Why would TRT reduce semen volume
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madman
Super Moderator
I would not place the blame solely on exogenous T as it is not the main driver here.
The most common sides when using exogenous T would be reduced fertility/spermatogenesis and testicular atrophy as exogenous T suppresses hypothalamic GnRH--> pituitary LH/FSH and the reduced LH/FSH will cause a major reduction intra-testicular testosterone (ITT).
Keep in mind the seminal vesicles and prostate are androgen-responsive accessory sex organs and are responsible for most of the fluid in semen
Seminal vesicles are considered the largest contributor to semen volume with the prostate contributing a substantial fraction and sperm/testicular secretions contributing a relatively small fraction.
So while use of exogenous T can profoundly suppress the testicular/sperm component testosterone can simultaneously maintain or increase activity/volume of the accessory-gland component.
The most likely cause of reduced semen volume would most likely be age, accessory-gland function, (aging prostate/seminal vesicles), ejaculation frequency, medications, and the physical properties of the semen.
Some men will notice a change in semen consistency/liquefaction (thick/gel) or clumpy which can make it look like there is less.
Also keep in mind weak pelvic floor muscles can contribute to that weak ejaculate causing the dribble. effect which can have a big impact on volume.
* Less than 5% of the volume of semen is actually sperm and the other 95+% is a cocktail of genital juices that provides nourishment, support, and safekeeping for sperm. 70% of the volume comes from the seminal vesicles, which secrete a thick, viscous fluid, and 25% from the prostate gland, which produces a milky-white fluid. A negligible amount is from the bulbo-urethral glands, which release a clear viscous fluid (pre-come) that has a lubrication function
* The average ejaculate volume is 2-5 cc (one teaspoon is the equivalent of 5 cc)
* As men get older, there are changes in the reproductive organs, particularly the prostate gland, one of the few organs in the body that enlarges with age
* The aging prostate and seminal vesicles produce less fluid; additionally, the ducts that drain the genital fluids can become clogged. In many ways, the changes in ejaculation parallel the changes in urination experienced by the aging male
* With aging, there is a decline in sensory nerve function, weakening of pelvic floor muscles, and diminished reproductive gland fluid production.
* The pelvic floor muscles play a key role in ejaculation
* Certain medications that are used to treat prostate enlargement profoundly affect ejaculatory volume. Additionally, the pelvic floor muscles—which play a vital role in ejaculation—weaken with aging.
madman
Super Moderator
Physiology of Ejaculation
Male ejaculate is a complex, non-homogenous, multi-role mixture of immune and glandular cells, salts, peptide and steroid hormones, carbohydrates, organic acids, lipids, mucus, nucleic acids, vitamins, minerals, urogenital microbial fora, and over 2000 unique proteins [9–12]. Although some components of semen are fully soluble, others bind directly to spermatozoa or are packaged into cargo-bearing vesicles that can then fuse with spermatozoa. Once inside the female reproductive tract, these non-spermatic components may serve to further stimulate ovulation, alter reproductive-tract pH, modulate immune activity, nourish spermatozoa, or provide other functions that are yet to be determined [11–13]. Table 1 describes normal macroscopic semen parameters as defined by current WHO guidelines [3••].
The composition of post-ejaculatory semen is highly variable between men and within individual men over the course of their lifetimes. However, approximately 90% of the semen is composed of fluid from the seminal vesicles, prostate, and bulbourethral gland, in descending order of percent contribution.[3••] As such, only a small fraction of the semen is composed of spermatozoa.
