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In this work, whether a two-bout exercise protocol can be used to make an objective, immediately available distinction between non-functional over reaching (NFO) and overtraining syndrome (OTS) was studied. Underperforming athletes who were diagnosed with the suspicion of NFO or OTS were included in the study. Recovery of the athletes was monitored by a sports physician to retrospectively distinguish NFO from OTS. Sports medicine laboratory The protocol was started and completed by 10 underperforming athletes. NFO was retrospectively diagnosed in five athletes, and OTS was diagnosed in five athletes. A two-bout maximal exercise protocol was used to measure physical performance and stressinduced hormonal reactions. Exercise duration, heart rate and blood lactate concentration were measured at the end of both exercise tests. Venous concentrations cortisol, adrenocorticotrophic hormone (ACTH), prolactin and growth hormone were measured both before and after both exercise tests. Maximal blood lactate concentration was lower in OTS compared with NFO, while resting concentrations of cortisol, ACTH and prolactin concentrations were higher. However, sensitivity of these measures was low. The ACTH and prolactin reactions to the second exercise bout were much higher in NFO athletes compared with OTS and showed the highest sensitivity for making the distinction. NFO might be distinguished from OTS based on ACTH and prolactin reactions to a two-bout exercise protocol. This protocol could be a useful tool for diagnosing NFO and OTS; however, more data should be collected before this test can be used as the gold standard.
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The goal in training competitive athletes is to provide training loads
that are effective in improving performance. At some stages during
the training process, athletes may experience an unexplainable de-
crease in performance. This might happen when prolonged exces-
sive training takes place concurrent with other stressors and insuf-
cient recovery. This unexplainable performance decrements can
result in chronic maladaptations that can lead to the overtraining
syndrome (OTS). A keyword in the recognition of OTS might be ‘‘pro-
longed maladaptation’’ not only of the athletic performance but also
of several biological, neurochemical and hormonal regulation mech-
anisms. When athletes deliberately use a short-term period (e.g.
training camp) to increase training load, they can experience short-
term performance decrement, without severe psychological or last-
ing other negative symptoms.1,2 This functional over reaching (FO)
will eventually lead to an improvement in performance after recov-
ery. However, when athletes do not sufciently respect the balance
between training and recovery, non-functional over-reaching (NFO)
can occur.1,2 At this stage, the rst signs and symptoms of prolonged
maladaptation such as performance decrements, psychological dis-
turbance (decreased vigour, increased fatigue) and hormonal distur-
bances are present, and the athlete will need weeks or months to
recover. The distinction between NFO and OTS is very difcult and
will depend on the clinical outcome and exclusion diagnosis.
The recent ‘‘consensus statement’’ of the European College of Sport
Science indicates that the difference between NFO and OTS is the amount
of time needed for performance restoration and not the type or duration
of training stress or degree of impairment.1 In essence, it is generally
thought that symptoms of OTS, such as fatigue, performance decline and
mood disturbances, are more severe than those of NFO. However, there
is no scientic evidence to either conrm or refute this suggestion.1 The
distinction between NFO and OTS is most of the time based on ‘‘time
to recover’’. Hence, there is a need for objective, immediately available
evidence that the athlete is indeed experiencing OTS.
Most of the literature agrees that FO, NFO and OTS must be viewed on
a continuum with a disturbance, an adaptation and nally a maladaptation
of the hypothalamic–pituitary–adrenal axis (HPA), resulting in an altered
Diagnosing overtraining in athletes using the two-bout
exercise protocol*
ABSTRACT
Objective. In this work, whether a two-bout protocol can be used
to make an objective, immediately available distinction between
non-functional over reaching (NFO) and overtraining syndrome
(OTS) was studied.
Design. Underperforming athletes who were diagnosed with the
suspicion of NFO or OTS were included in the study. Recovery
of the athletes was monitored by a sports physician to retrospec-
tively distinguish NFO from OTS.
Setting. Sports medicine laboratory.
Participants. The protocol was started and completed by 10 un-
derperforming athletes. NFO was retrospectively diagnosed in
ve athletes, and OTS was diagnosed in ve athletes.
Interventions. A two-bout maximal exercise protocol was used
to measure physical performance and stress induced hormonal
reactions.
Main outcome measurements. Exercise duration, heart rate and
blood lactate concentration were measured at the end of both ex-
ercise tests. Venous concentrations cortisol, adrenocorticotrophic
hormone (ACTH), prolactin and growth hormone were measured
both before and after both exercise tests.
Results. Maximal blood lactate concentration was lower in OTS
compared with NFO, while resting concentrations of cortisol,
ACTH and prolactin concentrations were higher. However, sen-
sitivity of these measures was low. The ACTH and prolactin re-
actions to the second exercise bout were much higher in NFO
athletes compared with OTS and showed the highest sensitivity
for making the distinction.
Correspondence to:
Romain Meeusen, Department of Human Physiology and Sports
Medicine, Faculty of Physical Education and Physical Therapy,
Vrije Universiteit Brussel, Pleinlaan 2, 1050 Brussels, Belgium;
rmeeusen@vub.ac.be
Accepted 14 July 2008, published online rst 14 August 2008
* This article was reproduced with permission from the BMJ Group.
It was originally published in the British Journal of Sports Medicine
2010;44:642-648.
R Meeusen,1 E Nederhof,1,2 L Buyse,1 B Roelands,1 G de Schutter,1 M F Piacentini3
1Department of Human Physiology and Sports Medicine, Faculty of Physical Education and Physical Therapy, Vrije Universiteit, Brussel,
Brussels, Belgium
2Center for Human Movement Sciences and University Center for Sports, Exercise and Health, University Medical Center Groningen, Univer-
sity of Groningen, Groningen, The Netherlands
3Department of Human Movement and Sports Science, Istituto Universitario di Scienze Motorie, Rome, Italy
EDITOR`S CHOICE
SAJSM VOL 22 NO. 4 2010 99
Conclusions. NFO might be distinguished from OTS based on
ACTH and prolactin reactions to a two-bout exercise protocol.
This protocol could be a useful tool for diagnosing NFO and OTS;
however, more data should be collected before this test can be
used as the gold standard.
hormonal response to intense training and competition.3–12 When
investigating hormonal markers of training adaptation, it is important to
target specic hormones for their information potential and to synchronise
their sampling in accordance with their response patterns.
