogen
synthesis in muscle, as well as mobilising amino
acids from skeletal muscle.I'"! The result is a de-
creased utilisation of glucose by muscle cells and
increased substrate availability. Like testosterone,
cortisol exerts most of its effects via cytosolic re-
ceptors which then interact with DNA in the nu-
clear region.[95]
Cortisol secretion from the adrenal gland is
regulated primarily by the hypothalamic-pituitary
axis .l96] Circulating levels of cortisol are detected
by the hypothalamus, which secretes cortico-
trophin releasing hormone (CRH) into the portal
circulation of the pituitary in response to low cor-
tisol levels.l 97] In turn, CRH signals the anterior
pituitary to release the peptide hormone adreno-
corticotropic hormone (ACTH).198] The precursor
of ACTH is the pro-opiomelanocortin (POMC)
molecule produced by the anterior pituitary. The
anterior pituitary itself can also detect increases
in circulating cortisol, resulting in decreased
ACTH release.l 98] ACTH is the most potent regu-
lator of cortisol release from the adrenal cortex.P?'
In addition, stress-sensitive catecholaminergic in-
nervation of the adrenal cortex, both splanchnic
and otherwise, appears to serve a small role in cor-
tisol regulation.U'P' Circulating adrenaline may
also contribute to cortisol regulation.Pf
Various resistance exercise protocols produce
exercise-induced cortisol increases.122-24,54,59,60,81]
The afternoon responses appear to be greater than
the morning responses, owing to circadian
rhythms.170,81] Although it has been suggested that
elevated cortisol levels may attenuate testosterone
responses ,180] no such relationship has been found
for exercise-induced responses after resistance ex-
ercise. Chronic resistance exercise does not pro-
duce a clear pattern of resting cortisol levels,
with no changes ,122,26,27] or decreased levels I26,62]
resulting . These decreased levels are often associ-
ated with decreased resistance training volumes.
© AdisInternaftonal Umited. All rights reserved.
115
In general, cortisol levels reflect long term
(~l month) training stresses.P'"
6.1 Resistance Exercise Overtraining
Increasing resistance training volume or in-
tensity produces greater resting cortisol lev-
els. 16,16,3,24,26,81] In addition, combining high in-
tensity resistance exercise with high intensity
endurance exercise also increases exposure to cir-
culating cortisoLl55] These responses could con-
tribute to replenishment of substrate stores, as
well as assist the skeletal-muscle tissue remodell-
ing process. On the other hand, exercise-induced
cortisol levels, which are also exercise-intensity
dependent, decrease when training volume is dou-
bled .123,24] It is possible that the presence of in-
creased resting levels of cortisol contribute to an
exhaustion of the hypothalamic-pituitary-adrenal
axis, thus preventing an adequate cortisol response
to such an acute stress.
In the presence of maximal intensity resistance
exercise overtraining.F'l no changes were ob-
served for resting levels of cortisol, while acute
levels actually decreased slightly after 2 weeks .
Such responses are contrary to high volume resis-
tance exercise and overtraining with highly aerobic
activities. It thus becomes apparent that some of
the classical signs of overtraining, based on data
from endurance athletes , cannot necessarily be
applied to overtraining resulting from highly an-
aerobic activities. Future research must address the
possible mechanism(s) of such a cortisol response,
whether it is due to adrenal cortex exhaustion, sym-
pathetic regulation,IIDO] or some other controlling
factor. Extremely high volumes of aerobic training
(i.e. long distance running up to 190 km/week and
70 kmlsession) have indicated impaired cortisol re-
sponses to hypoglycaemia, thus affecting substrate
availability and subsequent performances. 183]
Whether this occurs with high intensity resi stance
exercise overtraining is not known. Recent evi -
dence indicates that increased cortisol sampling
time s may be required to adequately determine ac-
tual resting and acute cortisol responses to a train-
ing stimulus.Uvl
Sports Med. 1997 Feb: 23 (2)
116
Furthermore, since cortisol has been reported
to decrease excitability of certain central nervous
sys tem neurons.l'P'J as well as help stabilise the
enzymes of adrenaline synthesi s, particularly
phenylethanolamine-N-methyltransferase and
dcpamine-f-hydroxylase.U 'F l its role in indirectly
modulating performance may be critical. The lack
of increased cortisol levels with high-intensity re-
sistance exercise overtraining has important impli-
cations for other areas of overtraining research,
since it has been shown that increased circulating
levels of cortisol may be associated with psycho-
logical depression.ll''U a condition sometimes as-
sociated with forms of overtraining.Pr' v'
7. Adrenocorticotropic Hormone (ACTH)
ACTH is a peptide originating from the anterior
pituitaryt 'P'l and is the primary regulator of adrenal
cortex secretion of cortisol.P?' Basophilic cells of
the anterior pituitary produce a precursor mole-
cule, POMC. [98] Enzymatic cleavage of POMC
molecules in the human anterior pituitary result in
equimolar secretion of ACTH and ~-lipotropin.l IOS]
The resulting ACTH molecule is 39 amino acids in
length, with the first 24 amino acids pos sessing full
biological activity.l '"! Therefore, the entire 39-
amino acid segment of ACTH is not necessary to
activate adrenal cortex secretion of cortisol. High
affinity binding of ACTH in the zona fasciculata
and zona glomerulosa of the adrenal cortex[ 106] re-
sults in synthesis and secretion of cortisol within
minutes via a cAMP mechanism.U'"! Secretion of
ACTH is very pulsatile,[108-1I0] with the resulting
increased cortisol secretion highly dependent on
increased ACTH pulse amplitude ,[108.1I0-112)
Secretion of ACTH is principally regulated by
corticotrophin-releasing hormone[96,II3J via portal
circulation from the hypothalamus, High affinity
binding of CRH in the anterior pituitary l1l4] acti-
vates a cAMP second messenger sys tem, resulting
in ACTH release. t'Pl Circulating corti sol acts
through negati ve feedback to modulate both
CRH! 97) and ACTH productionl'"! in the hypotha-
lamic-pitu itary axi s. Although evidence exi sts of
central catecholaminergic regulation of ACTH, cir-
© Adi s Inte rna tion a l Umited . All rights rese rved.
