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Endocrine response to masturbation-induced orgasm in healthy men following a 3-week sexual abstinence


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This current study examined the effect of a 3-week period of sexual abstinence on the neuroendocrine response to masturbation-induced orgasm. Hormonal and cardiovascular parameters were examined in ten healthy adult men during sexual arousal and masturbation-induced orgasm. Blood was drawn continuously and cardiovascular parameters were constantly monitored. This procedure was conducted for each participant twice, both before and after a 3-week period of sexual abstinence. Plasma was subsequently analysed for concentrations of adrenaline, noradrenaline, cortisol, prolactin, luteinizing hormone and testosterone concentrations. Orgasm increased blood pressure, heart rate, plasma catecholamines and prolactin. These effects were observed both before and after sexual abstinence. In contrast, although plasma testosterone was unaltered by orgasm, higher testosterone concentrations were observed following the period of abstinence. These data demonstrate that acute abstinence does not change the neuroendocrine response to orgasm but does produce elevated levels of testosterone in males.
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Michael S. Exton áTillmann H. C. Kru
Èger áNorbert
Bursch áPhilip Haake áWolfram Knapp áManfred
Schedlowski áUwe Hartmann
Endocrine response to masturbation-induced orgasm in healthy men
following a 3-week sexual abstinence
Abstract This current study examined the eect of a
3-week period of sexual abstinence on the neuroen-
docrine response to masturbation-induced orgasm.
Hormonal and cardiovascular parameters were exam-
ined in ten healthy adult men during sexual arousal
and masturbation-induced orgasm. Blood was drawn
continuously and cardiovascular parameters were
constantly monitored. This procedure was conducted
for each participant twice, both before and after a
3-week period of sexual abstinence. Plasma was sub-
sequently analysed for concentrations of adrenaline,
noradrenaline, cortisol, prolactin, luteinizing hormone
and testosterone concentrations. Orgasm increased
blood pressure, heart rate, plasma catecholamines and
prolactin. These eects were observed both before and
after sexual abstinence. In contrast, although plasma
testosterone was unaltered by orgasm, higher testos-
terone concentrations were observed following the
period of abstinence. These data demonstrate that
acute abstinence does not change the neuroendocrine
response to orgasm but does produce elevated levels of
testosterone in males.
Key words Abstinence áSexual arousal áOrgasm á
Prolactin áCatecholamines áCortisol á
Testosterone áCardiovascular
Although sexual abstinence is a common behavioral
pattern in humans, there has been little examination of
the psychological and physiological consequences of this
behavior. Nevertheless, limited data have demonstrated
that sexual abstinence may impact on the physiological
regulation of sexual function. Speci®cally, retrospective
studies have shown that features of semen quality are
reduced during long periods of sexual abstinence [5, 22].
In contrast, periods of abstinence between 12 h and
10 days have generally revealed enhanced sperm quality
parameters [9, 26, 28, 33], although this is not consistent
across all measures of sperm quality [28, 33]. Neverthe-
less, acute sexual abstinence is commonly employed prior
to clinical sperm donation to enhance sperm quality.
Despite knowing that acute abstinence aects repro-
ductive function, no data exist that examines the eect
of abstinence on the physiological response to sexual
arousal and orgasm. We have established a method for
examining the neuroendocrine response to masturba-
tion-induced orgasm in men and women [15±17, 24],
based upon a continuous blood sampling technique.
These investigations demonstrated that masturbation-
induced orgasm produced a pronounced increase in
cardiovascular responses and plasma catecholamine
concentrations. Furthermore, sexual arousal was char-
acterised by a large, persistent increase in concentrations
of plasma prolactin. Since hyperprolactinemia is known
to inhibit sexual arousal and function [13, 35], these data
suggest that prolactin may act as a peripheral and/or
central feedback signal in controlling sexual arousal
following orgasm.
Therefore, the purpose of this current study was
to investigate the eect of acute abstinence on the
physiological response to sexual arousal. Speci®cally, we
World J Urol (2001) 19: 377±382 ÓSpringer-Verlag 2001
The ®rst two authors made equal contributions to this work. This
study was partially supported by a grant from the Deutsche Fors-
chungsgemeinschaft (Sche 341/10±1).
M. S. Exton (&)áT. H. C. Kru
Èger áP. Haake
M. Schedlowski
Institut fu
Èr Medizinische Psychologie,
Ètsklinikum Essen, Hufelandstr. 55,
45122 Essen, Germany
Tel.: +49-201-723-4282; Fax: +49-201-723-5948
N. Bursch áU. Hartmann
Division of Clinical Psychiatry, Hannover Medical School,
30623 Hannover, Germany
W. Knapp
Division of Nuclear Medicine, Hannover Medical School,
30623 Hannover, Germany
examined the neuroendocrine responses to sexual
arousal and orgasm following separate periods of
regular sexual activity and sexual abstinence in healthy
men by using an established paradigm.
Materials and methods
Ten healthy male volunteers (mean age of 25.8  0.8 years, range
of 22±29 years) participated in this investigation. Participants were
screened by completing a general medical/health questionnaire and
gave their written consent before being admitted into the study. The
protocol for this study was approved by the Ethics Committee for
Investigations involving human subjects of the Hannover Medical
School, Germany. Individuals taking medication, abusing drugs/
alcohol, or exhibiting endocrinological, psychological or sexual
dysfunction/disorders were excluded from the study. All partici-
pants reported that they had an exclusively heterosexual orientation
and a relaxed attitude toward pornography. Further, all subjects
were currently in a stable relationship and reported having sexual
intercourse approximately 2±3 times per week.
Design and procedure
A repeated measures design was used so each participant viewed a
videotape and masturbated to orgasm on two separate days. Two
dierent videos were shown in a crossover design for the two
sessions. The ®rst session took place at 1630 hours on day 0.
Immediately after that ®rst session (day 0±day 20), the participant
refrained from any type of sexual activity. At 16:30 on day 21 each
subject once again participated in the sexual arousal paradigm. The
procedure of sexual arousal and orgasm both before (day 0) and
after (day 21) were identical, with each session lasting 2 h.
