Would LH-releasing hormone product have a place in pct? And at what doses?
first cut n paste from here
Luteinizing hormone (LH) and follicle-stimulating hormone (FSH) are called gonadotropins because stimulate the gonads - in males, the testes, and in females, the ovaries. They are not necessary for life, but are essential for reproduction. These two hormones are secreted from cells in the anterior pituitary called gonadotrophs. Most gonadotrophs secrete only LH or FSH, but some appear to secrete both hormones.
As describef for thyroid-simulating hormone, LH and FSH are large glycoproteins composed of alpha and beta subunits. The alpha subunit is identical in all three of these anterior pituitary hormones, while the beta subunit is unique and endows each hormone with the ability to bind its own receptor.
Physiologic Effects of Gonadotropins
Physiologic effects of the gonadotrophins are known only in the ovaries and testes. Together, then regulate many aspects of gonadal function in both males and females.
Luteinizing Hormone
In both sexes, LH stimulates secretion of sex steroids from the gonads. In the testes, LH binds to receptors on Leydig cells, stimulating synthesis and secretion of testosterone. Theca cells in the ovary respond to LH stimulation by secretion of testosterone, which is converted into estrogen by adjacent granulosa cells.
2nd link
3rd link
Full Version: LH-releasing hormone in PCT?
Looks like it does: http://books.google.com/books?id=kSvQ7ANeI...I0vTI&hl=en
LH = HCG (at least in terms of effect)
Using it during PCT will delay restoration of the HP part of the HPTA
GnRH and synthetic analogs are actually used to depress testicular function and after an initial 'flare' of increased T production everything shuts down and becomes insensitive.
Using it during PCT will delay restoration of the HP part of the HPTA
GnRH and synthetic analogs are actually used to depress testicular function and after an initial 'flare' of increased T production everything shuts down and becomes insensitive.
Benson: you have a thread on this, don't you?
If you use LH/hCG/hMG (we'll assume hCG as thats the most readily available and relatively cheap) all the way through PCT you will still be shutdown at the end of PCT, as you have been using an Exogenous Hormone to get the Leydig cells functioning. While it is natural test which has been produced, until your HPTA returns to normal you are still shutdown.
Now... That could be a week after PCT. It could be longer.
Jury is still out on this really, but its been suggested to use hCG at the end of the cycle in the gap between cycle and PCT, and in the earlt stages of PCT. Leaving Nolva and Clomid to do their job during PCT.
Use of hCG to keep the leydig cells ticking over on cycle is an option.
Now... That could be a week after PCT. It could be longer.
Jury is still out on this really, but its been suggested to use hCG at the end of the cycle in the gap between cycle and PCT, and in the earlt stages of PCT. Leaving Nolva and Clomid to do their job during PCT.
Use of hCG to keep the leydig cells ticking over on cycle is an option.
QUOTE (Benson @ Apr 2 2008, 12:20 PM) 
LH = HCG (at least in terms of effect)
Using it during PCT will delay restoration of the HP part of the HPTA
GnRH and synthetic analogs are actually used to depress testicular function and after an initial 'flare' of increased T production everything shuts down and becomes insensitive.
Using it during PCT will delay restoration of the HP part of the HPTA
GnRH and synthetic analogs are actually used to depress testicular function and after an initial 'flare' of increased T production everything shuts down and becomes insensitive.
Ok I understand what you are saying. I dont know the accuracy of your statement that LH-releasing hormone = HCG, since HCG has an FSH and TSH effect as well I believe. I never recommend HCG during pct.
But I guess let me rephrase my question: does LH-releasing hormone have a place in cycling AAS? I mean can it be used DURING cycle to allow for quicker recovery in pct?
bb
QUOTE (Tall @ Apr 2 2008, 01:29 PM)
If you use LH/hCG/hMG (we'll assume hCG as thats the most readily available and relatively cheap) all the way through PCT you will still be shutdown at the end of PCT, as you have been using an Exogenous Hormone to get the Leydig cells functioning. While it is natural test which has been produced, until your HPTA returns to normal you are still shutdown.
Now... That could be a week after PCT. It could be longer.
Jury is still out on this really, but its been suggested to use hCG at the end of the cycle in the gap between cycle and PCT, and in the earlt stages of PCT. Leaving Nolva and Clomid to do their job during PCT.
