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Comprehensive Review of the Anatomy and Physiology of Male Ejaculation: Premature Ejaculation Is Not a Disease

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Article selected to feature in Wiley's News Round-Up (it is a biweekly mailing sent to over 1,800 subscribing journalists). Wiley Press Release November 02, 2015 http://eu.wiley.com/WileyCDA/PressRelease/pressReleaseId-121651.html Human semen contains spermatozoa secreted by the testes and a mixture of components produced by the bulbo-urethral and Littre (paraurethral) glands, prostate, seminal vesicles, ampulla and epididymis. Ejaculation is used as a synonym for the external ejection of semen, but it comprises two phases: emission and expulsion. As semen collects in the prostatic urethra, the rapid preorgasmic distension of the urethral bulb is pathognomonic of impeding orgasm, and the man experiences a sensation that ejaculation is inevitable (in women, emission is the only phase of orgasm). The semen is propelled along the penile urethra mainly by the bulbocavernosus muscle. With Kegel exercises, it is possible to train the perineal muscles. Immediately after the expulsion phase the male enters a refractory period, a recovery time during which further orgasm or ejaculation is physiologically impossible. Age affects the recovery time: as a man grows older, the refractory period increases. Sexual medicine experts consider premature ejaculation only in the case of vaginal intercourse, but vaginal orgasm has no scientific basis, so the duration of intercourse is not important for a woman's orgasm. The key to female orgasm are the female erectile organs; vaginal orgasm, G-spot, G-spot amplification, clitoral bulbs, clitoris-urethra-vaginal complex, internal clitoris and female ejaculation are terms without scientific basis. Female sexual dysfunctions are popular because they are based on something that does not exist, i.e. the vaginal orgasm. The physiology of ejaculation and orgasm is not impaired in premature ejaculation: it is not a disease, and non-coital sexual acts after male ejaculation can be used to produce orgasm in women. Teenagers and men can understand their sexual responses by masturbation and learn ejaculatory control with the stop-start method and the squeeze technique. Premature ejaculation must not be classified as a male sexual dysfunction. It has become the center of a multimillion dollar business: is premature ejaculation - and female sexual dysfunction - an illness constructed by sexual medicine experts under the influence of drug companies? This article is protected by copyright. All rights reserved.
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REVIEW
Comprehensive Review of the Anatomy and
Physiology of Male Ejaculation:
Premature Ejaculation Is Not a Disease
VINCENZO PUPPO
1
*AND GIULIA PUPPO
2
1
Centro Italiano Di Sessuologia, Bologna, Italy
2
Department of Biology, University of Florence, Sesto Fiorentino, Italy
Human semen contains spermatozoa secreted by the testes and a mixture of
components produced by the bulbo-urethral and Littre (paraurethral) glands,
prostate, seminal vesicles, ampulla, and epididymis. Ejaculation is used as a
synonym for the external ejection of semen, but it comprises two phases:
emission and expulsion. As semen collects in the prostatic urethra, the rapid
preorgasmic distension of the urethral bulb is pathognomonic of impeding
orgasm, and the man experiences a sensation that ejaculation is inevitable (in
women, emission is the only phase of orgasm). The semen is propelled along
the penile urethra mainly by the bulbocavernosus muscle. With Kegel exer-
cises, it is possible to train the perineal muscles. Immediately after the expul-
sion phase the male enters a refractory period, a recovery time during which
further orgasm or ejaculation is physiologically impossible. Age affects the
recovery time: as a man grows older, the refractory period increases. Sexual
medicine experts consider premature ejaculation only in the case of vaginal
intercourse, but vaginal orgasm has no scientific basis, so the duration of inter-
course is not important for a woman’s orgasm. The key to female orgasm are
the female erectile organs; vaginal orgasm, G-spot, G-spot amplification, clito-
ral bulbs, clitoris-urethra-vaginal complex, internal clitoris and female ejacula-
tion are terms without scientific basis. Female sexual dysfunctions are popular
because they are based on something that does not exist, i.e. the vaginal
orgasm. The physiology of ejaculation and orgasm is not impaired in premature
ejaculation: it is not a disease, and non-coital sexual acts after male ejacula-
tion can be used to produce orgasm in women. Teenagers and men can under-
stand their sexual responses by masturbation and learn ejaculatory control
with the stop–start method and the squeeze technique. Premature ejaculation
must not be classified as a male sexual dysfunction. It has become the center
of a multimillion dollar business: is premature ejaculation—and female sexual
dysfunction—an illness constructed by sexual medicine experts under the influ-
ence of drug companies? Clin. Anat. 00:000–000, 2015. V
C2015 Wiley Periodicals, Inc.
Key words: semen; ejaculation; bulbocavernosus muscle; orgasm; sexual
dysfunction; dapoxetine
INTRODUCTION
Orgasm, a subjective experience of pleasure, is a
normal physiological function of humans. Male ejacula-
tion usually occurs simultaneously with orgasm. Ejacu-
lation is used as a synonym for the external ejection of
*Correspondence to: Vincenzo Puppo, Via Pistoiese 301/6,
50145 Florence, Italy. E-mail: dottvincenzopuppo@yahoo.it
Received 6 October 2015; Accepted 9 October 2015
Published online in Wiley Online Library (wileyonlinelibrary.com).