Experiments were conducted in a separate sound-attenuated
room equipped with a clinical bed, a color television and a video
cassette player. All leads, including the blood line, passed through
the wall into the adjacent room where the cardiovascular data and
blood samples were collected, allowing the subject to be completely
isolated throughout the experiment. At the beginning of each
session participants were placed on the bed in front of the video
screen. The cardiovascular monitor was then engaged 30 min prior
to the ®lm and a steady baseline reading was obtained before the
cannula was inserted (20 min before the beginning of the ®lm).
The session was composed of three sequences, each lasting 20 min.
The ®rst and last sections of the video tape were composed of
sections of an emotionally neutral documentary ®lm. However, the
middle section consisted of a 20 min pornographic ®lm that
showed dierent couples engaged in foreplay and sexual inter-
course. Blood sampling was initiated at the beginning of the ®lm.
After 10 min of the pornographic video had been watched (antic-
ipatory phase), subjects in the experimental session were required
to masturbate until orgasm. Blood was drawn continuously with
the samples divided into six 10 min intervals [15±17, 24]. Speci®-
cally, the ®rst two samples represented basal values (10, 20 min),
the third sample represented the response to ®lm-induced sexual
arousal (30 min), the fourth demonstrated the response to orgasm
(40 min) and the ®nal two samples showed the recovery phase (50,
60 min).
Apparatus and materials
Subjective sexual arousal
To provide a measurement for sexual arousal, participants com-
pleted a visual analogue scale (VAS) by rating their subjective level
of sexual arousal from `not at all sexually aroused' to `extremely
sexually aroused' [15±17, 24]. Subjective sexual arousal was mea-
sured at three time points±before, during and after the session±for
both controlled and experimental conditions.
Additionally, subjective assessment of the quality of the
orgasm was completed using 5-point Likert scales. These scales
examined the duration, intensity and speed of orgasm in absolute
value and as compared to a typical orgasm. These questions were
administered following both the experimental and controlled
Cardiovascular measures
The cardiovascular parameters heart rate (HR) and systolic and
diastolic blood pressure (BP) were monitored continuously via a
®nger cu connected to a blood pressure monitor (Critikon Cu &
Dinamap Vital Data Monitor; Critikon Ltd, USA) that was
located in the adjoining room. Cardiovascular activity was
recorded by computer every 30 s, and the HR and BP values were
averaged over 10 min intervals and analysed simultaneously with
the blood samples taken in 10 min interval.
Endocrine measures
For blood sampling, an IV cannula (Vaso®x Braunu
Èle, 18G) was
connected to a 1.25 m heparinized silicon tube (inner B2.0 mm,
Reichelt Chemie, Heidelberg, Germany) by a plastic three-way
stop-cock (Cook, Mo
Ènchengladbach, Germany). The silicon tubing
passed through the wall into the adjacent room and was positioned
through a peristaltic pump (Fresenius, Homburg, Germany). Blood
¯ow was adjusted to 2 ml/min, so that approximately 10 mls of
blood per 5 min were collected (i.e. more than 150 mls per session).
Blood was collected in EDTA tubes (Sarstedt, Nu
Germany), and the collection of each sample was delayed by the
time it took for blood to pass through the dead space in the tube.
Blood was stored on ice until the samples were centrifuged. Plasma
was stored in glass aliquots at )20 °C until it was time for the
hormone assays.
All samples from the one participant were analysed in duplicate
within the same assay for a particular hormone. Plasma prolactin
was evaluated by immunoradiometric assay (IBL, Hamburg,
Germany) and testosterone, LH, cortisol (Diagnostic System
Laboratories, Texas, USA) and catecholamines (IBL, Hamburg,
Germany) were assessed by radioimmunoassay. Inter and intra-
assay variability were 8.0% and 6.2%, respectively, for noradren-
aline; 5.1% and 4.0%, respectively, for adrenaline; 7.1% and 5.0%,
respectively, for prolactin; 7.9% and 5.2%, respectively, for
testosterone; 5.2% and 3.8%, respectively, for LH; and 4.3% and
2.8%, respectively, for cortisol.
Statistical analyses
Data from all subjects were analysed by 2-factor repeated measures
(condition x time) analyses of variance (ANOVA). If not stated
otherwise, only the condition x time interaction eect is reported.
An alevel of 0.05 was used for all ANOVAs. Post hoc simple eects
were evaluated by using paired samples t-tests with Bonferroni a
corrections made for multiple comparisons. Additionally, the
Wilcoxon test was completed for questionnaire data.
Subjective sexual arousal
Participants rated themselves as being signi®cantly
sexually aroused during the erotic ®lm (F(2, 16) 189.51,
P< 0.001; time eect) and greater subjective arousal
was observed following abstinence (F(1,8) 9.21,
P0.016; condition eect, Fig. 1a). Moreover, partici-
pants reported a longer duration (before, 2.1  0.3;
after, 3.5 0.3; Z )2.34, P0.019) and greater
intensity (before, 2.5 0.2; after, 3.7 0.3; Z )2.28,
P0.023) of orgasm following abstinence as compared
to the controlled session, whilst abstinence did not alter
the subjective speed to orgasm (before, 3.1 0.2; after,
3.5  0.2; Z )0.71, P> 0.05). Similar results were
revealed when subjects compared the orgasmic charac-
teristics to those of a typical orgasm (duration: before,
1.8  0.2; after, 3.1  0.4; Z )2.26, P0.023;
intensity: before, 2.1 0.2; after, 3.0 0.3; Z )1.73,
P0.080; speed: before, 3.1  0.2, after, 3.8  0.3;
Z)1.35, P> 0.05).
Prolactin, LH and testosterone response
to sexual arousal
Sexual arousal (timepoint: 30 min) and orgasm
(timepoint: 40 min) increased plasma prolactin levels
markedly in participants (F(5, 45) 5.80, P< 0.001;
time eect, Fig. 1b). However, no signi®cant dierence
was observed in this response before and after acute
abstinence (P> 0.05).
