THE-DET-OAK
IncreasedMyT @ ULV
anytime you raise your T level it goes up. besides protein synthesis, thats one of the main things T increases.
What gains to expect. Test Cyp
- Thread starter OnStar
- Start date
Great info guys.
I'm in my late 40's. I weight and cardio train 5 times a week and really try to watch what I eat. I also take a good daily vitaman and protien drinks 2 to 3x's a day.
I'll stick with the protocal and restest blood in 6 weeks from start.
I'm not trying to be the Hulk here just want to look good, feel better, and and keep it safe and healthy.
Thanks again guys
I'm in my late 40's. I weight and cardio train 5 times a week and really try to watch what I eat. I also take a good daily vitaman and protien drinks 2 to 3x's a day.
I'll stick with the protocal and restest blood in 6 weeks from start.
I'm not trying to be the Hulk here just want to look good, feel better, and and keep it safe and healthy.
Thanks again guys
juced_porkchop
Moderator
yep thats what id say. unless you had very low levels before
we may need to start a new thread about this, but to what extent do you feel this occurs? Honestly i have never heard this have any significance and I would assume any substantial increase would induce hyperplasia. How is the response signaled to the liver to send out more IGF-1?
Thoughts?
The first 6 months of being on testosterone I didn't have much in the realm of gains, but my bodyfat composition changed a lot. I didn't lose any weight, but the fat and water redistributes. I added some strength.
I have started back up after 4 months on clomid and metformin, which I lost some strength on, but in general made some health improvements.
This time I am feeling great, treating my diabetes while being on testosterone replacement therapy (TRT) is going really well. I also don't have gout, which was being brought on because of my diabetes.
Being on testosterone and training smart, you will add strength and muscle during a time that most people are losing muscle and adding fat.
I have started back up after 4 months on clomid and metformin, which I lost some strength on, but in general made some health improvements.
This time I am feeling great, treating my diabetes while being on testosterone replacement therapy (TRT) is going really well. I also don't have gout, which was being brought on because of my diabetes.
Being on testosterone and training smart, you will add strength and muscle during a time that most people are losing muscle and adding fat.
THE-DET-OAK
IncreasedMyT @ ULV
ARTICLES
Testosterone administration increases insulin-like growth factor-I levels in normal men
CJ Hobbs, SR Plymate, CJ Rosen and RA Adler
Department of Clinical Investigation, Madigan Army Medical Center, Tacoma, Washington 98493.
Although testosterone (T) administration can increase insulin-like growth factor-I (IGF-I) when administered to hypogonadal men, no studies have examined whether this occurs in normal men. The present study was undertaken to determine if an increase in IGF-I may be part of the anabolic effect of androgens. We enrolled 11 normal men in a randomized, double-blinded cross-over study. Subjects were assigned to receive either T enanthate (TE) (300 mg im, each week) or nandrolone (ND) decanoate (300 mg im, each week) for 6 weeks. After a washout period subjects were administered the alternate treatment. Pre- and posttreatment serum was analyzed for IGF-I by RIA after acid-ethanol extraction. Results expressed as mean +/- SEM (Table 1). IGF-binding protein-3 was measured by RIA and was unchanged in the TE treatment and decreased significantly after ND treatment. Although GH levels were not significantly different after either TE or ND treatment, they tended to increase after TE treatment (1.23 +/- 0.28 ng/mL vs. 3.3 +/- 1.03 ng/mL) but remained unchanged after ND treatment (1.68 +/- 0.68 ng/mL vs. 1.89 +/- 0.64 ng/mL). Serum total T levels increased 32 +/- 0.05 nmol/L in the TE-treated men, but fell by 7 +/- 0.02 nmol/L in the ND- treated men (P < 0.0001). Serum estradiol levels rose by 193.04 +/- 19.82 pmol/L in the TE-treated men although falling by 50.65 +/- 34.50 pmol/L in the ND-treated men (P < 0.0002). These data indicate that when normal men are given TE, serum IGF-I levels increase after 6 weeks of treatment. Treatment with ND did not change serum levels of IGF-I but did decrease the level of the major serum IGF-BP and therefore the level of bioavailable IGF-I may be increased in the ND group.
http://jcem.endojournals.org/cgi/content/abstract/77/3/776
Testosterone administration increases insulin-like growth factor-I levels in normal men
CJ Hobbs, SR Plymate, CJ Rosen and RA Adler
Department of Clinical Investigation, Madigan Army Medical Center, Tacoma, Washington 98493.