Fry & Kraemer
culating adrenaline or noradrenaline do not appear
to impact ACTH secretion.U'v' Afferent input from
skeletal muscle also appears to contribute to ACTH
levels.1117]
7.1 Resistance Exercise Overtraining
As with other pituitary hormones, no data exi st
regarding ACTH and resistance exercise overtrain-
ing . Evidence from overtraining with highly aero-
bic activities indicates that ACTH control of corti-
sol secretion diminishes with high volumes of
exercise.Fl that acute ACTH levels are attenuated
with increased exercise intensity.U'Iand that hypo-
thalamic dysfunction is a contributing factor.(83)
It has also been proposed that CRH pulsatility may
be altered with overtraining.U il When strength
performance has been decreased via maximal in-
tensity resistance exercise overtraining.F'l circu-
lating ACTH levels did not change either at rest or
after exerci se. This would suggest that the slight
decreases in acute cortisol levels previously re-
ported were not due to pituitary regulation . How-
ever, as with LH, no measures of ACTH pul satile
frequency or magnitude were recorded, which
could greatly affect the cortisol response.
8. Testosterone/Cortisol Ratio
In many ways, these 2 hormones exhibit con-
trasting phy siological properties. For this rea son ,
the ratio between the 2 (TES/CORT) has been used
in a number of training and overtraining investi-
gations. [6,7,20-24.26.27,47,60,62,79,81] Interpretation of
the meaning of the exercise-induced TES/CORT
ratio can be difficult since both testosterone and
cortisol contribute to the typically decreased acute
TES/CORT values .[22-24,11 8] Since the unbound
fraction of testo sterone is believed to be the bio-
logically active component, the ratio between free
testosterone and cortisol is sometimes monitored
(FfES/CORT).I6,62] It has been suggested that the
TES/CORT ratio is an indicator of the anabolic-
catabolic status of an individuaJ.l6,7] Thi s appears,
however, to be an oversimplification, and at best is
only a gross indirect measure of anabolic-catabolic
status. Regardless, this ratio has been po sitively
Sports Med. 1997 Fe b: 23 (2)
Resistance Exercise Overtraining
related to cha nges in phy sic al performance in
several studies)62,63,79, 119]
Exerci se-induced TES/CORT is not altered fol-
lowing 1 year of con sistent training.P?' Resting
ratio s also do not usuall y change with long term
training)22-24] Increases in TES/CORT have been
significa ntly correlated, however, with increased
streng th capabilities,[21 ,26,62,8I,l19] de sp ite the
sometimes non significant ab solute increases in
this ratio. This suggests that the TES/CORT ratio
may be a sensitive indicator of strength perfor-
mance . Few studies have monitored FTES/CORT
responses to resistance exercise, and no studies
have ob served exercise-induced FTES/CORT re-
sponses. No changes in resting FTES/CORT have
been ob served with normal resistance exercise
training volumes or detraining.l'Sl Since free tes-
tosterone has been demonstrated to be qu ite re-
sponsive to resistance exe rcise trainin g, it is likel y
that the FTES/CORT ratio may be more sensitive
to overtraining than the TES/CORT ratio .
