ArticlePDF Available

Abstract and Figures

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.
Content may be subject to copyright.
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*
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
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;
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
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
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
400 m
Triathlon Cycling Race
before testing
1 year 1 year At least 3
At least 2
At least
half a year
2–3 months 6 weeks 2 weeks 2 weeks 5 months
Duration re-
covery after
1 year Several
>5 years >3 years No full
1–2 months max 6
approx 12
1 month 3 months
Unable to
Unable to
of dizzi-
Unable to
Unable to
Unable to
dizziness and
during uphill
Unable to
races, bad
from train-
Unable to
and races
culty with
Unable to
and worse
race per-
Fatigue Severe Severe Severe Severe Severe Severe Severe Severe
Muscle sore-
Heavy and
painful legs
Heavy up-
per legs
Other symp-
11– 12 h
each night
Anorexia Psycho-
Gets up
to urinate,
14 h per
getting up,
5 kg in 5
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.
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.
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
Cutoff for
OTS OTS (%) NFO (%)
[La]max rst exercise test <8 mmol l-1 80 50
[La]max second exercise
<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
80 20
ACTH response to second
exercise test
100 80
PRL response to second
exercise test
100 100
GH response to second
exercise test
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
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.
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
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).
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.
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.
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
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.
Re f e r e n c e s
1. Meeusen R, Duclos M, Gleeson M, et al. Prevention, diagnosis and the
treatment of the Overtraining Syndrome. Eur J Sport Sci 2006;6:1–14.
2. Nederhof E, Lemmink KAPM, Visscher C, et al. Psychomotor speed: pos-
sibly a new marker for overtraining syndrome. Sports Med 2006;36:817–
3. Keizer H. Neuroendocrine aspects of Overtraining. In Kreider R, Fry AC,
O’Toole M, eds. Overtraining in sport 1998:145–68. Champaign (IL): Hu-
man Kinetics.
4. Lehmann M, Foster C, Keul J. Overtraining in endurance athletes: a brief
review. Med Sci Sports Exerc 1993;25:854–62.
5. Lehmann M, Foster C, Dickhuth HH, et al. Autonomic imbalance hypoth-
esis and overtraining syndrome. Med Sci Sports Exerc 1998;30:1140–5.
6. Lehmann M, Gastmann U, Baur S, et al. Selected parameters and mecha-
nisms of peripheral and central fatigue and regeneration in overtrained
athletes. In: Lehmann M, Foster C, Gastmann U, Keizer H, Steinacker
J, eds. Overload, performance incompetence, and regeneration in sport.
New York: Kluwer Academic/Plenum, 1999:7–25.
7. Lehmann M, Petersen KG, Liu Y, et al. Chronische und erscho¨pfende
Belastungen im Sport—Einuss von Leptin und Inhibin. [Chronic and ex-
hausting training in sports—inuence of leptin and inhibin] Dtsch Z Sport-
med 2001;51:234–43.
8. Meeusen R. Overtraining, indoor & outdoor. Vlaams tijdschrift voor Sport-
geneeskunde & Sportwetenschappen 1998;19:8–19.
9. Meeusen R. Overtraining and the central nervous system, the missing
link? In:Lehmann M, Foster C, Gastmann U, Keizer H, Steinacker J, eds.
Overload, performance incompetence, and regeneration in sport. New
York: Kluwer Academic/ Plenum publishers, 1999:187–202.
10. Meeusen R, Piacentini MF, Busschaert B, et al. Hormonal responses in
athletes: the use of a two bout exercise protocol to detect subtle differ-
ences in (over)training status. Eur J Appl Physiol 2004;91:140–6.
11. Urhausen A, Gabriel H, Kindermann W. Blood hormones as markers of
training stress and overtraining. Sports Med 1995;20:251–76.
12. Urhausen A, Gabriel H, Weiler B, et al. Ergometric and psychological
ndings during overtraining: a long-term follow-up study in endurance
athletes. Int J Sports Med 1998;19:114–20.