Use of hCG to keep the leydig cells ticking over on cycle is an option.
Now... That could be a week after PCT. It could be longer.
Jury is still out on this really, but its been suggested to use hCG at the end of the cycle in the gap between cycle and PCT, and in the earlt stages of PCT. Leaving Nolva and Clomid to do their job during PCT.
Use of hCG to keep the leydig cells ticking over on cycle is an option.
I think its a little disengenuous to say that yes your body is producing natural testosterone (& at a healthy male level) but you are 'shutdown'. I mean one of the primary functions of pct is to regain the body's natural test production. So while the cells might stop pushing out as much natty test once LH-rh is stopped, I would still prefer to enter PCT with the natural test levels of a normal healthy male instead of a 12yo girl.
bb
QUOTE (babyblu @ Apr 2 2008, 06:02 PM)
I think its a little disengenuous to say that yes your body is producing natural testosterone (& at a healthy male level) but you are 'shutdown'. I mean one of the primary functions of pct is to regain the body's natural test production. So while the cells might stop pushing out as much natty test once LH-rh is stopped, I would still prefer to enter PCT with the natural test levels of a normal healthy male instead of a 12yo girl.
bb
bb
Okay.
Normally....
Hypothalmus releases GnRH. GnRH starts the process to release LH. LH causes Leydig cells to release Test. Agreed...?
Add hCG into the mix and the feedback is broken. Exogenous LH (Read: hCG) circulating means the Hyptothalmus no longer needs to release GnRH, which then means no natural LH is released.
Therefore you are shutdown.
The assumption you are making is that you can go from testes which work with an exogenous dose of LH to testes which will work without that exogenous dose of LH.
But...
If you read my post I think we both want the same result, hence the 'hCG Pulse' pre/in initial stages of PCT, then leaving the clomid/nolva to do their job.
Does that make sense? I've got to go smash some Squat PBs, but I'll be back later
Yes I understant but based on your thoughts, the introduction of LH-releasing hormone (and please lets stick with this and NOT HCG b/c they are not the same) stimulates the body to produce MORE LH. So there would not be exogenous LH introduced into the body, which would then mean that GnRH is still produced by the hypothalmus.
I think we are on the same page but for clarity's sake lets NOT state it as testes that work w/exogenous LH vs. testes that will work w/o exogenous LH because again there is NO exegenous LH. Thats like saying injecting ghrp6 is the same as injecting HGH; its simply not the case. LH-releasing hormone causes the body to produce MORE LH. HCG mimics LH. I think the difference is important here.
bb
I think we are on the same page but for clarity's sake lets NOT state it as testes that work w/exogenous LH vs. testes that will work w/o exogenous LH because again there is NO exegenous LH. Thats like saying injecting ghrp6 is the same as injecting HGH; its simply not the case. LH-releasing hormone causes the body to produce MORE LH. HCG mimics LH. I think the difference is important here.
bb
QUOTE (babyblu @ Apr 2 2008, 07:13 PM)
Yes I understant but based on your thoughts, the introduction of LH-releasing hormone (and please lets stick with this and NOT HCG b/c they are not the same) stimulates the body to produce MORE LH. So there would not be exogenous LH introduced into the body, which would then mean that GnRH is still produced by the hypothalmus.
I think we are on the same page but for clarity's sake lets NOT state it as testes that work w/exogenous LH vs. testes that will work w/o exogenous LH because again there is NO exegenous LH. Thats like saying injecting ghrp6 is the same as injecting HGH; its simply not the case. LH-releasing hormone causes the body to produce MORE LH. HCG mimics LH. I think the difference is important here.
bb
I think we are on the same page but for clarity's sake lets NOT state it as testes that work w/exogenous LH vs. testes that will work w/o exogenous LH because again there is NO exegenous LH. Thats like saying injecting ghrp6 is the same as injecting HGH; its simply not the case. LH-releasing hormone causes the body to produce MORE LH. HCG mimics LH. I think the difference is important here.
bb
My appologies - I'd misread the above to assume you were using hCG which mimics LH, as opposed to using GnRH1.
Yes that sounds better. Question is - can you get your mitts on some GnRH1...?