The hypothalamus is under the control of several ‘‘higher’’ brain
centres and several neurotransmitters13 known to play a major role
in various neuroendocrine and behavioural functions, for example,
activation of the HPA axis, feeding and locomotion.14 Therefore, the
typical HPA axis-related hormones cortisol, adrenocorticotrophic
hormone (ACTH), prolactin (PRL) and human growth hormone (GH)
were targeted in the present study.
It should be emphasised that, depending on the training status,
the time the hormone measurements are taken (diurnal variation),
urinary, blood and salivary measures create a great variation in the
interpretation of the results. In pathological situations such as in major
depression,15,16 post-traumatic stress disorder,17 and probably also
in OTS,10 the glucocorticoids and the brain monoaminergic systems
apparently fail to restrain the HPA response to stress. Indeed, we
recently showed that a test protocol with two consecutive maximal
exercise tests separated by 4 h may give a good indication of the
HPA response to stress in well-trained and FO athletes relative to
a case of OTS.10 We found a suppression of the HPA response
to the second exercise bout in the OTS athlete as opposed to the
TABLE 1 Demographic data and reported symptoms of the patients
Subject 1 2 3 4 5 6 7 8 9 10
Sex Men Women Men Men Men Men Men Men Women Men
Age 18 17 38 36 31 46 21 35 23 22
Height (cm) 188 163 176 189 185 178 185 187 179
Weight (kg) 78.7 39 64 78 67.9 72.5 68.9 74.8 77.3 62.8
Sport Motor
cross
Distance
running
Distance
running
400 m
running
Distance
running
Triathlon Cycling Race
walking
Swim-
ming
Distance
running
Duration
symptoms
before testing
1 year 1 year At least 3
months
At least 2
months
At least
half a year
2–3 months 6 weeks 2 weeks 2 weeks 5 months
Duration re-
covery after
testing
1 year Several
years
>5 years >3 years No full
recovery
1–2 months max 6
months
approx 12
weeks
1 month 3 months
Performance
decrements
Unable to
complete
training
sessions
Unable to
perform
normal
training
because
of dizzi-
ness
Unable to
perform
normal
training
Unable to
perform
normal
training
Unable to
perform
normal
training
HRmax,<150,
dizziness and
dyspnoea
during uphill
cycling
Unable to
complete
races, bad
recovery
from train-
ing
Unable to
complete
normal
training
and races
Dif-
culty with
speed
training
Unable to
complete
normal
training
and worse
race per-
formance
Fatigue Severe Severe Severe Severe Severe Severe Severe Severe
Muscle sore-
ness
Heavy
legs
Heavy and
painful legs
Muscle
soreness
Hamstring
pain
Heavy up-
per legs
Other symp-
toms
Sleeps
11– 12 h
each night
psycho-
logical
problems
Anorexia Psycho-
logical
problems,
depres-
sion
Gets up
frequently
to urinate,
impo-
tence
Sleeping
distur-
bances
Psycho-
logical
problems
Sleeps
14 h per
day
Difculties
getting up,
gained
5 kg in 5
months
Diagnosis OTS OTS OTS OTS OTS NFO NFO NFO NFO NFO
NFO=non-functional overreaching, OTS=overtraining syndrome
100 SAJSM VOL 22 NO. 4 2010
normal responses. The question can be asked if this method is
also a valuable tool to make a distinction between NFO and OTS.
Therefore, we report the results of 10 patients who were referred to
our laboratory with the diagnosis of suspicion of NFO or OTS.
METHODS
Subjects
Ten patients who consulted a sports physician with complaints of
underperformance and fatigue participated in the present study.
The eight men and two women had an average height and weight
of 181±(8) cm and 68.4±(11.8) kg. All subjects were diagnosed by a
sports physician according to the latest guidelines for overtraining
diagnosis.1,18 A careful history including training history was taken,
completed by a physical examination and a blood draw to rule out
other possible causes for the complaints. Patients were diagnosed
as NFO or OTS retrospectively according to the severity of symp-
toms and the total duration of symptoms and underperformance (ie,
both before and after testing) when no medical explanation for the
condition could be found. It turned out that a cutoff of 1-year total
duration gave a good distinction between NFO and OTS patients.
Demographic data and reported symptoms can be found in table 1.
Data of subject 1 are the same as presented in an earlier publica-
tion.10 All subjects signed informed consent before participation.
Protocol
Two incremental graded exercise tests until exhaustion were per-
formed, with 4 h of rest in between. One hour before each test,
the athletes received a standardised meal (2315 kJ, 73% carbo-
hydrate, 19% protein, 8% fat). Athletes arrived in the laboratory at
07:00 after an overnight fast. The rst blood sample was collected
as they arrived. Immediately after the rst exercise test, the second
blood sample was drawn. The third and fourth blood samples were
drawn before and immediately after the second test. A schematic
overview of the protocol can be found in g 1. Because it is known
that venepuncture increases blood prolactin, going back to base-
line within 30 min, blood was drawn before and after each test (four
punctures) creating the same ‘‘stress’’ in each situation. The study
protocol was approved by the university ethical committee.
Exercise testing
Exercise tests were performed on a cycle ergometer (Lode Excalibur
Sport, Groningen, The Netherlands) or on a treadmill (Ergo ELG 55;
Woodway, Weil am Rhein, Germany) depending on the sport. Tests on
the cycle ergometer started with an initial workload of 80 W (subjects 6
and 7) or 30 W (subjects 4 and 9), the workload was increased by 40
W every 3 min. Tests on the treadmill started at 5.4 km h-1, the speed
was increased with 1.8 km h-1 each 3 min (subjects 1, 2, 3, 8 and 10).
One subject performed the treadmill test with an inclination of 1% (sub-
ject 5). The duration of each test was recorded in seconds. Subjects
wore a heart rate monitor (Polar Accurex Plus, Kempele, Finland) for
determination of maximal heart rate (HRmax) throughout the exercise
tests. After each exercise test, 20 ml of blood was drawn from the right
earlobe to determine maximal blood lactate concentration ([La]max)
with enzymatic analysis (EKF; Biosen 5030, Barleben, Germany).
Fig 1. Schematic overview of the protocol.