13. Meeusen R, De Meirleir K. Exercise and brain neurotransmission. Sports
Med 1995;20:160–88.
14. Wilckens T, Schweiger U, Pirke K. Activation of 5-HT1C-receptors sup-
presses excessive wheel running induced by semi-starvation in the rat.
Psychopharmacology 1992;109:77–84.
15. Dishman R. The norepinephrine hypothesis. In: Morgan WP, ed. Physical
activity & mental health. Washington: Taylor & Francis, 1997:199–212.
16. Porter R, Gallagher P, Watson S, et al. Corticosteriod–serotonin interac-
tions in depression: a review of the human evidence. Psychopharmacol-
ogy 2004;173:1–17.
17. Liberzon I, Taylor S, Amdur R, et al. Brain activation in PTSD in response
to traumarelated stimuli. Biol Psychiatry 1999;45:817–26.
18. Uusitalo ALT. Overtraining. Making a difcult diagnosis and implementing
targeted treatment. Phys Sportsmed 2001;29:35–50.
What is already known on this topic
The diagnoses NFO and OTS must be made based on an
exclusion diagnosis. The most important marker to distinguish
NFO from OTS is duration of recovery, which is only known
Athletes with NFO or OTS show a disturbed functioning of
the hypothalamic–pituitary–adrenal (HPA) axis, which parallels
disturbances in other stress-related syndromes.
What this study adds
The two-bout exercise protocol seems a useful tool for pro-
spectively diagnosing underperforming athletes, with an over-
shoot of adrenocorticotrophic hormone (ACTH) and prolactin
(PRL) after the second exercise bout in NFO athletes and a
suppression in OTS.
A possible explanation for the difference is hypersensitivity of
glucocorticoid receptors in NFO versus insensitivity in OTS.
SAJSM VOL 22 NO. 4 2010 105
19. Armstrong L, VanHeest J. The unknown mechanisms of the overtraining
syndrome. Clues from depression and psychoneuroimmunology. Sports
Med 2002;32:185–209.
20. Fry AC, Kraemer WJ, Ramsey LT. Pituitary–adrenal–gonadal respons-
es to highintensity resistance exercise overtraining. J Appl Physiol
21. Rietjens GJWM, Kuipers H, Adam JJ, et al. Physiological, biochemical
and psychological markers of strenuous training-induced fatigue. Int J
Sports Med 2005;26:16–26.
22. Nederhof E, Zwerver J, Brink M, et al. Different diagnostic tools in non-
functional overreaching. Int J Sports Med 2008;29:590–7.
23. Lehmann M, Gastmann U, Petersen KG, et al. Training-overtraining: per-
formance, and hormone levels, after a dened increase in training volume
versus intensity in experienced middle- and long-distance runners. Br J
Sports Med 1992;26:233–42.
24. Budgett R, Hiscock N, Arida RM, et al. The effects of the 5-HT2C ago-
nist mchlorophenylpiperazine on elite athletes suffering from unexplained
underperformance syndrome (overtraining). Br J Sports Med. Published
Online First 4 July 2008. doi:10.1136/bjsm.2008.046425
25. Holsboer F. The corticosteroid receptor hypothesis of depression. Neu-
ropsychopharmacology 2000;23:477–501.
26. Cizza G, Kvetnansky R, Tartaglia M, et al. Immobolisation stress rapidly
decreases hypothalamic corticotropin-releasing hormone secretion in
vitro in the male 344/N Fischer rat. Life Sci 1993;53:233–40.
27. Bremmer D. Does stress damage the brain? Biol Psychiatry 1999;45:797–
28. Joels M, Kvarst H, DeRijk R, et al. The coming out of the brain mineralo-
corticoid receptor. Trends Neurosci 2008;31:1–7.