DOI: 10.1002/ca.22655
V
V
C2015 Wiley Periodicals, Inc.
Clinical Anatomy 00:00–00 (2015)
semen, but it comprises two phases: emission, i.e. the
ejection into the prostatic urethra of spermatozoa
mixed with fluids secreted by accessory sexual glands
(by smooth muscle fiber contractions in the epididymis,
ductus deferens, seminal vesicles, and prostate); and
expulsion, i.e., the ejection of semen from the urethra
at the glands (by involuntary contractions of the stri-
ated perineal muscles). For sexual medicine experts,
ejaculatory disorders are the most common sexual dys-
functions in males (McMahon et al., 2013). The aim of
this review is to clarify the anatomy and physiology of
ejaculation and to assess whether premature ejacula-
tion (PE), the most common male sexual disorder, is
really a disease.
SEMEN
Semen contains spermatozoa secreted by the testes
(Fig. 1) and the seminal fluids, mainly produced by the
seminal vesicles and prostate (Fig. 2), which provide
the medium and vehicle for the spermatozoa (Chiarugi
and Bucciante, 1975). Human semen is a mixture of
components produced by several different glands.
These components are incompletely mixed during ejac-
ulation, so the initial ejaculate is not entirely homoge-
neous. The first portion of it consists of secretions from
the Cowper (bulbo-urethral) and Littre (paraurethral)
glands. The second portion derives from the prostate.
There follow small contributions from the ampulla and
epididymis and, finally, from the seminal vesicles,
which contribute the remainder, and majority, of the
ejaculate (Masters and Johnson, 1966; Owen and Katz,
2005; McDougal et al., 2012).
On average, there are 2–5 ml of semen per ejacu-
late, but the volume is progressively reduced with each
ejaculatory episode, and if more ejaculations occur at
short intervals the semen contains few spermatozoa.
On the other hand, if a male has been continent for sev-
eral days, a larger volume of semen is generally ejacu-
lated than after only a few minutes of continence. A
larger volume ejaculate is appreciated subjectively as
more sensually pleasurable than a lower volume. The
concentration of spermatozoa is highly variable and
also depends on the frequency of ejaculation. A count
of 20–120 million per milliliter is considered normal, so
there are 40–600 million spermatozoa in a single ejacu-
late; spermatozoa production slows down after age 40,
but it continues into the 80s and 90s. Seminal vesicle
secretions constitute 65–75% of the total volume,
prostate secretions 15–30%, and bulbo-urethral and
Littre glands secretions 1–5% (Mann, 1954; Masters
and Johnson, 1966; Masters et al., 1988; Owen and
Katz, 2005; Puppo, 2011; McDougal et al., 2012).
The spermatozoa mature in the epididymis, which
secretes potassium, sodium, and glycerylphosphoryl-
choline. The ampulla of the ductus deferens secretes a
yellowish fluid containing fructose, a sugar that nour-
ishes the spermatozoa. Seminal vesicle secretions pro-
duce a yellowish viscous fluid that contains amino acids,
citrate, phosphorus, potassium, enzymes, flavins, fruc-
tose, phosphorylcholine, prostaglandins, proteins, and
vitamin C. The prostate secretion is a thin whitish fluid
that contains acid phosphatase, citric acid, fibrinolysin,
prostate specific antigen, proteolytic enzymes, and zinc.
The bulbo-urethral gland secretion is thick and clear and
Fig. 1. Cross section through the testis (from Chiar-
ugi and Bucciante, 1975). 1, Tunica albuginea; 2, Septa;
3, Mediastinum; 4, Lobule; 5, Seminiferous tubules; 6,
Straight tubule; 7, Rete testis; 8, Efferent ductules; 9,
Conic ductusculosi; 10, Epididymis; 11, Ductus deferens.
Fig. 2. The accessory sexual glands (from Chiarugi
and Bucciante, 1975). 1, Urethra; 2, Prostate; 3, Seminal
vesicle; 4, Ampulla of ductus deferens; 5, Ductus defer-
ens; 6, Urinary bladder; 7, Bladder trigone; 8, Ureter; 9,
Peritoneum.
2 Puppo and Puppo
contains galactose, mucus, sialic acid, and plasminogen
activator (Mann, 1954; Owen and Katz, 2005).