The development of spermatozoa, a process known as spermatogenesis, begins at puberty with mature spermatozoa originating from germ cells found within the basement membrane of the seminiferous tubules of the testes. Sertoli cells, stimulated by follicle-stimulating hormone (FSH), and Leydig Cells, stimulated by luteinizing hormone (LH), both help to regulate spermatogenesis. Once puberty has begun, one cycle of spermatogenesis within the Sertoli cell epithelia begins every 13–16 days [14, 17, 18]; however, spermatogenesis is not consistently synchronous throughout all seminiferous tubules. Furthermore, the exact number of stages of spermatogenesis remains unclear and debated [14, 18]. After immotile spermatozoa are released into the tubules, they travel to the epididymis for further maturation and the development of functional motility. A fully mature sperm cell consists of a head, midpiece, and tail. The head contains the nucleus and is covered by the acrosome, which is filled with lysosomes that assist in fusion with an ovum. The midpiece of the spermatozoa contains abundant mitochondria to produce ATP production that provides energy for the sperm cell’s flagellum, or tail, which allows for propulsion [18]. The entire process of human spermatogenesis can vary in length, but previous studies estimate it at 42–76 days [14].
Mature spermatozoa are stored in the tail of the epididymis until the pelvic plexus receives sufficient sensory input from the hypogastric and pelvic nerves, in addition to the psychologically driven caudal paravertebral sympathetic chain, to initiate ejaculation [19]. The emission stage of ejaculation begins when the bladder neck is closed to prevent retrograde flow of the imminently passing ejaculate. This action coincides with the propulsion of sperm from the epididymis into the ductus (vas) deferens by smooth muscle contractions. From here, the sperm are carried through the spermatic cord towards the ejaculatory duct, where they mix with a clear fructose-rich solution from the seminal vesicle. As this new mixture passes through the prostate, an alkalinizing fluid is secreted which further thickens the fluid, now called semen, and protects the sperm from acidic conditions within the female reproductive tract. Finally, the semen passes through the bulbourethral glands which provide one final addition by releasing a fluid that both lubricates the urethral opening and clears it of any residual urine [11, 12, 14]. The final physiologic composition of the semen has now been produced and will be released in the next stage of ejaculation, termed expulsion.This refers to the ejection of semen through the urethral meatus, propelled by cyclic contractions of the striated pelvic muscles alongside those of the bulbospongiosus and ischiocavernosus muscles [20].
Volume
Retrograde ejaculation can be further described as complete, with no antegrade fraction, or incomplete, with minimal antegrade fraction [28]. Patients with retrograde ejaculation will have a post-orgasmic urinalysis that is positive for fructose and sperm [28]. Similar to anejaculation, retrograde ejaculation can be due to SCI and other neurologic disorders, although it can also be a side effect of certain medications or surgical procedures that relax the bladder neck [26]. As bladder neck closure and seminal emission are under the control of alpha-adrenergic receptors, antagonists of these receptors, such as tamsulosin or alfuzosin, may result in retrograde ejaculation [29]. Additionally, many antipsychotic medications, such asthioridazine, risperidone, iloperidone, and clozapine, have been associated with retrograde ejaculation due to their broad and difuse receptor antagonizing ability [30]. Surgeries, including transurethral prostatectomy and prostatic ablative procedures, are other common causes of anatomic retrograde ejaculation [30]. Various medications have been used to treat patients’ retrograde ejaculation and improve fertility, including midodrine, imipramine, and a combination of chlorpheniramine and phenylpropanolamine [28]. Electrovibration stimulation, sperm recovery from the urine, and surgical sperm retrieval can also be considered if pharmacologic therapy fails [28].
Hypospermia is defined as a semen volume of less than 1.4 mL on at least two separate semen analyses [3••]. Hypospermia can be an isolated finding but is also associated with other sperm abnormalities, such as oligospermia (low sperm count), asthenozospermia (reduced sperm motility), or teratozospermia (abnormal morphology of sperm) [31]. Lack of sexual abstinence prior to specimen collection commonly results in hypospermia [31]. As previously discussed, incomplete retrograde ejaculation can cause partial antegrade ejaculation and thus hypospermia [31]. Hormonal irregularities may also be a contributing factor, including hypogonadism, which decreases circulating levels of testicular androgens and leads to quantitative and qualitative alterations of multiple components of male ejaculate, resulting in hypospermia [31]. Similarly, hyperprolactinemia caused by prolactinomas or drugs, such as spironolactone, cimetidine, antipsychotics, and ketoconazole, can decrease androgen levels and result in hypospermia as a result of inhibitory feedback from elevated prolactin levels on the hypothalamic-pituitary-gonadal axis [31]. The bilateral or unilateral absence of the vas deferens, as can be seen in patients with cystic fibrosis, as well as obstructive abnormalities, such as prostatic cysts or post-surgical stenosis of the surgical tract, can also be associated with hypospermia [31]. Treatment of hypospermia is variable and depends on the specific etiology (Table 2).
