HPTA upregulation during BLAST and CRUISING..

[dr intensity]

hi guys,
i need to learn the right HPTA upregulation protocol for
1. Coventional blast and cruise ie
blast 12 weeks and 8 weeks cruise and then repeat.

and the one used for

2. DC style of HPTA upregulation.
blast 4 to 6 weeks and cruise 2 weeks.

there has been a lot of different types of information flowing around, so i am a bit confused.
what i have learnt for the Coventional blast and cruise is
1000iu hcg/week for the whole period along with 10mg nolvadex/day.

and for DC style of HPTA up regulation i have learnt 2 different approaches
1. blast 4 to 6 weeks with test + anabolic+ adex
and cruise 1st week 300mg clomid (day 1) then 200mg clomid (day2) then 150mg clomid (day 3) and then 100mg clomid for the rest of the cruise period, along with 300mg test p . and then repeat the blast and the cruise.

2. the other approach is use HCG + nolvadex + Arimidex + clomid during the cruise period with 50mg test p eod.(this one needs to be sorted out)


wud really appreciate your input
thank you

 

[PHIL HERNON]

Yes

You can do this.............use Naloxone.......but thats all I can say

 

[dr intensity]

why sir,
what wrong did i do...
Naloxone is a drug used to counter the effects of opioid overdose, for example heroin or morphine overdose.

please sir do not get angry just help me out.

 

[PHIL HERNON]

Oh man

why sir,
what wrong did i do...
Naloxone is a drug used to counter the effects of opioid overdose, for example heroin or morphine overdose.

please sir do not get angry just help me out.

Im not angry...........but I am not your trainer.....or doctor.........I was just pointing you in the right dierction...tryin gto help you....you need to research a bit deeper......

 

[dr intensity]

sir could you be a bit more specific.... i am not getting it...

 

[dr intensity]

In vivo evidence for a direct effect of naloxone on testicular steroidogenesis in the male rat.

Cicero TJ, Adams ML, O'Connor LH, Nock B.

Department of Psychiatry, Washington University School of Medicine, St. Louis, Missouri 63110.
Abstract

It has been suggested that endogenous opioid peptides (EOP) exert paracrine or autocrine effects in the testes. To assess this hypothesis, we examined whether naloxone, by blocking the effects of EOP, influenced serum testosterone levels, apart from its effects on LHRH/LH, in the intact male rat. We found that naloxone increased serum LH and testosterone levels over essentially the same time course and produced dose-dependent increases in serum testosterone levels even though LH levels were maximally elevated at all doses. These data are not consistent with the view that naloxone exerts its effects on testosterone exclusively by altering LHRH/LH release. Additional, perhaps more definitive, evidence of a direct effect of naloxone on testosterone's biosynthesis was provided by our observations that 1) naloxone generated increases in serum testosterone levels in male rats in which the naloxone-induced surge in LH was blocked by nembutal; and 2) intratesticular injections of naloxone increased serum testosterone levels without increasing LH. Although these data suggest that naloxone influences steroidogenesis independently of its effects on LH, we found that the antagonist failed to increase serum testosterone levels in hypophysectomized animals or when serum LH levels were allowed to reach undetectable levels in nembutal-blocked animals. Consequently, our data are consistent with the hypothesis that naloxone facilitates the effects of LH on testosterone's biosynthesis rather than exerting an independent effect of its own. Whether the effects observed in these studies represent a negative autocrine effect of EOP on Leydig cells or a paracrine effect on Sertoli cells remains to be determined. Nevertheless, our results provide, to our knowledge, the first in vivo evidence that EOP modulate testicular steroidogenesis in the intact animal.


is this what you meant, thank god..... i thought something else..

 

[PHIL HERNON]

Well

sir could you be a bit more specific.... i am not getting it...

These rec drug users shut down their pituitary..........no more LH, no more FSH, so no testosterone produced, no sperm produced.......why do you think they use Naloxone? Basically a u-opioid antagonist such as naloxone allows pulses of GnRH to occur so basically the hypothalmus can signal the pituitary to produce LH and FSH.....hence stimulating the Lydeg cells and sertoli cells...got it?