The semen is ejaculated in liquid form and is typically
translucent with a white, grey, or yellowish tint. It has a
creamy, sticky texture, its consistency resembling
mucilage or thin jelly. The later part of the ejaculated
semen coagulates immediately, forming globules. Right
after ejaculation the semen is rather thick, but it lique-
fies quickly. Liquefaction occurs over a period of 5 min
in vivo. After 15–30 min, the prostate-specific antigen
and plasminogen activator produced in the prostate
and present in the semen cause decoagulation of the
seminal coagulum. The liquefaction process allows the
spermatozoa to be released slowly from the coagulum
so they can be transported into the cervix and eventu-
ally upstream to the ovulated eggs. Overall, the process
of coagulation and liquefaction allows for appropriate
exposure of the spermatozoa to seminal fluid factors
that stimulate their motility and enhance their fertilizing
capacity, and then permits their orderly entry into
the upper female genital tract (Mann, 1954; Masters
et al., 1988; Balk et al., 2003; Owen and Katz, 2005;
McDougal et al., 2012).
The bulbo-urethral glands are two pea-sized struc-
tures connected to the urethra just below the prostate
gland. They produce a few drops of fluid, which some-
times appear at the tip of the penis during sexual
arousal but before ejaculation. It is mucoid in charac-
ter, usually totals no more than two or three drops,
and escapes involuntarily from urethral meatus. Some
men never notice this pre-ejaculatory fluid, while
others can produce a teaspoonful or more of this slip-
pery secretion. In some studies, pre-ejaculatory fluid
secreted by the bulbo-urethral glands during sexual
stimulation lacks spermatozoa so it cannot cause
pregnancy after coitus interruptus (Masters et al.,
1988; Fetissof et al., 1989; Puppo, 2011).
EMISSION PHASE OF EJACULATION
Emission is the first phase of the male ejaculation. It is
a sympathetic spinal cord reflex (T10–L2): stimuli from
the genitalia, essentially those reflecting the degree of
activation of sensory receptors mainly located in the
glans penis (Krause-Finger corpuscles), are integrated at
the spinal level and stimulate peristaltic contraction of
the accessory sexual glands. The emission phase is initi-
ated by contractions of the vasa efferentia of the testes.
At orgasm, spermatozoa starting from the epididymis up
the ductus deferens are propelled by its strong muscular
coats; their bulky vehicle is acquired from the seminal
vesicles along with reinforcements or emergency rations
of spermatozoa that may be stored there. The ductus
deferens contracts near-synchronously with the seminal
vesicles: the contents of the ampulla (outlet of the ductus
deferens) are discharged into the prostatic urethra
accompanied by simultaneous emission of seminal vesi-
cle secretions through the ejaculatory ducts (Fig. 3)
(Dickinson, 1949; Giuliano and Clement, 2005; Motofei
and Rowland, 2005; Palmer and Stuckey, 2008; Puppo,
2011; Rowland et al., 2010).
Ejaculatory ducts open in the seminal colliculus
(i.e., veru montanum), which is a prominence of the
dorsal surface of the prostatic urethra. Among them is
the male vagina (i.e., the prostatic utricle (Fig. 4);
“male vagina” is a more accurate term than “prostatic
utricle” because it is the homologue of the female
vagina). The ejaculatory ducts sometimes open into
the male vagina (Puppo, 2011, 2013).
During this phase the prostatic fluid is also dis-
charged into the prostatic urethra by regularly recurring
contractions, which can be palpated rectally. The effi-
ciency of the accessory sexual glands can become
Fig. 3. Emission phase (contractions of the epididy-
mis, ductus deferens, seminal vesicles, and prostate;
expansion of the urethral bulb) and expulsion phase
(bladder neck closure, penile/urethra/urethral bulb/peri-
neal muscle contractions; expulsion of semen) (from
Puppo, 2011). 1, Testis; 2, Bladder; 3, Ductus deferens;
4, Ampulla and seminal vesicle; 5, Ejaculatory duct; 6,
Prostate; 7, Prostatic urethra; 8, Anus; 9, External anal
sphincter; 10, Urogenital diaphragm; 11, Bulbocaverno-
sus muscle; 12, Bulb; 13, Penile urethra; 14, Corpus
cavernosum; 15, Glans penis.
Fig. 4. Ejaculatory ducts (from Puppo, 2011). 1,
Prostatic urethra; 2, Seminal colliculus; 3, Male “vagina”;
4, Ejaculatory duct; 5, Vaginal orifice; 6, Ejaculatory duct
orifice.
Anatomy and Physiology of Ejaculation 3
impaired during aging. Men over 60 years of age did not
demonstrate contractions of the prostate clinically dur-
ing ejaculation, and the amount of semen was reduced
(Masters and Johnson, 1966; Puppo, 2011).
As semen collects in the prostatic urethra, there is
simultaneously a two- to three-fold involuntary expan-
sion of the urethral bulb. The rapid preorgasmic
distension of the urethral bulb is pathognomonic of
impeding orgasm and the man experiences a sensa-
tion that ejaculation is inevitable, that is, the feeling
of having reached the limit of control. This subjective
experience has been described by many men as feel-
ing the ejaculation coming. The sense of inevitability
is accurate because at this point ejaculation cannot be
stopped. From the onset of this sensation there is a
brief interval (2–3 sec) during which the male feels
the ejaculation coming and can no longer constrain,
delay, or in any way control it. This subjective experi-
ence of inevitability develops as semen is collecting in
the prostatic urethra but before the actual emission
begins (Masters and Johnson, 1966; Masters et al.,
1988; Puppo, 2011).