Figure 2. Exercise duration, maximal heart rate and maximal
blood lactate concentrations during the rst (grey bars) and the
second (black bars) exercise test for the non-functional over-
reached (NFO) group and the overtraining syndrome (OTS)
group. Data are presented as means (SE).
Table 2 Sensitivity for the detection of OTS and NFO
Measure
Cutoff for
OTS OTS (%) NFO (%)
[La]max rst exercise test <8 mmol l-1 80 50
[La]max second exercise
test
<8 mmol l-1 100 67
[Cortisol]rest >175 mg l-1 80 60
[ACTH]rest >40 ng l-1 80 80
[PRL]rest >50 IU l-1 40 100
Cortisol response to second
exercise test
<200%
increase
80 20
ACTH response to second
exercise test
<200%
increase
100 80
PRL response to second
exercise test
<200%
increase
100 100
GH response to second
exercise test
<1000%
increase
40 40
[ACTH]rest, fasted morning adrenocorticotrophic hormone concentration;
[Cortisol]rest, fasted morning cortisol concentration; GH, human growth hormone;
[La]max, maximal blood lactate concentration; [PRL]rest, fasted morning prolactin
concentration.
SAJSM VOL 22 NO. 4 2010 101
102 SAJSM VOL 19 NO. 4 2007
102 SAJSM VOL 22 NO. 4 2010
Blood analysis
Samples were collected in prefrozen 4.5 ml K3 EDTA vacutainer
tubes (Becton Dickinson Vacutainer System Europe, Plymouth,
UK) and immediately centrifuged at 3000 rpm (Minifuge 2, Heraeus,
Germany) for 10 min, and plasma was frozen at -20˚C until further
analysis. Samples were assayed via RIA for cortisol (DiaSorin, Still-
water, Minnesota, USA), ACTH (Nichols Institute Diagnostics, San
Juan Capistrano, California, USA), PRL (Roche Diagnostics, Man-
nheim, Germany) and GH (Pharmacia & Upjohn Diagnostics, Upp-
sala, Sweden).
Hormonal concentrations were expressed both in absolute
(average (SE)) and relative values. For the relative hormone
concentrations, both pre-test values were set at 100%; both post-
test values were calculated by dividing through the pre-test value
and multiplying by 100%.
Data analysis
Data were analysed using three different methods: visual inspec-
tion, parametric statistics and calculation of sensitivity for both OTS
and NFO detection. Because the sample size was rather small (ie,
maximal 5 for each group), data were rst inspected visually. Para-
metric statistics and sensitivity calculation were used to support
conclusions from visual inspection of the data. For the purpose of
visual inspection, we created graphs with averages and SE for both
the OTS and the NFO groups. When visual inspection gave an in-
dication for group differences, parametric statistical analyses were
performed through ANOVA with repeated measures with one within
subjects factor (post-values for rst and second exercise test) and
one between-subjects factor (NFO or OTS) or through an independ-
ent samples t test. Those analyses were performed in SPSS V.15.0.
Sensitivity was also calculated for these variables by dividing the
number of correct OTS or NFO diagnoses by hormonal analysis by
the total number of OTS or NFO diagnoses according to the consen-
sus statement.1 Sensitivity was presented as a ratio. The denomina-
tor varies because of random missing values.
RESULTS
Exercise testing
Exercise duration, HRmax and [La]max are presented in g 2A, B,
and C. Visual inspection of the data led to the conclusion that there
is no difference in exercise duration and HRmax between the OTS
and the NFO patients. For [La]max, a much lower value was found
for the OTS patients in combination with a larger reduction from the
rst to the second test compared with the NFO patients. However,
parametric analysis did not indicate signicant differences. The main
effect of group gave an F ratio of 2.9 for [La]max and an F ratio <1
for exercise duration and HRmax, showing that almost three times
as much variance is explained by the group membership (ie, OTS vs
NFO) compared with random factors. In addition, sensitivity for OTS
detection with [La]max was high (table 2). With a cutoff of 8 mmol
l-1, four out of the ve OTS patients would have been diagnosed
correctly from the rst exercise test and four out of the four OTS
patients from the second exercise test. Sensitivity for NFO diagnosis
was lower, however (table 2). From the rst exercise test, a correct
diagnostic ratio of two out of four was found, for the second test, two
out of three.
Absolute hormone concentrations
In g 3A–D, absolute hormone concentrations are presented for the
NFO and the OTS groups. Visual inspection of the data led to the
conclusion that resting concentrations cortisol, ACTH and PRL were
higher for OTS patients compared with NFO. However, reactions to
exercise tests did not differ between the groups. Resting hormone
concentrations were tested with independent t tests. Only for ACTH,
the t test gave a value >2 (ie, t8= 2.6; p<0.05), meaning that only for
ACTH, the difference between the groups was more than twice as
large as the SE. Sensitivity of resting cortisol, ACTH and PRL was four
out of ve (cutoff 175 mg l-1), four out of ve (cutoff 40 ng l-1) and two
out of ve (cutoff 50 IU l-1), respectively (table 2). Sensitivity for detec-
tion of NFO was three out of ve, four out of ve and three out of ve
respectively for cortisol, ACTH and PRL, respectively (table 2).
Relative hormone concentrations
Hormonal responses to the two exercise bouts are presented in g
4A–D. Visual inspection led to the conclusion that there are no dif-
ferences in relative cortisol response between the NFO and the OTS
group. ACTH, PRL and GH responses are higher in the NFO group
compared with the OTS group, especially in the second exercise
bout. However, the SE of GH in the NFO group was probably too
large to draw clear conclusions. Indeed, the main effect of group
gave an F ratio of F1,7=1.4 for GH. For ACTH and PRL, F ratios were
F1,7=5.1 and F1,6=14.7, both signicant at p<0.05, conrming larger
responses for the NFO group. Visual inspection led to the conclusion
that this larger response was much more pronounced after the sec-
Figure 3. Cortisol, adrenocorticotrophic hormone (ACTH), pro-
lactin (PRL) and growth hormone (GH) concentrations before
and after the two exercise bouts for the NFO group (solid lines)
and the OTS group (dashed lines). Data are presented as mean
(SE).
Figure 4. Cortisol, ACTH, PRL and GH responses to the two ex-
ercise tests for the non-functional over-reached (NFO) group
(solid lines) and the OTS group (dashed lines). Data are pre-
sented as percentage increase from both baseline values (SE)
of the mean.