Although testosterone (T) administration can increase insulin-like growth factor-I (IGF-I) when administered to hypogonadal men, no studies have examined whether this occurs in normal men. The present study was undertaken to determine if an increase in IGF-I may be part of the anabolic effect of androgens. We enrolled 11 normal men in a randomized, double-blinded cross-over study. Subjects were assigned to receive either T enanthate (TE) (300 mg im, each week) or nandrolone (ND) decanoate (300 mg im, each week) for 6 weeks. After a washout period subjects were administered the alternate treatment. Pre- and posttreatment serum was analyzed for IGF-I by RIA after acid-ethanol extraction. Results expressed as mean +/- SEM (Table 1). IGF-binding protein-3 was measured by RIA and was unchanged in the TE treatment and decreased significantly after ND treatment. Although GH levels were not significantly different after either TE or ND treatment, they tended to increase after TE treatment (1.23 +/- 0.28 ng/mL vs. 3.3 +/- 1.03 ng/mL) but remained unchanged after ND treatment (1.68 +/- 0.68 ng/mL vs. 1.89 +/- 0.64 ng/mL). Serum total T levels increased 32 +/- 0.05 nmol/L in the TE-treated men, but fell by 7 +/- 0.02 nmol/L in the ND- treated men (P < 0.0001). Serum estradiol levels rose by 193.04 +/- 19.82 pmol/L in the TE-treated men although falling by 50.65 +/- 34.50 pmol/L in the ND-treated men (P < 0.0002). These data indicate that when normal men are given TE, serum IGF-I levels increase after 6 weeks of treatment. Treatment with ND did not change serum levels of IGF-I but did decrease the level of the major serum IGF-BP and therefore the level of bioavailable IGF-I may be increased in the ND group.
http://jcem.endojournals.org/cgi/content/abstract/77/3/776
THE-DET-OAK
IncreasedMyT @ ULV
Not only is insulin increased by T administration but sensitivity is also increased.
Men with diabetes usually need a lower dose of insulin while on TRT.
Men with diabetes usually need a lower dose of insulin while on TRT.
THE-DET-OAK
IncreasedMyT @ ULV
The liver and kidneys are connected to the endocrine system. Testosterone is basically a messenger signal that regulates many many things in our bodies. Anytime it is increased many things are affected, mostly they are sped up. Almost every cell in our bodies is affected by T.
http://www.steroidology.com/forum/anabolic-steroid-forum/152416-what-does-testosterone-do-body.html
Physiological effects
In general, androgens promote protein synthesis and growth of those tissues with androgen receptors. Testosterone effects can be classified as virilizing and anabolic, although the distinction is somewhat artificial, as many of the effects can be considered both.
* Anabolic effects include growth of muscle mass and strength, increased bone density and strength, and stimulation of linear growth and bone maturation.
* Androgenic effects include maturation of the sex organs, particularly the penis and the formation of the scrotum in unborn children, and after birth (usually at puberty) a deepening of the voice, growth of the beard and axillary hair. Many of these fall into the category of male secondary sex characteristics.
Testosterone effects can also be classified by the age of usual occurrence. For postnatal effects in both males and females, these are mostly dependent on the levels and duration of circulating free testosterone.
Early infancy
Early infancy androgen effects are the least understood. In the first weeks of life for male infants, testosterone levels rise. The levels remain in a pubertal range for a few months, but usually reach the barely detectable levels of childhood by 4***8211;6 months of age.[4][5] The function of this rise in humans is unknown. It has been speculated that "brain masculinization" is occurring since no significant changes have been identified in other parts of the body.[6][citation needed] Surprisingly, the male brain is masculinized by testosterone being aromatized into estrogen, which crosses the blood-brain barrier and enters the male brain, whereas female fetuses have alpha-fetoprotein which binds up the estrogen so that female brains are not affected.[7]
[edit] Pre-peripubertal
Pre- Peripubertal effects are the first visible effects of rising androgen levels at the end of childhood, occurring in both boys and girls.[vague]
* Adult-type body odour
* Increased oiliness of skin and hair, acne
* Pubarche (appearance of pubic hair)
* Axillary hair
* Growth spurt, accelerated bone maturation
* Hair on upper lip and sideburns.