8.1 Resistance Exerc ise Overtraining
Wh en resistance training volume or inten sity
are increased , resting TES/CORT will often de-
crease) 6,26,811 High calibre weightlifters, however,
showed no chan ges in the restin g ratios with in-
creased training volume, although the exercise-
induced respon ses became less variable after in-
creasing training volumep3,24] It has been
proposed that decreases of 30 % in the FTES/CORT
ratio, or values <0 .35 x 10- 3 indicate an over-
trained state,l7] although these characteristic s have
been ob serv ed in endurance athletes without evi-
dence of overtraining) 120] When strength has been
compromised due to maximal inten sity resistance
exercise overtraining, no changes have been evi-
dent in resting TES/CORT or FTES/CORT) 47]
Contrary to wha t might be expected, slight in-
creases in acute TES/CORT and FTES/CORT de-
veloped after 2 weeks in response to this overtrain-
ing protocol. Thi s again illu strates that various
overtrainin g protocol s and modalities produ ce dif-
ferent endocrine responses. As a result, several ofthe
© Ad is lnte rnotto no' Umited . All rig hts reserved.
117
commonly cited endo crine markers of overtr aining
may not apply to all situations.
9. Growth Hormone
Limited data are available concerning the role
of growth hormone on the aetiology of resistance
exercise overtrainin g. Growth hormone is a peptide
hormone of 191 amino acids including two di-
sulphide bonds. It is produced in, and secreted
from the acidophilic cell s of the anterior pituitary,
which contain from 5 to 10mg of growth horm one
at any one time in humans . Growth hormone is
secreted in a pulsatil e fashion, and is regulated by
the positive influ ences of growth hormone releas-
ing hormone, and the negative influences of
growth horm one inhibitory hormone, also known
as somatostatin.U'[ U Recent research has indicated
that numerous variants of gro wth horm one ex-
iSt.[1 22,1 23] Since not all of the se variants may
have identi cal immunoreactivity, previously used
methodologies may not have been sensitive to lev-
els of all types of growt h hormone, thus makin g
interpret ation of the data difficult at best. Al-
thou gh gro wth horm one can directly affec t a vari-
ety of tissues, many of its actions are actually due
to insulin-like grow th factors.[124] Besides influ-
encing grow th, growth hormone is also respon sible
for numerous metabolic action s. Of interest to the
study of overtraining is the potential effect of
growth hormone on skeletal muscle growth and
metabolism. Growth hormone enhance s amino
acid upt ake,[1 25] and accentuates lipolysis) 126] As
a result, amino acids are spared for anabolic purposes
in skeletal muscle, and glycolytic energy stores are
spared by preferential use of lipids . Such effects
can potentially influence maximal muscular force
production or muscul ar endurance performance.
As mention ed above, acute gro wth hormone
respon ses are relat ed to the metabolic properties
of the exerci se stress . As such, it is acutely se-
creted in an inten sit y-d ependent manner, with
gre ater resistanc e exe rcise intensities produ cing
higher circul ating !evels.[59,127] Some of the largest
exerci se-induced circ ulating growth horm one
le vel s ha ve been obs erv ed afte r hi gh int en sit y
Spo rts Me d . 1997 Fe b: 23 (2)
118
resistance,[23,24,59,60,128,129] with these levels re-
maining elevated for an extended time post exer-
cise,!60] Two resistance exercise training sessions
per day have not altered resting levels of growth
hormone after I day[130] or I week of such train-
ing,[27] Long term chronic resistance exercise of
over 2 years duration, however, may result in low-
ered resting and acute growth hormone levels,!60]
9.1 Resistance Exercise Overtraining
When resistance exercise training volume has
been dramatically increased (3 to 4 training ses-
sions/day), thus producing a state of overreaching,
both resting and acute growth hormone responses
have been attenuated,!23 ,24] Preliminary data from
high intensity resistance exercise overtraining
suggests that no changes in either resting or acute
growth hormone result, [personal observations] de-
spite alterations in numerous other physiological
systems.' 1,46-48] Although there is potential for
growth hormone to contribute to the physiological
and performance responses to overtraining, it does
not appear to be a major factor with maximal rela-
tive intensity resistance exercise overtraining. This
is further supported by the fact that the acute
growth hormone response to high relative intensity,
low repetition exercise (20 x I RM) is negli-
gible,! 11 81 High volumes of aerobic training have
produced impaired growth hormone responses to
hypoglycaemia, thus affecting substrate availabil-
ity and subsequent performances.l'"! Whether this
occurs with high intensity resistance exercise over-
training is not known. Further research is required
to more fully understand the role, if any, of growth
hormone during resistance exercise overtraining,
10. Adrenaline (Epinephrine)
Adrenaline is a circulating amine that acts as a
neurohormone, Circulating adrenaline originates
primarily from exocytosis in the chromaffin cells
of the adrenal medulla.U''U The effects of adrena-
line are quite dramatic, and affect numerous
physiological systems. In very general terms, cir-
culating adrenaline prepares the body for a 'fight-
or-flight' response .l' e!' Increased arousal , enhanced
© Adi s International Limited. All right s reserved.
Fry & Kraemer
cardiac output,l132] appropriate blood flow regula-
tion ,fI33] increased skeletal muscle force produc-
tion,l134] and greater energy substrate availabil-
it y l135 ,136] are a few of adrenaline's physiological
roles. The response of adrenaline to a 'fight or
flight' situation may provide insight on the adren-
aline response to an overtraining stimulus since
the body must respond to a stressor in both cases.
