Hormones (2019) 18:151–172

https://doi.org/10.1007/s42000-019-00115-7

REVIEW ARTICLE

The complex and bidirectional interaction between sex hormones

and exercise performance in team sports with emphasis on soccer
Nikolaos E. Koundourakis 1 & Andrew N. Margioris 2

Received: 17 March 2018 / Accepted: 7 January 2019 / Published online: 29 June 2019
# Hellenic Endocrine Society 2019

Abstract
A constant topic reported in the lay press is the effect of sex hormones on athletic performance and their abuse by athletes in their
effort to enhance their performance or to either boost or sidestep their hard, protracted, and demanding training regimens.
However, an issue that it is almost never mentioned is that the athletic training itself affects the endogenous production of
androgens and estrogens, while also being affected by them. Among sports, soccer is a particularly demanding activity, soccer
players needing to possess high levels of endurance, strength, and both aerobic and anaerobic capacity, with the very great
physiological, metabolic, physical, and psychological exertion required of the players being both influenced by sex steroids and,
reciprocally, affecting sex steroid levels. This review focuses on the currently available knowledge regarding the complex
relationship between athletic training and competition and sex steroid hormone adaptation to the demands of the exercise effort.
In the first part of the review, we will examine the effects of endogenous testosterone, estrogen, and adrenal androgens on athletic
performance both during training and in competition. In the second part, we will explore the reciprocal effects of exercise on the
endogenous sex hormones while briefly discussing the recent data on anabolic androgenic steroid abuse.

Keywords Sex steroids . Soccer . Androgens . Estrogen . Exercise performance

Introduction activity featuring a large variety of actions covering the whole

An almost daily topic of the lay press is the effect of sex
steroid hormones on athletic performance and the use and
abuse of anabolic steroids by athletes seeking to enhance their
performance and/or boost or sidestep the hard, protracted, and
demanding training regimens necessary for elite athletes.
However, an important point that is almost never mentioned
is that athletic training per se changes the endogenous produc-
tion of androgens and estrogens, a response to the body’s need
to adapt to the demands of training and competition, while it
often must also deal with exogenous supplementation, which
is liable to disrupt this adaptation process [1, 2]. Among the
different types of sports, soccer is a particularly demanding
* Nikolaos E. Koundourakis
nkoyndoy@hotmail.com
1
Lab of Clinical Chemistry-Biochemistry, Department of Laboratory
Medicine, School of Medicine, University of Crete, Heraklion, Crete,
Greece
2
Department of Clinical Chemistry, School of Medicine, University of
Crete, Heraklion, Crete, Greece
range of exercise training and conditioning. Aerobic and an-
aerobic, lactic and alactic metabolism are all part of the met-
abolic profile of soccer. Soccer players, especially profes-
sionals whether participating in training sessions or in games,
are continuously under physiological and psychological
stresses during both the preseason and in-season periods,
which last at least 10 months per year. This review focuses
on the currently available knowledge regarding the complex
relationship between athletic training and competition and sex
steroid hormones in the context of the body’s adaptation to the
demands of the exercise effort. The first part of the review will
constitute an examination of the effects of endogenous testos-
terone, estradiol, and adrenal androgens on athletic perfor-
mance both during training and in competition. The second
part will comprise an assessment of the reciprocal effects of
exercise on the endogenous sex hormones. The main focus of
interest is professional soccer. Although the available litera-
ture regarding individual sports is extensive, substantially less
evidence exists as regards soccer. In addition, the fact that
soccer training involves diverse kinds of conditioning makes
it of special interest as concerns the bidirectional association
of soccer training/competition and sex steroid levels. A soccer
player needs to achieve high levels of endurance, including
152 Hormones (2019) 18:151–172

anaerobic and strength and power performance, parameters
that have been reported to affect and to be affected by the
products of the hypothalamic–pituitary–gonadal (HPG) axis
[3]. Indeed, the evidence to date suggests that these high de-
mands of exercise performance are influenced by sex steroids
and that they reciprocally affect sex steroid levels.
Sex steroids
The biochemistry of sex hormones is well understood and is
summarized in Fig. 1. Sex steroids are discrete chemical sub-
stances which in males are synthesized and excreted by the
gonads and the adrenal cortex. The many mechanisms of sex
steroid action operate by acting on receptors (androgen and/or
estrogen receptors) that ultimately regulate genomic (direct
regulation of gene transcription) and nongenomic (interaction
with signal transduction molecules) processes in target cells.
The interaction of sex steroids with their receptors affects the
activity of cells, tissues, and organs [3], the interaction being
triggered by the activation of enzyme systems, alteration in
membrane permeability, initiation of muscle contraction, and
relaxation and stimulation of protein synthesis.
Exercise and gonadal sex steroids:
a reciprocal relationship
Sex steroids affect exercise performance, while, recipro-
cally, exercise also affects the production of sex steroids.
Moreover, exercise training regimes affect the production
of gonadal sex steroids depending on the age of athletes,
their training status, and the mode, intensity, and volume
of their exercise training program, as well as several other
independent factors (Fig. 2) [1–5]. The close and bidirec-
tional association between exercise and gonadal steroids
forms a complex and delicate balance, one which should
not be disrupted by the administration of synthetic ste-
roids. Gonadal steroids play a major role in the physiolo-
gy of muscles. They are also heavily involved in neuro-
muscular coordination and adaptation to the demands of
strenuous exercise regimes, resulting in enhanced exercise
performance and increased ability to perform adequately
during both the training and competition periods [2, 3, 5].
The majority of the scientific evidence on this subject focuses
on individual athletes, particularly those participating in endur-
ance and resistance sports, while fewer data are available regard-
ing athletes in team sports, including in professional soccer.

Fig. 1 Sex steroids’ biochemistry CHOLESTEROL P450scc

PREGNENOLONE

P450c17

17 0H PREGNENOLONE

P450c17

17β-HSD-1
Sulfatase
DHEA
ANDROSTENEDIOL
17β-HSD-2
DHEAS Sulfotransferase

17β-HSD-4 3β-HSD-1

3β-HSD-2
17β-HSD-3

ANDROSTENDIONE TESTOSTERONE
17β-HSD-2
Aromatase 5α-reductase-1
Aromatase
5α-reductase-2

17β-HSD-1 5α-reductase-3

ESTRONE ESTRADIOL DIHYDROTESTOSTERONE

17β-HSD-2

17β-HSD-4
Hormones (2019) 18:151–172 153

Fig. 2 Parameters that affect sex Training status of the

steroid response to exercise Exercise volume Diet composion
individual

Rate of sex steroid

Exercise load
producon and removal
Parameters affecng
sex steroid response
to exercise
Exercise intensity Changes in the paern of
distribuon

Exercise duraon Exercise mode Psychological stress

Effects of sex steroids on exercise
performance
Despite the major role played by gonadal sex steroids in de-
termining patterns of sexual behavior and function, the notion
of their importance, and particularly that of androgens, with
regard to boosting exercise performance could well be, in our
view, grossly overestimated (Fig. 3). Because of the confu-
sion, much of this due to exaggerated reports in sports jour-
nalism on this subject, the use and abuse of gonadal steroids,
and especially that of androgens, has gained considerable at-
tention among the athletic population. Most of the experimen-
tal work published in this area involves testosterone, with its
effects on exercise performance being shown to be both direct
and indirect and, for the most part, bidirectional.
Effect of testosterone on muscles
Testosterone affects a variety of parameters that play crucial
roles in the ability to perform efficiently during exercise, this
involving, inter alia, the nervous and the musculoskeletal sys-
tems. As concerns the muscles, testosterone exerts a direct
anabolic effect, inducing muscle growth and increasing mus-
cle mass [6, 7] via its direct stimulatory effect on muscle
protein synthesis [8, 9]. In addition, testosterone alters the
cross-sectional area of both type I and II muscle fibers [10].
Data from animal studies suggest that testosterone may also
have a strong influence on skeletal muscle contraction, known
as excitation–contraction coupling, and on fast twitch muscle
fibers. These effects of testosterone on muscle physiology
result in an induction of explosive exercise performance [7,
11], which, as a consequence, leads to high levels of muscle
activity coupled with short duration of contraction time [8, 12,
13]. Of note, there is a well-documented link between muscle
mass, muscle strength, and exercise performance, and, in par-
ticular, of the type involving explosive movements, including
jumps, sprints, acceleration, deceleration, and rapid changes
of direction, all of which are of vital importance for most
athletic events, including soccer [14, 15]. In professional soc-
cer players, sprinters, and elite team athletes, a direct relation-
ship between testosterone levels and vertical jump height and
power output has been observed, suggesting that this andro-
gen affects the development of type II muscle fibers [12, 13].
Effect of testosterone on neuromuscular coordination
The effect of testosterone on athletic performance also in-
volves acceleration of neuromuscular transmission [16, 17].
Indeed, testosterone increases the number of acetylcholine
receptors at the neuromuscular junction [11], thus accelerating
neuromuscular coordination. Regarding the latter, several
studies have observed that both vertical jump and sprint per-
formance are influenced by neuromuscular features [18, 19]
and that optimal neuromuscular coordination is essential for

Fig. 3 Proposed physiological Intracellular calcium

Erythropoiesis
effects of androgens on exercise regulaon
performance

Regulaon of Body fat regulaon

Proposed
metabolism
physiological effects of
sex steroids
Skeletal muscle Ancatabolic effect
anabolism