Viscosity
After ejaculation, semen coagulates and then gradually liquefies. However, in 12–29% of men, in a process likely related to infection, inflammation, dysfunction of male sex glands, or in diseases directly affecting male fertility, semen may be hyper viscous [33]. Semen hyperviscosity can be diagnosed by using a wide-bore pipette to dispense a drop of semen by gravity and measuring a thread length of more than 2 cm long [33]. The causes of semen hyperviscosity may contribute to infertility, and it has been postulated that hyperviscosity itself may be a contributing factor due to the impairment of normal sperm movement [33]. Esfandiari et al. [34] investigated the effect of increased seminal viscosity on patients undergoing in vitro fertilization and found that couples with seminal hyperviscosity experienced significantly lower fertilization rates, clinical pregnancy rates, and implantation rates. Hyperviscous semen can be treated by in vitro dilution of semen and directly by overhydration, prostatic massage, and parenteral hyaluronidase with some success [33]. Additionally, mucolytic agents, anti-inflammatory agents, and antibiotics have been used for the management of hyper viscous sperm depending on the etiology [33].
Currently, there exists very limited literature related to hyperviscosity, or over-liquefaction, of semen. In a study using physical analysis of ejaculate to estimate the diagnostic potential and to predict the function of the seminal vesicles and prostate, 3.6% of semen samples analyzed had hyperviscous semen and were associated with biochemical markers that suggested impaired secretory activity of the seminal vesicles [35].
Male ejaculate is a complex, non-homogenous, multi-role mixture of immune and glandular cells, salts, peptide and steroid hormones, carbohydrates, organic acids, lipids, mucus, nucleic acids, vitamins, minerals, urogenital microbial fora, and over 2000 unique proteins [9–12]. Although some components of semen are fully soluble, others bind directly to spermatozoa or are packaged into cargo-bearing vesicles that can then fuse with spermatozoa. Once inside the female reproductive tract, these non-spermatic components may serve to further stimulate ovulation, alter reproductive-tract pH, modulate immune activity, nourish spermatozoa, or provide other functions that are yet to be determined [11–13]. Table 1 describes normal macroscopic semen parameters as defined by current WHO guidelines [3••].
The composition of post-ejaculatory semen is highly variable between men and within individual men over the course of their lifetimes. However, approximately 90% of the semen is composed of fluid from the seminal vesicles, prostate, and bulbourethral gland, in descending order of percent contribution.[3••] As such, only a small fraction of the semen is composed of spermatozoa.
The development of spermatozoa, a process known as spermatogenesis, begins at puberty with mature spermatozoa originating from germ cells found within the basement membrane of the seminiferous tubules of the testes. Sertoli cells, stimulated by follicle-stimulating hormone (FSH), and Leydig Cells, stimulated by luteinizing hormone (LH), both help to regulate spermatogenesis. Once puberty has begun, one cycle of spermatogenesis within the Sertoli cell epithelia begins every 13–16 days [14, 17, 18]; however, spermatogenesis is not consistently synchronous throughout all seminiferous tubules. Furthermore, the exact number of stages of spermatogenesis remains unclear and debated [14, 18]. After immotile spermatozoa are released into the tubules, they travel to the epididymis for further maturation and the development of functional motility. A fully mature sperm cell consists of a head, midpiece, and tail. The head contains the nucleus and is covered by the acrosome, which is filled with lysosomes that assist in fusion with an ovum. The midpiece of the spermatozoa contains abundant mitochondria to produce ATP production that provides energy for the sperm cell’s flagellum, or tail, which allows for propulsion [18]. The entire process of human spermatogenesis can vary in length, but previous studies estimate it at 42–76 days [14].