Wouldnt have started the thread unless I couldnt 
The question really is, how much would a person need to run?
bb
The question really is, how much would a person need to run?
bb
Some good info here:
http://www.mindandmuscle.net/forum/index.php?showtopic=29121
Benson's thread, also interesting:
http://www.mindandmuscle.net/forum/index.php?showtopic=32175
http://www.mindandmuscle.net/forum/index.php?showtopic=29121
Benson's thread, also interesting:
http://www.mindandmuscle.net/forum/index.php?showtopic=32175
yes good info. i am looking at a lypholized lh-rh peptide that would be injectable like hcg.
bb
bb
"At the pituitary, GNRH1 stimulates the synthesis and secretion of the gonadotropins follicle-stimulating hormone (FSH) and luteinizing hormone (LH). These processes are controlled by the size and frequency of GNRH1 pulses, as well as by feedback from androgens and estrogens. Low frequency GNRH1 pulses lead to FSH release, whereas high frequency GNRH1 pulses stimulate LH release."
The key word is PULSE. Unless you have sophisticated machinery (hitherto unknown on this planet) that will allow you to administer GnRH in a pulsatile fashion, you WILL completely shut down your HPTA. As Benson noted, because we are unable to mimic the natural pulsatile rhythm, administration of these peptides is actually used as an experimental protocol for inducing reversible hypogonadic states (i.e., to replicate castration).
EDIT: Your post below only confirms that you are thinking of using what I thought you were (although Luteinizing is spelled wrong - classy). Im going to laugh if you take this in the face of these warnings... unless, of course, chemical castration is your goal.
The key word is PULSE. Unless you have sophisticated machinery (hitherto unknown on this planet) that will allow you to administer GnRH in a pulsatile fashion, you WILL completely shut down your HPTA. As Benson noted, because we are unable to mimic the natural pulsatile rhythm, administration of these peptides is actually used as an experimental protocol for inducing reversible hypogonadic states (i.e., to replicate castration).
EDIT: Your post below only confirms that you are thinking of using what I thought you were (although Luteinizing is spelled wrong - classy). Im going to laugh if you take this in the face of these warnings... unless, of course, chemical castration is your goal.
Human Leutenizing hormone Releasing Hormone
Ultra Pure
Catalog No: CRL603A Size: 5.0 mg
CRL603B Size: 10.0 mg
CRL603C Size: 20.0 mg
Description: Synthetic Human Leutenizing Hormone Releasing Hormone is a single, non-glycosylated, polypeptide chain containing 10 amino acids and having a molecular mass of 1182.4 Daltons.
Physical Appearance: Sterile filtered white lyophilized (freeze-dried) powder.
Formulation: The Human Leutenizing Hormone Releasing Hormone was lyophilized from a concentrated (1mg/ml) solution with no additives.
Solubility: It is recommended to reconstitute the lyophilized Leutenizing Hormone Releasing Hormone in sterile ddH2O not less than 100μg/ml, which can then be further diluted to other aqueous solutions. Note: Always centrifuge vial before opening.
Stability: Lyophilized Human Leutenizing Hormone Releasing Hormone, although stable at room temperature for 3 weeks, should be stored desiccated below -18°C. Upon reconstitution, Human Leutenizing Hormone Releasing Hormone should be stored at 4°C between 2-7 days and for future use below -18°C. For long term storage it is recommended to add a carrier protein (0.1% HSA or BSA). Please prevent freeze-thaw cycles.
Purity: Greater than 98.0% as determined by:
(a) Analysis by RP-HPLC.
(B) Mass Spectral Anaylsis {MALDI-TOF exhibits correct Mw}.
Amino Acid
Sequence: Glu-His-Trp-Ser-Tyr-Gly-Leu-Arg-Pro-Gly-NH2
NOT FOR HUMAN USE. FOR RESEARCH ONLY. NOT FOR DIAGNOSTIC OR THERAPEUTIC USE.
Ultra Pure
Catalog No: CRL603A Size: 5.0 mg
CRL603B Size: 10.0 mg
CRL603C Size: 20.0 mg
Description: Synthetic Human Leutenizing Hormone Releasing Hormone is a single, non-glycosylated, polypeptide chain containing 10 amino acids and having a molecular mass of 1182.4 Daltons.
Physical Appearance: Sterile filtered white lyophilized (freeze-dried) powder.