The actions of adrenaline are manifested by inter-
actions at either a- or ~-adrenergic membrane re-
ceptors in target tissues.UV'
The secretion-coupling process of the adrenal
chromaffin cells is regulated primarily by innerva-
tion from the greater splanchnic nerve via the su-
prarenal plexus, with some contribution from the
coeliac plexus.l138] In this manner, higher centres
can carefully control this important neurohormone.
In addition, the adrenal medulla is entirely encap-
sulated by the cortex. As a result, the chromaffin
cells are exposed to cortisol that is secreted in the
cortex,!139,140] Cortisol contributes to adrenaline
regulation by inducing enzymes of adrenaline
synthesis, especially phenylethanolamine-N-
methyltransferase. lI02,141]
Adrenergic receptors are found on most peri -
pheral tissues of the body, indicating the important
fun ction of circulating adrenaline. The known
signs and symptoms of overtraining involve many
different physiological systems, most of which
are under adrenergic regulation to some extent. Of
particular interest to resistance exercise over-
training is the potential for circulating adrenaline
to modify skeletal muscle force production and
substrate availability, thus influencing both maxi-
mal muscular strength and local muscular endur-
ance, Several physiological mechanisms exist for
such a compromise of muscular performance. With
in vitro muscle preparations, exposure to adrena-
line or ~ agonists produces increased muscle force
production in both fast twitch fl42] and slow
twitchl1431 muscle. Both muscle fibre types appear
to be equally sensitive to a-adrenergic stimulation.
Such stimulation has been associated with in-
creased intramuscular cAMP,!144] Thi s in turn may
be responsible for increased transmembrane
Sports Med. 1997 Feb: 23 (2)
Resistanc e Exercise Overtraining
transport of Na" and K+,1145] thu s altering Cat"
tran sients and muscle contractility.U v' l It is the-
ori sed that the increase in extracellular K+ that oc-
cur s during muscle act ivity signals increas ed sym-
pathoadrenal act ivit y via afferent feedback .U'["
The increa sed adrenaline stimulates greater K+
uptake and Na" efflux via ~ stimulation, resulting
in greater muscle contractility. Thi s theory is sup-
ported in part by increased pla sma K+ during ~
blockade'!146] Adrenaline also increase s glyco-
genolysis in exercising skeletal muscle [1 36] via ~
stimulation.UVl The resulting increase in cAMP
activates glycogen phosphorylase and inactivates
glycogen synthase.!135] When ~ stimulation is
blocked, pho sphorylase activity is not affected'! 142]
In addition , a stimulation increases glycogeno-
ly sis by increased phosphofructokinase activ-
ity.!1 48J It should be noted, however, that decreased
glycogenolytic activity doe s not always affect ex-
ercise performance. P! l
Interactions between neural and endocrine fac-
tor s are readil y apparent in the adrenal gland.[149]
Symp athetic neural activity vi a acetylcholine
stimulates catecholamine secretion and release.[IOO]
Differential responses are also obser ved for activa-
tion of muscarinic or nicotinic cholinergic recep-
tors in the adrenal medulla,1140J thu s pro viding
further mech ani sm s for adaptation. It ha s been
rep orted that neural stimulation of the medulla
controls catecholamine level s abo ve basal levels,
while corti sol levels help to maintain basal levels.1102]
The se various adrenaline regulatory mechanisms
may be differentially activated during the course
of overtraining. For this rea son , both resting and
exerci se-induced levels of adrenaline mu st be
monitored and compared to the respon ses of other
physiological sys tems .
Greater sympathoadrenal acti vit y occurs with
anaerobic exercise than with aerobic exercise,1150]
and it is known that adrenaline levels are positi vely
related to anaerobic exercise intensity.!56,15l J
Lon g te rm we ight training produces grea ter
adr enal ine respon ses at the same relati ve exercise
intensity (i.e . % RM ), thu s maximum effort pro-
duces a grea ter adrenaline response.I'<' Thi s results
© Ad is Inte rnatio na l Umited. All rights reserved .
119
in greater maximal adrenaline level s in chronically
resi stance trained individuals. Chronic resistance
training also produces a decreased adrenaline re-
sponse at absolute exercise intensities.l' Vl The se
adaptations are somewhat similar to tho se ob-
served with endurance training. Perturbations to
the adrenergic system, such as high intensity resis-
tance exercise overtraining, are evident from alter-
ations from thi s pattern of adrenaline respon se.