[edit] Pubertal
Pubertal effects begin to occur when androgen has been higher than normal adult female levels for months or years. In males, these are usual late pubertal effects, and occur in women after prolonged periods of heightened levels of free testosterone in the blood.
* Enlargement of sebaceous glands. This might cause acne.
* Phallic enlargement or clitoromegaly
* Increased libido and frequency of erection or clitoral engorgement
* Pubic hair extends to thighs and up toward umbilicus
* Facial hair (sideburns, beard, moustache)
* Loss of scalp hair (Androgenetic alopecia)
* Chest hair, periareolar hair, perianal hair
* Leg hair
* Axillary hair
* Subcutaneous fat in face decreases
* Increased muscle strength and mass[8]
* Deepening of voice
* Increase in height
* Growth of the Adam's apple
* Growth of spermatogenic tissue in testes, male fertility
* Growth of jaw, brow, chin, nose, and remodeling of facial bone contours
* Shoulders become broader and rib cage expands
* Completion of bone maturation and termination of growth. This occurs indirectly via estradiol metabolites and hence more gradually in men than women.
[edit] Adult
Adult testosterone effects are more clearly demonstrable in males than in females, but are likely important to both sexes. Some of these effects may decline as testosterone levels decrease in the later decades of adult life.
* Libido and clitoral engorgement/penile erection frequency
* Regulates acute HPA response under dominance challenge[9]
* Mental and physical energy
* Maintenance of muscle trophism
* The most recent and reliable studies have shown that testosterone does not cause or produce deleterious effects on prostate cancer. In people who have undergone testosterone deprivation therapy, testosterone increases beyond the castrate level have been shown to increase the rate of spread of an existing prostate cancer.[10][11][12]
* Recent studies have shown conflicting results concerning the importance of testosterone in maintaining cardiovascular health.[13][14] Nevertheless, maintaining normal testosterone levels in elderly men has been shown to improve many parameters which are thought to reduce cardiovascular disease, risk such as increased lean body mass, decreased visceral fat mass, decreased total cholesterol, and glycemic control.[15]
* Under dominance challenge, may play a role in the regulation of the fight-or-flight response[16]
Testosterone regulates the population of thromboxane A2 receptors on megakaryocytes and platelets and hence platelet aggregation in humans[17][18]
Reference ranges for blood tests, showing adult male testosterone levels in light blue at center-left.
Testosterone is necessary for normal sperm development. It activates genes in Sertoli cells, which promote differentiation of spermatogonia.
In animals (grouse and sand lizards), higher testosterone levels have been linked to a reduced immune system activity. Testosterone seems to have become part of the honest signaling system between potential mates in the course of evolution.[19][20]
[edit] Brain
As testosterone affects the entire body (often by enlarging; men have bigger hearts, lungs, liver, etc.), the brain is also affected by this "sexual" advancement;[3] the enzyme aromatase converts testosterone into estradiol that is responsible for masculinization of the brain in a male fetus.[citation needed][dubious ***8211; discuss]
There are some differences in a male and female brain (the result of different testosterone levels), one of them being size: the male human brain is, on average, larger; however, in females (who generally do not have as high testosterone levels) the corpus callosum is proportionally larger and women also have more dendritic connections between brain cells. This means that the effect of testosterone is a greater overall brain volume, but a decreased connection between the hemispheres.[21]
A study conducted in 1996 found no immediate short term effects on mood or behavior from the administration of supraphysiologic doses of testosterone for 10 weeks on 43 healthy men.[8]
Literature suggests that attention, memory, and spatial ability are key cognitive functions affected by testosterone in humans. Preliminary evidence suggests that low testosterone levels may be a risk factor for cognitive decline and possibly for dementia of the Alzheimer***8217;s type,[22][23] a key argument in Life Extension Medicine for the use of testosterone in anti-aging therapies. Much of the literature, however, suggests a curvilinear or even quadratic relationship between spatial performance and circulating testosterone,[24] where both hypo- and hypersecretion of circulating androgens have negative effects on cognition and cognitively-modulated aggressivity, as detailed above.