Enhanced muscle
An-inflammatory
repair aer exercise
effect
induced damage
154
these types of activities [20, 21]. Furthermore, it has been
documented that strength gains without accompanying mus-
cle hypertrophy are a neural adaptation to an increase in the
neuromuscular coordination of the muscles involved [22]. The
aforementioned evidence clearly demonstrates that the impact
of testosterone on exercise performance depends in part on its
effect on neuromuscular coordination of the muscles involved
in each specific task.
Effect of testosterone on behavior and aggression
Testosterone may affect athletic performance not only via its
anabolic effects on muscles and the enhancement of neuro-
muscular coordination, but also via its behavioral effects.
Extensive bibliography exists documenting a link between
testosterone levels and masculine behavior and aggression in
healthy men and women. Indeed, testosterone levels have, in
general, been associated with aggressiveness, initiative, lead-
ership, and professional success [23, 24]. In addition, in un-
dergraduate female students, high salivary testosterone corre-
lates with an action-oriented profile, while those with lower
testosterone viewed themselves as conventional individuals
possessing a caring attitude coupled with an anxious and de-
jected disposition [25]. Furthermore, high testosterone levels
have been associated with high dominance scores, strong
personality characteristics, and professional rank [26].
Likewise, serum testosterone levels correlate with scores
of verbal aggression and anger [27]. A similar association
has also been documented between testosterone and ag-
gressiveness in experimental animal models [28, 29].
Based on these findings, it could be speculated that higher
levels of endogenous testosterone may enhance overall
athletic performance by boosting drive, initiative, and ag-
gressiveness during both training and competition.
Effect of testosterone on body fat
The beneficial effects of testosterone on athletic perfor-
mance also involve metabolism and energy balance, testos-
terone exerting major effects on fat metabolism and on its
regional distribution [30]. It has been observed that testos-
terone is an important determinant of regional fat distribu-
tion [30] and testosterone decline is related to fat mass
increase [31, 32]. The latter observation is of great signif-
icance since it is well documented that body fat mass af-
fects exercise performance. Diet protocols that lower body
fat composition (fat mass/fat-free mass) reduce the energy
cost of running [33]. In sports, including soccer, body fat
mass inversely correlates with sprint tests [34], neuromus-
cular performance in general, and aerobic endurance ca-
pacity. In conclusion, serum testosterone levels and body
fat mass interact with each other, and both affect athletic
performance, either independently or in combination.
Hormones (2019) 18:151–172
Effect of testosterone on exercise recovery
Another mechanism via which testosterone improves athletic
performance appears to be its beneficial effects on recovery
rate following both extensive training and athletic competition
[35]. The mechanism(s) via which testosterone accelerates the
recovery phase after exercise may involve innate immunity
mechanisms. It should be noted here that extensive training
and strenuous athletic competitions induce an inflammatory
response. Testosterone exerts suppressive effects on both hu-
moral and cellular immunity, acting as a natural anti-
inflammatory agent. Testosterone suppresses the inflammato-
ry response in macrophages, lymphocytes, and the vascular
endothelium via its receptor expressed on all these types of
cells. In fact, testosterone appears to suppress the secretion of
several cytokines, while cytokines impair the synthesis and
secretion of testosterone [36].
A second mechanism via which testosterone acceler-
ates the recovery period following strenuous athletic ac-
tivity is its capacity to ameliorate the effects of exercise-
induced hypercortisolism, which exerts a catabolic effect
on muscle metabolism mainly by suppressing protein syn-
thesis [37]. Via its ability to ameliorate muscle catabolism
and its induction of proteinosynthesis within the muscles,
testosterone appears to enable accelerated recovery from
exercise training stress.
Effect of testosterone on the oxygen-carrying
capacity of the blood and energy availability
Testosterone also boosts stamina and endurance by increasing
the oxygen-carrying capacity of the blood: it has been ob-
served that testosterone enhances red blood cell production
via stimulation of erythropoietin synthesis and secretion as
well as by directly stimulating bone marrow hemopoesis and
the acceleration of iron incorporation into erythrocytes [38].
Furthermore, testosterone increases energy through its regula-
tion of hepatic and muscle glycogen stores during endurance
exercise and its enhancement of lipolysis [39]. In addition, it
has been shown that testosterone facilitates catecholamine-
induced lipolysis in a dose-dependent manner, an effect
achieved by physiological concentrations of testosterone
[40]. Enhanced lipolysis diminishes the rate of glycogen con-
sumption, exerting a beneficial adaptation to these types of
activities, since carbohydrate sparing ensures energy provi-
sion throughout the duration of strenuous events. It should
be stressed that the effects of testosterone on glucose signaling
take place in both the liver and muscles [41]. Finally, testos-
terone can also affect muscle performance and recovery by
means of calcium signaling. Calcium triggers muscle contrac-
tions via its interaction with the proteins actin and myosin.
Testosterone affects intracellular calcium trafficking, thereby
Hormones (2019) 18:151–172
enhancing an important component of muscle contraction and
thus exercise performance [42].
Dehydroepiandrosterone, dehydroepiandrosterone
sulfate, and exercise performance
In humans, dehydroepiandrosterone (DHEA), which is pro-
duced by the zona reticularis of the adrenal gland, represents
the most abundantly circulating steroid hormone. DHEA is
decreased by certain diseases, by obesity, as well as with ag-
ing. DHEA exerts direct effects mainly on the central nervous
system by binding to specific membrane receptors [43], while
it also activates nuclear receptors following its conversion into
testosterone by the enzymes 17beta-hydroxysteroid dehydro-
genase and 3beta-hydroxysteroid dehydrogenase/Δ5–4 isom-
erase (3β-HSD). These enzymes, as well as P450arom and 5-
reductase, are expressed in skeletal muscles that locally con-
vert DHEA to testosterone and its biologically active form,
dihydrotestosterone [44]. Acute aerobic exercise induces the
expression of all the above enzymes in the muscles in both
sexes [45]. Resistance training restores declines in muscle sex
steroid hormone steroidogenesis in older men [46]. Apart
from acting as a testosterone precursor in the muscles and
many other tissues of the body, DHEA can also affect exercise
performance via its neuroprotective effects on neurons as
well as its effect on neurogenesis and neural survival [47].
Most of the beneficial effects of DHEA on muscles take
place within minutes from the beginning of exercise, as
several studies have reported [46–52]. These immediate
effects, including the acute rise of DHEA, on muscle
physiology appear to be an ultra-fast adaptation to meet
the musculoskeletal demands of exercise.
In regard to its sulfate, dehydroepiandrosterone-sulfate
(DHEA-S), there are some findings indicating that its levels
are linearly related to muscle strength and increased physical
performance in elderly individuals [46, 53, 54]. In addition,
the fact that older adults with low DHEA-S levels are poor
responders to demands of exercise training adaptations sug-
gests that optimal levels of this sulfate are needed for such
adaptations [47]. However, while the above observations are
applicable in the elderly, there is no scientific evidence, to the
best of our knowledge, that DHEA-S exerts any direct effect
on exercise performance capacity in athletes. Another mech-
anism via which DHEA-S could hypothetically affect exercise
performance is its proposed neuroprotection effects on neurite
growth and neuroneogenesis, as well as its ability to protect
neuronal cells against apoptosis and its antagonistic effects on
oxidants and glucocorticoids. DHEA-S has been observed to
have anti-inflammatory and immunomodulating effects and to
influence catecholamine synthesis and secretion [55].
Therefore, apart from its suggested effect on the optimal func-
tion of the nervous system, which is an essential regulatory
parameter for exercise performance, DHEA-S might also play
155
a key role in exercise-induced muscle damage, acting as an
antioxidant and in muscle repair via its anticatabolic effects,
which could in turn translate to enhanced recovery after exer-
cise training stress. However, these hypotheses remain purely
speculative, since no evidence as yet exists to support a ben-
eficial effect of the aforementioned mechanisms on exercise
performance in athletes. On the other hand, DHEA-S levels
have been linked to optimal body composition status [56] and
low DHEA-S [57] with increased waist-to-hip ratio.
Accordingly, DHEA-S could affect exercise performance ca-
pacity through changes in body weight and body fat [58].
Furthermore, it has been suggested that DHEA-S affects mus-
cle metabolism during exercise. Hernández-Morante et al.
[56], in a study on 85 obese patients, demonstrated for the first
time in vitro that DHEA-S stimulates lipolysis preferably in
subcutaneous fat in women and in visceral fat in men.
Interestingly, DHEA-S may also affect cognitive function
[59]. Indeed, Moffat et al. [60] measured endogenous levels
of DHEA-S and related them to quantified cognitive status,
which could be an important parameter in several sports.
Lastly, there is evidence showing that both DHEA and its
sulfate may affect the capacity to perform efficiently during
exercise via another indirect mechanism. Similar to the case of
testosterone, data exist linking these adrenal androgens to ag-
gression and behavior, with DHEA and DHEA-S having been
shown to correlate with an expansive, aggressive, and egocen-
tric personality [61]. This being the case, hypothetically, in-
creased levels of these weak adrenal androgens could provoke
high levels of aggressiveness; thus, a facilitation of neural
input during maximal explosive effort may occur.
Δ4-Androstenedione (Δ4-dione) and exercise
performance
Δ4-Dione is produced by the adrenal glands and the go-
nads. Δ4-Dione has no biological effect on its own but
exerts its effects via its conversion into testosterone and
estradiol [52]. Evidence regarding the effects of exoge-
nous Δ4-dione on strength and fat mass [62, 63] comes
from a review paper that summarized several studies.
Interestingly, despite the different daily dosages of Δ4-
dione used in these studies, no effect on muscle strength
or size or body fat was evident. Based on the biochemis-
try of Δ4-dione, it is possible to assume that exogenous
use of Δ 4-dione could elevate testosterone in healthy
young males. However, it has been shown that the re-
quired doses for this effect are quite high, i.e., in excess
of 300 mg per day. Such high doses of Δ4-dione may
cause a mixed bag of actions, since it can be converted
to both testosterone and estadiol, the latter inducing the
development of a female phenotype, including body fat
distribution and muscular changes.
156
Estrogens and exercise performance
Estrogens exert various beneficial effects on athletic perfor-