10.1 Resistance Exercise Overtraining
Maximal intensity re sistance exercise over-
training has resulted in no changes to pre- exercise
adrenaline level s, but acute level s are significantly
increased within I week of initiating the over-
training protocol.t ' f The lack of altered pre-
exercise adrenaline is contrary to reports that this
is characteristic of a general state of overtrain-
ing .!1 6,1 531 The ele vated exercise-induced adrena-
line re sponse (>7000 pmol/L) indicate s an en-
hanced ac ute activation of the adrenal medulla
with thi s form of overtraining. It should be noted,
however, that these levels are comparable to levels
pre viously reported for re sist ance trained indi-
viduals who were not overtrained.!61 ,1 54J
Therefore, it appears that an increase in the
acute adrena line response , and not the abso lute
acute adrenaline levels, that indicate an overtrained
state with high inten sity resistance exerci se. This
is quite different from the parasympathetic over-
training syndrome of endurance athletes,lll,1 2,43]
and as has been previously suggested when com-
paring aerobic and anaerobic activities,[155] the
overtraining respon se of the sympathetic nervous
system may vary between anaerobic and aerobic
acti vities. Since numerou s other symptoms of a
sympathetic overtraining syndrome were not
evident,II ,1 6,1 8,46,47,153) such an augmented acute
adrenal ine re sponse ma y be simply the initial
step in a phy siological continuum of overtraining
adapt ations.
Longer term use of the maximal intensity
re sistance exercise overtraining protocol ma y
have eventuall y affected re sting catecholamine
le vel s, much like those see n with overtrained
Sports Med. 1997 Feb: 23 (2)
120
endurance athletes.IS.9-1I ] A theoretical sequence of
events ma y proceed from augmented acute adren-
aline,[46] progressing to augmented resting lev-
els,IISS] and culminating in a con stant depression of
adrenaline as indicated by attenuated nocturnal uri-
nary excretion of adrenaline.Pl
De spite the fact that exercise-induced adrena-
line wa s elevated in the presence of maximal inten-
sity resi stan ce exerci se overtraining ,146] mu scle
strength performance was not enhanced. I!' Control
subj ec ts in thi s study exhibited strong correlations
(r :? 0.79 ) between changes in several mu scular
strength performances (isokinetic and involuntary
stimula ted quadriceps strength) and changes in
acute adrenaline levels, but no significant correla-
tions were ob served for the overtrained individu-
als .146] Thi s indicates a po ssible downregulation of
skeletal mu scle ~ receptors for the overtrained in-
dividual s, coinciding with peripheral mal adapta-
tion s sugg es ted by several mu scular performance
me asures) I ] The elev ated acute adr en alin e level s
ma y, how ever, ha ve contributed to the slightly el-
evated acute testo sterone level s ob served with thi s
type of overtra ining, since acute testosterone
sec retio n by the teste s are under adrenergic regula-
tion .IIS6,IS7]
11. Noradrenaline (Norepinephrine)
Mo st of circ ulating noradrenaline originate s
from spillov er from peripheral sympathetic nor-
adrenergic sy naps es, thu s it reflects neuro-
transmitter activity)lS8] Up to 80 % of noradrena-
line released from a neuron bouton will either be
metaboli sed by catechol-O-methyltransferase IIS9]
or monoamine-oxidase.U'v' or taken up by the pre-
synaptic nerve terminal .U''!' The remaining no r-
adrenaline spill s over to the circulation , thu s re-
presenting an indirect me asure of sympathetic
nervou s activ ity) 162, 163] Small amounts of nor-
adrenaline are sec reted by the adre nal medull a
(~2 0 % of adrena li ne secretio n) , altho ug h the se
amounts do not contribute grea tly to circulating
Ievel s. IIS7] Noradrenaline is involved in preparing
the body for ' fight-or-fli ght' situations by the same
mechani sm s pre viou sly listed for adrenaline.1136]
© Ad is Inte rnat io nal Limited . All rig hts rese rved .
Fry & Kraemer
Al so like adrenal ine, noradrenaline elicits its
phy siologic al resp on ses by interacting with a and
~ receptors in the target tissue s)1 37] No radrenaline
secretion occurs when an action potential permits
Ca'" to enter the neuron bouton.IIM] Therefore, the
stimulus-secreti on patterns of noradrenaline re -
lea se is regulated by the higher brain centres.
Like adrenaline, noradrenaline levels are po si-
tivel y related to exercise intensities,IISI] alth ough
increased duration of exercise also contributes to
greater noradrenaline levels) S6] Th e actual pattern
of adrenaline and noradrenaline secretion differ
with variou s exercise intensities,IS6] indicating
that the se 2 catecholamines reflect different phy s-
iological responses to the exerci se stress. Circulat-
ing post-exercise noradrenaline at the same relative
intensity (i.e . %RM ) will increase with long term
train ing,168] while lev el s decrease at the same
absolute inten sities.I'Vl As with adren aline, these
exerci se-induced response s of noradrenaline to re-
sistance exerci se are similar to tho se observed with
aerobic training .
11,1 Resistance Exercise Overtraining
Circulating noradrenaline level s are an indirect
measure of sympathetic nervou s sy stem ac tivity.