Formulation: The Human Leutenizing Hormone Releasing Hormone was lyophilized from a concentrated (1mg/ml) solution with no additives.
Solubility: It is recommended to reconstitute the lyophilized Leutenizing Hormone Releasing Hormone in sterile ddH2O not less than 100μg/ml, which can then be further diluted to other aqueous solutions. Note: Always centrifuge vial before opening.
Stability: Lyophilized Human Leutenizing Hormone Releasing Hormone, although stable at room temperature for 3 weeks, should be stored desiccated below -18°C. Upon reconstitution, Human Leutenizing Hormone Releasing Hormone should be stored at 4°C between 2-7 days and for future use below -18°C. For long term storage it is recommended to add a carrier protein (0.1% HSA or BSA). Please prevent freeze-thaw cycles.
Purity: Greater than 98.0% as determined by:
(a) Analysis by RP-HPLC.
(B) Mass Spectral Anaylsis {MALDI-TOF exhibits correct Mw}.
Amino Acid
Sequence: Glu-His-Trp-Ser-Tyr-Gly-Leu-Arg-Pro-Gly-NH2
NOT FOR HUMAN USE. FOR RESEARCH ONLY. NOT FOR DIAGNOSTIC OR THERAPEUTIC USE.
QUOTE (Mr.Kite @ Apr 3 2008, 06:57 AM)
Im going to laugh if you take this in the face of these warnings... unless, of course, chemical castration is your goal.
"chemical castration" is a bit severe...the leydig cells will still be producing T and the gonads will be healthy. the only "shutdown" experienced will be at the hypothalmus, and as i understand that is generally corrected naturally within days of coming off HCG or a similar LH/FSH mimic. the severe shutdown most people experience on steroid cycles is due to extended suppression of LH/FSH which makes the testes atrophy, which takes much longer to correct.
question though - wouldnt a GnRH-stimulating peptide (not a mimetic, but a stimulator), being at the top of the food chain, cause a suppression-free supply of T? all the necessary glands would be functioning...maybe they would desensitize, but there's probably a protocol to avoid it...anyway, i'm just thinking out loud.
QUOTE (thebrakes @ Apr 3 2008, 07:26 PM)
"chemical castration" is a bit severe...
That is the term commonly used for the administration of a GnRh agonist...the action is in the pituitary and after the initial hormone flare, the pituitary is completely desensitized and stops stimulating the testes which then atrophy. It is reversible.
QUOTE (thebrakes @ Apr 3 2008, 04:26 PM)
"chemical castration" is a bit severe...the leydig cells will still be producing T and the gonads will be healthy. the only "shutdown" experienced will be at the hypothalmus, and as i understand that is generally corrected naturally within days of coming off HCG or a similar LH/FSH mimic. the severe shutdown most people experience on steroid cycles is due to extended suppression of LH/FSH which makes the testes atrophy, which takes much longer to correct.
question though - wouldnt a GnRH-stimulating peptide (not a mimetic, but a stimulator), being at the top of the food chain, cause a suppression-free supply of T? all the necessary glands would be functioning...maybe they would desensitize, but there's probably a protocol to avoid it...anyway, i'm just thinking out loud.
question though - wouldnt a GnRH-stimulating peptide (not a mimetic, but a stimulator), being at the top of the food chain, cause a suppression-free supply of T? all the necessary glands would be functioning...maybe they would desensitize, but there's probably a protocol to avoid it...anyway, i'm just thinking out loud.
I clearly stated that it would be temporary chemical castration, but it is chemical castration nonetheless while the aftereffects of the GnRH administration are still in effect.
And what do you mean the "only shutdown"? If the hypothalamus is desensitized by over stimulation of GnRH (which is what happens with these long acting synthetics that are not administered in a pulsatile pattern), the hypothalamus drastically reduces the number of receptors, leading to a long term suppression from a lack of LH secretion (GnRH is not similar to HCG). If you are suppressed at any stage in the cascade it WILL trickle down to the leydig cells and cause a cessation of T production.
I'll just cite a single pubmed study to drive the point home. You guys should really take an upper level class on the hormonal systems... I mean this review explicitly says that people prefer the use of GnRH to castration just because they like their balls, not because there is much of a difference in effect.
QUOTE
Management of advanced prostate cancer: can we improve on androgen deprivation therapy?