mance via their effects on exercise-induced inflammation and
muscle damage, as well as muscular recovery and repair rates
[64]. More specifically, estradiol exerts a significant effect on
muscle membrane stability while at the same time ameliorating
exercise-induced muscle damage [65]. In particular, certain in-
tensive exercise protocols can cause skeletal muscle damage,
resulting in an efflux in the circulation of high quantities of
muscle cell proteins and enzymes, including creatine kinase
(CPK), lactate dehydrogenase, aspartate aminotransferase,
and myoglobin [66]. CPK is the most commonly measured
marker of muscle damage [67, 68]. Female athletes respond
to intensive exercise by significantly lower levels of muscle
CPK compared to male athletes [69, 70], this reduction being
attributed by some to the protective role of estradiol in muscle
cell membranes that have suffered exercise-induced damage
[36]. The protective effect of estrogens on muscle membranes
is also enhanced by their moderate antioxidant potential [71].
Finally, estrogens may protect muscles from damage and ac-
celerate their recovery from athletic injuries via their well-
known anti-inflammatory effect on the vascular endothelium.
Indeed, administration of estradiol attenuates the vascular ex-
pression of inflammatory mediators and neutrophil infiltration
(an essential component of innate immunity) following injury
[72]. Estrogens also attenuate the induction of myeloperoxidase
activity in skeletal muscle following exercise [73].
Estrogen as a modulator of intermediate metabolism
of muscle cells
In addition to the beneficial effects of estrogens on muscle dam-
age, inflammation, and repair, another potential performance-
enhancing mechanism is their regulation of intermediate metab-
olism. Estrogens conserve tissue glycogen during submaximal
exercise, an effect resulting in a significant improvement of
exercise performance [74]. These data indicate that estradiol
replacement spares tissue glycogen during submaximal exercise,
a study by Kendrick et al. having demonstrated the contribution
of these glycogen-sparing effects to significant improvement in
exercise performance [74]. Furthermore, it has been suggested
that estrogen controls lipolysis by upregulating alpha2A-
adrenergic receptors directly in human adipose tissue through
estrogen receptor alpha [75]. The above evidence thus leads to
the conclusion that estrogens may positively affect exercise per-
formance capacity by regulating muscle metabolism.
Effects of endurance exercise on androgens
In general, endurance exercise training seems to have signif-
icant effects on the major male reproductive hormone,
Hormones (2019) 18:151–172
testosterone. A growing body of evidence suggests that basal
testosterone levels are lowered in endurance-trained males
[64, 65]. The mechanism of this effect is currently speculative,
but it may be related to HPG axis dysfunction. The effects of
exercise in significantly reducing testosterone levels as well as
in disrupting the HPG axis possibly do not appear until after
months or years of endurance exercise training. Potentially,
the lowered testosterone levels of the endurance-trained male
could disrupt their anabolic and androgenic functions/
processes [76, 77]. From a reproductive point of view,
this effect of endurance training on testosterone produc-
tion may explain the lower libido and the subfertility
problems of these athletes [77]. However, to date, there
are only limited findings to indicate that any consistent
disruption of the testosterone-dependent processes in the
male occurs due to endurance training [76].
The question of whether regular endurance exercise alters
basal DHEA and DHEA-S cannot be answered at this time
given the contradictory findings [78]. Indeed, in a quite re-
cently published, elegant, and well-written review, the authors
examine the literature on the effect of exercise on adrenal
androgens [78], stating correctly that the physiological signif-
icance of DHEA and DHEA-S on exercise has only recently
been recognized. It now appears that several published reports
on the effect of exercise training and competition on adrenal
androgen production in elite athletes have found alterations of
their production, while others are unable to document any
such effect [78, 79]. It has been observed that pituitary
ACTH is the principal effector of exercise-induced DHEA
and DHEA-S production, since simultaneous administration
of exogenous glucocorticoids blunts the responses of these
steroids to exercise [78]. It has also been suggested that
exercise-induced increase in adrenal androgens may be due
to a decrease of extracellular fluid and thus of the volume of
their distribution as a result of loss of fluids during intense
exercise [78]. The observed discrepancies could also be relat-
ed to the initial physical aptitude of the subjects and/or the
short duration of the training program. A long period of train-
ing may be needed, i.e., of at least 1 year, to increase basal
values. It should be noted that in most studies, 8 to 24 weeks
of exercise training significantly improved physical perfor-
mance capacity and body composition [78] despite the lack
of change in DHEA-S. It could also be hypothesized that the
observed discrepancies in the literature are due to high and
low responders to exercise. Notably, it has recently been re-
ported that individuals with low DHEA-S levels appear to be
poor responders in terms of exercise training adaptations,
whereas those with high DHEA-S levels were observed to
have improved reactive time and locomotive function in re-
sponse to training [47].
The existing literature concerning the effects of short- and
long-term endurance exercise training on Δ4-dione levels is
extremely limited. Only two studies, to the author’s
Hormones (2019) 18:151–172
knowledge, sought to shed some light on the effects of chronic
exercise on Δ4-dione levels. However, the results of both
studies [80, 81] failed to show any effect on Δ4-dione con-
centration after short (2-week) or long (40-week) marathon
and bicycle training programs, respectively, the results hence
suggesting that endurance exercise training does not enhance
adrenal function in regard to Δ4-dione. However, caution is
advised if one attempts to extrapolate the latter findings to the
case of competitive athletes because of the higher age of the
participants employed in the aforementioned two studies and
the fact that there was no definition of the magnitude (inten-
sity, volume, and duration) of the endurance exercise training
performed by these individuals.
Effects of resistance exercise on androgens
In contrast to endurance exercise, there is evidence suggesting
that resistance exercise has the ability to positively affect en-
dogenous testosterone production [82–85]. This effect seems
to be related to the training regime used, the training status of
the subjects, and the examined time intervals [82–85]. Indeed,
acute resistance exercise is a powerful stimulator of testoster-
one and cortisol production in lean adult individuals [86]. A
well-designed acute resistance exercise protocol among
healthy, sedentary, untrained men, categorized into three age
groups (20–26, 38–53, and 59–72 years old), caused an acute
elevation of total and free testosterone immediately postexer-
cise, which returned to baseline within 15 min of its cessation
[87]. The authors conclude that aging does not attenuate tes-
tosterone response to acute resistance exercise. Similarly,
acute resistance exercise increased serum free and total testos-
terone [88] in a population of untrained individuals.
Furthermore, since resistance training has been suggested to
increase muscle steroidogenesis [82], the fact that some stud-
ies failed to observe an effect of resistance–strength training
on testosterone levels may be a result of increased
extrasplanchnic utilization and increased uptake by peripheral
target tissue (e.g., skeletal muscle) during this period by the
target organs, and not an unaffected HPG axis. In addition, the
level of training stimulus administered and the volume of
training load employed could also play an important regula-
tory role in testosterone response to resistance training [5].
Finally, there are many experimental and procedural con-
straints that may complicate the interpretation of hormonal
findings, such as blood sampling method, diurnal variations
in hormone concentrations, hormone detection methodology,
and research protocol [82].
There is to date little evidence as to the effects of resistance
training on testosterone precursors and metabolites. More spe-
cifically, little is as yet known about the response of DHEA
and DHEA-S [78, 79] to resistance training periods, while no
evidence exists with regard to the effect of Δ4-dione. Based
157
on the available evidence, firm conclusions cannot be drawn
regarding the response of adrenal androgens to resistance
training in young healthy male athletes. This is because in this
group, the response of these androgens to resistance training,
as also in the case of testosterone, appears to be affected by
several factors: the latter include the training status of the
participants, the specific training regime used, and both the
age and the sex of the participants [81, 85].
Effects of endurance exercise on estradiol
and prolactin
Compared to androgens, there are few studies examining
the effect of endurance exercise training on estrogens
[89–91]. According to the available data coming from
studies that have examined the responses of the main es-
trogen estradiol (E2), it remains unclear whether endur-
ance exercise does, in fact, affect its levels: some authors
have reported alterations in its levels due to endurance
training, while others failed to support these findings
[89, 90]. However, it can be speculated that the different
study designs, the training status of the subjects [5], and
the time point of the athletic season when the measure-
ment was performed [88] could have interfered with the
findings of these studies. Moreover, uncontrolled and/or
variable dietary intake could also have added to the ob-
served discrepancies [92].
Regarding prolactin (PRL), in general, its response to ex-
ercise reveals large interindividual differences. One explana-
tion for the existing discrepancies is the fact that its levels
depend partly on intracellular glucose availability [93]. The
exercise-induced rise in PRL seems to be significant only in
better-trained individuals [94] or those training at higher exer-
cise intensities (> 90% VO2max in untrained people). As a
result of training, the release of PRL is reported to be en-
hanced or starts at lower exercise intensities, but these effects
could not be confirmed in all studies [93]. The exercise re-
sponse may be associated with an anaerobic lactic contribu-
tion [95], this possibly corroborating the hypothesis that an-
aerobic lactic exercise is an important trigger mechanism in-
ducing overtraining syndrome [96]. Furthermore, PRL, simi-
lar to cortisol, has been found to respond as a stress hormone
[1, 96]. Accordingly, differences in training volume and inten-
sity and the training status of the participants executing the
specific training regimes could add to these contradictions.
Effects of resistance exercise on estradiol
and prolactin
Limited evidence exists regarding the responses of both estra-
diol and PRL to resistance exercise. Häkkinen et al. [97] in an
158
early study examined the effects of a 24-week resistance train-
ing program on E2 and PRL levels. No alteration was ob-
served in any of the examined hormones. Notably, the authors
suggested that this kind of training has no lasting endocrino-