Mea surement of nor adrenaline, when co mpared
with response s of other ph ysiological variables,
provide insight on ce ntral regulation of numerous
phy siological sys tems . Furthermore, determining
the time course of adaptation of the sympathetic
nervous system with an overtraining stimulus will
help clarify the role of central control to the aetiol-
ogy of intensity-spe cific resistance exerci se over-
training. As far as resistance exercise overtraining
responses are concerned, circulating noradrenaline
level s have only been studied in response to maxi-
mal intensit y resistanc e exercise overtraining.t'f
As with adrenalin e, pre-exerci se nor adrenalin e did
not cha nge with th is type of overtraining, but acut e
le vel s were dramat icall y elevated after only I
week. The resulting le vel s (>70 nmollL) were
gre ater th an have been previously reported with
resistance exerc ise,161.IS2.ls4.16S] most likely due in
Sports Med. 1997 Fe b: 23 (2)
Resistance Exercise Overtraining
part to differences in the exercise stresses , and the
sampling times .
In many ways, the responses of noradrenaline
to maximal intensity resistance exercise over-
training are very similar to those' of adrenaline.
These data add further support to the presence of a
sympathetic overtraining syndrome with such an
overtraining protocol, although it is only evident
with the exercise-induced responses. Although the
changes in noradrenaline were positively corre-
lated with changes in several strength measures
(isokinetic and involuntary stimulated quadriceps
strength; r ~ 0.88) for the overtrained individuals,
changes in noradrenaline were negatively related
to changes in IRM performance on the training
exercise.l 461 Not only does this further support the
possibility of downregulation of skeletal muscle ~
receptors, but it suggests that changes in exercise-
induced noradrenaline may be a marker of high
intensity resistance exercise overtraining before
IRM performances actually decrease.(1,46]
12. Peptide F
Peptide F originates primarily from the chro-
maffin cell s of the adrenal medulla, and is appar-
ently cosecreted with the more abundant adrena-
line.l166.1 67] It is a proenkephalin fragment,
containing a [Met]enkephalin at either end.l l68J
Peptide F, however, is not a precursor to [Metjen-
kephalin, but is the apparent end-product of post-
translational processing unique to the chromaffin
cells of the adrenal medulla.l l681The physiological
function of peptide F is not entirely known, but it
has been associated with immune function .[169,1 70j
In addition, by comparing circulating levels of
adrenaline and peptide F, alterations in secretory
patterns of the chromaffin cell s becomes evi-
dent.[53.56.1711
Chronic exercise programmes can result in
altered catecholamine levels.!66-68] Since pro-
enkephalin peptide F is cosecreted with adrenaline,
chronic training may also affect peptide F level s.
Indeed, endurance trained individuals have
shown evidence of chromaffin cell secretion pat-
terns coordinated with the acute training stress.l!"!'
© Adis tntemotionol Umited . A ll rig hts reserved.
121
These individuals preferentially secreted adrena-
line during maximal treadmill exercise, while un-
trained individuals showed no such coordinated
pattern. With the onset of some type s of resistance
exercise overtraining, adrenal chromaffin cell
function may be compromised. Although the half-
life of peptide F is ~15 min[ 1721 while the half-life
of adrenaline is just a few seconds, chromaffin cell
secretory activity can be monitored by comparing
circulating adrenaline and peptide F levels when
sampling occurs within seconds post exercise. The
inability of adrenal chromaffin cells to adequately
release adrenaline can have profound effects on
many physiological systems, such as altered
skeletal muscle function in the periphery.I' <'v'
12.1 Resistance Exercise Overtraining
When maximal intensity resistance exercise
overtraining is induced, no changes have been ob-
served for circulating peptide F levels at rest or
after exercise.[481 As previously mentioned, such
an overtraining protocol results in increased acute
levels of adrenaline. The fact that the circulating
ratio between peptide F and adrenaline changes
with this type of overtraining, suggests that the
secretory patterns of adrenal chromaffin cell s are
altered during this type of overtraining. It is
pos sible that such a response is a physiological at-
tempt to preserve adrenaline secretory capabilities
during stressful training , when the body most
needs it.
13. Additional Indicators of Overtraining
Although not circulating hormones, there are
several blood-borne compounds that have been
suggested as po ssible physiological markers of
overtraining and/or overreaching.If In general,
the scientific evidence is equivocal concerning
their use in this manner.
13.1 Creatine Kinase
Skeletal muscle di sruption may be indirectly
asse ssed by level s of circulating creatine kinase.