Mature spermatozoa are stored in the tail of the epididymis until the pelvic plexus receives sufficient sensory input from the hypogastric and pelvic nerves, in addition to the psychologically driven caudal paravertebral sympathetic chain, to initiate ejaculation [19]. The emission stage of ejaculation begins when the bladder neck is closed to prevent retrograde flow of the imminently passing ejaculate. This action coincides with the propulsion of sperm from the epididymis into the ductus (vas) deferens by smooth muscle contractions. From here, the sperm are carried through the spermatic cord towards the ejaculatory duct, where they mix with a clear fructose-rich solution from the seminal vesicle. As this new mixture passes through the prostate, an alkalinizing fluid is secreted which further thickens the fluid, now called semen, and protects the sperm from acidic conditions within the female reproductive tract. Finally, the semen passes through the bulbourethral glands which provide one final addition by releasing a fluid that both lubricates the urethral opening and clears it of any residual urine [11, 12, 14]. The final physiologic composition of the semen has now been produced and will be released in the next stage of ejaculation, termed expulsion.This refers to the ejection of semen through the urethral meatus, propelled by cyclic contractions of the striated pelvic muscles alongside those of the bulbospongiosus and ischiocavernosus muscles [20].
Volume
Retrograde ejaculation can be further described as complete, with no antegrade fraction, or incomplete, with minimal antegrade fraction [28]. Patients with retrograde ejaculation will have a post-orgasmic urinalysis that is positive for fructose and sperm [28]. Similar to anejaculation, retrograde ejaculation can be due to SCI and other neurologic disorders, although it can also be a side effect of certain medications or surgical procedures that relax the bladder neck [26]. As bladder neck closure and seminal emission are under the control of alpha-adrenergic receptors, antagonists of these receptors, such as tamsulosin or alfuzosin, may result in retrograde ejaculation [29]. Additionally, many antipsychotic medications, such asthioridazine, risperidone, iloperidone, and clozapine, have been associated with retrograde ejaculation due to their broad and difuse receptor antagonizing ability [30]. Surgeries, including transurethral prostatectomy and prostatic ablative procedures, are other common causes of anatomic retrograde ejaculation [30]. Various medications have been used to treat patients’ retrograde ejaculation and improve fertility, including midodrine, imipramine, and a combination of chlorpheniramine and phenylpropanolamine [28]. Electrovibration stimulation, sperm recovery from the urine, and surgical sperm retrieval can also be considered if pharmacologic therapy fails [28].
Hypospermia is defined as a semen volume of less than 1.4 mL on at least two separate semen analyses [3••]. Hypospermia can be an isolated finding but is also associated with other sperm abnormalities, such as oligospermia (low sperm count), asthenozospermia (reduced sperm motility), or teratozospermia (abnormal morphology of sperm) [31]. Lack of sexual abstinence prior to specimen collection commonly results in hypospermia [31]. As previously discussed, incomplete retrograde ejaculation can cause partial antegrade ejaculation and thus hypospermia [31]. Hormonal irregularities may also be a contributing factor, including hypogonadism, which decreases circulating levels of testicular androgens and leads to quantitative and qualitative alterations of multiple components of male ejaculate, resulting in hypospermia [31]. Similarly, hyperprolactinemia caused by prolactinomas or drugs, such as spironolactone, cimetidine, antipsychotics, and ketoconazole, can decrease androgen levels and result in hypospermia as a result of inhibitory feedback from elevated prolactin levels on the hypothalamic-pituitary-gonadal axis [31]. The bilateral or unilateral absence of the vas deferens, as can be seen in patients with cystic fibrosis, as well as obstructive abnormalities, such as prostatic cysts or post-surgical stenosis of the surgical tract, can also be associated with hypospermia [31]. Treatment of hypospermia is variable and depends on the specific etiology (Table 2).