Anderson J, Abrahamsson PA, Crawford D, Miller K, Tombal B.
Malmö University Hospital, Lund University, Sweden.
Gonadotrophin-releasing hormone (GnRH) agonists are currently the mainstay in the management of advanced prostate cancer. Used either as monotherapy or combined with antiandrogens, GnRH agonists suppress serum testosterone levels and thus slow the growth of the tumour cells that depend on testosterone for growth. GnRH agonists have largely replaced orchidectomy in the management of advanced prostate cancer, because patients are reluctant to undergo surgical castration. However, can we do better in androgen-deprivation therapy? There is some evidence to suggest that GnRH agonists do not achieve the level of testosterone suppression attained with orchidectomy, or as rapidly, factors which could be expected to affect overall survival. Together, these observations highlight the need to develop newer agents that can achieve rapid, profound and sustained testosterone suppression, equivalent to that with orchidectomy. Preliminary data for the GnRH blocker, degarelix, suggest that this new agent might overcome the shortcomings associated with GnRH agonists. Further clinical data are therefore awaited with much interest.
Anderson J, Abrahamsson PA, Crawford D, Miller K, Tombal B.
Malmö University Hospital, Lund University, Sweden.
Gonadotrophin-releasing hormone (GnRH) agonists are currently the mainstay in the management of advanced prostate cancer. Used either as monotherapy or combined with antiandrogens, GnRH agonists suppress serum testosterone levels and thus slow the growth of the tumour cells that depend on testosterone for growth. GnRH agonists have largely replaced orchidectomy in the management of advanced prostate cancer, because patients are reluctant to undergo surgical castration. However, can we do better in androgen-deprivation therapy? There is some evidence to suggest that GnRH agonists do not achieve the level of testosterone suppression attained with orchidectomy, or as rapidly, factors which could be expected to affect overall survival. Together, these observations highlight the need to develop newer agents that can achieve rapid, profound and sustained testosterone suppression, equivalent to that with orchidectomy. Preliminary data for the GnRH blocker, degarelix, suggest that this new agent might overcome the shortcomings associated with GnRH agonists. Further clinical data are therefore awaited with much interest.
Just do a PubMed search for "GnRH Androgen Deprivation" and you will find a host of other studies that use GnRH administration as a protocol for inducing androgen deprivation for the treatment of various diseases (or basic level research). And thats why I am so sure of myself on this point. Scientists arent researching what the effects of the administration are, that is already known, rather they commonly use it for this purpose. Inject GnRH at your own risk.
EDIT: Benson beat me to it. But read what I wrote. Let it sink in. It is the truth.
LH-rh is not a 'long acting synthetic':
DISAPPEARANCE OF LH-RELEASING HORMONE IN MAN AS DETERMINED BY RADIOIMMUNOASSAY
AKIRA ARIMURA11Endocrine and Polypeptide Laboratory and Endocrinology Section of the Medical Service, Veterans Administration Hospital and Department of Medicine, Tulane University School of Medicine, New Orleans; Hospital General del Centro Medico Nacional, IMSS, Mexico, D. F., ABBA J. KASTIN11Endocrine and Polypeptide Laboratory and Endocrinology Section of the Medical Service, Veterans Administration Hospital and Department of Medicine, Tulane University School of Medicine, New Orleans; Hospital General del Centro Medico Nacional, IMSS, Mexico, D. F., D. GONZALEZ-BARCENA11Endocrine and Polypeptide Laboratory and Endocrinology Section of the Medical Service, Veterans Administration Hospital and Department of Medicine, Tulane University School of Medicine, New Orleans; Hospital General del Centro Medico Nacional, IMSS, Mexico, D. F., JORGE SILLER11Endocrine and Polypeptide Laboratory and Endocrinology Section of the Medical Service, Veterans Administration Hospital and Department of Medicine, Tulane University School of Medicine, New Orleans; Hospital General del Centro Medico Nacional, IMSS, Mexico, D. F., ROBERT E. WEAVER11Endocrine and Polypeptide Laboratory and Endocrinology Section of the Medical Service, Veterans Administration Hospital and Department of Medicine, Tulane University School of Medicine, New Orleans; Hospital General del Centro Medico Nacional, IMSS, Mexico, D. F. AND ANDREW V. SCHALLY11Endocrine and Polypeptide Laboratory and Endocrinology Section of the Medical Service, Veterans Administration Hospital and Department of Medicine, Tulane University School of Medicine, New Orleans; Hospital General del Centro Medico Nacional, IMSS, Mexico, D. F.1Endocrine and Polypeptide Laboratory and Endocrinology Section of the Medical Service, Veterans Administration Hospital and Department of Medicine, Tulane University School of Medicine, New Orleans; Hospital General del Centro Medico Nacional, IMSS, Mexico, D. F.