29. Kuipers H, Keizer H. Overtraining in elite athletes. Sports Med 1988;6:79–
... Furthermore, using heart rate monitors during training sessions in rugby, a sport marked by contact, impact, and wrestle drills, as well as a lot of resistance and anaerobic efforts, is challenging and often inappropriate. Fortunately, the session-RPE method for assessing training has been a popular tool for monitoring training periodization in numerous sports during the last decade (16), and several investigators have adopted this strategy (5,6,8,16). The session-RPE was used in this investigation because of its simplicity, low cost, and applicability in various sports, including soccer, rugby union, basketball, and other individual sports (5,6,16). ...
... Furthermore, using heart rate monitors during training sessions in rugby, a sport marked by contact, impact, and wrestle drills, as well as a lot of resistance and anaerobic efforts, is challenging and often inappropriate. Fortunately, the session-RPE method for assessing training has been a popular tool for monitoring training periodization in numerous sports during the last decade (16), and several investigators have adopted this strategy (5,6,8,16). The session-RPE was used in this investigation because of its simplicity, low cost, and applicability in various sports, including soccer, rugby union, basketball, and other individual sports (5,6,16). ...
... Fortunately, the session-RPE method for assessing training has been a popular tool for monitoring training periodization in numerous sports during the last decade (16), and several investigators have adopted this strategy (5,6,8,16). The session-RPE was used in this investigation because of its simplicity, low cost, and applicability in various sports, including soccer, rugby union, basketball, and other individual sports (5,6,16). ...
... Einen originellen Ansatz verfolgte die Arbeitsgruppe um Meeusen et al. (2010) auf der Suche nach einer Unterscheidung zwischen den einzelnen Überlastungsstadien anhand der hormonellen Antwort bei zwei aufeinanderfolgenden erschöpfenden stufenweise ansteigenden Tests: Ein NFOR ging im Vergleich zum FOR mit einer gesteigerten Ausschüttung von ACTH, Prolaktin und Wachstumshormon nach dem zweiten Test einher, während ein Übertrainingssyndrom durch einen deutlich ausgeprägten hormonellen Anstieg nach dem ersten Test gefolgt von einer vollständig supprimierten Reaktion auf den zweiten Test charakterisiert war. ...
Unter einem „Übertrainingssyndrom“ versteht man einen unerwarteten Abfall der Leistungsfähigkeit ohne organisch krankhaften Befund, der auch nach einer längeren Regenerationsphase nachweisbar ist. Es existiert kein einzelner zuverlässiger Marker zur Diagnose von chronischen Überlastungszuständen. Die Diagnose eines Übertrainingssyndroms ist eine klinische Ausschlussdiagnose. Zur Prävention sind standardisierte Leistungstests und Fragebögen zur Erfassung der subjektiven Befindlichkeit mit Kenntnis individueller Basiswerte geeignet. Eine angemessene Ernährung, Kälteanwendungen, adäquater Schlaf sowie eine präventive individuelle Trainingsplanung und -dokumentation scheinen geeignete Möglichkeiten, die Erholung zu unterstützen und somit die Qualität des Trainings zu gewährleisten. Dieser Beitrag ist Teil der Sektion Sportmedizin, herausgegeben vom Teilherausgeber Holger HW Gabriel, innerhalb des Handbuchs Sport und Sportwissenschaft, herausgegeben von Arne Güllich und Michael Krüger.
... Ils arrivent au labo à sept heures, à jeun, avec une première prise de sang, qui sera réalisée à nouveau avant et à la fin de chaque test d'exercice. Meeusen et al. ont utilisé ce protocole dans trois études, lesquelles permettent de confirmer l'intérêt du TOP test pour discriminer OTS et NFO[31][32][33]. Les trois études confirment que le NFO est caractérisé par une hyperréponse de la prolactine et de l'ACTH (sans augmentation du cortisol) au premier test et l'OTS par une moindre réponse de l'ACTH au second test. ...