In older men, the emission phase can be foreshort-
ened to the extent that all sensation of ejaculatory
inevitability is lost or lengthened. In this situation, the
male’s ejaculatory process is one of sudden second-
phase expulsion of semen through the urethral mea-
tus without distinct first-phase warning contractions of
the accessory glands of reproduction. In other word,
instead of a two-phase, well-differentiated ejaculatory
process, the elderly male may have a single-phase
expulsion of semen, the accessory glands of reproduc-
tion contracting simultaneously with the expulsive
penile contractions rather than preceding them by
2–3 sec (Masters and Johnson, 1966; Masters et al.,
1988; Puppo, 2011).
In women, emission is the only phase of orgasm.
Jannini et al. in 2012 stated: “The phenomenon of
female ejaculation refers to an expulsion of fluid from
the urethra that is different from urine.” Shafik et al.
in 2009 stated that the female orgasm was not
associated with the appearance of fluid from the
vagina or urethra.
In the vaginal vestibule, the external orifice of the
urethra is seen with the paraurethral (Skene’s) ducts
opening on both sides. The intraurethral (Skene’s)
glands are regarded as the female “prostate.” Secre-
tions from these glands are expelled through the ure-
thral meatus or through the orifices of the paraurethral
ducts into the vaginal vestibule, which corresponds to
the dorsal wall of the male penile urethra (while the
labia minora correspond to its ventral wall); female
“prostate” secretion during orgasm corresponds to
the emission phase of male ejaculation. From a physio-
logical point of view, the term “female emission” is
more accurate than “female ejaculation” (however, in
a few women there is a powerful emission): it corre-
sponds to the emission of seminal fluid into the pros-
tatic urethra in the male. The lack of an ejaculation
phase in the female could explain why women have no
refractory period and are able to experience multiple
orgasms (Puppo, 2011, 2013; Puppo and Puppo,
2015b).
EXPULSION PHASE OF EJACULATION
Expulsion is the second phase of the male ejacula-
tion. The organs participating in the expulsion phase
comprise the bladder neck and urethra as well as the
perineal muscles, creating the physical force that pro-
pels the semen and accounts for the spurting of it dur-
ing ejaculation (Fig. 3) (Masters and Johnson, 1966;
Puppo, 2011).
Normal antegrade ejaculation is initiated by bladder
neck closure; the internal sphincter of the bladder
remains sealed to prevent semen from flowing back-
ward into the bladder and to ensure that it moves for-
ward, precluding any mixing of urine and semen. The
external urinary sphincter is relaxed, which allows the
seminal fluid to flow into the distended bulb, whence
it is propelled along the penile urethra and from the
urethral meatus (Masters and Johnson, 1966; Giuliano
and Clement, 2005; Puppo, 2011).
Expulsion is a parasympathetic spinal cord reflex
mediated by somatic nerves (S2–S4). Stimulation of
the glans sensory receptors is relayed by the puden-
dal nerve afferent fibers to S4, and then to the hypo-
gastric plexus at the T10–L2 sympathetic ganglia.
Sensory information is relayed centrally to the brain,
where three ejaculatory centers are situated. Two are
in the hypothalamus (the medial preoptic area and
the paraventricular nucleus) and one in the midbrain
(the periaqueductal grey). These centers integrate the
peripheral events of seminal emission, ejaculation and
orgasm. Their efferent dopamine output is modulated
by the nucleus paragigantocellularis. Neurotrans-
mitters involved in these centers include noradrena-
line, g-aminobutyric acid, oxytocin, nitric oxide,
serotonin and estrogen. Expulsion is triggered by
dopamine acting on the D2 receptors of central and
spinal efferent fibers, which relay information down to
the sympathetic ganglia at T10–L2 and sacral fibers.
This stimulates pudendal nerve fibers from the S2–S4
region of the spinal cord. Rhythmic contractions of the
perineal muscles are controlled by parasympathetic
nerves, which override the sympathetic nerves
(Palmer and Stuckey, 2008).
Histologically, the perineal muscles are striated
muscles; physiologically they are mixed muscles, i.e.,
they can undergo both voluntary and involuntary
reflex contractions. The most important are: the
ischiocavernosus muscle (muscle of erection), bulbo-
cavernosus (BC) muscle (muscle of male ejaculation),
external sphincter muscle of the anus (the contrac-
tions of which enhance the sensations of orgasm; in
younger men they occur regularly during orgasm but
they decrease in frequency as the male ages), striated
urethral sphincter muscle, transverse perineal
muscles, levator muscle of the prostate, and puborec-
talis muscle (Puppo, 2011, 2013).