Contrary to what has been postulated in outdated studies and by certain sections of the media, aggressive behaviour is not typically seen in hypogonadal men who have their testosterone replaced adequately to the eugonadal/normal range. In fact, aggressive behaviour has been associated with hypogonadism and low testosterone levels and it would seem as though supraphysiological and low levels of testosterone and hypogonadism cause mood disorders and aggressive behaviour, with eugondal/normal testosterone levels being important for mental well-being. Testosterone depletion is a normal consequence of aging in men. One consequence of this is an increased risk for the development of Alzheimer***8217;s Disease.[25][26]
[edit] Biochemistry
[edit] Biosynthesis
Human steroidogenesis, showing testosterone near bottom.
Like other steroid hormones, testosterone is derived from cholesterol.[27] The largest amounts of testosterone are produced by the testes in men. It is also synthesized in far smaller quantities in women by the thecal cells of the ovaries, by the placenta, as well as by the zona reticularis of the adrenal cortex in both sexes.
In the testes, testosterone is produced by the Leydig cells.[28] The male generative glands also contain Sertoli cells which require testosterone for spermatogenesis. Like most hormones, testosterone is supplied to target tissues in the blood where much of it is transported bound to a specific plasma protein, sex hormone binding globulin (SHBG).
Factors affecting testosterone levels
* Loss of status or dominance in men.[16]
* Implicit power motivation predicts an increased testosterone release in men.[29]
* Aging reduces testosterone release.[30]
* Hypogonadism
* Sleep (REM dream) increases nocturnal testosterone levels.[31]
* Resistance training increases testosterone levels,[32] however, in older men, that increase can be avoided by protein ingestion.[33]
* Zinc deficiency lowers testosterone levels[34] but over supplementation has no effect on serum testosterone.[35]
* Licorice. The active ingredient in licorice root, glycyrrhizinic acid has been linked to small, clinically non-significant decreases in testosterone levels.[36] In contrast, a more recent study found that licorice administration produced a substantial testosterone decrease in a small, female-only sample.[37]
[edit] Metabolism
Testosterone is reduced to 5***945;-dihydrotestosterone (DHT) by the cytochrome P450 enzyme 5-alpha reductase [38] or converted into estradiol by aromatase (CYP19A1).[39]
[edit] Mechanism of action
The effects of testosterone in humans and other vertebrates occur by way of two main mechanisms: by activation of the androgen receptor (directly or as DHT), and by conversion to estradiol and activation of certain estrogen receptors.[40][41]
Free testosterone (T) is transported into the cytoplasm of target tissue cells, where it can bind to the androgen receptor, or can be reduced to 5***945;-dihydrotestosterone (DHT) by the cytoplasmic enzyme 5-alpha reductase. DHT binds to the same androgen receptor even more strongly than T, so that its androgenic potency is about 5 times that of T.[42] The T-receptor or DHT-receptor complex undergoes a structural change that allows it to move into the cell nucleus and bind directly to specific nucleotide sequences of the chromosomal DNA. The areas of binding are called hormone response elements (HREs), and influence transcriptional activity of certain genes, producing the androgen effects. It is important to note that if there is a 5-alpha reductase deficiency, the body (of a human) will continue growing into a female with testicles.
Androgen receptors occur in many different vertebrate body system tissues, and both males and females respond similarly to similar levels. Greatly differing amounts of testosterone prenatally, at puberty, and throughout life account for a share of biological differences between males and females.
The bones and the brain are two important tissues in humans where the primary effect of testosterone is by way of aromatization to estradiol. In the bones, estradiol accelerates maturation of cartilage into bone, leading to closure of the epiphyses and conclusion of growth. In the central nervous system, testosterone is aromatized to estradiol. Estradiol rather than testosterone serves as the most important feedback signal to the hypothalamus (especially affecting LH secretion). In many mammals, prenatal or perinatal "masculinization" of the sexually dimorphic areas of the brain by estradiol derived from testosterone programs later male sexual behavior.
The human hormone testosterone is produced in greater amounts by males, and less by females. The human hormone estrogen is produced in greater amounts by females, and less by males. Testosterone causes the appearance of masculine traits (i.e., deepening voice, pubic and facial hairs, muscular build, etc.) Like men, women rely on testosterone to maintain libido, bone density and muscle mass throughout their lives. In men, inappropriately high levels of estrogens lower testosterone, decrease muscle mass, stunt growth in teenagers, introduce gynecomastia, increase feminine characteristics, and decrease susceptibility to prostate cancer, reduces libido and causes erectile dysfunction and can cause excessive sweating and hot flushes. However, an appropriate amount of estrogens is required in the male in order to ensure well-being, bone density, libido, erectile function, etc.