Correspondence: Dr A. Arimura, Department of Medicine, Tulane University School of Medicine, New Orleans, Louisiana, U. S. A.
Abstract
The disappearance of LH-releasing hormone (LH-RH) administered i.v. together with inulin was measured by radioimmunoassay. The half-time disappearance of 3.6 min for LH-RH was significantly shorter than the half-time of 14.2 min found for the inulin. On the assumption that diffusion and distribution into the extracellular space and excretion are quantitatively similar for LH-RH and inulin, the part of the half-life of LH-RH due to metabolic breakdown can be calculated to be about 4.8 min. Peak LH and FSH values were found to occur later. The results suggest that most of the immunoreactive LH-RH is no longer present in the blood at the time of maximal gonadotropin release and that this is because of rapid metabolism as well as diffusion and excretion.
This article is cited by:
WILLIAM F. CROWLEY, JR., MARCO FILICORI, NANETTE SANTORO and DANIEL SPRATT. (1987) Approaches to the Study of GnRH in Humans: Implications for Design of Effective Therapiesa. Annals of the New York Academy of Sciences 519:1, 269–286
Summary Abstract and References Full Article PDF
DISAPPEARANCE OF LH-RELEASING HORMONE IN MAN AS DETERMINED BY RADIOIMMUNOASSAY
AKIRA ARIMURA11Endocrine and Polypeptide Laboratory and Endocrinology Section of the Medical Service, Veterans Administration Hospital and Department of Medicine, Tulane University School of Medicine, New Orleans; Hospital General del Centro Medico Nacional, IMSS, Mexico, D. F., ABBA J. KASTIN11Endocrine and Polypeptide Laboratory and Endocrinology Section of the Medical Service, Veterans Administration Hospital and Department of Medicine, Tulane University School of Medicine, New Orleans; Hospital General del Centro Medico Nacional, IMSS, Mexico, D. F., D. GONZALEZ-BARCENA11Endocrine and Polypeptide Laboratory and Endocrinology Section of the Medical Service, Veterans Administration Hospital and Department of Medicine, Tulane University School of Medicine, New Orleans; Hospital General del Centro Medico Nacional, IMSS, Mexico, D. F., JORGE SILLER11Endocrine and Polypeptide Laboratory and Endocrinology Section of the Medical Service, Veterans Administration Hospital and Department of Medicine, Tulane University School of Medicine, New Orleans; Hospital General del Centro Medico Nacional, IMSS, Mexico, D. F., ROBERT E. WEAVER11Endocrine and Polypeptide Laboratory and Endocrinology Section of the Medical Service, Veterans Administration Hospital and Department of Medicine, Tulane University School of Medicine, New Orleans; Hospital General del Centro Medico Nacional, IMSS, Mexico, D. F. AND ANDREW V. SCHALLY11Endocrine and Polypeptide Laboratory and Endocrinology Section of the Medical Service, Veterans Administration Hospital and Department of Medicine, Tulane University School of Medicine, New Orleans; Hospital General del Centro Medico Nacional, IMSS, Mexico, D. F.1Endocrine and Polypeptide Laboratory and Endocrinology Section of the Medical Service, Veterans Administration Hospital and Department of Medicine, Tulane University School of Medicine, New Orleans; Hospital General del Centro Medico Nacional, IMSS, Mexico, D. F.
Correspondence: Dr A. Arimura, Department of Medicine, Tulane University School of Medicine, New Orleans, Louisiana, U. S. A.
Abstract
The disappearance of LH-releasing hormone (LH-RH) administered i.v. together with inulin was measured by radioimmunoassay. The half-time disappearance of 3.6 min for LH-RH was significantly shorter than the half-time of 14.2 min found for the inulin. On the assumption that diffusion and distribution into the extracellular space and excretion are quantitatively similar for LH-RH and inulin, the part of the half-life of LH-RH due to metabolic breakdown can be calculated to be about 4.8 min. Peak LH and FSH values were found to occur later. The results suggest that most of the immunoreactive LH-RH is no longer present in the blood at the time of maximal gonadotropin release and that this is because of rapid metabolism as well as diffusion and excretion.