Jannini et al. in 2015 stated: “The pelvic floor
muscles actively collaborate to achieve ejaculation,
with from three to seven contractions... pelvic floor
motoneurons, produces the pelvic floor contractions
characteristic of ejaculation,” but the semen is
expelled the full length of the penile urethra under
strong pressure created by the involuntary but coordi-
nated contractions of the perineal muscles. The
4 Puppo and Puppo
semen is propelled from the prostatic urethra along
the penile urethra mainly by the BC muscle, which
covers the urethral bulb. It is situated in the anterior
region of the perineum, i.e. penile region (Figs. 5 and
6) (Masters and Johnson, 1966; Chiarugi and Buc-
ciante, 1975; Puppo, 2006, 2011).
“At orgasm, the BC muscle contracts rhythmically.
It is suggested that the muscle helps ejaculation by
acting as a ‘pump.’ On contraction, the muscle might
compress and evacuate the contents of the bulbous
urethra to the exterior. On relaxation of the muscle,
the intraurethral pressure drop probably ‘sucks’ the
semen from the posterior into the bulbous urethra.
The intrabulbar urethral fossa might act as a ‘recepta-
cle’ in which the semen pools to be ejected by BC
muscle contraction. The rhythmic BC muscle contrac-
tion, with its pumping action, might result in ejecting
the semen in jets. The BC muscle functions also to
evacuate the urine that remains in the urethra at the
end of micturition. When the bladder empties its con-
tents, the urine remaining in the urethra seems to be
evacuated by repeated voluntary contraction of the
BC muscle. The latter compresses the bulbous urethra
and probably empties the urethra of urine in spurts”:
the BC muscle can be considered the muscle of ejacu-
lation (Shafik, 1995).
The urethral bulb also contracts regularly as an aid
to the propulsive mechanism. The first two or three
ejaculatory contractions of the penile urethra project
the semen content under such pressure that the initial
portions of the ejaculate can be expelled 30–60 cm
from the urethral meatus if the penis is unencum-
bered by vaginal containment. The expulsive penile
contractions start at intervals of 0.8 sec. After the first
three or four major expulsive efforts the contractions
are rapidly reduced in both frequency of recurrence
and expulsive force. Minor contractions of the penile
urethra continue for several seconds in an irregularly
recurring manner, projecting a minimal amount of
seminal fluid under little if any expulsive force. The
terminal intercontractile intervals are extended to sev-
eral seconds (Masters and Johnson, 1966; Masters
et al., 1988).
The man over 50 years of age exhibits markedly
reduced ejaculation, 15–30 cm being the average
distance over which the semen can be expelled. The
older the male, the fewer the expulsive contractions
and the weaker the expulsive force propelling the
semen. The ejaculatory contractions that produce sig-
nificant expulsive force are reduced in number to one
or two at the most. The intercontractile intervals rap-
idly lengthen, particularly after the second expulsive
contraction of the penile musculature (Masters and
Johnson, 1966; Masters et al., 1988).
In the aging male, particularly if his erection has
been long-maintained, the semen seeps from or
escapes the urethral meatus without significant ejacu-
latory pressure, and the experience can be one of
seepage rather than semen expulsion. A final drop or
two of semen can seep from the urethral meatus with-
out expulsive force. The male ejaculatory experience,
once initiated by contractions of the accessory glands
of reproduction, cannot be constrained or delayed
until semen expulsion has been completed. Expulsion
occurs when the process reaches the point of the
ejaculatory inevitability, the point of no return: it is a
reflex response to the presence of semen in the bul-
bous urethra. Semen does not appear externally until
several seconds after the point of ejaculatory inevita-
bility because of the distance it has to travel through
the urethra (Masters and Johnson, 1966; Masters
et al., 1988; Puppo, 2011).
Men cannot have multiple orgasms or a rapid series
of ejaculations: immediately after ejaculation the
male enters a refractory period, a recovery time dur-
ing which further orgasm or ejaculation is physiologi-
cally impossible. There is great variability in the
length of the refractory period both among males and
within individuals; it can last anywhere from a few
minutes to many hours. Many males below the age of
30, but relatively few thereafter, have the ability to
ejaculate frequently and are subject to only very short
Fig. 5. Ischiocavernosus and bulbocavernosus mus-
cle (from Puppo, 2006). 1, Corpus cavernosum; 2, Cor-
pus spongiosum of the urethra; 3–4, Ischiocavernosus
muscle; 5, Bulbocavernosus muscle.
Fig. 6. Urethral bulb covered by bulbocavernosus
muscles (from Puppo, 2006). 1, Ischiocavernosus mus-
cle; 2, Bulbocavernosus muscle; 3, Houston muscle; 4,
Fibrous septum.
Anatomy and Physiology of Ejaculation 5
refractory periods. Younger men typically recover
more quickly than older men. Age affects the recovery
time: as a man grows older, the refractory period
increases. It can last for extended periods particularly
after the age of 60, when there is less physical need
to ejaculate (Masters and Johnson, 1966; Masters
et al., 1988; Puppo, 2011).