Sexual arousal (timepoint: 30 min) and masturba-
tion-induced orgasm (timepoint: 40 min) did not aect
testosterone concentrations either before or after absti-
nence (P> 0.05). However, a signi®cant increase in
basal testosterone levels were observed following the
period of abstinence (F(5, 45) 6.72, P0.029; con-
dition eect, Fig. 1c). A signi®cant dierence between
the conditions was observed at the 20 min baseline pe-
riod, with this dierence remaining throughout the ses-
sion. Increased testosterone was further accompanied by
a small increase in plasma LH following abstinence;
however this change did not reach statistical signi®cance
(P> 0.05; data not shown).
Cardiovascular response to sexual arousal
Sexual arousal (timepoint: 30 min) and orgasm
(timepoint: 40 min) increased heart rate (F(5, 45)
=14.18, P< 0.001; time eect), systolic blood pressure
(F(5, 45) 16.35, P< 0.001; time eect) and diastolic
blood pressure in participants (F(5, 45) 18.11,
P< 0.001; time eect, Fig. 2). However, no signi®cant
dierence was observed in any of these responses before
and after acute abstinence (all P> 0.05).
Sympathoadrenal response to sexual arousal
Sexual arousal (timepoint: 30 min) and orgasm (time-
point: 40 min) increased both adrenaline (F(5,45)
=7.95, P< 0.001; time eect) and noradrenaline
(F(5,45) 10.90, P< 0.001; time eect) in participants
(Fig. 3). However, no signi®cant dierence was observed
in either of these responses before and after acute ab-
stinence (P> 0.05). Sexual arousal and masturbation-
induced orgasm did not aect cortisol concentrations
either before or after abstinence. However, re¯ecting
circadian rhythm, cortisol levels decreased consistently
over time during both sessions (F(5, 45) 4.66,
P0.02; time eect).
Fig. 1a±c Subjective sexual arousal before, during and after sexual
arousal; plasma prolactin (ng/ml) and testosterone (ng/ml) concen-
trations during baseline (10, 20 min), in response to ®lm-induced
sexual arousal (30 min), following orgasm (40 min), and recovery
after orgasm (50, 60 min). Each subject participated before sexual
abstinence (h) and following 3 weeks of abstinence (j)(Data
displayed as mean SE). Subjective sexual arousal was increased
by masturbation-induced orgasm (a). Furthermore, this response was
enhanced following sexual abstinence. Plasma prolactin concentra-
tions (b) were signi®cantly elevated by sexual arousal and orgasm
both before and after sexual abstinence. In contrast, plasma
testosterone concentrations (c) were unaected by sexual arousal
and orgasm both before and after sexual abstinence. However, plasma
testosterone was signi®cantly elevated after abstinence when com-
pared to basal values (Data displayed as mean SE)
The current study demonstrated that 3 weeks of sexual
abstinence elevated basal testosterone concentrations
and increased both subjective sexual arousal and sub-
jective interpretation of the quality of the orgasm.
However, despite these subjective reports, acute absti-
nence did not alter the well-characterised cardiovascular
and endocrine responses to orgasm.
Sexual arousal and masturbation-induced orgasm
produced pronounced increases in sympathetic activity,
which were re¯ected by increased heart rate, blood
pressure and plasma catecholamine concentrations.
Furthermore, orgasm produced a pronounced increase in
plasma prolactin concentrations. These results mirrored
previous data obtained by studying masturbation in
both men and women [15, 24], which have been shown
to be orgasm speci®c [16].
We have suggested that prolactin secretion following
orgasm may act as a peripheral and/or central feedback
signal in controlling post-orgasm sexual arousal. This
position is supported by a wealth of data from studies of
animals and humans that demonstrate the marked
inhibitory eect that hyperprolactinemia has on sexual
arousal and behavior [11, 13, 30, 32, 35], as well as a
decrease in inhibition following the normalization of
circulating prolactin [13, 35].
Prolactin may also act as an acute negative controller
of sexual function by inhibiting the function of sexual
Fig. 2a±c Cardiovascular activity during baseline (10, 20 min), in
response to ®lm-induced sexual arousal (30 min), following orgasm
(40 min) and recovery after orgasm (50, 60 min). Each subject
participated before sexual abstinence (h) and following 3 weeks of
abstinence (j) (Data displayed as mean SE). Heart rate (beats/
min; a), systolic blood pressure (mm Hg; b) and diastolic blood
pressure (mm Hg; c) were signi®cantly elevated by sexual arousal
and orgasm before and after sexual abstinence
Fig. 3a±c Plasma adrenaline (pg/ml), noradrenaline (pg/ml), and
cortisol (ng/ml) concentrations during baseline (10, 20 min), in
response to ®lm-induced sexual arousal (30 min), following orgasm
(40 min), and recovery after orgasm (50, 60 min). Each subject
participated before sexual abstinence (h) and following 3 weeks of
abstinence (j) (Data displayed as mean SE). Adrenaline (a)
and noradrenaline (b) concentrations were signi®cantly elevated by
sexual arousal and orgasm both before and after sexual abstinence.
In contract, plasma cortisol concentrations (c) were unaected by
sexual arousal and orgasm both before and after sexual abstinence
organs. Although not extensively examined, some data
clearly demonstrate that acute increases in prolactin
inhibit erectile function by hindering the smooth muscle
relaxation of the corpus cavernosum [4]. Alternatively,
acute increases in prolactin may contribute to a sexual-
satiation mechanism following orgasm by means of
feedback to the central nervous system (CNS) structures
that control sexual arousal [10, 21, 29].
Should prolactin act as a negative regulator of sexual
arousal, increased prolactin secretion may be expected
to accompany increased sexual arousal produced by
abstinence. However, the current data show that acute
abstinence does not alter the prolactin response to
masturbation-induced orgasm. Nevertheless, although it
is clear that the prolactin response is orgasm dependent,
the magnitude of the response may be independent of
the quality of the orgasm. Alternatively, the subjective
scores used presently may not provide an accurate
assessment of physiological quality of the orgasm. Thus,
future studies should incorporate a more complete
assessment of orgasm quality, by integrating a more
robust measurement of orgasmic characteristics (e.g.
exact timing of orgasm duration, erectile response).