 

[dr intensity]

These rec drug users shut down their pituitary..........no more LH, no more FSH, so no testosterone produced, no sperm produced.......why do you think they use Naloxone? Basically a u-opioid antagonist such as naloxone allows pulses of GnRH to occur so basically the hypothalmus can signal the pituitary to produce LH and FSH.....hence stimulating the Lydeg cells and sertoli cells...got it?

thankyou sir,
i appreciate

 

[Huge_C2]

These rec drug users shut down their pituitary..........no more LH, no more FSH, so no testosterone produced, no sperm produced.......why do you think they use Naloxone? Basically a u-opioid antagonist such as naloxone allows pulses of GnRH to occur so basically the hypothalmus can signal the pituitary to produce LH and FSH.....hence stimulating the Lydeg cells and sertoli cells...got it?

The only thing to look into is to what degree if any at all does this effect the rest of the body?? Have read some good things on this inb the last half hour but nothing to show other effects.. I did however read its used to some degree to raise blood pressure..

 

[PHIL HERNON]

Well

The only thing to look into is to what degree if any at all does this effect the rest of the body?? Have read some good things on this inb the last half hour but nothing to show other effects.. I did however read its used to some degree to raise blood pressure..

I guess some don't feel good at all on this drug............but what bodybuilder ever claimed to feel good? haahhahah

 

[musicmann89]

I guess some don't feel good at all on this drug............but what bodybuilder ever claimed to feel good? haahhahah

LOL

 

[hawkmoon]

Eric M. Potratz on HPTA and u-opiod

Suppression of the HPTA (Hypothalamus, Pituitary, Testicular Axis) is seemingly unavoidable during a steroid cycle. What I will be presenting in this article is a new idea to the world of AAS users. This exciting new concept addresses the possibility of limiting and possibly preventing suppression of the (HPTA) during cycle. More specifically, I will show you how to actively modulate the hypothalamus & pituitary pulse generator during cycle and how this can prime our endocrine system for a quicker, smarter, and healthier recovery from anabolic androgenic steroids (AAS).

For a moment, let’s forget the concept of “post cycle therapy”, and embrace the idea of “on cycle therapy” – active therapy throughout a steroid cycle. The HPTA involves a constant biological interplay of responses and feedback loops that can ultimately become shutdown and degraded during AAS administration. However, research suggests suppression of the hypothalamus and pituitary may be preventable during steroid use. Before we delve into the details, lets first take a quick recap on the HTPA and how it responses to AAS.

HPTA – The basics

When the hypothalamus senses low hormone levels, it secretes gonandotropin releasing hormone (GnRH). This GnRH then travels a short distance to the nearby pituitary gland to stimulate the release of the gonadotrophins -- luteinizing hormone (LH) and follicle stimulating hormone (FSH). These gonadotrophins travel all the way down to the testes, to activate their respective leydig and seritoli cells. LH initiates testosterone production by stimulating the leydig cell receptor (steroidogenesis), while FSH initiates sperm production by stimulating the sertoli cell receptor (spermatogenesis).

AAS’s inhibit hormone production just as your body’s own hormones do. Testosterone interacts with the androgen receptor (AR) and estrogen interacts with the estrogen receptor (ER). When these hormones are in high concentration, they cause the hypothalamus to decrease its release of GnRH, which decreases LH and FSH production from the pituitary. (1) This cuts off the signal to the testis and halts all hormone production. This process is a daily event for the rhythmic endocrine system. Spikes in LH & FSH are followed by spikes in testosterone, and spikes in testosterone result in a reduction of LH & FSH release until testosterone levels decline and LH & FSH is released again. The caveat with most steroids, is that hormone levels remain chronically high (24/7) and do not allow release of LH or FSH, thus leaving the pituitary and testis in a dormant state for as long as the steroids are administered.

While low-dose on-cycle hCG is a good protocol to mimic LH and keep the testes from atrophy, (discussed here) it won’t help prevent pituitary atrophy. We forget that the pituitary is susceptible to the same degradation and atrophy as the testes. That is, when the GnRH secretion from the hypothalamus stops (during a steroid cycle), the pituitary reduces its number of GnRH receptors and becomes less and less responsive to GnRH stimulation as time goes on. (11) This is analogous to atrophy of the testis, during absence of an LH or FSH signal. On the other hand, both the pituitary and testis will decrease receptor concentration during over stimulation as well, as its been found from too much hCG use or too much GnRH stimulation.(12,13) The point here, is that only minor stimulus is required for the preservation of sensitivity in the endocrine organs. Perhaps a completely neglected and suppressed pituitary (or testes) may explain the lack of full and prompt recovery for many steroid users, despite adherence to a “tried and true” PCT regimen. So the question is – How can we prevent suppression of the testes, and better yet, how can we prevent suppression of the pituitary?