SAJSM VOL 22 NO. 4 2010 103
ond exercise bout. Indeed, parametric results pointed in the direction
of an interaction effect between test and group for ACTH and PRL
(F1,7=4.1; p=0.084; F1,6=4.0; p=0.092).
Sensitivity of ACTH and PRL for the detection of OTS was four
out of four and ve out of ve, respectively (table 2; cutoff, 200%
at the second exercise test) and for the detection of NFO was four
out of ve and three out of three, respectively. Sensitivity of cortisol
(cutoff, 200% at the second test) and GH (cutoff, 1000%) for the
detection of OTS was four out of ve and two out of ve, and for the
detection of NFO, one out of ve and two out of four, respectively
(table 2).
DISCUSSION
Results of the present study show that ACTH and PRL responses
to a double maximal exercise bout are sensitive for the diagnosis of
OTS and NFO. Cortisol and GH responses were much less sensitive
measures as were resting hormone concentrations. Maximal lactate
concentrations at both exercise tests showed a high sensitivity for
the detection of OTS, but almost half of the NFO patients did not
reach [La]max of 8 mmol l-1 either.
Subjects
One of the difculties in diagnosing OTS is that this should be based
on ‘‘exclusion criteria’’.1,18 Although, in recent years, the knowledge
of central pathomechanisms of the OTS has signicantly increased,
there is still a strong demand for relevant tools for the early diagnosis
of OTS. By calculating sensitivity for detection of NFO and OTS, a
good indication of the value of the different measures for the diagno-
sis of unexplainable underperformance is obtained (table 2).
Ten patients were referred to the laboratory with a possible
diagnosis of having OTS. Based on the criteria used in the consensus
statement of the ECSS,1 the decision was made to perform a double
maximum test with these athletes. One of the criteria to dene an
athlete as OTS is that recovery from the status will take months, or
even years.1,2 In the present study, an arbitrary cutoff of 1 year was
used. Those patients who needed more than 1 year for recovery
were retrospectively diagnosed with OTS, the others with NFO.
There seemed to be a good distinction between the patient groups
based on this criterion, as the OTS patient with the shortest recovery
time (1) experienced underperformance and other symptoms for
2 years, whereas the NFO patient with the longest recovery time
(10) had NFO for 8 months. In addition, although subjective, there
seemed to be a good parallel with the severity of the symptoms.
Lactate
One almost overall nding, at least in endurance and strength-
endurance athletes having OTS, is a diminished maximal lactate
concentration, whereas submaximal values remain unchanged or
slightly reduced.10,12 This is conrmed in the present study where
OTS patients did not reach maximal lactate concentrations above 8
mmol l-1. Two out of the four NFO patients did not reach [La]max of 8
mmol l-1 at the rst exercise test either (for one patient [La]max was
missing). Thus, although low [La]max has frequently been described
as a diagnostic marker for OTS, from these results, it does not seem
sensitive enough to distinguish OTS from NFO.
Absolute hormone concentrations
Resting hormone concentrations have been a topic of many stud-
ies and discussions. It has been suggested that conicting results
were, at least partly, because of a lack of standardization in both the
way overtraining was measured and in the hormone measurement
protocols used. Results from the present study show that variability
in resting hormone concentrations is also present within groups of
NFO and OTS patients. The arguments for contradictory ndings are
not valid within this study where blood was drawn at the same time
of day always after an overnight fast. However, the diurnal varia-
tion in cortisol cannot be ruled out with this protocol because tests
are separated by 4 h. However, each test was done with the same
protocol and timing so that the data were collected in a standardised
manner. One possible reason why the cortisol levels do not show the
same pattern as ACTH might be because of this diurnal variation.
Therefore, it must be concluded that resting hormone concentrations
are not sensitive enough, at least not to diagnose unexplained un-
derperformance in athletes. It has been suggested that hormonal
reactions to stress tests are more sensitive.1,11
The symptoms associated with OTS, such as changes in emotional
behaviour, prolonged feelings of fatigue, sleep disturbances and
hormonal dysfunctions are indicative of changes in the regulation
and coordinative function of the hypothalamus.8,19 Previous
studies have shown different results for stress-induced hormonal
responses.6,20,21 Results from a previous study10 and the present
study show that contradictory ndings cannot solely be explained by
different measurement methods and/or denitions used. From gs 3
and 4, it is clear that hormonal responses to one single exercise bout
are not sensitive enough to distinguish NFO from OTS.
Relative hormone concentrations
The only measures that accurately distinguished NFO from OTS
were increases in ACTH and PRL concentrations after a second
maximal exercise bout. The OTS athletes showed a very small or
no increase in ACTH and PRL concentrations after the second exer-
cise bout; the NFO athletes showed very large increases. This is a
conrmation of our previous studies with this protocol.10 ,22 The use
of two bouts of maximal exercise to study neuroendocrine variations
showed an adapted exercise-induced increase of ACTH, PRL and
GH to a two-exercise bout.10
The fact that GH did not perform as well as both other pituitary
hormones in the present study could be the result of the large inter-
individual variation in the NFO group. One of the NFO athletes had
a very low resting value before the second exercise test and showed
an increase of 12 000%. Cortisol concentrations after the second
exercise test seem also quite good markers for OTS but poor when
it comes to distinguish NFO from OTS. Although almost all OTS
athletes showed a reduced increase in the response of cortisol to
the second exercise bout, almost none of the NFO athletes showed
an overshoot (table 2). This result is similar to earlier ndings.10,22
In an earlier study, we found that in order to detect signs of OTS
and distinguish them from normal training responses or FO, this
method may be a good indicator not only of the recovery capacity
of the athlete but also of the ability to normally perform the second
bout of exercise.10 The test could, therefore, be used as an indirect
measure of hypothalamic– pituitary capacity. It was hypothesised
that on the NFO–OTS continuum, a hypersensitivity of the pituitary
is followed by an insensitivity or exhaustion afterwards.10,22 Results
from the present study conrm this hypothesis. The NFO athletes
showed a very high response to the second exercise bout, at least in
ACTH and PRL, whereas the OTS athletes showed suppression.