Endocrine system - Wikipedia, the free encyclopedia
http://www.steroidology.com/forum/anabolic-steroid-forum/152416-what-does-testosterone-do-body.html
Physiological effects
In general, androgens promote protein synthesis and growth of those tissues with androgen receptors. Testosterone effects can be classified as virilizing and anabolic, although the distinction is somewhat artificial, as many of the effects can be considered both.
* Anabolic effects include growth of muscle mass and strength, increased bone density and strength, and stimulation of linear growth and bone maturation.
* Androgenic effects include maturation of the sex organs, particularly the penis and the formation of the scrotum in unborn children, and after birth (usually at puberty) a deepening of the voice, growth of the beard and axillary hair. Many of these fall into the category of male secondary sex characteristics.
Testosterone effects can also be classified by the age of usual occurrence. For postnatal effects in both males and females, these are mostly dependent on the levels and duration of circulating free testosterone.
Early infancy
Early infancy androgen effects are the least understood. In the first weeks of life for male infants, testosterone levels rise. The levels remain in a pubertal range for a few months, but usually reach the barely detectable levels of childhood by 4***8211;6 months of age.[4][5] The function of this rise in humans is unknown. It has been speculated that "brain masculinization" is occurring since no significant changes have been identified in other parts of the body.[6][citation needed] Surprisingly, the male brain is masculinized by testosterone being aromatized into estrogen, which crosses the blood-brain barrier and enters the male brain, whereas female fetuses have alpha-fetoprotein which binds up the estrogen so that female brains are not affected.[7]
[edit] Pre-peripubertal
Pre- Peripubertal effects are the first visible effects of rising androgen levels at the end of childhood, occurring in both boys and girls.[vague]
* Adult-type body odour
* Increased oiliness of skin and hair, acne
* Pubarche (appearance of pubic hair)
* Axillary hair
* Growth spurt, accelerated bone maturation
* Hair on upper lip and sideburns.
[edit] Pubertal
Pubertal effects begin to occur when androgen has been higher than normal adult female levels for months or years. In males, these are usual late pubertal effects, and occur in women after prolonged periods of heightened levels of free testosterone in the blood.
* Enlargement of sebaceous glands. This might cause acne.
* Phallic enlargement or clitoromegaly
* Increased libido and frequency of erection or clitoral engorgement
* Pubic hair extends to thighs and up toward umbilicus
* Facial hair (sideburns, beard, moustache)
* Loss of scalp hair (Androgenetic alopecia)
* Chest hair, periareolar hair, perianal hair
* Leg hair
* Axillary hair
* Subcutaneous fat in face decreases
* Increased muscle strength and mass[8]
* Deepening of voice
* Increase in height
* Growth of the Adam's apple
* Growth of spermatogenic tissue in testes, male fertility
* Growth of jaw, brow, chin, nose, and remodeling of facial bone contours
* Shoulders become broader and rib cage expands
* Completion of bone maturation and termination of growth. This occurs indirectly via estradiol metabolites and hence more gradually in men than women.
[edit] Adult
Adult testosterone effects are more clearly demonstrable in males than in females, but are likely important to both sexes. Some of these effects may decline as testosterone levels decrease in the later decades of adult life.
* Libido and clitoral engorgement/penile erection frequency
* Regulates acute HPA response under dominance challenge[9]
* Mental and physical energy
* Maintenance of muscle trophism
* The most recent and reliable studies have shown that testosterone does not cause or produce deleterious effects on prostate cancer. In people who have undergone testosterone deprivation therapy, testosterone increases beyond the castrate level have been shown to increase the rate of spread of an existing prostate cancer.[10][11][12]
* Recent studies have shown conflicting results concerning the importance of testosterone in maintaining cardiovascular health.[13][14] Nevertheless, maintaining normal testosterone levels in elderly men has been shown to improve many parameters which are thought to reduce cardiovascular disease, risk such as increased lean body mass, decreased visceral fat mass, decreased total cholesterol, and glycemic control.[15]
* Under dominance challenge, may play a role in the regulation of the fight-or-flight response[16]
Testosterone regulates the population of thromboxane A2 receptors on megakaryocytes and platelets and hence platelet aggregation in humans[17][18]
Reference ranges for blood tests, showing adult male testosterone levels in light blue at center-left.