logical effects on the pituitary. Similarly, two recent studies
conducted at the same laboratory also found that resistance
training had no effects on the serum levels of E2 and
PRL [98, 99]. Based on the available evidence, it seems
that resistance training has no effect on the endogenous
levels of these sex steroids. However, the thus far limited
bibliography on this subject means that further research is
needed to determine whether resistance training does not,
in fact, affect E2, and PRL levels. Regarding PRL specif-
ically, because of indications that it may be a stress hor-
mone, future studies should examine in particular its re-
sponse to different types of strength training [1, 96].
Gonadotropin response to exercise
A good deal of research has been devoted to examining go-
nadotropin response to exercise, especially in females [1],
without methodological constraints. However, the studies ex-
amining gonadotropin response to resistance and/or endur-
ance exercise in professional athletes are fewer; moreover,
since they report contradictory findings, mainly as concerns
LH but also regarding FSH [1, 4], interpretation of these re-
ports is subject to methodological limitations. The main lim-
iting parameter is that in the vast majority of the available
studies, blood sampling was obtained only once, at a specific
time point, for determination of gonadotropin levels. Though
the findings are not insignificant, since they provide some
insight into gonadotropin response to exercise and its role in
testosterone response [4], given that they come from a single
measurement of gonadotropin levels, they should be
interpreted with caution considering gonadotropin’s high pul-
satile secretory profile [1, 4]. In order to draw safe and accu-
rate conclusions regarding LH and FSH response to different
types of exercise, information should be provided concerning
their biological activity and behavior. Although this is actually
an issue for future interventions/research, some parameters
should be taken into consideration. The first and perhaps most
important step would be implementation of a series of mea-
surements aiming to capture their pulsatile response. In addi-
tion, it would be very helpful to measure gonadotropin-
releasing hormone (GnRH) levels, since this decapeptide is
responsible for inducing pituitary synthesis and secretion of
both LH and FSH [1, 4]. Furthermore, measurements of tes-
tosterone and estrogen concentrations should be concomitant-
ly performed, since these sex steroids complete a negative
feedback loop by inhibiting the release of GnRH [1, 4].
Lastly, other parameters that are strongly related to LH and
FSH levels should be carefully scrutinized. In particular,
Hormones (2019) 18:151–172
researchers should strictly verify and meticulously determine
whether athletes are participating in well-controlled training
regimes that do not lead to extreme overreaching and
overtraining and that they are not subjected to rapid body
weight losses and/or fasting during the studies; also of impor-
tance is clarification as to whether the subjects are meeting
their energy requirements through adequate energy intake
which has been fine-tuned to match their total caloric expen-
diture [1]. The available evidence regarding the above two
hormones is presented in detail in the following two sections.
Effects of endurance exercise
on gonadotropins
Due to the inconsistent findings regarding E2 and PRL, go-
nadotropin LH response to endurance training is not as yet
clear [4]. In general, LH levels in endurance trained versus
untrained individuals vary, and further research is needed to
determine the reason for these discrepancies. However, it
could be speculated that they are due to differences in testos-
terone levels among the study participants, given that LH re-
sponse is thought to be related to TT behavior [76, 82], as well
as to methodological issues, such as blood sampling methods,
hormone detection methodology, and research protocol.
Furthermore, according to Hall et al. [100], since pulsatile
release and the amplitude characteristics of LH were not de-
termined in these studies, the observed findings did not define
LH responses to endurance training. Similar observations
have been reported regarding the other gonadotropin,
FSH. These discrepancies could also be attributed to the
different training regimes used, the training status of the
participants, and the mode of training activity. In addition,
changes in FSH might also be related to alterations in TT
levels, which have been reported to stimulate FSH secre-
tion [101] and, furthermore, pulsatile release and the am-
plitude characteristics of this estrogen [100].
Effects of resistance exercise
on gonadotropins
Regarding resistance exercise and gonadotropins, the majority
of studies have examined LH response to resistance training,
apparently based on indications that this hormone plays a
significant role as a regulator of testosterone secretion.
Häkkinen et al. [97] examined the effects of a 24-week pro-
gressive resistance training program on the hormonal profile
of 21 males. The training regime employed failed to induce
any changes in LH serum levels by the end of the study com-
pared to baseline. Similarly, a 2-week training period, an 8-
week period [102], and 28 days of resistance training 4 times/
week [98] in elite weightlifters, healthy young male subjects,
Hormones (2019) 18:151–172
and resistance-trained athletes, respectively, failed to find any
effects of LH on the resistance training programs. In contrast,
Busso et al. [103] showed that a 6-week training period for
elite weightlifters resulted in increased LH levels.
Interestingly, this finding was concomitant with a decrease
in TT levels, suggesting that the reduction in serum levels
was not mediated by an impairment of hypothalamic–
pituitary function. The results of a 2012 study have added to
the controversy by reporting increased LH levels after a period
of 11 weeks in elite weightlifters [104]. In general, it could be
maintained that resistance training does not seem to affect the
pituitary in regard to LH response. The above discrepancies
could be attributed once again to the pulsatile release and
amplitude characteristics of LH [100] and the participants’
basal levels of testosterone, since, according to some authors,
LH levels are affected by the levels of this major androgen.
Furthermore, the participants’ training status could also
play a role, since untrained or less trained individuals
have been shown to have a higher response in regard to
testosterone, which could in turn be translated to alter-
ation in LH [97, 104, 105]. Concerning the latter hypoth-
esis, it should be mentioned that concomitant increases in
testosterone and LH levels during a long period of resis-
tance training or uncorrelated changes of these two hor-
mones have been reported [97, 104, 105].
Regarding the other gonadotropin, FSH, to our knowledge,
only three early studies [97, 102, 106] from the same labora-
tory have examined the effects of resistance exercise training
on gonadotropin serum levels. The authors of all three studies
reported that prolonged resistance training does not alter rest-
ing FSH levels in this specific type of activity. However, it
should be noted that in none of these studies did the authors
consider pulsatile secretion of FSH, an omission that could
imply the limited value of the aforementioned observations.
These findings should therefore be treated with caution.
Elements of the physiology of soccer
Soccer is a rigorous sport in which the players have to exercise
and perform at greatly uneven intensities distributed over time
in a highly discontinuous manner [107]. As a sport, it is char-
acterized as a high-intensity intermittent exercise which re-
quires players to be able to carry out complicated tasks requir-
ing aerobic and anaerobic competence, exhibit endurance and
explosive power, and handle strength loads of diverse inten-
sity. During soccer competitions and training, aerobic loading
is high, and it has been suggested that the main metabolic
functions rely predominantly on aerobic pathways [108].
However, although aerobic metabolism dominates the energy
supply, anaerobic energy, and in particular the ability of the
neuromuscular system to produce maximal strength and
159
power and their derivatives (sprints, jumps, and acceleration),
appears to be of crucial importance [109].
Indicative of the high aerobic requirements needed in
soccer is the finding that during a 90-min game of soccer,
the players cover a distance of 9–12 km [110]. In addition,
elite-level players play and/or train at an average intensity
close to the lactate threshold, which corresponds to an inten-
sity of approximately 87–90% of maximal heart rate, while
there is a constant change of activity every few seconds
[111]. During the endurance context of the game, each player
is required to perform approximately 1000 to 1400 activities
of short duration [108, 111, 112]. Moreover, during the
game, a high-intensity run occurs approximately every 70 s
(10 to 30 activities) at maximal speed, while the game will
also include about 10 headers, 15 tackles, 50 involvements
with the ball, 30 passes, and approximately 50 turns, and
sustaining forceful contractions to maintain balance and
control of the ball against defensive pressure [110].
It is evident from the above that anaerobic pathways are
highly taxed in soccer. However, due to the acyclic nature of
the sport, during competitions and training periods, there is
interaction between all three energy systems, aerobic, alactic
anaerobic, and lactic anaerobic. The dominant system at any
time depends on the intensity of the activity performed at the
specific moment. The fact that soccer training and competition
are dominated by speed acceleration, jumping, changing of
direction and breaking [110], which, in order to be performed
efficiently, require adequate aerobic levels (as indicated by
maximal oxygen consumption [VO2max]), demonstrates the
crucial importance of endurance, strength, power, and both
muscular hypertrophy and neural adaptations in this sport.
Regarding the latter two mechanisms, they have both been
shown to play a central role in the development of muscle
strength in soccer players [110]. However, it has been clearly
demonstrated that adequate performance during soccer train-
ing and/or competitions does not depend solely on sufficient
conditioning but also on other important parameters. Among
these, circulating adrenal and gonadal sex steroid levels are
hypothesized to be of great importance due to their effects on a
variety of factors that are directly or indirectly related to the
ability to perform efficiently during aerobic and anaerobic
types of activities.
Soccer and sex steroids: a bidirectional
relationship
Soccer implements aerobic, anaerobic, and strength loads,
which vary in intensity and volume, enabling the players to
achieve competitive success [110]. Therefore, soccer can be
characterized neither as a strictly endurance event nor as a
strictly strength and power event, making it more difficult to
evaluate and assess the hormonal responses to exercise
160
training and competition due to the variety of training
stimuli. There is uncertainty regarding the expected pat-
tern of response of sex steroids in these variables and,
therefore, concerning their usefulness in determining the
appropriateness of training loads, the impact of training
and competition volumes on change in these measure-
ments, and the relationships between change in measure-
ment variables and performance.
To date, few reports exist, which moreover are often con-