This article is cited by:
WILLIAM F. CROWLEY, JR., MARCO FILICORI, NANETTE SANTORO and DANIEL SPRATT. (1987) Approaches to the Study of GnRH in Humans: Implications for Design of Effective Therapiesa. Annals of the New York Academy of Sciences 519:1, 269–286
Summary Abstract and References Full Article PDF
Effects of treatment with LH releasing hormone before the early increase in LH secretion on endocrine and reproductive development in bull calves
RK Chandolia, A Honaramooz, PM Bartlewski, AP Beard, and NC Rawlings
Between 6 and 20 weeks of age an early increase in LH secretion has been reported in Hereford bull calves. Delaying this early increase in LH secretion delays testicular development. This study was designed to determine whether a premature increase in LH secretion during the early postnatal period enhances testicular development. Ten age- and body weight-matched Hereford bull calves were divided into two groups. One group (n = 5) received 200 ng LH releasing hormone (LHRH) i.v. every 2 h for 14 days, between 4 and 6 weeks of age. On the basis of blood samples taken every 15 min for 10 h, mean serum LH and testosterone concentrations and LH pulse frequency were increased by LHRH treatment (P < 0.05). Serum concentrations of FSH were not significantly influenced by treatment (P > 0.05). In treated animals at 24 weeks of age, mean serum testosterone concentrations and LH pulse amplitude were increased (P < 0.05). The concentrations of spermatozoa in electroejeculates collected at 52 weeks of age were greater in LHRH-treated compared with control calves. Testicular growth was enhanced by LHRH treatment and histological evaluation of the testis at 54 weeks of age showed increased spermatogenesis and also larger numbers of Sertoli cells per tubule cross-section as a result of LHRH treatment. We conclude that treatment with LHRH before the early increase in LH secretion altered testicular development and suggest that the early increase in LH secretion in bull calves may be critical for initiating and regulating the progression of reproductive maturation.
RK Chandolia, A Honaramooz, PM Bartlewski, AP Beard, and NC Rawlings
Between 6 and 20 weeks of age an early increase in LH secretion has been reported in Hereford bull calves. Delaying this early increase in LH secretion delays testicular development. This study was designed to determine whether a premature increase in LH secretion during the early postnatal period enhances testicular development. Ten age- and body weight-matched Hereford bull calves were divided into two groups. One group (n = 5) received 200 ng LH releasing hormone (LHRH) i.v. every 2 h for 14 days, between 4 and 6 weeks of age. On the basis of blood samples taken every 15 min for 10 h, mean serum LH and testosterone concentrations and LH pulse frequency were increased by LHRH treatment (P < 0.05). Serum concentrations of FSH were not significantly influenced by treatment (P > 0.05). In treated animals at 24 weeks of age, mean serum testosterone concentrations and LH pulse amplitude were increased (P < 0.05). The concentrations of spermatozoa in electroejeculates collected at 52 weeks of age were greater in LHRH-treated compared with control calves. Testicular growth was enhanced by LHRH treatment and histological evaluation of the testis at 54 weeks of age showed increased spermatogenesis and also larger numbers of Sertoli cells per tubule cross-section as a result of LHRH treatment. We conclude that treatment with LHRH before the early increase in LH secretion altered testicular development and suggest that the early increase in LH secretion in bull calves may be critical for initiating and regulating the progression of reproductive maturation.
BB, in men, there is no real functional difference between using LhRh and hCG and you would be unwise to either after your cycle was done because it would likely delay your HP recovery and keep you dependent on exogenous stimulation for your T production.
QUOTE (Benson @ Apr 4 2008, 02:55 AM)
BB, in men, there is no real functional difference between using LhRh and hCG and you would be unwise to either after your cycle was done because it would likely delay your HP recovery and keep you dependent on exogenous stimulation for your T production.
No.
There is a difference. One has its effects at the hypothalamus, and one has its effects at the pituitary. I think we can all agree that those are different subcortical structures (I hope). They respond to their (respective) hormones differently, require different patterns of hormone release, and down regulate receptors differently.