A closer look –

There are several ways that steroids can inhibit LH & FSH release from the pituitary based on the receptors they occupy, and this is important to understand if you plan on blocking AAS induced suppression. For instance, it appears that AAS which bind strictly to the AR only inhibit LH & FSH release by suppressing GnRH release from the hypothalamus (ie Primobolan, Proviron, Anavar or Masteron). (34,37,39) However, AAS which possess estrogenic (ER) or progestogenic (PR) activity inhibit LH & FSH by directly down-regulating the GnRH receptors on the pituitary, while also reducing GnRH release from the hypothalamus. (35,38) Therefore, progestin based AAS such as trenbolone and nandrolone are “double suppressive” because they are binding to the AR and PR and suppressing LH & FSH by two different mechanisms. (36) The same can be said for steroids that aromatize, such as testosterone or methandrostenolone since they can activate both AR and ER receptors.

Evidence suggests that estradiol is about 200x more suppressive than testosterone on a molar basis (37), and that administration of Arimidex can greatly reduce testosterone’s suppression of LH release. (42) However, since progesterone based AAS’s such as nandrolone and trenbolone are inherently progestogenic based on their hormone structure, there is no way to prevent them from activating the PR. Therefore, it’s virtually pointless to try to block the suppression from progestin based anabolics. However, we can block suppression from the ER by using either non-aromatizing AAS’s or aromatase inhibitors. So this now leaves us with suppression of LH & FSH via the AR, but this suppression can be blocked, and that’s exactly what I’m going to show you.

When it comes to suppression of the hypothalamus, there is more than a simple on/off switch for the hypothalamus control center. Evidence suggests that there isn’t even a direct AR or ER receptor on GnRH secreting neurons. (2-6) Meaning, steroid hormones do not directly influence GnRH release from the hypothalamus, but actually communicate through an intermediary. (7)

It was well summarized here by A. J Tilbrook et al,

“It follows, that the actions of testicular steroids on GnRH neurons must be mediated via neuronal systems that are responsive to steroids and influence the activity of GnRH neurons.”

And again here by FJ Hayes et al,

“It was thus postulated that estrogen-receptive neurons were acting as intermediaries in the non-genomic regulation of GnRH by estrogen”

There is a network of neurogenic intermediaries in the hypothalamus governing GnRH release from steroid hormone influence. More specifically, it is the combined efforts of neuro-active peptides and catecholamines which send the message of “suppression” to the GnRH neurons once activated by steroid hormones. (16) These primary messengers are known as a group of neuro-active peptides called endogenous opioid peptides (EOP’s). (7,16) The EOP’s consist of the three main peptides -- b-endorphin, dynorphin, and enkephalins, which act upon their respective u-opioid, k-opioid, and s-opioid receptors. It appears that the most influential EOP in GnRH modulation is b-endorphin, acting upon the u-opioid receptor. (8-10) For this reason, b-endorphin will be the main focus of the article (although there are other minor intermediates involved.)

When steroid hormones reach the hypophysial portal, they activate the EOP’s, which suppress GnRH and consequently suppress LH & FSH. We know that steroid hormones must communicate with these opioid receptors in order for them to inhibit the release of GnRH from the GnRH neurons, since the GnRH neurons do not have their own AR or ER receptors. What’s most interesting here is that the suppression on GnRH neurons can actually be intercepted by a u-opioid receptor antagonist – such as naloxone, and the orally active congers naltrexone, and nalmefene.