flicting, on the acute and long-term effects of soccer on sex
steroids [103, 105, 113–116]; most are, in addition, of limited
utility in that they examine only its effects on testosterone
levels. Changes in adrenal and gonadal sex steroids appear
to depend on the duration of the training program, the type
of exercise, the training status of the players, as well as the
intensity, duration, and volume of the exercise programs
employed [5, 117]. It should be noted that physical training
can be understood as a stress process that affects several phys-
iological systems. In this process, another steroid hormone,
cortisol (C), plays a role as a stress indicator. Most of the
available soccer studies examining the effect of long-term
training and/or competitions on sex steroids have also evalu-
ated C response as well as the T/C ratio as a reflection of the
balance between anabolic and catabolic processes.
Association between sex steroid levels
and soccer performance indices
The suggested beneficial effects of sex steroids on a variety of
parameters related to the ability to perform efficiently during
exercise raised the question of whether sex steroids, and main-
ly endogenous testosterone levels, are associated with soccer
performance indices. Published studies on the effects of sex
steroids on parameters of soccer performance are few and
limited in scope, while the findings are inconsistent.
A study by Bosco et al. [12] supports the generally pro-
posed notion that circulating testosterone levels are associated
with explosive exercise performance. In particular, the authors
reported that a significant relationship exists between TT
levels and both vertical jumping height and power output in
professional male soccer players. Based on their findings and
the well-established fact that explosive jumping performance
is positively related to the percentage of FT fibers in leg ex-
tensor muscles [118], the authors hypothesized that this ana-
bolic hormone influences the development of type II fibers.
Furthermore, a negative correlation was observed between
endurance capacity and TT levels, which, the authors
conjectured, must be related to the different distribution of
muscle fibers of various types in the athletes who were tested.
The latter hypothesis was based on the observation that sig-
nificant differences have been found between the distributions
of FT and ST fibers in endurance and sprint-type athletes
Hormones (2019) 18:151–172
[119]. Further confirmation regarding these findings came
from a study by the same group [13], the aim being to test
hormonal response to brief periods of supramaximal exercise
in professional soccer players. The authors reported that a
positive correlation was evident between average power out-
put during jumping and average jumping height and testoster-
one in professional soccer players, findings that were in agree-
ment with the postulated association between explosive per-
formance and testosterone levels. Of note, a limitation of this
type of experimental protocol is testosterone measurement at
only one time point, producing an incomplete estimation of
the adaptation curve of this type of athletic performance.
In contrast to the aforementioned evidence, a recent study
by Kraemer et al. [120] failed to confirm these findings. The
authors examined whether the antagonistic relationship be-
tween anabolic and catabolic processes during a soccer season
can affect performance. Twenty-five male collegiate soccer
players were studied throughout a season (11 weeks) to inves-
tigate the effects of long-term training and competition on
testosterone levels. Baseline testing was performed 1 week
before the first competitive game (T1), four assessments were
made during the season (i.e., weeks 3, 7, 8, and 9; T2–T5), and
a further assessment was made 1 week following the end of
the competitive period (T6) to determine whether any dramat-
ic recovery occurred. Subjects were grouped as starters (S)
and nonstarters (NS). When correlations between testosterone
levels and performance characteristics were explored, a sig-
nificant relationship was found in the NS between testosterone
and vertical jump performance at T5, but this was not a con-
sistent finding, since no other correlation was evident at the
other time points in either S or NS. The authors also observed
in the players categorized as S significant correlations between
testosterone concentrations and knee flexion at 1.05 rad sec21
for T6, knee flexion at 5.25 rad sec21 for T1 and T6, and peak
isometric torque at T1 and T3. However, similar to jumping
ability, these correlations were not evident in the same pattern
throughout the study in both S and NS; therefore, they did not
constitute an effect of circulating TT levels on isometric
strength and comprised only a random finding. Similar find-
ings were reported by Gorostagia et al. [121]. The authors
examined the hormonal responses over the course of 11 weeks
of training and soccer competition in 21 regional soccer
players and the association between TT and C as well as the
load-vertical jumping height curve (with different external
loads), sprint, and endurance running performance. A control
group and an explosive-type strength-training group were
used to examine this question. No significant correlations
were observed between the individual changes in performance
parameters and the individual changes in serum hormone con-
centrations from weeks 0 to 11 in either group, indicating that
the main androgen, TT, does not seem to be associated with
the jumping, sprinting, and aerobic capacity of soccer players.
Only a significant inverse correlation was observed in the
Hormones (2019) 18:151–172
experimental group between the individual relative increase in
countermovement jump (CMJ) height with the use of 40 kg
external load and the individual relative changes in the serum
testosterone/cortisol ratio, from weeks 0 to 4, 4 to 8, and 8 to
11. These findings indicate that those players with a larger
decrease in the testosterone/cortisol ratio may be more likely
to produce major explosive strength gains than those with
smaller decreases in the testosterone/cortisol ratio. However,
since these correlations were observed only in the experimen-
tal group, they could not be attributed to soccer training but
were rather the result of the specific strength-training regime
used in this study: this further supports the notion that
strength-training alterations may lead to modifications in
anabolic/catabolic processes [1, 4]. The findings from a recent
study in elite under 15 (U15) and under 17 (U17) soccer
players are in agreement [122]. Testosterone levels and per-
formance (CMJ test with a bar of 30% of body mass on
the athlete’s shoulders) were assessed on three occasions,
T1: beginning of the competitive season, T2: end of the
regular season, and T3: end of the playoffs. No significant
correlation was identified between the relative changes in
T concentration and power performance in both groups.
The findings of this study suggest that T changes and
power changes are not related.
These observations are supported by two studies from our
laboratory [123, 124]. We have observed that during presea-
son and at different time points during the competition season,
there was no correlation of TT, FT, 3a-diol-G, DHEA-S, Δ4-
androstenedioe, LH, FSH, E2, and PRL with the ergometric
evaluation of soccer performance. We failed to observe any
relationship between sex steroids and exercise performance
despite the observed changes in performance parameters,
TT, and 3a-diol-G levels during the entire study. Notably,
throughout these two studies, in order to exclude some of
the parameters that could affect endogenous sex steroid levels,
a controlled dietary intake was followed, and furthermore,
training load was constantly monitored in order to avoid any
overtraining or overreaching effect. Our findings clearly sug-
gest that adrenal and gonadal sex steroids do not seem to
directly affect soccer performance.
The observed discrepancies in the literature could addition-
ally be a result of changes in the rate of production and re-
moval of both sex steroids, as well as to changes in the pattern
of their distribution, especially in the studies that have closely
examined the association between sex steroids and perfor-
mance indices. Furthermore, it should be mentioned that
among different soccer teams, there can be significant differ-
ences in the intensity, volume, and load of the employed train-
ing programs, which could in turn lead to modifications in
endogenous hormonal production [5].
However, we could not exclude the possibility that sex
steroids may have favorably affected exercise performance
via the aforementioned proposed indirect mechanisms.
161
Indeed, it has been suggested that sex steroids have the ability
to indirectly affect exercise capacity by a variety of mecha-
nisms, such as (a) an effect on intracellular calcium release
[42] and inhibition of the anticatabolic effects of glucocorti-
coids; (b) anti-inflammatory effects and thus enhanced recov-
ery after strenuous exercise; (c) activation of the glucose me-
tabolism-related signaling pathway in skeletal muscle
[103] and thus enhanced carbohydrate utilization during
exercise, the latter stimulating catecholamine-induced li-
polysis [40] in a dose-dependent manner and providing a
massive availability of energy during exercise; (d) altered
muscle damage and repair after exercise; and lastly, (e)
due to increased aggression, a facilitation of neural input
during maximal explosive effort.
Effect of soccer on sex steroid production
Sex steroid response to soccer competitions
Although limited in number, several studies have examined
the effects of soccer competition stress on sex steroids
(Table 1). Notably, the majority of the available evidence
has examined the main androgen, testosterone, while very
scarce or no data exist concerning the other sex steroids.
Aizawa et al. [125] examined the changes of pituitary, adrenal,
and gonadal hormones during competition among female soc-
cer players. The authors observed that levels of C and PRL
increased significantly during competition compared with
precompetition. Levels of LH increased significantly during
competition and those of DHEA-S changed significantly,
whereas levels of T and FSH were unchanged. The authors
concluded that hormonal changes reflect physical and mental
stress during competition. By contrast, TT levels were found
to increase in men and women, members of intercollegiate
varsity soccer teams, after league matches [126]. Similar re-
sults were reported by Celani and Grandi [114]. The authors
found a significant rise of serum testosterone following stren-
uous soccer games in ten well-trained but nonprofessional
soccer players. In a subsequent study conducted by the same
authors, differences were examined between professional and
nonprofessional soccer players [114]. In nonprofessional
players, the 90-min game resulted in increased TT and PRL
levels, thus providing confirmation of the findings of their
previous study. However, the results of the professional soccer
players revealed increased PRL levels, though TT and the
gonadotropins LH and FSH remained unchanged.
Interestingly, the LH response of the nonprofessional players
was higher compared to their professional colleagues. The
authors attributed these differences between nonprofessional
and professional soccer players to the higher physical and
emotional stress of the nonprofessional players [127]. The
latter changes seem to be related to the stress induced by the
circulating catecholamines and glucocorticoids [127, 128],
162 Hormones (2019) 18:151–172