In contrast to previous data using punctual blood
sampling [8, 34], sexual arousal in the current paradigm
induced elevations in plasma testosterone concentrations
that did not reach statistical signi®cance. However, basal
testosterone levels were elevated throughout the session
following abstinence when compared to values obtained
prior to abstinence. Enhanced testosterone may have
been a physiological response to re-initiate sexual
activity throughout the abstinence period, since
increasing testosterone concentrations have been shown
to stimulate the initiation of coital and other partnered
sexual activity [19, 20]. However, this appears unlikely
because baseline testosterone levels at the beginning of
the video sequence were similar before and after absti-
On the other hand, the increased testosterone
concentrations may have resulted from enhanced sensi-
tivity to anticipatory cues, since testosterone secretion
increases in anticipation of sexual interaction [18]. Thus,
the increase in testosterone following abstinence may
have resulted from increased anticipation of the erotic
®lm. Although initial basal testosterone values (10 min
timepoint) were not altered by abstinence, the dierence
between conditions that appeared after the start of the
session (20±60 min) support this position.
Such anticipatory or preparatory sex hormone re-
sponses are suggested by several other studies [3, 25, 31]
and seem to re¯ect more general appetitive responses in
the expectation of the potentially rewarding conse-
quences of sexual activity. As appetitive responses are
behaviors that represent a central motivational state for
contact with a goal object [2], increased testosterone
concentrations may represent an enhancement of the
aective properties of the goal object by sexual absti-
nence. Furthermore, a close interaction exists between
steroid hormones and the brain systems involved in
reward. Speci®cally, acute increases in testosterone have
possible neural rewarding qualities [2]; this eect is
potentially mediated by dopaminergic systems [14]. With
regard to our current results, one can speculate that
sexual abstinence has a twofold eect on this interaction
pattern: It may enhance the anticipated rewarding
properties of re-initiated sexual activity and it may lower
the threshold at which testosterone produces rewarding
eects. Both factors may interact to trigger the elevated
testosterone levels observed following abstinence.
The enhanced subjective qualities of sexual arousal
and orgasm intensity following sexual abstinence may
also be explained by increased testosterone concentra-
tions. Indeed, elevated levels of testosterone in men are
known to enhance nocturnal erections [12], probably by
acting on peripheral neurons that control copulatory
re¯exes [23]. Additionally, some evidence suggests that
testosterone stimulates the erectile response to experi-
mentally-induced sexual arousal; however, this position
remains equivocal [7]. Nevertheless, increased testoster-
one elevates feelings of sexual arousal and libido [1, 6],
and increases both orgasmic frequency [27] and coital
initiation [20]. Thus, our data suggest that testosterone
may have in¯uenced the subjective assessment of sexual
arousal either by directly modifying genital reactions, or
alternatively, by manipulating the CNS structures that
regulate sexual motivation and arousal.
Summarizing, the current study demonstrated that
masturbation-induced orgasm produces pronounced
elevated cardiovascular responses and plasma concen-
trations of catecholamines and prolactin. Although
these responses were unaltered by acute abstinence from
sexual activity, abstinence increased subjective sexual
arousal and the quality of the orgasm, as well as basal
testosterone concentrations. Thus, although acute
abstinence enhances subjective sexual arousal it has
little impact on the acute neuroendocrine response to
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... In particular, whether and to what extent OT administration affects appetitive, consummatory, and refractory aspects of sexual behaviour in humans has not yet been systematically investigated. Thus, in the present study the effects of acute intranasal OT administration on measures of sexual behaviour and endocrine parameters in healthy young males were examined using a previously established experimental paradigm (Krueger et al., 1998(Krueger et al., , 2002(Krueger et al., , 2003aExton et al., 1999Exton et al., , 2000Exton et al., , 2001. In a double-blind, placebo-controlled, balanced cross-over design, sexual arousal, and orgasm were induced by an erotic film and masturbation. ...
... The documentary was neutral in content, without violent or stirring scenes, and therefore consisted of travel stories or natural science films, whereas the erotic sequences showed heterosexual couples stimulating each other and having intercourse. All visual stimulations were established in previous studies (Krueger et al., 1998(Krueger et al., , 2003a(Krueger et al., , 2006Exton et al., 1999Exton et al., -2001. Subjects completed questionnaires before, in the middle/after orgasm (in retrospect) and immediately after the sessions. ...
... We therefore assume that the effects of OT on HPA-axis activity depend on the additional influence of psychosocial interaction, which was not provided in the current paradigm where sexual activity took place alone in a laboratory setting without a sexual partner. Future studies will extend the paradigm by incorporating sexual interaction with a partner in the laboratory (Exton et al., 2001) as well in a naturalistic setting. ...
... However, to date there is no scientific evidence to support this assumption. When coitus and masturbation are analysed in respect to their effect on acute hormone responses, they are mainly associated with the release of endorphins, dopamine, oxytocin and prolactin [12][13][14][15][16][17][18][19][20][21][22]. After orgasm, various studies have shown that prolactin levels increase, whereas oxytocin and dopamine levels decrease significantly [12][13][14][15][16][17][18][19]23]. ...
... When coitus and masturbation are analysed in respect to their effect on acute hormone responses, they are mainly associated with the release of endorphins, dopamine, oxytocin and prolactin [12][13][14][15][16][17][18][19][20][21][22]. After orgasm, various studies have shown that prolactin levels increase, whereas oxytocin and dopamine levels decrease significantly [12][13][14][15][16][17][18][19]23]. The effect of sexual activity on the hormone concentrations of testosterone (total and free), estrogen, cortisol and luthenizing hormone (LH) has not yet been fully investigated and understood. ...