Viscosity
After ejaculation, semen coagulates and then gradually liquefies. However, in 12–29% of men, in a process likely related to infection, inflammation, dysfunction of male sex glands, or in diseases directly affecting male fertility, semen may be hyper viscous [33]. Semen hyperviscosity can be diagnosed by using a wide-bore pipette to dispense a drop of semen by gravity and measuring a thread length of more than 2 cm long [33]. The causes of semen hyperviscosity may contribute to infertility, and it has been postulated that hyperviscosity itself may be a contributing factor due to the impairment of normal sperm movement [33]. Esfandiari et al. [34] investigated the effect of increased seminal viscosity on patients undergoing in vitro fertilization and found that couples with seminal hyperviscosity experienced significantly lower fertilization rates, clinical pregnancy rates, and implantation rates. Hyperviscous semen can be treated by in vitro dilution of semen and directly by overhydration, prostatic massage, and parenteral hyaluronidase with some success [33]. Additionally, mucolytic agents, anti-inflammatory agents, and antibiotics have been used for the management of hyper viscous sperm depending on the etiology [33].
Currently, there exists very limited literature related to hyperviscosity, or over-liquefaction, of semen. In a study using physical analysis of ejaculate to estimate the diagnostic potential and to predict the function of the seminal vesicles and prostate, 3.6% of semen samples analyzed had hyperviscous semen and were associated with biochemical markers that suggested impaired secretory activity of the seminal vesicles [35].
Vince
Super Moderator
My understanding is TRT reduces semen volume mainly by shutting down the hormonal signals that tell the testicles to function and produce fluid.
madman
Super Moderator
No.
Sperm/testicular secretions play a small role as <5% of the semen volume is sperm.
Majority of semen volume is produced by the seminal vesicles (70%) and prostate (25%).
Again even though the hpta is highly suppressed exogenous T can simultaneously maintain or increase activity/volume of the accessory-gland component (seminal vesicles and prostate).
The main function of LH is to stimulate the Leydig Cells in the testes to produce intra-testicular testosterone (ITT) and the main function of FSH stimulate the Sertoli/germ cells to produce sperm.
Again as I stated in my previous reply the most common sides when using exogenous T would be reduced fertility/spermatogenesis and testicular atrophy as exogenous T suppresses hypothalamic GnRH--> pituitary LH/FSH and the reduced LH/FSH will cause a major reduction intra-testicular testosterone (ITT).
However, there are some interesting statements in this thread. Are they accurate?
It turns out that Intratesticular Testosterone (ITT) levels in a healthy man are naturally 40 to 100 times higher than the testosterone levels measured in a routine blood test. I am told that the testicles drain into a localized network of pelvic veins that pass directly by the prostate and seminal vesicles on their way back up to the main circulatory system. Through a process called local vascular shunting (or portal transfer), extremely high concentrations of this local testosterone diffuse directly into these nearby target glands (prostate and seminal vesicles).
When a man is on TRT monotherapy without hCG, his internal testicular production (ITT) shuts down, entirely drying up this hyper-concentrated local vascular shunt. The prostate and seminal vesicles are forced to function on much lower systemic blood levels, drastically reducing their fluid output. This leaves behind only the clear secretions of the bulbourethral glands. This localized androgen deficit is why TRT frequently causes clear ejaculate, and why adding hCG restores volume & colour.
Vince
Super Moderator
Seminal Vesicles (65% to 70%): Provide the largest portion of fluid. This fluid contains fructose for sperm energy, proteins, and prostaglandins.
madman
Super Moderator
LH/FSH are not the direct acute stimulators of seminal-vesicle/prostate fluid secretion and you do not need the very high intra-testicular testosterone (ITT) concentration itself to maintain accessory-gland fluid production.
What is critical here is the very high ITT is essential for spermatogenesis but is not itself required for the accessory sex glands to receive androgen stimulation.
Exogenous T and its metabolite DHT would suffice.
The seminal vesicles make up the majority (70%) of semen and the secretion is androgen dependant (T/DHT) signalling through the AR.