With Kegel exercises, it is possible to train the peri-
neal muscles (“pelvic floor exercises” is an incorrect
term). Strengthening these muscles can be important
for improving the oxygenation and trophism of all of
them, so the muscle tone needed for their function is
maintained. Kegel exercises are important for pre-
venting urinary incontinence, and they can reduce the
lengthening of the refractory period and prevent the
weakening of the expulsive force of semen that occur
in all men over 50 years of age (Puppo, 2006, 2011).
Orgasm without ejaculation is common in boys
before puberty and can occur if the prostate is dis-
eased or when certain drugs are used. Anejaculation
is the inability to ejaculate despite an erection
(McDougal et al., 2012; Meng et al., 2013; McMahon
et al., 2013). Males experience nocturnal ejaculation,
the highest incidence and frequency of this occurring
during the late teens. Nocturnal ejaculation provides a
physiological safety-valve for accumulated sexual ten-
sion that has not been released in any other fashion
(Masters et al., 1988). Ejaculation can sometimes
occur without orgasm, for example in certain types of
neurological illness (Masters et al., 1988). In retro-
grade ejaculation, the bladder neck does not close off
properly during orgasm so semen spurts backward
into the bladder. This occurs in some men with multi-
ple sclerosis or diabetes or after certain types of pros-
tate surgery (Rowland et al., 2010; McDougal et al.,
2012).
PREMATURE EJACULATION IS NOT A
DISEASE/SEXUAL DYSFUNCTION
Premature ejaculation (PE) has been defined as a
male sexual dysfunction characterized by ejaculation
that always or nearly always occurs prior to or within
1 min of vaginal penetration and the inability to delay
the event, with negative personal consequences
(American Psychiatric Association, 2013; McMahon
et al., 2013; Tiefer, 2014).
Hatzimouratidis et al. in 2015 stated: “Erectile dys-
function and premature ejaculation are the two main
complaints in male sexual medicine.” Byun et al. in
2013 stated: “In men PE is more common than
delayed ejaculation. Timed intercourse imposes a sub-
stantial degree of stress on men. Physicians and clini-
cians should acknowledge the potentially harmful
effects of timed intercourse on the physical and men-
tal health of men. The impact of impending timed
intercourse on sexual dysfunction and the behavior of
male partners have only recently been investigated.
Jannini et al. in 2015 stated: “the term ‘premature
ejaculation’ would be introduced later in 1917 by a
psychoanalyst. In the beginning, PE was considered
as psychogenic in nature. PE is considered as a
psycho-neuro-endocrine and urologic disorder affecting
the couple.” Yang et al. in 2013 stated: “In spite of
the increasing interest in PE in the field of sexual
medicine, our knowledge about the prevalence, etiol-
ogy, diagnosis, and treatment of PE is scarce.” Buvat
in 2011 stated. “Although the characteristics of PE
are established, the exact etiology is largely
unknown. Most of the proposed biological and psy-
chological etiologies of PE are supported by little
evidence.”
IS PE REALLY A MALE SEXUAL
DYSFUNCTION/DISEASE?
Sexual medicine experts consider PE only in the
case of vaginal intercourse. PE is limited to heterosex-
ual men engaging in vaginal intercourse, as few rele-
vant studies have been conducted on homosexual
men or during other forms of sexual activity (McMa-
hon et al., 2013).
Lee et al. in 2013 stated: “The epidemiology of PE
has not been firmly established, and the lack of robust
epidemiological studies renders its true prevalence
unknown. PE males felt that they did not satisfy their
partners in terms of the partners’ sexual satisfaction
and frequency of orgasm, in comparison with non-PE
males.”
Until a few decades ago, PE did not entail discom-
fort for males during vaginal intercourse because
orgasm was not essential for female sexual satisfac-
tion. Until the mid-twentieth century, many people
(including some medical authorities) believed that
women were not capable of orgasm. This belief
undoubtedly reflected a cultural bias: sex was seen as
something the man did to the woman for his own
gratification. Women were told for centuries to do
their wifely duties by making themselves available to
their husbands for sex (Masters and Johnson, 1966;
Masters et al., 1988).
PE is considered the cause of the partner’s failure
to achieve vaginal orgasm, with negative psychologi-
cal consequences for the male, but vaginal orgasm
does not exist. The key to female orgasm are the
female erectile organs, i.e. the clitoris, vestibular
bulbs and pars intermedia, labia minora, and corpus
spongiosum of the female urethra. Vaginal orgasm, G-
spot, G-spot amplification, clitoral bulbs, clitoral or
clitoris-urethra-vaginal complex, internal clitoris and
female ejaculation (O’Connell et al., 2005, 2008;
Rubio-Casillas and Jannini, 2011; Jannini et al., 2012;
Buisson and Jannini 2013; Jannini et al., 2014; Oakley
et al., 2014; Vaccaro et al., 2014; Graziottin and
Gambini, 2015; Herold et al., 2015; Levin, 2015; Pan
et al., 2015; Pauls, 2015; Vaccaro, 2015) are terms
without scientific basis and should not be used by
urologists, gynecologists, sexologists, sexual medicine
experts, women, or the mass media (Puppo, 2013;
Puppo and Puppo, 2015b).