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Background: Hormones like testosterone play a crucial role in performance enhancement and muscle growth. Therefore, various attempts to increase testosterone release and testosterone concentration have been made, especially in the context of resistance training. Among practitioners, sexual activity (coitus and masturbation) a few hours before training is often discussed to result in increases of testosterone concentration and thus promote muscle growth. However, there is no evidence to support this assumption and the kinetics of the testosterone and cortisol response after sexual activity have not been adequately investigated. Therefore, the aim of this pilot-study was to examine the kinetics of hormone concentrations of total testosterone, free testosterone and cortisol and their ratios after masturbation. In a three-arm single blinded cross-over study, the effects of masturbation with visual stimulus were compared to a visual stimulus without masturbation and the natural kinetics in healthy young men. Results: The results showed a significant between-condition difference in free testosterone concentrations. Masturbation (p < 0.01) and a visual stimulus (p < 0.05) may seem to counteract the circadian drop of free testosterone concentrations over the day. However, no statistical change was observed in the ratios between total testosterone, free testosterone and cortisol. Conclusions: It can be assumed that masturbation may have a potential effect on free testosterone concentrations but not on hormonal ratios. However, additional studies with larger sample sizes are needed to validate these findings.
... Hyperstimulation and/or frustration created by a similar situation may promote frequent SSB as documented in feral-domestic cats (Yamane 2006). Deprivation of member(s) of the opposite sex generates sexual strain that can be relaxed by different behavioural outlets including onanism, SSB, or interspecific sexual behaviours (Exton et al. 2001;Yamane 2006;Sakaguchi et al. 2007). A positive impact of abstinence (a proxy of frustration) on both T levels and sexual motivation has been documented in humans (Exton et al. 2001;Sakaguchi et al. 2007). ...
... Deprivation of member(s) of the opposite sex generates sexual strain that can be relaxed by different behavioural outlets including onanism, SSB, or interspecific sexual behaviours (Exton et al. 2001;Yamane 2006;Sakaguchi et al. 2007). A positive impact of abstinence (a proxy of frustration) on both T levels and sexual motivation has been documented in humans (Exton et al. 2001;Sakaguchi et al. 2007). Yet, nonadaptive SSB may simply reflect behavioural mistakes, such as inaccurate sexual partner discrimination (Scharf and Martin 2013). ...
Two populations, island and mainland, of promiscuous sexually coercive Hermann tortoises (Testudo hermanni, a species with delayed maturity ~10 years) from the Prespa Region in Macedonia were scrutinized. Prior maturity, tortoises first grow slowly, thereafter gradually increase growth speed, variation in body size and survival probability (mean annual survival rate: 0.30 to 0.70). Potential for indeterminate growth, progressive hardening of the carapace and a survival plateau at the age of five (0.90) promote inter-individual variations in growth trajectories and a wide range of adult asymptotic sizes. Our data question the classical notion of a given size at maturity; instead progressive raise of testosterone levels suggests that maturity is established in growing males ranging from 115 to 140mm in body length. In the Testudo genus females are larger than males; asymptotic estimates of body size show that the studied populations make no exception. Yet, the largest island tortoises are males. With ~100 individuals/ha and an operational sex ratio (OSR ♂/♀) of ~11, male sexual coercion provokes cloacal injuries to females and reduces their body-condition, increasing female mating costs. Male adult survival (0.97) is greater compared to female survival (0.84). Island females do not live long, are discouraged from reproduction and low recruitment further exacerbates OSR-bias, eventually leading to population extinction. Where females suffer and are underrepresented, frustrated males exhibit frequent same-sex sexual behaviours along with extravagant sexual behaviours. The results are discussed in a conservation framework.
... However, coitus failed to alter plasma concentration of LH and FSH (Lee et al., 1974;Stearns et al., 1973). In men, LH and FSH concentrations were unaltered by sexual activity (Exton et al., 2001a;Krüger et al., 1998Krüger et al., , 2003a). It appears that most data speak against any release of the gonadotropins in response to sexual incentive stimuli or sexual activity. ...
Sexual incentive stimuli activate sexual motivation and heighten the level of general arousal. The sexual motive may induce the individual to approach the incentive, and eventually to initiate sexual acts. Both approach and the ensuing copulatory interaction further enhance general arousal. We present data from rodents and humans in support of these assertions. We then suggest that orgasm is experienced when the combined level of excitation surpasses a threshold. In order to analyze the neurobiological bases of sexual motivation, we employ the concept of a central motive state. We then discuss the mechanisms involved in the long- and short-term control of that state as well as those mediating the momentaneous actions of sexual incentive stimuli. This leads to an analysis of the neurobiology behind the interindividual differences in responsivity of the sexual central motive state. Knowledge is still fragmentary, and many contradictory observations have been made. Nevertheless, we conclude that the basic mechanisms of sexual motivation and the role of general arousal are similar in rodents and humans.
... The majority of previous studies investigated changes of the HPA axis as a result of sexual behavior. It was reported that plasma cortisol levels were both unaffected during film-induced sexual arousal as well as during sexual arousal and orgasm in healthy volunteers [29,30]. Later studies revealed a positive correlation between baseline salivary cortisol and sexual arousal, using an imagined sexual social situation exercise in healthy volunteers [17]. ...
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Purpose of ReviewCompulsive sexual behavior disorder has been recently included in the 11th revision of the International Classification of Diseases (ICD-11), and the possible contribution of neurochemical and hormonal factors have been reported. However, relatively little is known concerning the neurobiology underlying this disorder. The aim of this article is to review and discuss published findings in the area.Recent FindingsEvidence suggests that the neuroendocrine systems are involved in the pathophysiology of compulsive sexual behavior. The hypothalamus-pituitary adrenal axis, the hypothalamus-pituitary–gonadal axis, and the oxytocinergic system have been implicated.SummaryFurther studies are needed to elucidate the exact involvement of neuroendocrine and hormonal systems in compulsive sexual behavior disorder. Prospective longitudinal studies are particularly needed, especially those considering co-occurring psychiatric disorders and obtaining hormonal assessments in experimental circumstances with appropriate control groups.