Résumé Démarrer une activité physique et sportive (APS) régulière selon les recommandations de l’Organisation mondiale de la santé ou, à l’autre extrémité du spectre de l’APS, être un athlète très entraîné, voire de haut niveau, ne modifie pas les concentrations hormonales basales, mesurées au repos, à distance de la dernière session d’APS. Chez les sujets âgés (60-80 ans), certaines hormones (testostérone, S-DHEA) peuvent être augmentées avec l’entraînement mais leurs valeurs restent dans les limites physiologiques. C’est pourquoi un sujet entraîné, voire très entraîné, présente un profil hormonal normal. Les valeurs hormonales anormales ont a priori une valeur pathologique et nécessitent d’être explicitées.
... They reported a 118% and 73% reduction in the response of cortisol and adrenocorticotrophic hormone (ACTH; a precursor hormone to cortisol) in the athletes in response to the second maximal cycling bout after the 10-day training period compared to before the training period (Meeusen et al., 2004). Meeusen et al. (2010) also reported that athletes in a state of OTS (classified according to the duration and severity of symptoms and underperformance experienced) show little or no exerciseinduced increases in ACTH in response to the second maximal exercise bout in their exercise stress test. This suggests that the exercise-induced response of the HPA hormones, specifically cortisol and ACTH, may be lowered following periods of intensified training. ...
Full-text available
Background: Intensified training coupled with sufficient recovery is required to improve athletic performance. A stress-recovery imbalance can lead to negative states of overtraining. Hormonal alterations associated with intensified training, such as blunted cortisol, may impair the immune response. Cortisol promotes the maturation and migration of dendritic cells which subsequently stimulate the T cell response. However, there are currently no clear reliable biomarkers to highlight the overtraining syndrome. This systematic review and meta-analysis examined the effect of intensified training on immune cells. Outcomes from this could provide insight into whether these markers may be used as an indicator of negative states of overtraining. Methods: SPORTDiscus, PUBMED, Academic Search Complete, Scopus and Web of Science were searched until June 2022. Included articles reported on immune biomarkers relating to lymphocytes, dendritic cells, and cytokines before and after a period of intensified training, in humans and rodents, at rest and in response to exercise. Results: 164 full texts were screened for eligibility. Across 57 eligible studies, 16 immune biomarkers were assessed. 7 were assessed at rest and in response to a bout of exercise, and 9 assessed at rest only. Included lymphocyte markers were CD3 ⁺ , CD4 ⁺ and CD8 ⁺ T cell count, NK cell count, NK Cytolytic activity, lymphocyte proliferation and CD4/CD8 ratio. Dendritic cell markers examined were CD80, CD86, and MHC II expression. Cytokines included IL-1β, IL-2, IL-10, TNF-α and IFN-γ. A period of intensified training significantly decreased resting total lymphocyte ( d= − 0.57, 95% CI − 0.30) and CD8 ⁺ T cell counts ( d= − 0.37, 95% CI − 0.04), and unstimulated plasma IL-1β levels ( d= − 0.63, 95% CI − 0.17). Resting dendritic cell CD86 expression significantly increased ( d = 2.18, 95% CI 4.07). All other biomarkers remained unchanged. Conclusion: Although some biomarkers alter after a period of intensified training, definitive immune biomarkers are limited. Specifically, due to low study numbers, further investigation into the dendritic cell response in human models is required.
... In the diagnosis of OTS, stimulation tests of ACTH, GH, and prolactin can be helpful. In such tests, the rise of hormone levels after stimulation is reduced, however, more research is needed to evaluate their diagnostic value [35,36]. In a study conducted among 51 men aged 18-50 years old, of which 14 presented OTS, OTS patients typically presented elevation of estradiol level, and decrease of testosterone level. ...