If a woman has an orgasm through clitoral stimula-
tion but not during intercourse, it does not meet the
criteria for a clinical diagnosis of female orgasmic dis-
order. If the orgasmic difficulties are the result of
inadequate sexual stimulation, these cases should not
be diagnosed as a disorder of female orgasm
6 Puppo and Puppo
(American Psychiatric Association, 2013). “Female
sexual dysfunctions are popular because they are
based on something that does not exist, i.e., the vagi-
nal orgasm. There are no medications for female sex-
ual dysfunction because it is impossible to use drugs
to increase the desire of vaginal intercourse. Hypoac-
tive sexual desire disorder is an example of a condi-
tion that was sponsored by industry to prepare the
market for a specific treatment. Flibanserin is an anti-
depressant, but the mechanism by which the drug
improves sexual desire is not known. Addyi has not
been shown to enhance sexual performance, it was
found to be modestly effective in improving sexual
desire during clinical trials: women should fully under-
stand the risks associated with the use of Addyi before
considering treatment” (Puppo and Puppo, 2015a).
The female sexual function index (FSFI) questionnaire
is the most widely used measure of female sexual
dysfunction; however, it does not assess female sex-
ual function but primarily assesses vaginal inter-
course. The FSFI must not be used to assess female
sexual dysfunctions (Puppo, 2015). In all women,
orgasm is always possible if the female erectile organs
are effectively stimulated during masturbation, cunni-
lingus, or partner masturbation, or during vaginal
intercourse if the clitoris is simply stimulated with a
finger (Puppo, 2011, 2013).
Many men think prolonged intercourse is the key to
orgasms, but it is not helpful for women. PE does not
occur if both partners agree that the quality of their
sexual encounters is not influenced by efforts to delay
ejaculation, and some females may be grateful to get
it over with quickly. Male ejaculation does not auto-
matically mean the end of sex for most women.
Touching and kissing can be continued almost indefi-
nitely; non-coital sexual acts after male ejaculation
can be used to produce orgasm in women (Puppo and
Puppo, 2015b; Puppo et al., 2015).
As a matter of fact, the vaginal orgasm has no sci-
entific basis, so the duration of penile-vaginal inter-
course is not important for a woman’s orgasm. Sexual
dysfunctions are conditions in which the ordinary
physical responses of sexual function are impaired: it
is important for men (and sexual medicine experts,
endocrinologists, urologists, andrologists, and sexolo-
gists) to understand that in “premature” ejaculation
the physiology of ejaculation and orgasm is not
impaired, and that PE is normal in adolescent males
especially during their first sexual encounters.
Sansone et al. stated in 2015: “It should be clear
that PE is often associated with endocrine diseases.”
Jannini et al. in 2015 stated: “PE is still far from being
fully understood. All cases of PE thus are or become
psychogenic, even where PE is a symptom of an
organic etiology. The epidemiology of PE is dramati-
cally influenced by its definition. Pharmaceutical
industry-sponsored population studies, limited by the
possible conflict of interest but with the merit of huge
enrollments, show a 20% prevalence. Dapoxetine is
the unique, first-line, officially approved pharmaco-
therapy for PE.” PE during vaginal intercourse is not a
male sexual dysfunction/disease, therefore it cannot
be associated with endocrine diseases and drug ther-
apy must be not used.
Jannini et al. in 2015 stated: “E.A. Jannini has
received personal fees from Menarini, Bayer, Ibsa,
GSK, and Pfizer.” PE has become the center of a multi-
million dollar business: is PE—and female sexual dys-
function—an illness constructed by sexual medicine
experts under the influence of drug companies?
Moon du et al. in 2015 stated: “Feasibility and effi-
cacy of glans penis augmentation for PE. The patho-
physiology of premature ejaculation is poorly
understood.” The pathophysiology of PE is poorly
understood because it is not a disease, so glans penis
augmentation is not medically indicated. Men must be
informed about the lack of data supporting the effi-
cacy of this procedure and its complications. Clinicians
who receive requests for glans penis augmentation, or
for medical treatment for PE, must discuss with the
patient the reason for his request and examine him
for physical signs or symptoms that could indicate a
need for surgical intervention or drugs. A patient’s
concern regarding the appearance of his genitalia can
be alleviated by a discussion of the wide range of nor-
mal genitalia and reassurance that the appearance of
the penis differs significantly from man to man.
Human body functions must be studied in the sub-
ject: questionnaires about male ejaculation must
assess masturbation, and the questions should not
include the words “intercourse” and “satisfaction.” I
warn colleagues to maintain a high level of profession-
alism: unscientific definitions and questionnaires must
not be used. A new definition could be: PE is a sexual
dysfunction when the ability to delay ejaculation dur-
ing masturbation is diminished or lacking, and ejacu-
lation occurs before the person wishes it, with
negative personal consequences (Puppo et al., 2015).