... Here, the authors reported that abstinence led to an increase in basal testosterone level, yet did not alter the typical cardiovascular and endocrine responses to orgasm. Therefore they concluded that abstinence has an insufficient impact on endocrine responses (Exton et al., 2001). To note, this study also had a small sample size. ...
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Despite its relevance for human sexuality, literature on potential effects of ejaculation frequency and masturbation on general and mental health outcomes is sparse. Reasons for this knowledge gap include a general lack of interest, but also methodological challenges and still existing superstition. This paper reconciles literature from various fields to extract relevant information on how ejaculation frequency effects general and mental health outcomes. Culture-bound syndromes have been reported in countries still strictly tabooing or condemning masturbation. Masturbatory guilt describes a phenomenon in individuals experiencing a discrepancy between moral standards and own behavior with respect to masturbation. Abstinence is one aspect under study in the area of fertility treatment. Specific time frames and their respective implications on quality of sperm remain inconclusive. Limited temporal resolution capacities hamper the precise study of brain structures directly activated during ejaculation. The relation between ejaculation frequency and hormonal influences remains poorly understood. Future research that specifically addresses ejaculation frequency and potential mental and general health outcomes is needed. In contrast to extracting knowledge as a byproduct from other studies with a different focus, this enables sound study designs and could provide evidence-based results which could then be further discussed and interpreted.
... The activation of the hypothalamus-pituitary-adrenal axis and this can lead to a suppression of luteinizing hormone release because of the dysregulation of homeostasis (stress) and triggers an adaptive stress response (G¹dek-Michalska et al., 2013). Our study results were discrepancy with concluded of (Exton et al., 2001) that orgasm in humans did not acutely affect testosterone levels in the blood. It was also argued that sex in men did not have any effects on testosterone levels but rather it could positively influence the production of testosterone (Dabbs and Mohammed, 1992. ...
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This study was to shed light on levels of testosterone and cortisol hormones in male dromedary camels during the mating time, by collection the blood samples using the manual method and compared with the remote-controlled blood sampling (RBS) method, to assess whether either these methods had affected changes in the concentration of the hormones or not. The blood samples were collected from fifteen adult male camels, via two experiment with one-day intervals: first experiment by manual method during three periods (pre-mating, mating, and post-mating) one hour between each period, and the second experiment by the RBS in the same protocol. The serum testosterone and cortisol concentrations of all animals were determined via ELISA technique. The result which appearance a significant difference in the mating time used RBS compared with manual method. These findings might be due to the withdrawal of blood remotely which could cause a reduction of excitement in animals using the manual blood sampling at the presence of veterinarians, so it was considered as an ideal method to measure hormonal concentrations, especially in experiments which need accurate results.
... Masturbation is an activity that both tends to lower receptivity to testosterone, as well as release serotonin to end an orgasm, creating a subjective feeling of sexual satiety and preventing immediate sexual arousal following orgasm in men (Corona et al., 2009; for a relevant study on male rates, see Phillips-Farfán, Lemus, & Fernández-Guasti, 2007) While one early study found heightened levels of testosterone immediately after masturbating (Purvis et al., 1976) and returning to normal shortly thereafter, a more relevant study found significantly heightened levels of testosterone in males who had avoided masturbating for three weeks (Exton et al., 2001). In other words, banning masturbation increases testosterone, which may be associated with higher rates of violence, impulsivity, and rape. ...
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Policies regarding masturbation among incarcerated men vary throughout the United States. To describe the state of these policies, a systematic review of prison masturbation policies was conducted. The review revealed that masturbation among incarcerated men is banned in most U.S. prisons (sometimes in all cases, and other times only when it is intended to disturb others, and/or is public). Furthermore, many states’ Departments of Corrections have made these policies difficult for the public to identify. Prison masturbation bans have been defended on the grounds that they reduce STI transmission, help maintain order, prevent hostile work environments for female prison staff, assist in prison rape prosecutions, and assist in rehabilitating incarcerated people. By reviewing the available social science and endocrinological research on masturbation, those justifications are found to have minimal basis in scientific evidence. Conversely, the evidence does suggest the masturbation bans could potentially be linked with higher rates of violence, rape, exploitation, sex offender recidivism, insomnia, stress, depression, and suicide. Instead of being rooted in evidence, bans on prison masturbation seem to be primarily motivated by sex-negativity and the desire to retributively punish incarcerated people. To alleviate these harms, this article suggests allowing incarcerated men to masturbate within specifically identified circumstances, and/or to lessen existing punishments for masturbation. Potential problems with the implementation of the suggested policy are discussed, and a call is made to make inmate handbooks, which contain most of these policies, available to the public. Unique opportunities for penological and sexological research are identified.
... Yet in a recent review, Ayad, van der Horst, and Du Plessis (2018, p. 245) called for a revision of this recommendation based upon finding superior sperm quality in shorter abstinence periods. On the level of physiological outcomes, thus, there is currently no evidence for any beneficial effects of abstinence from masturbation (notwithstanding endocrinological effects like an increase in serum testosterone; Exton et al., 2001;Jiang, Jiang, Zou, & Shen, 2003). ...
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Despite the lack of evidence for negative health effects of masturbation, abstinence from masturbation is frequently recommended as a strategy to improve one’s sexual self-regulation. We adopted a framework of perceived problems with pornography to collect first hints about whether abstinence from masturbation stems from a psychological and behavioral “addiction” or conflicting attitudes. In an online questionnaire survey recruited via a non-thematic Reddit thread (n = 1063), most participants reported that they had tried to be abstinent from masturbation. As visible from zero-order correlations and multiple linear regression, motivation for abstinence was mostly associated with attitudinal correlates, specifically the perception of masturbation as unhealthy. While there were associations with hypersexuality, no significant correlation with behavioral markers such as maximum number of orgasms was found. Higher abstinence motivation was related to a higher perceived impact of masturbation, conservatism, and religiosity and to lower trust in science. We argue that research on abstinence from masturbation can enrich the understanding of whether and how average frequencies of healthy behavior are pathologized.