TT, total testosterone; FT, free testosterone; 3a-diol-G, 3α androstanediol glucuronide; C, cortisol; DHEA-S, dehydroepiandrosterone-sulfate; Δ4, Δ4 -androstenedione; E2, estradiol; LH, luteinizing
TT ↑ in the S group; no change for FT in both groups
↑ C, ↑ PRL during competition vs pre; ↑ LH during
competition vs pre; no changes in TT, DHEA-S,
both known to impair Leydig cell function [127]. Thus, any

SD: TT ↑, PRL ↑; no changes in LH, FSH levels

TT ↓ at half-time C ↑ during the match / normal
possible impairment in Leydig cell steroidogenesis could be
the result of the unchanged TT levels in professional soccer

levels at 45 and 90 min after the match

PF: PRL ↑; no changes in TT, LH, FSH

athletes in response to the soccer match. In line with the latter

TT ↑; no changes in LH, FSH, PRL

C ↑ and T/C ↓ until 48 h recovery

findings regarding testosterone, the authors of three other

C ↑ postgame, no change in TT
studies failed to observe any alterations in plasma T (including

FSH during competition.

free T) concentration immediately after and 72 h after a soccer
competition [115, 129, 130].
Conversely, in the study by Sotiropoulos et al. [116], TT
concentration decreased, while C concentration increased sig-
nificantly, resulting in a > 50% drop of the T/C ratio. These

Results
data suggest that high-intensity intermittent exercise of long
duration, such as a soccer match, increases C, decreases TT
concentration and, as a consequence, results in a decreased T/

TT, DHEA-S, C, LH, FSH,

C ratio, indicating that a soccer match places considerable
stress on the endocrine system, leading to a catabolic environ-

TT, LH, FSH, PRL

TT, LH, FSH, PRL
ment. Similar results in regard to TT were reported by Lupo

Measurements
et al. [131] after the first half of a soccer competition. In 18
trained football players, blood samples were collected before a

PRL

TT, C
TT, C

TT, C

Experimental group (played in the game; n = 14) or a TT, C

football match, at half-time, at the end, and 45 and 90 min
after the end of the match. TT levels showed a decrease in the

match, at half-time, at the end, and 45 and 90 min

Blood samples 14–15 h from the end of both a cus-

rest period. Cortisol and Δ4-androstenedione levels increased

tomary training session and a strenuous football

Players performed an official match and data were

Blood samples were obtained before (pre), during

control group (did not participate in the game;

3 days of competition (competition), and after

Saliva samples before and after league matches

Blood samples were collected before a football
immediately after the match but returned to control levels 45

Blood samples collected after a 90-min match

collected 72 h before and 24, 48, and 72 h
and 90 min after the end of the match, respectively. It is sug-
gested that during this type of exercise, anabolic and catabolic
hormones may be simultaneously activated. These hormonal
responses appear to be reflective of the metabolic demands of
Experimental design details

competition (post-3 days)

after the end of the match

soccer [1] coming from high-intensity activities alternating

with periods of lower-intensity activities.
It is evident that there is variability in these hormonal re-
sponses after soccer competitions. These discrepancies are in

hormone; FSH, follicle-stimulating hormone; PRL, prolactin; ↑, increase; ↓, decrease

postmatch

n = 10)
accordance with observations from other studies in different
match

sports [1, 4]. Explanations for the discrepancies have been pro-
posed in other observational studies concerning different sports, 10 age-matched, healthy, sedentary controls (SD)
which took into consideration that there is great variability with-
Men and women university’s intercollegiate varsity

10 trained nonprofessional soccer players (PF) and

in soccer games in regard to intensity, volume, the opponents’

ability, environmental parameters (e.g., exercise in high temper-
atures, at a high altitude, etc.), training status of the players, and
the fact that nominal time and actual playing time can differ
Sex steroid response to soccer competitions

7 male professional soccer players

7 high-level male soccer players

substantially with every soccer game. Another possible mech-

18 trained male soccer players

9 elite female soccer players

24 elite male soccer players

anism could be related to modifications in the action of the

hypothalamic–pituitary–adrenal axis (HPA) on testicles or ad-
renals in response to the balance between exercise and recovery
[132, 133]. Inappropriate physiological loading would likely
soccer team
Participants

result in increased C due to oversecretion of adrenocorticotro-

phic hormone as a response to the increased sensitivity of the
HPA to stress [4, 5]. According to Tremplay et al. [5], hormonal
responses to exercise depend on the intensity and volume of the
Edwards et al. [126]

Ispirlidis et al. [115]

Aizawa et al. [125]

performed activities and the training status of the participants, a

Celani and Grandi

Grand and Celani

Lupo et al. [131]

Silva et al. [129]