There are two other studies that have measured prolactin in
relation to overtraining. Lehmann et al23 showed that an increase
in training volume, rather than intensity, led to more symptoms
associated with overtraining. They also observed a close-to-
signicant exercise-induced decrease in plasma prolactin in the
104 SAJSM VOL 22 NO. 4 2010
increased intensity group but no change because of increased
volume. Budgett et al24 observed a more marked plasma prolactin
response to a neuroendocrine challenge in athletes with unexplained
underperformance syndrome. They also observed a higher resting
plasma prolactin in unexplained underperformance syndrome
athletes than healthy controls. These authors also state that prolactin
could prove useful in monitoring the individual response to training
and recovery.
Behind the seemingly uniform acute hormonal response to
exercise, explaining the disturbance to the neuroendocrine system
caused by OTS is not that simple. There are several similarities with
other intensive and chronic stress situations. There is compelling
evidence for the involvement of HPA axis abnormalities in chronic
stress situations such as post-traumatic stress disorder17 and
depression25 and probably also during NFO and OTS. In chronic
stress situations, the number of ACTH and cortisol secretion pulses
is increased, which is also reected in elevated urinary cortisol
production.25
Chronic stress and the subsequent chronic peripheral
glucocorticoid secretion plays an important role in the desensitisation
of higher brain centre response during acute stressors because it
has been shown that in acute (and also chronic) immobilisation, the
responsiveness of hypothalamic corticotrophin-releasing hormone
(CRH) neurons rapidly falls.26 These adaptation mechanisms
could be the consequence of changes in neurotransmitter release,
depletion of CRH and/or desensitisation of hypothalamic hormonal
release to afferent neurotransmitter input.26 Indeed, concentrations
of CRH are elevated, the number of CRH-secreting neurons in the
limbic brain regions is increased and the number of CRH binding
sites in the frontal cortex is reduced secondary to increased CRH
concentrations following chronic stress.25
Another very important brain area that mediates, and in
turn is affected by the stress response, is the hippocampus.27
The consequences of impaired regulation of cortisol secretion
are manifold, ranging from effects in peripheral tissues (eg,
osteoporosis) to changes in the central nervous system.28 Most of
the effects seen in chronic stress situations can be explained by
the occupation of the two glucocorticoid receptors in the brain. In
normal situations, the mineralocorticoid receptor will be occupied,
whereas the glucocorticoid receptor has lower afnity for the natural
ligand corticosterone (cortisol) than the mineralocorticoid receptor
and is extensively activated only after stress and at the peaks of
the circadian rhythm. One of the main functions of glucocorticoid
receptors is to normalise brain activity some hours after an organism
has been exposed to a stressful event and to promote consolidation
of the event for future use.25,28 To this purpose, corticosteroids feed
back in precisely those circuits that are initially activated by the
stressor and are enriched in glucocorticoid receptors: limbic forebrain
neurons and the paraventricular nucleus of the hypothalamus.
When stress is chronically induced, as in NFO and OTS, two
specic mechanisms could occur: rst, when corticosteroid levels are
chronically too high, a hypersensitivity of the receptors will occur, this
can lead to a disinhibition of CRH producing neurons, which in turn
will lead to an intensied release of ACTH (as seen in the second
exercise bout in the NFO athletes). When the chronic stress situation
continues and glucocorticoid receptors are chronically activated
(which occurs in post-traumatic stress disorder17 and depression),25
a blunted ACTH response to CRH will occur.28
From the data mentioned previously, it can be concluded that
in NFO and OTS, the neuroendocrine disorder is a hypothalamic
dysfunction rather than a malfunction of the peripheral hormonal
organs29 and that the distinction between NFO and OTS can be
characterised by hypersensitivity versus insensitivity of glucocorticoid
receptors. The interactive features of the periphery and the brain
could be translated into possible immunological, psychological and
endocrinological disturbances.
Competing interests: None.
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What is already known on this topic
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What this study adds
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... The two-bout exercise protocol (Meeusen et al., 2004;2010) might help to distinguish FOR from NFOR/OTS (Kreher, 2016) based on hypothalamic-pituitary-adrenal axis (HPA) dysfunction (Meeusen et al., 2010). The protocol involves two graded exercise tests to exhaustion with a 4-hour rest between bouts (Meeusen et al., 2008), and involves measures of adrenocorticotropic hormone (ACTH) and prolactin (PRL), measured at four time points: baseline, immediately after completion of the first test, prior to the second test, and immediately after the second test. ...
... The two-bout exercise protocol (Meeusen et al., 2004;2010) might help to distinguish FOR from NFOR/OTS (Kreher, 2016) based on hypothalamic-pituitary-adrenal axis (HPA) dysfunction (Meeusen et al., 2010). The protocol involves two graded exercise tests to exhaustion with a 4-hour rest between bouts (Meeusen et al., 2008), and involves measures of adrenocorticotropic hormone (ACTH) and prolactin (PRL), measured at four time points: baseline, immediately after completion of the first test, prior to the second test, and immediately after the second test. ...
... The protocol involves two graded exercise tests to exhaustion with a 4-hour rest between bouts (Meeusen et al., 2008), and involves measures of adrenocorticotropic hormone (ACTH) and prolactin (PRL), measured at four time points: baseline, immediately after completion of the first test, prior to the second test, and immediately after the second test. Statistically significantly increased ACTH and prolactin concentrations in NFOR appear to differentiate between athletes with OTS (Meeusen et al., 2010), however, further studies are required to establish valid and reliable boundaries (Cadegiani et al., 2017a). ...
Chapter
Careful programming and manipulation of training and recovery are required for optimal performance. Functional overreaching (FOR) occurs after well-timed periods of relatively large training loads and adequate restoration. However, excessive training loads and insufficient recovery can result in non-functional overreaching (NFOR) or the overtraining syndrome (OTS). FOR: Short-term reduction in performance lasting several days to weeks with subsequent performance improvement after a period of recovery. NFOR: Performance decrease is observed over a period of several weeks to months with no subsequent performance improvement. OTS: Long-term maladaptation resulting in reduced performance capacity observed over a period of several weeks, months or years with no subsequent performance improvement. (Definitions taken from Halson and Jeukendrup, 2004; Meeusen et al., 2013) A robust, multifactorial testing battery is recommended to identify potential deleterious effects on training and performance. At the time of writing there is no single-standard test to guide decision making; practitioners should therefore develop an individualised battery of assessments based on the needs analysis of the sport and the individual athlete. We specifically suggest a combination of objective performance metrics and physiological responses to fixed-intensity exercise, alongside psychophysiological, subjective responses to evaluate the risk of long-term performance decline and maladaptation caused by NFOR/OTS. For a more general consideration of athlete wellbeing, see Chapter 15.2.