Such assessments must be differentiated from
Sports Med . 1997 Fe b: 23 (2)
122
studies of severe muscle damage where circulating
activity levels of creatine kinase have approached
34000 IUIL)173] Use of creatine kinase as an indi-
rect marker of muscle disruption, however, has not
been typically monitored in the presence of actual
performance decrements due to overtraining or
overreaching. Greater endurance training volumes
have been associated with muscle disruption as in-
dicated by increased circulating levels of creatine
kinase, although these levels are considerably
lower than observed with muscle damage)9.1 3.14]
When maximal intensity resistance exercise over-
training resulted in decreased IRM,II] the resulting
circulating creatine kinase activity of approxi-
mately 600 IU/L was comparable to levels ob-
served after a typical resistance exercise session)174]
Such creatine kinase levels suggest low degrees of
skeletal muscle disruption, and most likely did not
contribute to the attenuated strength.Ul It remains to
be seen how creatine kinase activity levels respond
in the presence of high volume resistance exercise
overtraining.
13.2 Lactate
Decreased blood lactate responses at a given
work rate have been suggested as a marker of
parasympathetic overtrainiug.I'<' >!"! Lactate re-
sponses to exercise have been shown to either
decrease,19.13.15.23.24] or stay the same[38,42] when
training volumes increase. A decreased acute lac-
tate response has also been observed in the presence
of maximal intensity resistance exercise overtrain-
ing.l!' A problem with using such a physiological
response as a marker of overtraining is that de-
creased acute lactate at the same submaximal exer-
cise intensity is a normal training adaptation for
both endurance and resistance exercise,[175.176]
therefore it is important to determine the exercise
lactate response during maximal efforts.I!" It is
known that muscle glycogen decreases with pro-
longed periods of swimming overtraining, which
may be due in large part to dietary considera-
tions.[49] Such decreased glycogen levels may also
contribute to the lowered lactate response reported
for increased resistance exercise training volumes.
© Ad is lnte rnon onol lirnlted. All righ ts reserved.
Fry & Kraemer
Recent evidence with endurance exercise suggests
that the lactate/ratings of perceived exertion ratio
during maximal endurance exercise is attenuated
with overtraining.U?' but it is not known ifthe same
response occurs with resistance exercise overtrain-
ing. When acute lactic acid decreased with high
intensity resistance exercise overtraining, the total
amount of external work performed (joules) at the
same relative intensity (%IRM) also decreased.I!'
Whether this relationship was causal, however,
could not be determined.
13.3 Ammonia
At rest, ammonia is primarily produced from
dietary protein, and is immediately detoxified to
urea by the liver)177) During exercise, circulating
ammonia is derived primarily as a product from the
skeletal muscle purine nucleotide cycle)I78] It
should be noted, however, that a number of clinical
conditions may contribute to circulating levels of
ammonia.UY' thus making the interpretation of
ammonia levels difficult. Preliminary data indi-
cated that I week of increased resistance exercise
training volume may result in elevated ammonia
levels,[180] but 2 separate follow-up studies have
not supported such a response in highly trained
elite weightlifters)153.1 81] Although skeletal mus-
cle degradation due to overtraining may result in
amino acid deamination and a resulting increase in
circulating ammonia, this has yet to be scientifi-
cally demonstrated.
14. Conclusions
Much of the scientific data available on
resistance exercise overtraining have been extra-
polated from scenarios where actual physical per-
formances have not been adversely affected or
have been recovered from in a matter of several
days.[22-24.26,27,8I,119] As such, these data demon-
strate what may occur during phases of stressful
training or short term overtraining, called over-
reaching. Few scientific data are available on ac-
tual cases of decreased performances due to over-
training , Descriptive or cross-sectional data are
available for endurance types of activity,[44,83) and
Spo rts Moo. 1997 Fe b : 23 (2)
Resistance Exercise Overtraining 123

longitudinal studies have been performed for

highly aerobic trainingP-Il,43 1In the area of highly High Typical High
training overtraining training
anaerobic exercise, suggested signs and symptoms volume scenario Intensity
of overtraining have been derived from either over- Combination of
Sets x %
training with highly aerobic activities or from em- reps excessive Repetition
training volume maximum
pirical reports from coaches and athletes. Little Total
and intensity
scientifically obtained longitudinal data are avail- training

able on the physiological responses to performance

sessions
Low I Low

decrements due to resistance exercise overtrain-
ing.[1,46-481 Although the phenomenon of over-
training appears to be a relatively common prob-
lem among coaches and athletes, 120,23) overtraining
is extremely difficult to elicit in a controlled
scientific setting for either endurancel" 10,43] or re-
sistancell .22-251 exercise. A confounding factor is
the semantics of terminology in the area of over-
training. Numerou s reviews and articles have been
written that have used a confusing mixture of ter-
minology and definitions as to what actually con-
stitutes overtraining. This confusion has led to
compilations of suggested definitions,l33,1201 Al-
though stressful training of any type produces
many physiological responses, overtraining occurs
only when actual physical performances are ad-
versely affected and cannot be reversed without
long term rest and recovery.