Testosterone is necessary for normal sperm development. It activates genes in Sertoli cells, which promote differentiation of spermatogonia.
In animals (grouse and sand lizards), higher testosterone levels have been linked to a reduced immune system activity. Testosterone seems to have become part of the honest signaling system between potential mates in the course of evolution.[19][20]
[edit] Brain
As testosterone affects the entire body (often by enlarging; men have bigger hearts, lungs, liver, etc.), the brain is also affected by this "sexual" advancement;[3] the enzyme aromatase converts testosterone into estradiol that is responsible for masculinization of the brain in a male fetus.[citation needed][dubious ***8211; discuss]
There are some differences in a male and female brain (the result of different testosterone levels), one of them being size: the male human brain is, on average, larger; however, in females (who generally do not have as high testosterone levels) the corpus callosum is proportionally larger and women also have more dendritic connections between brain cells. This means that the effect of testosterone is a greater overall brain volume, but a decreased connection between the hemispheres.[21]
A study conducted in 1996 found no immediate short term effects on mood or behavior from the administration of supraphysiologic doses of testosterone for 10 weeks on 43 healthy men.[8]
Literature suggests that attention, memory, and spatial ability are key cognitive functions affected by testosterone in humans. Preliminary evidence suggests that low testosterone levels may be a risk factor for cognitive decline and possibly for dementia of the Alzheimer***8217;s type,[22][23] a key argument in Life Extension Medicine for the use of testosterone in anti-aging therapies. Much of the literature, however, suggests a curvilinear or even quadratic relationship between spatial performance and circulating testosterone,[24] where both hypo- and hypersecretion of circulating androgens have negative effects on cognition and cognitively-modulated aggressivity, as detailed above.
Contrary to what has been postulated in outdated studies and by certain sections of the media, aggressive behaviour is not typically seen in hypogonadal men who have their testosterone replaced adequately to the eugonadal/normal range. In fact, aggressive behaviour has been associated with hypogonadism and low testosterone levels and it would seem as though supraphysiological and low levels of testosterone and hypogonadism cause mood disorders and aggressive behaviour, with eugondal/normal testosterone levels being important for mental well-being. Testosterone depletion is a normal consequence of aging in men. One consequence of this is an increased risk for the development of Alzheimer***8217;s Disease.[25][26]
[edit] Biochemistry
[edit] Biosynthesis
Human steroidogenesis, showing testosterone near bottom.
Like other steroid hormones, testosterone is derived from cholesterol.[27] The largest amounts of testosterone are produced by the testes in men. It is also synthesized in far smaller quantities in women by the thecal cells of the ovaries, by the placenta, as well as by the zona reticularis of the adrenal cortex in both sexes.
In the testes, testosterone is produced by the Leydig cells.[28] The male generative glands also contain Sertoli cells which require testosterone for spermatogenesis. Like most hormones, testosterone is supplied to target tissues in the blood where much of it is transported bound to a specific plasma protein, sex hormone binding globulin (SHBG).
Factors affecting testosterone levels
* Loss of status or dominance in men.[16]
* Implicit power motivation predicts an increased testosterone release in men.[29]
* Aging reduces testosterone release.[30]
* Hypogonadism
* Sleep (REM dream) increases nocturnal testosterone levels.[31]
* Resistance training increases testosterone levels,[32] however, in older men, that increase can be avoided by protein ingestion.[33]
* Zinc deficiency lowers testosterone levels[34] but over supplementation has no effect on serum testosterone.[35]
* Licorice. The active ingredient in licorice root, glycyrrhizinic acid has been linked to small, clinically non-significant decreases in testosterone levels.[36] In contrast, a more recent study found that licorice administration produced a substantial testosterone decrease in a small, female-only sample.[37]
[edit] Metabolism
Testosterone is reduced to 5***945;-dihydrotestosterone (DHT) by the cytochrome P450 enzyme 5-alpha reductase [38] or converted into estradiol by aromatase (CYP19A1).[39]
[edit] Mechanism of action
The effects of testosterone in humans and other vertebrates occur by way of two main mechanisms: by activation of the androgen receptor (directly or as DHT), and by conversion to estradiol and activation of certain estrogen receptors.[40][41]
Free testosterone (T) is transported into the cytoplasm of target tissue cells, where it can bind to the androgen receptor, or can be reduced to 5***945;-dihydrotestosterone (DHT) by the cytoplasmic enzyme 5-alpha reductase. DHT binds to the same androgen receptor even more strongly than T, so that its androgenic potency is about 5 times that of T.[42] The T-receptor or DHT-receptor complex undergoes a structural change that allows it to move into the cell nucleus and bind directly to specific nucleotide sequences of the chromosomal DNA. The areas of binding are called hormone response elements (HREs), and influence transcriptional activity of certain genes, producing the androgen effects. It is important to note that if there is a 5-alpha reductase deficiency, the body (of a human) will continue growing into a female with testicles.