finding that accounts for the difference in observed hormonal

responses after a soccer game.
[127]
[114]
Table 1

It should be noted that reasons other than physiological

Study

stress, such as psychological factors, could affect sex steroid

Hormones (2019) 18:151–172
responses after competitions. Individuals losing an athletic
competition (loss of status) would experience a greater degree
of stress, which would influence their postcompetition TT,
DHEA-S, and C levels [134]. According to these authors, in
men, androgens generally increase following victory and de-
crease following defeat, while C has a reverse response [132].
In addition, several studies have shown that other factors, like
context [135], individual differences, e.g., power motivation
[136], social anxiety [137], and motivation to win [138], as
well as cognitive appraisal [139], can play an important role in
predicting postcompetition testosterone changes. However, it
must be mentioned that effects on changes in men’s testoster-
one brought about by winning or losing are not always ob-
served [138, 140].
Sex steroid responses to soccer training
Several published reports, most of them examining the re-
sponse of testosterone, suggest that soccer training induces
the production of sex steroids. Filaire et al. [132] reported that
salivary testosterone in 17 France national team players was
significantly reduced during a period of poor performance in
the competitive season. Similarly, decreased levels of andro-
gens, TT, and DHEA-S were also reported, implying that the
decreased androgen levels had a negative effect on perfor-
mance, possibly due to a decreased anabolic environment. A
recent study in elite under 15 (U15) and under 17 (U17) soccer
players also observed decreased saliva TT levels at the end of
the competitive period as compared to the beginning of the
season [122]. According to the authors, the observed reduc-
tion in T concentration in both the U15 and under U17 groups
over the study period could be attributed to variation in the
training content and could perhaps be related to an inappro-
priate balance between stress and recovery. Studies from other
laboratories that have examined a variety of team sports, in-
cluding soccer, are in agreement with these findings.
Decreased levels of the androgens TT, FT [141–144], and
DHEA-S [141] were also reported. However, the mechanisms
for these changes remain unclear. One explanation could be
interactive modifications of the HPA axis [145], dependent
upon modifications of hormonal uptake by their target organs
or even alterations in their catabolism [146, 147].
Different results were reported by Celani and Grandi [114].
The authors examined the effects of a 3-month regular training
program on the pituitary testicular axis in nonprofessional
male soccer players. Basal serum levels of T and also the
gonadotropins, LH, FSH, and PRL, were measured before
and after the experimental period. No alterations were evident
for any of the measured parameters. In support of these find-
ings, Hoffman et al. [90] found that an intercollegiate soccer
season did not affect total TT serum levels. Throughout the
competitive season, circulating TT concentrations remained at
baseline levels, suggesting that in male soccer players, a
163
season of intercollegiate soccer had minimal effect on the
adrenal–testicular axis. Interestingly, starters had an average
of 11.8% greater resting TT concentrations than nonstarters
throughout the season. This observation could imply a possi-
ble effect of the extra intensive competition load on total T
levels on basic players compared to nonstarters. Although this
difference was statistically insignificant, it is interesting in the
light of the observation that elevated TT levels were negative-
ly correlated to fatigue [148].
In another study examining responses to a season of soccer
match play, 20 professional players were tested at four points
throughout a season after periods of different volumes and
intensities of training [133]. These authors reported that TT
remained unchanged throughout the study, while resting sali-
vary C was significantly elevated at the end of the season,
having risen in a progressively increasing manner from base-
line toward the end-point measurement. Both TT and C levels
had returned to normal by the commencement of the follow-
ing season, and TT/C was relatively unchanged except for a
nonsignificant decrease at the end of the season compared to
baseline. The change in TT/C was found to be nonsignificant;
however, it may represent further evidence of the potential
benefit of this measure for monitoring responses in team sport
athletes over long-term training periods. The nonsignificant
decrease in TT in conjunction with the elevations in C levels
provides further evidence of the type of response that may be
expected throughout a season of high-level team sport com-
petition. It seems that in this study, the recorded TT, C, and
TT/C values point to progression toward a catabolic state in
the final phase of the competitive season. This may be related
to the extended nature of competitive seasons and the accu-
mulation of periods of less than optimal recovery over time.
In contrast, an early study by Carli et al. [149] showed that
TT levels increased significantly during a competitive soccer
season. The authors examined the impact of a season of semi-
professional soccer competition on both TT and C. They ob-
served that TT levels increased at the 3-week mark, although
beyond this time, levels were not different from pretraining
values. It was hypothesized that the observed increase in cir-
culating TT was possibly related to the increased need for
glycogen storage and replenishment in response to exercise
training stress. In addition, the authors observed that C in-
creased as a response to training, with rises occurring 12 weeks
after the commencement of training and at the end of the
season (24 weeks). In agreement are the findings of another
study by Kraemer et al. [120]. The authors examined hormon-
al responses during 11 weeks of football training in starters
and nonstarters. Analysis of their results showed that while TT
concentration was low, though within normal values, at base-
line, there was evidence of a significant increase in TT levels
in both groups after the end of the study, implying a positive
trigger on the pituitary–gonadal axis regarding TT. The only
difference between groups occurred at the 3-week
164
measurement, with nonstarters displaying higher levels.
Interestingly, C was higher in nonstarters than in starters at
baseline 1 week prior to the commencement of the season.
At week 8, starters showed an increase in C. Testosterone/
cortisol was elevated in the nonstarter group at the end of
the season compared to baseline and after 3 weeks of compe-
tition. An important finding of this study was that both starters
and nonstarters suffered performance decrements throughout
the season, suggesting that responses are independent of
match play. In other words, training may have a larger impact
on performance variables and hormonal markers than compe-
tition. However, it should be mentioned that the observed rise
in TT at the end of their study was tentatively attributed not to
soccer training but rather to the results of the reduction in
training stress. The latter hypothesis lends further confirma-
tion to the suggestion that TT levels are negatively correlated
to fatigue [148]. In agreement are the findings of Gorostiaga
et al. [121]. The purpose of their study was to examine the
effects of explosive strength and soccer training after a period
of 11 weeks. The authors observed that a progressive train-
ing program, which is relatively common practice in soc-
cer, including full squad, vertical jump, and sprinting ex-
ercises, resulted in increased TT levels. In addition, this
increase was accompanied by improvements in low load
portions in load-vertical jumping strength, suggesting a
close relationship between TT levels and performance.
Variations in TT in response to soccer training were report-
ed by Handziski et al. [143]. The aim of their study was to
evaluate changes in a number of hormonal parameters during
a competition half-season. Thirty male professional soccer
players were tested three times, prior to the preparation phase,
before the competition phase (conditioning phase) during a
week of tapering in which intensity and volume of exercise
was reduced, and after finishing the completion phase.
Interestingly, analysis of the results revealed that after the
conditioning phase, both TT levels and TT/C increased sig-
nificantly, whereas C levels decreased, pointing to an in-
creased anabolic environment, this implying that soccer
players were able to recover quickly from the stresses of train-
ing [120]. Conversely, after the competition phase, both TT
and TT/C serum levels were significantly decreased, whereas
C levels were increased. The increase in TT and TT/C after the
conditioning phase could be due to the training workload
used, i.e., decreased volume of training and intensity, since
androgen levels have been reported to be affected by both
these parameters. By contrast, the significant decrease in TT
levels, accompanied by increased C levels and thus a de-
creased TT/C ratio, could be connected to the volume and
intensity of previous working loads [143] (numbers of com-
petitions). Recent studies conducted at our laboratory have
evaluated the effect of seasonal soccer training on all adrenal
and gonadal sex steroids [124,150]. We examined sex steroid
responses over an entire soccer season (preseason and
Hormones (2019) 18:151–172
competition period) in three professional soccer teams which
differed in strength-training volume and load. Analysis of our
results revealed that regular soccer training alone does not
affect circulating sex steroid levels. In contrast, we observed
that a combination of soccer training with strength sessions
over a season increases TT and FT but does not affect DHEA-
S, Δ4-androstenedione, LH, E2, FSH, and PRL. The observed
gonadal androgen increases were in proportion to the strength-
training volume, i.e., the higher the volume (3 sessions/week
vs 2 sessions/week), the more pronounced the elevations.
Furthermore, we observed that the program that was charac-
terized by the higher strength training volume in our study (3
sessions/week) provided sufficient stimulus for an increase in
circulating 3a-diol-G levels. This metabolite has strong andro-
genic activity, estimated at 75% of the bioactivity of testoster-
one [151]. A significant amount of 3a-diol-G also derives
from DHEA-S and androstenedione. Τhe elevation of 3a-
diol-G levels indicates a positive anabolic effect, since this
metabolite is a marker of the total androgen pool and an indi-
cator of peripheral activation of androgens [152].
To date, the available literature does not provide clear-cut
conclusions regarding the effects of soccer training/
competition on the production of gonadal sex steroids.
Nevertheless, it now appears that the magnitude of the effects
of soccer on gonadal sex steroids depends on the exercise
mode and training status of the subjects as well as the inten-
sity, duration, and volume of training [120]. The latter data are
further confirmed by the studies of Pacobahyba et al. [153]
and Gorostiaga et al. [121] as well as the study from our
laboratory [123] showing that alterations in training volume
and load and the specific exercise activities employed during
soccer training may affect sex steroid levels. Furthermore, it
should be mentioned that inadequate or adequate recovery
from exercise, increased energy demands, and insufficient
substrate replenishment occurring at intervals throughout the
long-term training period could also be responsible for fluctu-
ations in hormonal responses and thus the observed discrep-
ancies in the available literature [4] (Table 2).
Anabolic androgenic steroids and athletes
Anabolic steroids are synthetic derivatives of the main andro-
gen, testosterone, including testosterone itself, which is the
primary male sex hormone [154]. These agents have been
chemically modified to maximize the anabolic (nitrogen re-
tention and protein synthesis) and minimize the androgenic
(masculinizing) effects [155]. However, none of the currently
available drugs are purely anabolic: the two effects are insep-
arable [156], which accounts for their being named anabolic
androgenic steroids (AAS).
AAS have well-documented and valid medical/therapeutic
uses in diseases such as male hypogonadism, certain types of
Table 2 Sex steroid response to soccer training

Study Participants Experimental design details Measurements Results

Filaire et al. [132] 17 male soccer players The initial testing was performed 1 day following TT, FT TT ↓ at T3 and T4; no changes for FT
the start of season training (T1). They were then
performed before and after a high-intensity train-
ing program (T2 and T3, respectively) and
16 weeks after T3 (T4)
Hormones (2019) 18:151–172

Filaire et al. [133] 20 professional soccer players
Celani and Grandi [114] 7 professional soccer players
Grandi and Celani [127] 10 trained non-professional soccer players Testing was performed prior the beginning of the
and 10 age-matched, healthy, sedentary
controls
Gorostiaga et al. [121] 8 experimental (S) and 11 control (C) re- 11-week in-season training; the strength training
gional soccer players
Kraemer et al. [120] 25 male collegiate soccer players
Pacobahyba et al. [153] 24 U20 soccer players
Koundourakis et al. [123] 67 male professional soccer players
members of 3 teams
Koundourakis et al. [124] 45 male professional soccer players
Handziski et al. [143] 30 professional soccer players
4 occasions throughout a season after periods of
different volumes and intensities of training
Players were examined after a 30-day rest period
and after 12 weeks
seasonal training (after a 30-day rest period), and
after 12 weeks
program in the S group consisted of two training
sessions each week; players of the S group also
performed some light strengthening exercises
(loads of 40–60% of one maximum repetition)
11-week period in-season, with variations in volume
Nonlinear periodization program (G1) and
nonperiodized program (G2), both for 12 weeks,
3 times/week
Players were members of 3 teams with different
strength training protocols: team A (high-strength
training stress); team B (moderate-strength
training stress); team C (low-strength training
stress). Measurements were performed at 4
points. 1: beginning of preseason; 2: at
mid-season; 3: at the end of the season
Measurements were performed at the beginning
(pre) and at the end (post) of a 6-week off-season
period
Measurements were period performed at
half-season: before the preparation phase (phase
I), before the competition phase (phase II; after
previous phase), and after finishing the
competition phase (phase III)
TT, C No changes in TT throughout the season; C ↑
only at the end of the season
TT, LH, FSH, PRL No changes in TT, LH, FSH, and PRL levels
(long-term effects on basal levels)
TT, LH, FSH, PRL No changes in TT, LH, FSH, and PRL levels
(long-term effects on basal levels)
TT, FT TT ↑ in the S group only; no changes for FT in
both groups
TT TT ↑ at the end of the study
TT TT ↑ at the end of the study in both G1 and G2
compared to baseline; TT ↑ in G1 vs G2
TT, FT, 3a-diol-G Team A: TT ↑ at 2 vs 1 and 3 vs 1 and 2;
3a-diol-G ↑ at 3 vs 1 and 3 vs 2; no changes
observed for DHEA-S, Δ4, FT; no changes in
both teams B and C
TT, FT, DHEA-S, Δ4, No changes in any of the examined hormones
3a-diol-G, Ε2, LH
FSH, PRL
T, C Phase II: TT ↑, C ↓, TT/C ↑
Phase III: TT ↓, C ↑, TT/C ↓