A critical finding of the literature cited in the
present review is that there are differences in the
physiological responses to anaerobic and aerobic
overtraining. As such, many ofthe signs and symp-
toms of overtraining that have been suggested by
overtraining with highly aerobic activitiesI8.28,381
(see table II) do not necessarily apply to resistance
exercise overtraining. Although this has been pre-
viously suggested,11 8,33 1 it is only now becoming
evident from scientific investigation, and must be
considered when comparing other types of over-
training with high intensity resistance exercise
overtraining. To compound this problem, different
resistance exercise training protocols produce a
variety of neuroendocrine responses .153,54,58.59,118]
The net result, with regards neuroendocrines, is
that there appear to be different aetiologies of
overtraining for high volumes and high relative
intensities of resistance exercise overtraining. Al-
I
training training
intensity volume
High volume, Low volume,
low intensity .4--------.. high intensity
overtraining overtraining
Fig. 2. Contributions of relative resistance exercise training in-
tensity (% repetition maximum) and training volume (sets x rep-
etitions) resulting in overtraining/overreaching.
though typical resistance exercise training proto-
cols usually include various combinations of high
volumes (sets x repetitions) and high relative in-
tensities (%RM), most scientific studies have fo-
cused on one extreme or the other (see fig. 2). From
an investigator's perspective, such an approach is
necessary. To completely understand the develop-
ment of resistance exercise overtraining, each of
the contributing factors (i.e. training volume and
intensity) must be studied in isolation. Only then
can the entire picture involving all the contributing
factors be elucidated.
At this point, it can be clearly seen that dis-
tinctly different physiological responses occur for
resistance exercise overtraining due to increased
training volume and increased training intensity
(fig. 3). With increased resistance exercise training
volumes, many of the neuroendocrine responses
are somewhat similar to those observed with en-
durance exercise overtraining or overreaching
(compare table I and fig. 3). However, when rela-
tive resistance training intensity is increased, a
very different neuroendocrine response exists.
The net result is that many of the classical neuro-
endocrine markers for overtraining are not appro-
priate for identifying high intensity resistance
exercise overtraining. It has been suggested that
endurance (i.e. highly aerobic) activities may

© Adis International Umited. All rightsreserved. Sports Med. 1997 Feb; 23(2)
 124 Fry & Kraemer

Resistance exerc ise tation s to heavy resistance exerci se (i.e. >70 %

overtrain ing/overreaching

I \
lRM ) include a complex interaction between the
neuromuscular and neuroendocrine systems of the
body.l53.54.135.1521Each ofthese systems depends in
Increased Increased
training volume training int ensity part on the other for optimal adaptation. Likewise,
the development of an overtraining syndrome in-
Testosterone J. Rest and acute No change or slight i
rest and acute cludes many interactions between the neuro-
muscular and neuroendocrine systems.
luteinising Unknown No change (?)
hormone From a practical standpoint, what are the train-
ing implications of these neuroendocrine responses
Cortisol TRest and acute No change or slight J. to overtraining? How can the coach, athlete, or re-
rest and acute
creationallifter avoid the dreaded phenomenon of
ACTH Unknown No change (?) overtraining? It is well known that changes in the
training stresses will influence the neuroendocrine
Testosterone/ J. Rest and acute No change environmentp·21.621 The problem centres on the
cortisol ability to adjust the acute resistance exercise train-
Growth hormone No change or No change (?) ing variables (i.e. exercise choice, order, volume,
J. rest and acute
resistance or load, and rest)[501 in a manner that
Adrenaline Unknown t Acute avoids overtraining.
(epinephrine)
Such a training programme requires appropriate
Noradrenaline Unknown t Acute manipulation of these variables resulting in train-
(norepinephrine)
ing periodisation.[50,1 82]This training concept finds
Peptide F Unknown No change its roots in the General Adaptation Syndrome as
propo sed by Selye.[321 By dosing the training
stresses in a variable manner, the athlete can avoid
Creatine kinase Unknown Normal training
values long term disruption of the body' s homeosta-
sis,l35,1 83) Short term stressful training (i.e. over-
lactate I Acute J. Acute
reaching ) is sometimes desirabl e provided the
No change or
training stresses are properly prescribed(fig, I). It is
Ammonia Unknown
slight Trest the responsibility of the coach to make sure exces-
sive training stresses are not applied to the athlete,
Fig. 3. Comparison of endocrine and blood-borne variable re-
thus ensuring the avoidance of overtraining.Uf Fu-
sponses to resistan ce exerci se overtraining and overreaching
(rest = resting hormo nal concentrations; acute =
ho rmo nal ture research will continue to shed light on the nu-
concentrations in resp onse to a resistance exer cise stimulus). merous and comple x physiological mechanisms
=
Abbreviation and symbols: ACTH ad renocorticotrophic hor-
contributing to resistance exercise performance
=
mone ; (?) data difficult to interpret because of the pulsatility of
=
the respective hormones; l' increase; .J, decrease. = decrements due to overtraining.

produce overtraining dominated by parasympa- References

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