Full-text available
Introduction: Overtraining syndrome (OTS) is a state of excess sportsmen's overload caused by too high an intensity of training. The main cause of OTS is too big a training load. Also, they are other risk factors like restrictive diets, inordinate stress, and inflated expectations of a family and a coach. Description of the state of knowledge: despite numerous hypotheses like dysregulation of hypothalamus and pituitary, inflammatory hypothesis, and glycogen hypothesis the exact cause of OTS is not fully understood. None of these hypotheses explains completely all of the symptoms. In diagnosis, several laboratory tests are required to exclude other diseases. After it, because of possible systemic character diagnostic process of OTS is still problematic. One of the diagnostic methods relies on the measurement of hormone levels. Another potential diagnostic method is the measurement of saliva immunoglobulins and other anti-viral proteins. Also, the measurement of serum cell-free DNA can be used. After the onset of OTS, the most important treatment method is rest, which should last for 6-12 weeks or longer. Nowadays, treatment options are looking for shortenings this time. These options are anti-inflammatory drugs and repeated hypoxia-hyperoxia exposure combined with low-intensity training. Since the only well-established treatment method is prolonged rest, prevention is the most important aspect of OTS management. Adequate education of young athletes and their parents is also important. Summary: Overtraining syndrome is a serious problem that concerns many athletes. This problem not only affects results and careers but also sportsmen’s life. Because of the wide scope of symptoms, which can be often nonspecific making the correct diagnosis can be difficult.
... 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]. ...
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.
Excessive physical exercise (overtraining, OT) charactered by long-term and excessive training results in the damage of multiple vital tissues including hippocampus which plays a critical role in learning and memory. A combination of dasatinib (D) plus quercetin (Q) (D+Q) belongs to senolytic drugs which selectively kill senescent cells in vitro and vivo. In this study, the rats that suffered a five-week excessive swimming training were subjected to the oral administration of D+Q. D+Q alleviated the decline in exercise performance of OT rats during the swimming training, and prevented learning and memory deficits in Morris water maze, Y-maze and novel object recognition tests after excessive swimming training. Analytical results by SA-β-gal staining and western blotting showed that D+Q significantly reduced senescent cells with repressed expression of senescence-related proteins, p53 and p21, in hippocampus. Nissl and immunohistochemical staining showed that D+Q significantly attenuated neuronal loss caused by apoptosis. Interestingly, we observed elevated level of cleaved caspase 3, an apoptosis executor protein, in p21 positive hippocampus cells by D+Q treatment in immunofluorescent staining, suggesting that senescent cells were induced to apoptosis in D+Q-treated rats. The positive control drug, silibinin, showed similar protective effect against OT, but did not induce the apoptosis of senescent cells, suggesting a difference in the protective mechanisms. These results indicated that D+Q alleviates overtraining-induced deficits in learning and memory through elimination of senescent cells and reduction of apoptotic cell number.
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.
Full-text available
مقياس التقييم الشخصي واحد من اهم المقاييس التي تستخدم قيم الاحمال التدريبة وفقا لادار الشخص لاثر الحمل التدريبي علية. حيث ساهم هذا المقياس في العديد من الدراسات في كشف اثر الحمل الفعلي على الرياضيين.
Full-text available
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.
Full-text available
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.
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.
Overtraining is an imbalance between training and recovery. Short term overtraining or ‘over-reaching’ is reversible within days to weeks. Fatigue accompanied by a number of physical and psychological symptoms in the athlete is an indication of ‘stateness’ or ‘overtraining syndrome’. Staleness is a dysfunction of the neuroendocrine system, localised at hypothalamic level. Staleness may occur when physical and emotional stress exceeds the individual coping capacity. However, the precise mechanism has yet to be established. Clinically the syndrome can be divided into the sympathetic and parasympathetic types, based upon the predominance of sympathetic or parasympathetic activity, respectively. The syndrome and its clinical manifestation can be explained as a stress response. At present, no sensitive and specific tests are available to prevent or diagnose overtraining. The diagnosis is based on the medical history and the clinical presentation. Complete recovery may take weeks to months.
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)
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.
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.
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.