... Second, basal plasma stress hormone levels (i.e., cortisol, norepinephrine, and epinephrine) likely will not reliably distinguish athletes with OTS from healthy individuals (Cadegiani and Kater, 2017). Thus, measuring stress hormone levels during exercise may be a valid and more revealing approach (Meeusen et al., 2010;Meeusen et al., 2013). Third, few of the neuroendocrine assessments of athletes with OTS have involved validated and widely recognized standardized tests that are endorsed by professional endocrinology societies. ...
... (2000); Reichenberg et al. (2001);Leonard. (2006) Wittert (1996); Armstrong and VanHeest (2002); Meeusen et al. (2010); Cadegiani and Kater (2020) (Epstein, 1997;Leonard, 2006;Zunszain et al., 2011;Hughes et al., 2016) Resolution requires weeks or months of rest (OTS and MD) a chronic stress may result in increased glucocorticoid secretion at rest, delayed reduction/termination of the stress response, facilitated or sensitized responses to novel stressors, or hyporesponsiveness in extreme cases (Siever et al., 1986;Herman, 2013;Jacobson, 2014). Abbreviations, HPA, hypothalamic-pituitary-adrenal axis; SAM, sympathetic-adrenalmedullary axis; ACTH, adrenocorticotrophic hormone Frontiers in Network Physiology | www.frontiersin.org ...
... The 2013 joint consensus statement of the European College of Nutrition and the American College of Sports Medicine (Meeusen et al., 2013) noted that the fatigue and underperformance associated with nonfunctional overreaching (Figure 1) can be attributed, at least in part, to a low muscle glycogen concentration. This document also noted that 1) chronic energy deficiency and glycogen depletion amplify stress hormone (cortisol, norepinephrine/noradrenaline, epinephrine/adrenaline; Figure 2) and cytokine responses to exercise and may be determinants of emerging OTS, and 2) dietary carbohydrate supplementation may reverse the symptoms of nonfunctional overreaching (Meeusen et al., 2010). These two theoretical concepts were supported by research that reported reduced signs, symptoms, and performance decrements in runners who consumed a higher amount of carbohydrate for 7 days (5.4-8.5 g/kg body mass) during two iterations of strenuous training (Achten et al., 2004). ...
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The phenomenon of reduced athletic performance following sustained, intense training (Overtraining Syndrome, and OTS) was first recognized more than 90 years ago. Although hundreds of scientific publications have focused on OTS, a definitive diagnosis, reliable biomarkers, and effective treatments remain unknown. The present review considers existing models of OTS, acknowledges the individualized and sport-specific nature of signs/symptoms, describes potential interacting predisposing factors, and proposes that OTS will be most effectively characterized and evaluated via the underlying complex biological systems. Complex systems in nature are not aptly characterized or successfully analyzed using the classic scientific method (i.e., simplifying complex problems into single variables in a search for cause-and-effect) because they result from myriad (often non-linear) concomitant interactions of multiple determinants. Thus, this review 1) proposes that OTS be viewed from the perspectives of complex systems and network physiology, 2) advocates for and recommends that techniques such as trans-omic analyses and machine learning be widely employed, and 3) proposes evidence-based areas for future OTS investigations, including concomitant multi-domain analyses incorporating brain neural networks, dysfunction of hypothalamic-pituitary-adrenal responses to training stress, the intestinal microbiota, immune factors, and low energy availability. Such an inclusive and modern approach will measurably help in prevention and management of OTS.
... Stages of effort, overreaching and overtraining (32). Table 2 Neurobiological basis: Overtraining, Hypothalamus-Pituitary-Adrenocortical (HPA) Axis, Depression and Immune System Several pathophysiological pathways have been studied in the context of OTS (38). ...
... A connection between overtraining and symptoms of depression could also be traced to neurobiological factors (5). The regulation of stress hormones plays a role in both overtraining and depression (32). This is caused by dysregulation of the hypothalamus-pituitary-adrenocortical (HPA) axis, the body's major stress hormone system. ...
Article
Overtraining is characterized by a mismatch between exerted strain and exercise tolerance. Overtraining is generally not sufficiently feared nor is enough attention paid to its prevention. As a result, the first warning signals and symptoms are often either perceived too late or there is a delay in the correct interpretation of signs. This often leads to negative consequences over months, which, in turn, can lead to more frequent injuries as well as Depression. Due to the increasing professionalism and density of competition in competitive sports, overtraining occurs more frequently as athletes are left with a shorter period of time to recover. In order to treat overtraining, it is first necessary to identify the syndrome. Symptoms are often disregarded and trainers and athletes attempt to compensate for poor performance with excessive training. This leads to a vicious cycle with significant reduction of the overall performance of the athlete as a consequence. Psychological parameters can also be signs of non-func-tional overload. Examples include restlessness, irritability, emotional instability, recurring states of fear, emerging indifference or reduced performance motivation. However, disturbed cognitive processes as an impairment of central elements of movement control can also occur. As part of sports psychiatric support, conspicuous psychological parameters can be recorded and contextualised. The Synergetic Navigation System (SNS) is available for systematic recording and corresponding process management. The Synergetic Navigation System (SNS) can be used as an instrument for load, training and competition control to prevent non-functional overload and overtraining. It is also suitable for promoting performance and preventing injuries as well as stabilizing the psychological structure. Key Words: Mental Health Symptoms, Mental Disorders, Injury Prevention, Exercise Intolerance, Synergetic Navigation System (SNS)
... Our results support this conjecture as both SFMS-Q and training logs scores showed significant changes from pre-to mid-season whereas, no significant changes were demonstrated in cortisol levels during the same time. As it has already been pointed out, the difficulty in distinguishing NFOR from OTS is a pivotal challenge facing athletes and coaches [3,9,[31][32][33]. Recently, Sghir et al. stated that there is a significant relationship between overtraining, as measured by SFMS-Q, and factors such as level of practice, the number of hours of training outside the main discipline, the history of injury or illness over the past six months, the notion of an altitude training, and menstrual disorder in more than 150 athletes of team and individual sports from both sexes [4]. ...