Oh and by the way, BabyBlu, Lh-RH = GnRH. Just incase you were confused about the relevance of my previous posts to your post. You are using a different name for the same
chemical, but that doesnt change how your brain works (in response to the administration of Lh-RH).
I just realized however, that I was thinking of GnRH receptor agonists and not GnRH itself (and there should be a big difference in effect). I'll have to look over the data again and get back to you on what the effects of GnRH itself will have.
Kite: I understand. I started with 'LH-rh' and stay consistent with my nomenclature, because some people seem to have errenously introduced 'hcg'.
Benson: never said that I would use LH-rh in my PCT. Where does that come from? The title I guess but I guess I should have titled the thread: "LH-rh as a recovery tool" for use DURING cycle. I specifically am refering to using this ON-CYCLE (like one would use hcg). I never recommend using hcg in PCT nor would I consider using LH-rh in PCT.
There seems to be a lot of confusion about the topic, so let me REFINE: The use of LH-rh DURING cycle to maintain the body's natural production of test, which subsequently/hopefully will allow the body an easier recovery in PCT.
bb
Benson: never said that I would use LH-rh in my PCT. Where does that come from? The title I guess but I guess I should have titled the thread: "LH-rh as a recovery tool" for use DURING cycle. I specifically am refering to using this ON-CYCLE (like one would use hcg). I never recommend using hcg in PCT nor would I consider using LH-rh in PCT.
There seems to be a lot of confusion about the topic, so let me REFINE: The use of LH-rh DURING cycle to maintain the body's natural production of test, which subsequently/hopefully will allow the body an easier recovery in PCT.
bb
boy htis htread is confusing. GnRH agonists are certainly different from HCG. which one are you talking about?
QUOTE (liorrh @ Apr 6 2008, 10:16 AM)
boy htis htread is confusing. GnRH agonists are certainly different from HCG. which one are you talking about?
It seems like he is not really talking about either. He is talking about GnRH itself, which of course is a GnRH agonist, but its not one of the long acting synthetics that is used for chemical castration. As I result I don't really know what the effects on the pituitary will be. My guess is that its still nothing to fuck around with.
From the pituitary gland we have LH and FSH
In simplified terms of action on the testicles:
LH = HCG
FSH = HMG
From the Hypothalimus (master gland) we have LHRH (Gonadorelin or GnRH).
This acts upon the pituitary to release LH and FSH. There is no equivalent to LHRH.
Long acting analogs of LRHR will cause inhibition as will frequent dosing of LHRH.
Dosing E3D of LHRH worked very well for me. 2.5mg per injection. Injecting ED caused rapid inhibition.
I bought 100mg for a very good price, alliquoted the desired dose into 1cc insulin syringes and stuck them in the freezer.
In simplified terms of action on the testicles:
LH = HCG
FSH = HMG
From the Hypothalimus (master gland) we have LHRH (Gonadorelin or GnRH).
This acts upon the pituitary to release LH and FSH. There is no equivalent to LHRH.
Long acting analogs of LRHR will cause inhibition as will frequent dosing of LHRH.
Dosing E3D of LHRH worked very well for me. 2.5mg per injection. Injecting ED caused rapid inhibition.
I bought 100mg for a very good price, alliquoted the desired dose into 1cc insulin syringes and stuck them in the freezer.
QUOTE (Mr.Kite @ Apr 4 2008, 07:11 AM)
There is a difference. One has its effects at the hypothalamus, and one has its effects at the pituitary. I think we can all agree that those are different subcortical structures (I hope). They respond to their (respective) hormones differently, require different patterns of hormone release, and down regulate receptors differently.
he said "no real functional difference", by which i imagine he meant that both lead to eventual stimulation of the testes to produce T. had he thought they were completely interchangable from a chemical standpoint, i doubted he'd have chosen the words he did. anywho.
i am interested in the thread content, thanks guys, it's educational....many of us dont have time for classes on this...
how long does the chemical castration last from one GnRH injection? and do they use a modified analog structure to make it last longer? i find it odd that the pituitary can be stimulated by GHRH to kick out GH, with very little, if any, downregulation afterwards, but the hypothalamus does it so quickly...and doesnt the first dose of GnRH cause a large surge in T?
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