... 32 However, other investigators have suggested that the eurypeptides (the prime of component the EL) may have played eminent role in liberating the bound-form of testosterone from sex hormone-binding globulin that might raise free form of sex hormone in the serum. 33,34 ...
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Rats who were exposed to high fat diet for a specific duration displayed significant degenerative changes involving the testicular cells and structures. The supplement of eurycoma longifolia appears to protect the cells from damages.
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This study evaluated the effects of chronic treatment with cabergoline (CAB), a new, potent and long-lasting ergoline-derived dopamine agonist, on seminal fluid parameters and sexual and gonadal function in hyperprolactinemic males in comparison with the effect of bromocriptine (BRC) treatment. Seventeen males with macroprolactinoma were treated with CAB at a dose of 0.5-1.5 mg/week (n = 7), or BRC at a dose of 5-15 mg/day (n = 10) for 6 months. Baseline prolactin (PRL) was 925.7 +/- 522.6 microg/l in the CAB-treated group and 1059.4 +/- 297.6 microg/l in the BRC-treated group. All the patients suffered from libido impairment, ten from reduced sexual potency, and six had infertility. In five patients provocative bilateral galactorrhea was found. Seminal fluid analysis, functional seminal tests and penis rigidity and tumescence, measured by nocturnal penile tumescence (NPT) using Rigiscan equipment, were assessed before and after 1, 3 and 6 months of CAB or BRC treatment. Hormone profiles were assessed before and after 15, 30, 60, 90 and 180 days of both treatments. Before treatment, all patients had a low sperm count with oligoasthenospermia, reduced motility and rapid progression with an abnormal morphology and decreased viability, and a low number of erections. After 1 month, serum PRL levels were significantly reduced in both groups of patients (20.6 +/- 6.6 microg/l during CAB and 256.3 +/- 115.1 microg/l during BRC treatment) and were normalized after 6 months in all patients (CAB: 7.9 +/- 2.2 microg/l; BRC: 16.7 +/- 1.8 microg/l). After 6 months, a significant increase of number, total motility, rapid progression and normal morphology was recorded in patients treated with both CAB and BRC. An increase in the number of erections during the first 3 months of both treatments was noted by NPT. However, the improvements in seminal fluid parameters and sexual function were more evident and rapid in patients treated with CAB. The number of erections was normalized after 6 months of treatment in all patients submitted to CAB treatment, and in all patients but one treated by BRC. In addition, a significant increase of serum testosterone (from 3.7 +/- 0.3 to 5.3 +/- 0.2 microg/l) and dihydrotestosterone (from 0.4 +/- 0.1 to 1.1 +/- 0.1 nmol/l) was recorded. At the beginning of treatment, mild side-effects were recorded in two patients after CAB and mild-to-moderate side-effects in five patients after BRC administration. The treatment with CAB normalized PRL levels, improving gonadal and sexual function and fertility in males with prolactinoma, earlier than did BRC treatment, providing good tolerability and excellent patient compliance to medical treatment.
Sexual problems are highly prevalent in both men and women and are affected by, among other factors, mood state, interpersonal functioning, and psychotropic medications.The incidence of antidepressant-induced sexual dysfunction is difficult to estimate because of the potentially confounding effects of the illness itself, social and interpersonal comorbidities, medication effects, and design and assessment problems in most studies. Estimates of sexual dysfunction vary from a small percentage to more than 80%. This article reviews current evidence regarding sexual side effects of selective serotonin reuptake inhibitors (SSRIs). Among the sexual side effects most commonly associated with SSRIs are delayed ejaculation and absent or delayed orgasm. Sexual desire (libido) and arousal difficulties are also frequently reported, although the specific association of these disorders to SSRI use has not been consistently shown. The effects of SSRIs on sexual functioning seem strongly dose-related and may vary among the group according to serotonin and dopamine reuptake mechanisms, induction of prolactin release, anticholinergic effects, inhibition of nitric oxide synthetase, and propensity for accumulation over time. A variety of strategies have been reported in the management of SSRI-induced sexual dysfunction, including waiting for tolerance to develop, dosage reduction, drug holidays, substitution of another antidepressant drug, and various augmentation strategies with 5-hydroxytryptamine-2 (5-HT2), 5-HT3, and [small alpha, Greek]2 adrenergic receptor antagonists, 5-HT1A and dopamine receptor agonists, and phosphodiesterase (PDE5) enzyme inhibitors. Sexual side effects of SSRIs should not be viewed as entirely negative; some studies have shown improved control of premature ejaculation in men. The impacts of sexual side effects of SSRIs on treatment compliance and on patients' quality of life are important clinical considerations. (J Clin Psychopharmacol 1999;19:67-85)
DURING the past two years I have had to spend periods of several weeks on a remote island in comparative isolation. In these conditions I noticed that my beard growth diminished, but the day before I was due to leave the island it increased again, to reach unusually high rates during the first day or two on the mainland. Intrigued by these initial observations, I have carried out a more detailed study and have come to the conclusion that the stimulus for increased beard growth is related to the resumption of sexual activity.
Erections in response to erotic films and fantasies were measured in eight hypogonadal men, with and without androgen replacement, and eight age-matched controls. Erections to films in the hypogonadal men did not differ from those of the controls and were not affected by androgen replacement. Erections to fantasy were significantly smaller and slower to develop in the hypogonadal men and did show significant improvement during androgen replacement. These preliminary results suggest that erections to certain types of stimuli are relatively independent of androgens, whereas the response to fantasy may be androgen dependent. The implications of these findings are discussed.