The prostate contributes the other (25%) and its secretion is also androgen dependant (T/DHT) with Ts metabolite DHT playing a strong role here.
Think of the 5ARis (finasteride/dutasteride) as one of the most common side-effects is reduced ejaculate volume.
As you would know the main function of LH is to stimulate the Leydig Cells in the testes to produce intra-testicular testosterone (ITT) and the main function of FSH is to stimulate the Sertoli/germ cells to produce sperm
Sperm is made in the seminiferous tubules of the testes and in order for such this is where FSH + very high intra-testicular testosterone (ITT) is needed.
ITT is extraordinarily high compared with serum T because LH stimulates Leydig cells to produce testosterone directly within the testis and the high concentration is crucial for normal spermatogenesis not the activity/volume of the accessory-glands (seminal vesicles and prostate).
The seminal vesicles and prostate respond primarily to androgen exposure in the systemic circulation and within the gland itself.
Yes some men on T therapy do experience a noticeable reduction in ejaculate volume but it is not a given because semen volume isn't controlled by one hormone or one tissue.
It depends on accessory-gland function, androgen exposure, age, ejaculation frequency, hydration, medications, obstruction, individual physiology.
If youn sift through the literature low ejaculate volume is a multifactorial and may reflect accessory-gland or seminal-tract dysfunction, androgen deficiency, medications, age, ejaculation interval, ejaculatory/seminal-tract obstruction, retrograde ejaculation or impaired emission, and individual variation.
Also keep in mind there are many men including me that have never had an issue with ejaculate volume on a T only protocol.
The only thing that ever had any noticeable impact for me was being dehydrated or ejaculating too frequently.
If anything my force and orgasms are more intense and I can still shoot big loads on a T only protocol.
There are lots of older men nattty or on solo T therapy that have BPH (inflammation) or weak pelvic floor muscles (dribblers) which can easily have a negative impact on semen volume.
Throw in retrograde ejaculation too.
Aging in and of itself can play a big role.
* As men get older, there are changes in the reproductive organs, particularly the prostate gland, one of the few organs in the body that enlarges with age
* The aging prostate and seminal vesicles produce less fluid; additionally, the ducts that drain the genital fluids can become clogged. In many ways, the changes in ejaculation parallel the changes in urination experienced by the aging male
* With aging, there is a decline in sensory nerve function, weakening of pelvic floor muscles, and diminished reproductive gland fluid production.
* The pelvic floor muscles play a key role in ejaculation
* Certain medications that are used to treat prostate enlargement profoundly affect ejaculatory volume.
* Additionally, the pelvic floor muscles—which play a vital role in ejaculation—weaken with aging.
EFFECT OF LONG-TERM TESTOSTERONE OENANTHATE ADMINISTRATION ON MALE REPRODUCTIVE FUNCTION: CLINICAL EVALUATION, SERUM FSH, LH, TESTOSTERONE, AND SEMINAL FLUID ANALYSES IN NORMAL MEN (1975)
Keep in mind n=7 study.
Seven healthy men 250 mg testosterone enanthate weekly for 21 weeks, with serial measurements of LH, FSH, testosterone, sperm concentration, motility, morphology, seminal fructose, and seminal fluid volume.
“ the serum FSH and LH were rapidly suppressed after the initiation of the TOe therapy.”
“ The mean sperm concentration fell to values below three million spermatozoa per ml.”
“ In contrast, the mean seminal fluid volume and serum androstenedione levels did not change significantly during TOe administration.”
madman
Super Moderator
Yes as I already stated in my opening reply the seminal vesicles are the largest contributor to ejaculate volume.
madman
Super Moderator
Could not upload another file to my original post as six is max!
The gist is laid out in my previous reply (post #8).
Vince
Super Moderator
Yes, usually between 25% to 40% men on TRT remain fertile. I really don't know how true that is, but my semen definitely is lower on trt then before TRT.
It definitely has not lowered my libido. Even with the lower semen/ sperm sex is still awesome.
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