Teenagers must understand that PE is absolutely
normal at their age. Men with PE have no negative
personal consequences during masturbation: there is
no such thing as PE when orgasm and ejaculation are
attained by masturbation. However, masturbation pro-
vides a safe means of sexual experimentation,
improving sexual self-confidence.
Jannini et al. in 2015 stated: “From the early 1900s
until the 1990s, PE was considered a psychological
problem, and it was treated primarily with behavioral
therapies such as the squeeze technique and stop–start
technique.” Sexologists and sexual medicine experts
must acknowledge two specific methods called the
Fig. 7. The squeeze technique (from Puppo, 2011).
A: Coronal squeeze. B: Basilar squeeze.
Anatomy and Physiology of Ejaculation 7
stop–start method and the squeeze technique that help
recondition the ejaculatory reflex during masturbation.
In the stop–start method the male stimulates the penis
manually until he feels that he is rapidly approaching
ejaculation, and then he stops all stimulation until the
sense of ejaculatory urgency disappears. Stimulation
then begins again, and the stop–start cycle is repeated
several times before the man is allowed to ejaculate
(Semans, 1956; Glina et al., 2007; Puppo, 2011). In
the squeeze technique the man puts his second and
third fingers on the frenulum of the penis and places his
thumb just below the coronal ridge on the opposite side
(Fig. 7A). Firm pressure is applied for about 4 sec and
then abruptly released. The squeeze technique reduces
the urgency to ejaculate. It must begin in the early
phase of masturbation and continue periodically, every
few minutes. With the basilar squeeze, the squeezing is
at the base of the penis (Fig. 7B) (Masters et al., 1988;
Puppo, 2011).
CONCLUSIONS
Sexual health is a fundamental and universal human
right, and sexual pleasure, including autoeroticism, is a
source of physical and psychological wellbeing that con-
tributes to human happiness. Knowledge of the anat-
omy and physiology of male ejaculation is essential in
the field of men’s sexual health. Men must also know
the changes in their sexual response that occur physio-
logically with aging and train their perineal muscles
with Kegel exercises.
The man with PE is often embarrassed or depressed
about his plight, which he regards as reflecting poorly
on his manhood. Sexual medicine experts, endocrinolo-
gists, urologists, andrologists, and sexologists must
acknowledge that PE is not a disease and must not be
classified as a male sexual dysfunction, and that it is
normal for any healthy adolescent man owing to his
inexperience in sexual matters. Teens and men can
understand their sexual response during masturbation
and learn ejaculatory control with the stop–start
method and the squeeze technique. They will then be
able to gain better control during intercourse. Also, dur-
ing lovemaking, the duration of vaginal intercourse is
not important.
Sexual medicine experts and sexologists must
know that vaginal orgasm does not exist and ensure
that proper sex education is provided in schools and
by the mass media. They must define having sex/
making love as a situation in which orgasm occurs for
both partners with or without vaginal intercourse: a
definition for all human beings.
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Anatomy and Physiology of Ejaculation 9
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... [1][2][3][4][5][6][7][8] For the efficient expulsion of sperm from the urethral meatus, coordination of an intricate sequence of neurophysiological events and contraction of numerous smooth and striated muscle groups are required, as well as the absence of anatomical obstruction. [1][2][3][4][5][6][7][8] Specific muscles are involved in each phase of ejaculation. [1][2][3][4][5][6][7][8] In the emission phase, seminal fluid is secreted into the prostatic urethra (PSU) by sequential epithelial secretion and smooth muscle contractions in the epididymis, ductus deferens, seminal vesicles (SVs), prostate, ejaculatory ducts (EDs), and there is simultaneous closure of the bladder neck and the external urethral sphincter and contraction of the periurethral musculature. ...
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... As males reach puberty, they start to engage in sexual intercourse, which alters their ejaculation time and perceived ejaculation control with the passage of time. Therefore, premature ejaculation is (PE) should not be considered or defined as pathological [1]. ...
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... The compressive narrowing of the sulcus would also affect the transport dynamics of semen. Crocodiles do not have proximal muscles that drive semen in pressurized emissions as mammals do (Puppo & Puppo, 2016); instead, semen is moved steadily along the groove by peristaltic pressures from alternately contracting smooth muscles lateral to the sulcus groove (Johnston et al., 2014). We have shown evidence of orthogonally placed smooth muscles that could provide coordinated peristaltic semen propulsion. ...
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... Nombre de facteurs biologiques a été évoqué, pouvant expliquer l'EP, avec notamment la possibilité d'une hypersensibilité du gland, une représentation corticale du nerf pudendal, des troubles de la neurotransmission sérotoninergique centrale de l'érection et d'autres comorbidités sexuelles, telles qu'une éventuelle prostatite, une iatrogénie, des drogues récréatives, un syndrome de la douleur pelvienne chronique ou une dysthyroïdie. . . Et cependant, aucune de ces étiologies n'a pu être vérifiée par des études à grande échelle [22]. Toutes ces avancées nous font-elles donc aller vers une surmédicalisation de l'EP ? ...
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