Androgen receptors occur in many different vertebrate body system tissues, and both males and females respond similarly to similar levels. Greatly differing amounts of testosterone prenatally, at puberty, and throughout life account for a share of biological differences between males and females.
The bones and the brain are two important tissues in humans where the primary effect of testosterone is by way of aromatization to estradiol. In the bones, estradiol accelerates maturation of cartilage into bone, leading to closure of the epiphyses and conclusion of growth. In the central nervous system, testosterone is aromatized to estradiol. Estradiol rather than testosterone serves as the most important feedback signal to the hypothalamus (especially affecting LH secretion). In many mammals, prenatal or perinatal "masculinization" of the sexually dimorphic areas of the brain by estradiol derived from testosterone programs later male sexual behavior.
The human hormone testosterone is produced in greater amounts by males, and less by females. The human hormone estrogen is produced in greater amounts by females, and less by males. Testosterone causes the appearance of masculine traits (i.e., deepening voice, pubic and facial hairs, muscular build, etc.) Like men, women rely on testosterone to maintain libido, bone density and muscle mass throughout their lives. In men, inappropriately high levels of estrogens lower testosterone, decrease muscle mass, stunt growth in teenagers, introduce gynecomastia, increase feminine characteristics, and decrease susceptibility to prostate cancer, reduces libido and causes erectile dysfunction and can cause excessive sweating and hot flushes. However, an appropriate amount of estrogens is required in the male in order to ensure well-being, bone density, libido, erectile function, etc.
Endocrine system - Wikipedia, the free encyclopedia
Last edited:
cjw2021
Pro Bodybuilder
Nice research. I love deca but absolutely hate enanthate. I saw it pretty interesting how DECA lowered estrogen so much. I feel sorry for all the men in these studies that they load up on DECA and don't add an ancillary testosterone to...lol so they are like neutering the men and not telling them.
skitzz
New member
Hey OAK,
How do you calculate what a person's T level will be based on their doseage? Like in the sample above, you say that a person in the low 200-400 range will bump their T levels up to 1200 if they dose at 200mg a week.
Reason I ask is this would be helpful in mapping out what your doseage would have to be to see decent gains. Even a somewhat educated guess is better than just taking what everyone else is taking.
THE-DET-OAK
IncreasedMyT @ ULV
honestly its just a guess. Im prolly guessing low in that example. Ive just seen and read blood tests and that usually where it falls. that is the peak m speaking of in that example as well.
In the study i mentioned it actually gives their ranges.
One thing to remember is it all depends on the realtionshiop to when the blood was drawn and when your last injection was.
for example most guys get their trough around 6-800 on 125-150mg a week. this test should have been taken the day before their next injection in order to get the trough. so the person that doses once a week @ 150mg will prolly land around 800 the day before their next shot. since cyp has about a 7 day half-life in most men you can guess that his T levels were double what the test showed the day after their most recent injection. this case it would have been 1600.
in the study 300mg-600mg of T. the 300 group had T levels at like 1500. this test was taken according to the half-life like it is in most study's. so we can assume their T levels reached a peak of 3000.
lets say the same person who was injecting 150mg a week does 75mg 2x a week. this means you would have your blood test done 3 days after injection. his levels may be at 1000 when tested but his peak would only go up to 12-1300.
When on testosterone replacement therapy (TRT) you want your trough to be around 600 to be extra cautious.
reading the numbers is one thing, finding out where you like yours are another.
Last edited:
THE-DET-OAK
IncreasedMyT @ ULV
lol I know poor bastards lol
Similar threads