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Objectives This study aimed to investigate the changes in subjective and objective variables related to the overtraining syndrome and correlation between these variables during a full season of female soccer league. Methods Twelve female soccer players voluntarily participated in this study. In a longitudinal study design, cortisol concentrations and scores of the Société Française de Médicine du Sport questionnaire were measured at pre-, mid-, and post-season. In addition, resting heart rate, length of sleep and scores of Likert-type training logs including quality of sleep, tiredness sensation, training willingness, appetite, competitive willingness, and muscle soreness were recorded during seven consecutive days at pre-, mid-, and post-season. Results The results showed a significant increase in cortisol levels from pre- to post-season (P = 0.009). A significant increment was also seen in scores of the SFMS questionnaire from pre- to mid-season (P = 0.009), mid- to post-season (P = 0.0001), and pre- to post-season (P = 0.0001). The SFMS-Q scores were 7.58, 10.8, and 21.08, at pre-, mid-, and post-season respectively. Likewise, the resting heart rate demonstrated a significant surge from pre- to mid-season (P = 0.006), mid- to post-season (P = 0.0001), and pre- to post-season (P = 0.0001). Moreover, the scores of all the Likert-type training logs were significantly decreased from pre- to post-season (P < 0.05). Conclusion These results indicate a shift towards overtraining syndrome on the training-overtraining continuum in female soccer players during a full season. Besides, these findings accentuate the importance of concomitant use of both subjective and objective measures of the overtraining syndrome and that a longitudinal approach is essential to gain an accurate estimation of athletes’ status in response to any alterations in the training load.
... Another possible and direct reason may be that central fatigue has been suggested to be related to neurotransmitters such as serotonin and dopamine (Dobryakova et al., 2015). In previous studies, dopamine has been shown to increase during exhausting exercise (Fisher et al., 2004;Petzinger et al., 2007), and a reduced level of dopamine was reported in fatigued rats (Meeusen et al., 2010). In addition, Petzinger et al. have shown that exercise may influence activity-dependent processes in the basal ganglia through alterations in dopaminergic neurotransmission and have demonstrated that exercise-induced behavioral benefits may be due to changes in cortical hyper-excitability normally observed in the dopaminedepleted state (Petzinger et al., 2010). ...
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The strength of lower extremity is important for individuals to maintain balance and ambulation functions. The previous studies showed that individuals with Parkinson's disease suffered from fatigue and strength loss of central origin. The purpose of this study was to investigate the effect of lower extremities' cycling training on different components of force and fatigue in individuals with Parkinson's disease. Twenty-four individuals (13 males, 11 females, mean age: 60.58 ± 8.21 years) diagnosed with idiopathic Parkinson's disease were randomized into training and control groups. The maximum voluntary contraction (MVC) force, voluntary activation level (VA), and twitch force of knee extensors were measured using a custom-made system with surface electrical stimulation. The general, central, and peripheral fatigue indexes (GFI, CFI, and PFI) were calculated after a fatiguing cycling protocol. Subjects received 8 weeks of low resistance cycling training (training group) or self-stretching (control group) programs. Results showed that MVC, VA, and twitch force improved (p < 0.05) only in the training group. Compared to the baseline, central fatigue significantly improved in the training group, whereas peripheral fatigue showed no significant difference in two groups. The cycling training was beneficial for individuals with Parkinson's disease not only in muscle strengthening but also in central fatigue alleviation. Further in-depth investigation is required to confirm the effect of training and its mechanism on central fatigue.
... When training is prolonged and leads to excessive strain on athletes, it can lead to inadequate recovery and a reduction in the positive physiological adaptations of training, which can further lead to overtraining and performance decrements. 17,18 While coaches expressed a desire to assess their athletes' workloads, it is important to note that challenges currently exist regarding the most effective methods for assessing athlete workload. Heart rate has historically been the most commonly used outcome for evaluating internal training loads 19,20 but heart rate monitoring has limitations during weight, interval, intermittent, and plyometric training. ...
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Workload plays important roles in sports-related injury and athletic performance by influencing exposure to external injury risk factors and potential events, promoting changes in fitness level, which involves positive adaptations to training that may lead to improved performance, and/or stimulating fatigue which leads to negative effects in the body that may increase the risk of injury and negatively affect performance. In addition to the physical stress and significant time required for practice and training, student athletes also face subjective stressors. The total workload affects injury risk, but acute changes or spikes in external and/or internal loads seem to affect injury risk the most. These also may lead to poor recovery practices that may affect physical and academic performance. It is important for the medical team, coaches, parents, and the student athlete to understand the vulnerability of this population to increased amounts of workload and its positive and negative effects.
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Successful training must involve overload but also must avoid the combination of excessive overload plus inadequate recovery. Athletes can experience short term performance decrement, without severe psychological, or lasting other negative symptoms. This Functional Overreaching (FOR) will eventually lead to an improvement in performance after recovery. When athletes do not sufficiently respect the balance between training and recovery, Non-Functional Overreaching (NFOR) can occur. The distinction between NFOR and the Overtraining Syndrome (OTS) is very difficult and will depend on the clinical outcome and exclusion diagnosis. The athlete will often show the same clinical, hormonal and other signs and symptoms. A keyword in the recognition of OTS might be ‘prolonged maladaptation' not only of the athlete, but also of several biological, neurochemical, and hormonal regulation mechanisms. It is generally thought that symptoms of OTS, such as fatigue, performance decline, and mood disturbances, are more severe than those of NFOR. However, there is no scientific evidence to either confirm or refute this suggestion. One approach to understanding the aetiology of OTS involves the exclusion of organic diseases or infections and factors such as dietary caloric restriction (negative energy balance) and insufficient carbohydrate and/or protein intake, iron deficiency, magnesium deficiency, allergies, etc. together with identification of initiating events or triggers. In this paper we provide the recent status of possible markers for the detection of OTS. Currently several markers (hormones, performance tests, psychological tests, biochemical and immune markers) are used, but none of them meets all criteria to make its use generally accepted. We propose a “check list” that might help the physicians and sport scientists to decide on the diagnosis of OTS and to exclude other possible causes of underperformance.