The psychoneuroendocrine responses to sexual arousal have not been clearly established in humans. However, we have demonstrated previously that masturbation-induced orgasm stimulates cardiovascular activity and induces increases in catecholamines and prolactin in blood of both males and females. We presently investigated the role of orgasm in producing these effects. Therefore, in this study parallel analysis of prolactin, adrenaline, noradrenaline, and cortisol concentrations, together with cardiovascular variables of systolic/diastolic blood pressure and heart rate were undertaken during film-induced sexual arousal in nine healthy adult men and nine healthy adult women. Blood was drawn continuously via an indwelling cannula and connected tubing system passed through a mini-pump. In parallel, the cardiovascular parameters were recorded continuously via a computerised finger-cuff sensor. Subjective sexual arousal increased significantly in both men and women during the erotic film, with sexual arousal eliciting an increase in blood pressure in both males and females, and plasma noradrenaline in females only. In contrast, adrenaline, cortisol and prolactin levels were unaffected by sexual arousal. These data further consolidate the role of sympathetic activation in sexual arousal processes. Furthermore, they demonstrate that increases in plasma prolactin during sexual stimulation are orgasm-dependent, suggesting that prolactin may regulate a negative-feedback sexual-satiation mechanism.
Data regarding the neuroendocrine response pattern to sexual arousal and orgasm in man are inconsistent. In this study, ten healthy male volunteers were continuously monitored for their cardiovascular and neuroendocrine response to sexual arousal and orgasm. Blood was continuously drawn before, during and after masturbation-induced orgasm and analyzed for plasma concentrations of adrenaline, noradrenaline, cortisol, luteinizing hormone (LH), follicle stimulating hormone (FSH), prolactin, growth hormone (GH), β-endorphin and testosterone. Orgasm induced transient increases in heart rate, blood pressure and noradrenaline plasma levels. Prolactin plasma levels increased during orgasm and remained elevated 30 min after orgasm. In contrast, none of the other endocrine variables were significantly affected by sexual arousal and orgasm. © 1998 Elsevier Science Ltd. All rights reserved.
The stimuli from a receptive female and/or copulation itself leads to the release of dopamine (DA) in at least three integrative hubs. The nigrostriatal system promotes somatomotor activity; the mesolimbic system subserves numerous types of motivation; and the medial preoptic area (MPOA) focuses the motivation onto specifically sexual targets, increases copulatory rate and efficiency, and coordinates genital reflexes. The previous (but not necessarily concurrent) presence of testosterone is permissive for DA release in the MPOA, both during basal conditions and in response to a female. One means by which testosterone may increase DA release is by upregulating nitric oxide synthase, which produces nitric oxide, which in turn increases DA release. Hormonal priming in females may also increase DA release in the MPOA, and copulatory activity may further increase DA levels in females. One of the intracellular effects of stimulation of DA D1 receptors in the MPOA of male rats may be increased expression of the immediate-early gene c-fos, which may mediate longer term responses to copulation. Furthermore, increased sexual experience led to increased immunoreactivity to Fos, the protein product of c-fos, following copulation to one ejaculation. Another intracellular mediator of DA’s effects, particularly in castrates, may be the phosphorylation of steroid receptors. Finally, while DA is facilitative to copulation, 5-HT is generally inhibitory. 5-HT is released in the LHA, but not in the MPOA, at the time of ejaculation. Increasing 5-HT in the LHA by microinjection of a selective serotonin reuptake inhibitor (SSRI) increased the latency to begin copulating and also the latency to the first ejaculation, measured from the time the male first intromitted. These data may at least partially explain the decrease in libido and the anorgasmia of people taking SSRI antidepressants. One means by which LHA 5-HT decreases sexual motivation (i.e. increases the latency to begin copulating) may be by decreasing DA release in the NAcc, a major terminal of the mesolimbic system. Thus, reciprocal changes in DA and 5-HT release in different areas of the brain may promote copulation and sexual satiety, respectively.
Previous data have indicated that orgasm produces marked alterations in plasma prolactin concentrations in men and women. Thus, the current study aimed to extend these data by examining prolactin response to coitus in healthy males and females. Ten pairs of healthy heterosexual couples participated in the study. Blood was drawn continuously for 20 min before, during, and until 60 min following sexual intercourse and orgasm. Plasma was subsequently analysed for prolactin concentrations. Coitus-induced orgasm produced a marked elevation of plasma prolactin in both males and females. Plasma prolactin concentrations remained elevated 1 h following orgasm. These data, together with previous evidence that masturbation-induced orgasm produces pronounced, long-lasting increases in plasma prolactin concentrations in both males and females, suggest a role for acute prolactin alterations in modifying human sexual desire following orgasm.
Despite the widespread use of androgen in the treatment of hypogonadal men, its efficacy in restoring sexual behavior to hypogonadal patients has not been established in appropriately controlled behavioral studies. Accordingly, testosterone enanthate or vehicle was injected once every 4 weeks im in a double blind experiment. The subjects were six adult males, aged 32-65 yr, two with gonadal failure and four with secondary hypogonadism. Two doses of testosterone (100 and 400 mg) were administered for approximately 5 months, with the treatments varied at random within and among subjects. Details of sexual activity and experience were followed by the use of daily logs. Frequencies of erections, including nocturnal erections and coitus, showed significant dose-related responses to androgen treatment which closely followed the fluctuations in the circulating testosterone level. As indicated by the Profile of Mood States test, behavioral responses did not appear to be mediated by changes in mood. We concluded that the stimulatory effects of testosterone on sexual activity are rapid, reliable, and not due to a placebo effect. To maintain plasma testosterone and adequate sexual function within normal levels, even high doses of testosterone enanthate should be given no less frequency than once every 3 weeks.
The hypothesis is tested that luteinizing hormone (LH) and follicle stimulating hormone (FSH( may be released from the anterior pituitary in response to a psychological state of sexual arousal. LH levels in 10 male volunteers were found to be higher after viewing a sexually arousing film than after a control film. The magnitude of LH response was found to be positively correlated with the subjective evaluation of sexual arousal. FSH levels tended in the same direction bu the predominant and unexpected finding for this hormone was that levels were consistently lower during the first session, when anxiety was high, and higher during the second session, when anxiety was less, whether control or stimulus film had been shown. This study is analogous to those demonstrating the responsiveness of other anterior pituitary hormones to specific psychological states.