TT, total testosterone; FT, free testosterone; 3a-diol-G, 3α androstanediol glucuronide; C, cortisol; DHEA-S, dehydroepiandrosterone-sulfate; Δ4, Δ4 -androstenedione; E2, estradiol; LH, luteinizing
hormone; FSH, follicle-stimulating hormone, PRL, prolactin; ↑, increase; ↓, decrease
165
166
anemias, osteoporosis, and breast cancer and for producing
anticatabolic effects in muscle wasting syndromes [154,
155]. However, for approximately the past 80 years, they have
been extensively used for nontherapeutic purposes, AAS be-
ing some of the most commonly employed performance-
enhancing drugs among athletes [154]. The huge popularity
of these agents among the athletic population is based on
expectations that AAS administration can exert a number of
powerful effects on the human body [157], providing both
acute and long-term benefits in exercise performance and ca-
pacity. Initially, AAS were employed only by athletes partic-
ipating in sports requiring strength and high levels of peak
power. However, their use and abuse has extended also to
those participating in endurance activities, the athletes’ aim
being to achieve positive alterations in the rheological proper-
ties of the blood as well as enhanced recovery after exercise
[155]. Based on the available recommendations and setting
aside those reports that are of low quality and lack consistency,
solid evidence, and scientific support [154], in general, ath-
letes who abuse AAS are aiming for certain potential benefits
that can be both physiological and psychotropic. Regarding
the physiological aspects, they wish to benefit from a number
of ergogenic effects, such as increased anabolism via nitrogen
retention and protein synthesis, decreased catabolism via glu-
cocorticoid antagonist action and/or inhibition of myostatin,
increased blood flow and oxygen transport to the exercising
muscles and thus enhanced endurance capacity, and augment-
ed recovery after exercise [157–160]. They also want to take
advantage of a possible stimulatory effect on other anabolic
agents, and specifically on human growth hormone and insu-
lin growth factor-1 [154, 155]. As to the desired psychotropic
effects, these include increases in motivation, aggression, and
positive mood, along with a state of euphoria, all of which are
likely to aid them during training and competitions [154, 155].
However, despite the general consensus among athletes that
they do indeed benefit from nonpharmaceutical AAS admin-
istration, evidence supporting the ergogenic effect of AAS on
exercise performance capacity among healthy athletic individ-
uals remains scant [155, 157]. Admittedly, the scientific data
suffer from inconsistency among the various studies. For
example, discrepancies exist in study designs and meth-
odologies, including differences in administration strate-
gies and periods, assorted training protocols [159], the
lack of placebo, of control groups, and/or of a double-
blind design, as well as methodological flaws in the doses
used [157, 161–164]. There are even reports combining
discussion of AAS abuse with that of abuse of other licit
or illicit substances, making it difficult to accurately dis-
criminate between the observed effects [155, 157].
However, two issues in particular limit our ability to scien-
tifically validate the perception of athletes regarding the ergo-
genic effects of AAS. Firstly, there is the fact that AAS abuse
involves supraphysiological doses that are considerably
Hormones (2019) 18:151–172
greater, approximately 100- to even 1000-fold in excess of
medically used doses, and secondly, athletes typically com-
bine several AAS agents [154, 155]. The presence of these
two factors, apart from arousing serious ethical concerns
among researchers, also makes it impossible to replicate what
athletes actually use. Studies on doping are therefore unlikely
to reproduce the performance effects that administration of
supraphysiological doses is claimed to achieve [155–157].
Taking into account all the aforementioned limitations, it is
not surprising that many studies have failed to detect any
ergogenic effects of AAS leading to performance benefits.
However, recent well-designed studies using modestly
supraphysiological doses of AAS have shown that they do
indeed possess ergogenic effects [155], with evidence clearly
supporting the positive effects of AAS on muscle anabolism
and lean body muscle and strength-related measures, such as 1
repetition maximum on bench press and squat and isokinetic
strength in active healthy individuals [154, 155]. The studies
further indicate that the observed effects are dose-dependent
[154, 155]. In support of the latter findings, there are indica-
tions that supraphysiologic doses of testosterone, combined or
not with strength training, increase fat-free mass as well as
muscle size and strength in normal men, although it is not
clear whether these effects are actually translated to increased
exercise performance [6]. Specifically regarding soccer, there
are to date no studies examining anabolic agent supple-
mentation on exercise performance parameters. To the
best of our knowledge, the only evidence comes from a
study examining the effects of another anabolic agent,
DHEA, on body composition parameters. The authors re-
ported that supplementation in youth soccer players [165]
failed to induce any positive effect of this steroid
prohormone on lean body mass and body fat percentage,
questioning its efficacy at least in this athletic population.
Although the effects on muscle anabolism, lean body mass,
and strength are unequivocal, this is not the case as regards the
existing evidence for other ergogenic physiological effects of
AAS administration on healthy active individuals [155]. Some
findings indicate that AAS users may enhance performance
through positive effects on erythropoiesis, red blood cell count,
hematocrit, hemoglobin, vasodilation, blood flow, and even
positively altered capillary density within skeletal muscle after
long-term AAS abuse [1, 155]. The benefit of all these adapta-
tions could hypothetically be increased oxygen and nutrient
supply during exercise and faster removal of the metabolic
by-products [1, 154]. These effects could, also hypothetically,
enhance aerobic capacity. However, although the above results
have been clearly seen in animal studies as well as in studies in
elderly individuals with mobility issues [1, 154, 155], with the
results applying to some but not all examined aerobic capacity
measures, the same results were not observed in active healthy
males: the actual efficacy of AAS agents as concerns aerobic
related performance is thus disputable [166].
Hormones (2019) 18:151–172
Regarding the suggestion that AAS promote recovery via
their anticatabolic effects [167], the available literature does
not support this notion. This idea was initially based on
evidence coming from animal studies showing that andro-
gens can bind to glucocorticoid receptors [158, 168, 169],
thereby blocking the catabolic actions of hormones, such as
cortisol involved in tissue breakdown during and after ex-
ercise, which effects could, in turn, speed recovery from
exercise. However, this anticatabolic action has not in fact
been clearly demonstrated [158]. The available studies on en-
hanced recovery examined indirect parameters of exercise
stress [157], such as CPK concentration and lactate concen-
trations [154, 170, 171]: they furthermore provide inconsistent
findings [154, 155]. Notably, a study has reported a higher
androgen/cortisol ratio [172] after a strength-training regime
in athletes who were on AAS compared to nonusers; however,
since there is minimal research into these findings, substantial
conclusions cannot be drawn.
Apart from the reported physiological effects, there are
findings suggesting that AAS administration results in several
acute and long-term psychotropic effects that could enhance
performance, such as increased motivation, aggression, deter-
mination and cognition, elevation of mood, and euphoria
[154, 155]. However, in conjunction with the above positive
effects, several other negative effects have been observed,
such as increased irritability, mood swings, distractibility
[173], maniac episodes, and even cognitive deficits, notably
in visuospatial memory, which is vital for athletic performance
[174], especially in team sports. The latter effects throw fur-
ther doubt on the presumed benefits of AAS for enhancing
performance. Lastly, some evidence suggests that AAS have
also been shown to play a role in neuroprotection and nerve
regeneration, although adverse neurotoxicity has also been
described with prolonged use [175], which could ultimately
result in a worsening of athletic performance. However, the
latter finding is not alone among the suspected negative effects
of AAS administration. There is a plethora of data indicating
that AAS abuse can result in a number of reversible or irre-
versible life-threatening disorders. More specifically, it has
been reported that AAS abuse is correlated with numerous
side effects that can induce cardiovascular, hepatic, muscular,
endocrine, skeletal, immune, reproductive, and renal dysfunc-
tions, debilitating psychological symptoms, and, in some
cases, even increased mortality [176, 177]. Given the huge
risks, it appears strange that AAS are so widely abused by
athletic and nonathletic populations: one would assume that
no potential or even proven ergogenic benefit that could
provide an advantage during one or several competitions
is worthwhile sacrificing one’s health for. It is clear that
tools to support AAS doping prevention should be imple-
mented, these including educational and/or screening par-
adigms [154] to reduce AAS abuse and even eliminate
nontherapeutic AAS administration.
167
Conclusion
To sum up, it is evident that, currently, inconsistent scientific
evidence exists regarding the behavior of sex hormones in
response to both soccer competition and short- or long-term
soccer training periods.
Soccer is a sport involving a wide range of actions covering
a broad array of exercise conditioning and during which aer-
obic and anaerobic, lactic and alactic metabolism is activated.
Players, especially professionals, are continuously (training
and competition) under physiological and psychological stress
for approximately a 10-month period. Thus, the nature of the
sport itself could be a reason for the equivocal scientific evi-
dence. A soccer player needs high levels of various types of
endurance, anaerobic and strength and power performance,
parameters that have all been reported to modulate the balance
and secretion of sex steroids in different ways [4]. Many of the
scientific uncertainties seem likely to be related to the com-
plex and variable nature of the exercise and psychological
stress experienced by soccer players. Furthermore, none of
the studies covering either competitions or training periods
have reported in detail on the physiological stress the subjects,
i.e., the players, were under, their mood states (especially as
regards competitions), their psychological profile (capability to
cope in extreme situations/conditions), their training status, the
volume, intensity, and duration of exercise, sufficient or inade-
quate recovery from exercise, and nutritional parameters, nor
was there sufficient reference to environmental factors (e.g., air
temperature) which could lead to fluctuations in hormonal re-
sponses. Moreover, the studies varied greatly in experimental
design. Even when descriptions were included of volume, in-
tensity, and load of exercise, the studies employed different
terminology [178], thus adding to the many inconsistencies. It
is also possible that well-trained athletes may respond differ-
ently. In sum, all these factors or any one of them can exert a
different effect on the pituitary–adrenal axis, or can lead to
imbalances in the anabolic–catabolic ratio and, in general, dif-
ferent modulations of the pattern of basal hormone secretion.
Today, a much more detailed analysis is possible of the
exact load players need to cope with during both competition
and long-term training periods (time motion analysis; global
positioning system [GPS]) [179, 180]. Thus, what is required
in order to examine the acute and long-term training effects on
sex steroids is regular and accurate analysis during competi-
tions, along with interpretation of week-to-week training loads
as concerns the multiple kinds of activities used and the train-
ing, volume, and duration of exercise, with clear definitions of
the nature of the exercise stimulus.
Regarding AAS abuse, the well-demonstrated side ef-
fects heavily outweigh any perceived benefits they may
provide. Undoubtedly, educational and/or screening para-
digms should be implemented in order to eliminate non-
therapeutic AAS administration.
168
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