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Overtraining syndrome is a serious problem marked by decreased performance, increased fatigue, persistent muscle soreness, mood disturbances, and feeling 'burnt out' or 'stale.' The diagnosis of overtraining is usually complicated, there are no exact diagnostic criteria, and physicians must rule out other diseases before the diagnosis can be made. An orthostatic challenge shows promise as a diagnostic tool, but the subjective feelings of the patient remain one of the most reliable early warning signs. Prevention is still the best treatment, and certain subjective and objective parameters can be used by athletes and their trainers to prevent overtraining. Further studies are needed to find a reliable diagnostic test and determine if proposed aids to speed recovery will be effective.
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Persistant psycho-physical performance incompetence can be understood as ultimative, negative feedback regulation to prevent profound destruction. Chronic overload causes a sports-specific, individually different pattern of metabolic, non-metabolic, hormonal, immunological, and neuronal error signals and their integration / coordination in the hypothalamic neuronal network. Consequences can consist of an inhibition of efferent ergotropic sympathoneuronal, -adrenal, thyrotropic, somatotropic, gonadotropic, and neuronal axes. The adrenocorticotropic axis seems to be hiphasically regulated with increased ACTH release in an early state and blunted release in an advanced state of overload. A reduction in beta-adrenergic, neuromuscular, myofibrillar, and energetic capacities of skeletal muscles can precede or parallel the down-regulation of axes. This can in part be understood as steroid myopathy dependent on excess cortisol release during exhaustive, prolonged exercise. Under conditions of severe metabolic load, a significant decrease in circulating fat tissue hormone leptin was observed. This may represent a significant hormonal error signal which signals the brain a negative triglyceride balance dependent on prolonged β 3 adrenoreceptor stimulation. An increase in circulating leptin is again observed during sufficient regeneration periods. Leptin deficiency is, among others, coupled to increased hypothalamic neuropeptide y activity and inhibition of neuro-endocrine axes except for the adrenocorticotropic axis in an early overload state. Inhibition of gonadotropic axis, supplementary also of thyrotropic and somatotropic axes, and exercise-dependent excess cortisol release compromizes spermatogenesis and results in decreased release of Sertoli cell hormone inhibin B, (Granulosa cell hormone in women; selective inhibition of FSH release), as additionally shown in overloaded elite athletes. An increase of inhibin B was also seen during regeneration. Leptin and inhibin B represent an afferentendocrine part of a regulation loop between peripheral tissues and hypothalamus, the highest coordination and integration center of the organism.
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reexamines the norepinephrine hypothesis advanced as an explanation for the reductions in depression and anxiety reported by humans following physical activity / provide an overview of past and present views of how norepinephrine modulates brain–behavior relationships that are important for depression and anxiety / summarize studies of the effects of exercise on norepinephrine within the context of brain–behavior integration / suggest some areas where research is especially needed (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Chapter
From a physiological standpoint, exercise can impose a significant amount of stress on an organism. Muscular activity requires coordinated integration of many physiological and biochemical systems. Such integration is possible only if the body’s various tissues and systems can communicate with each other. The nervous system is responsible for most of this communication through central command and peripheral adjustments. Regular exercise or training will result in better performance, however this ‘challenge of homeostasis’ can lead to an disturbed balance between training and recovery. This stress is counteracted by several adaptive and regulation mechanisms. The physiological responses to any disturbance of the body’s equilibrium and its ‘feed-forward’and ‘feed-back’ from and to the brain is primarily the responsibility of the endocrine system . The endocrine and nervous system work in concert to initiate and control movement and all physiological processes it involves. When all facets of the central nervous and neuroendocrine system are performing in harmony, the ability to coordinate and regulate key physiological and metabolic functions, under the perturbations imposed by physical exercise, is quite remarkable. To date, relatively little attention has been placed on the role of the central nervous system in overtraining and fatigue during exercise and training. This chapter will focus on the possible involvement of the central nervous system in the onset of fatigue during exercise and the role of neurotransmitters and neuromodulators in possible mechanisms that underlie overtraining.
Chapter
Definition, types, symptoms, findings, underlying mechanisms, and frequency of overtraining and overtraining syndrome have been described in an introductory article to the present volume. During the past 10 years, our increasing knowledge in this field has also been discussed in different original and review articles well as presented at the 1996 Memphis Overtraining and Overreaching in Sports Conference and summarized in a book project. Aim of this present overview, which was presented during the 1997 Reisensburg Castle workshop, is an additional up-dating of our knowledge considering mechanisms underlying overtraining-related performance incompetence in affected athletes with respect to further results obtained in this field during the past 2 years. Particular emphasis has been given to the time-course of regeneration subsequent to overtraining as far as it is known at present. From an operational standpoint, the thesis was followed that findings such as impairment of neuromuscular function depressed β-adrenergic receptor density related depressed lipolysis, glycogenolysis, glycolysis, and heart rate response as well as depressed intrinsic sympathetic activity depressed turnover in contractile proteins depressed adrenocortical and pituitary-hypothalamic responsiveness in an advanced stage or iron deficiency can explain performance incompetence in overtrained athletes, whereas appropriate regeneration should be indicated by their normalization.
Article
Corticotropin-Releasing-Hormone (CRH) is the principal secretagogue for plasma ACTH and corticosterone secretion and plays an important role in coordinating a variety of physiological and behavioral responses to stress. To explore whether there is a rapid change in the secretory response of the hypothalamic CRH neuron during acute stress, we report here a study of the effects of KCl and norepinephrine (NE) on CRH release in vitro from rat hypothalami explanted after 5, 30, 60, and 120 minutes of immobilization. We also measured the plasma levels of ACTH, β-endorphin, corticosterone, prolactin, GH, and TSH at these intervals. As the duration of immobilization increased, KCl and NE-induced CRH release in vitro progressively fell. After reaching a maximal rise after 30 minutes of immobilization, plasma ACTH, β-endorphin, and prolactin progressively fell in plasma, whereas corticosterone remained elevated up to 120 minutes; TSH and GH secretion rapidly declined and remained suppressed. Taken together, these data suggest that during immobilization stress, the responsiveness of the hypothalamic CRH neuron rapidly falls, owing either to CRH depletion and/or desensitization to NE, and this is paralleled by a concomitant decrease in pituitary-adrenal responsiveness.