This is accomplished by blocking the u-opioid receptor and preventing the inhibitory effects of b-endorphin upon the GnRH releasing neuron. It should be noted that this “antagonism” of suppression is not due to antagonism of the AR or ER itself, since u-opioid antagonists to not bind to hormone receptors. (15,32)

The effect of a u-opioid receptor antagonist on the HPTA is demonstrated here --



Essentially, a u-opioid antagonist such as naloxone takes the brakes off of GnRH release and allows pulses of GnRH to occur as if no steroid hormones are present. (17) Naloxone, and related u-opioid antagonists have consistently proven to block the suppressive effects of testosterone, DHT, and estrogen administration in both animals and humans. (18-25) It also appears that these drugs have the ability to increase pituitary sensitivity to GnRH. (26,27)

U-opioid antagonists have long been used for treatment of opioid dependence; not only to control cravings of narcotics, but to restore a suppressed endocrine system. (28,29) It’s well known that strong opioid based drugs such as methadone, cocaine, heroin and alcohol can suppress GnRH and therefore suppress LH & FSH. It seems that this decease of GnRH, LH & FSH is due to the same EOP mechanisms seen with AAS induced suppression. (33) In alcoholics, cocaine and heroin users, naltrexone and naloxone have been used to restore LH and testosterone levels. (28,29) Naltrexone has even been proposed as a treatment for male impotence and erectile dysfunction. (30,31)

Naloxone, naltrexone and nalmefene seem progressively more powerful in their potency to block b-endorphin, respectively. (14,18) Naloxone lacks oral bioavailability therefore injection is required. An injectable preparation could easily be made with BA water due to the water solubility of the compound. A 40mg subcutaneous injection would be a typical dose of naloxone. Naltrexone is orally active, with a safe and effective oral dose being about 100mg for a 220lb male. (18) While a lower dose of about 25-50mg of nalmefene would seemingly have the same benefit. (20,24) Increasing the dose of these drugs will surely increase the likelihood of side-effects without notably increasing the benefit. A twice a week dosing protocol would seem appropriate with these drugs, as only to increase GnRH and LH release enough to prevent pituitary and testicular shutdown – Just enough to keep them in the “ball game” so to speak. Also, a twice a week dosing protocol would most likely limit the increased opioid sensitivity induced by the long-term use of the drugs.

A word of caution: The opioid antagonists mentioned in this article are recognized as safe and non-toxic at the given dosages; however they can cause severe withdrawal symptoms in opiate users (methadone, morphine, cocaine, and heroin addicts.) Caution is also advised when using opioid antagonists prior to sedation or surgery as they can reduce effectiveness of anesthetics. Temporary nausea, headache or fatigue, are occasional side-effects associated with the use of these drugs. Naltrexone has been reported to heighten liver enzymes, while naloxone and nalmefene do not appear to have this issue. At any rate, a twice a week protocol for 4-16 weeks is unlikely to cause any liver issues that may be associated with naltrexone. Contrary to popular believe, opioid antagonists do NOT have any addictive properties.

A few point to consider -

For those who choose to embark on an opioid antagonist protocol several things should be considered.



Remember, progestin based anabolics such as trenbolone and nandrolone are “double suppressive” because they desensitize the pituitary directly by PR activation. It also appears that no opioid receptor antagonist or aromatase inhibitor can prevent suppression via the PR. Therefore, trenbolone or nandrolone are going to cause unavoidable inhibition of HTPA function by causing suppression via the ER, AR and PR. (40,41) If one hopes for a prompt and full recovery post cycle, perhaps progestin based anabolics are better avoided, or at least limited in duration of use.
As it was pointed out earlier in this article, estrogen has a markedly stronger effect on suppression of LH release compared to androgens since estrogen suppresses the hypothalamus and pituitary. Usage of an AI such as anastrozole, letrozole, or exemestane (Aromasin) can reduce estrogen and greatly reduce suppression on GnRH, LH and FSH release by preventing excessive ER activation in the hypothalamus and desensitization of the pituitary GnRH receptors. (35,37,38) Anastrozole has ~50% maximal total estrogen suppression at 1mg/day. Exemestane has ~50% maximal total estrogen suppression at 25mg/day. While letrozole has ~60% at 1mg/day. These are averages based on compiled data from several studies. Similar estrogen suppression can also been seen from only twice a week administration of these AI’s. (43-47)


References

1. Hypothalamic Gonadotropin-Releasing Hormone: Basic and Clinical Aspects.
Yen SSC
Raven Press, New York, pp 245–280 (1991)

2. Absence of androgen receptors in LHRH immunoreactive neurons.
Huang X, Harlan RE.
Brain Res 1993; 624:309–311

3. Augmented hypothalamic proopiomelanocortin gene expression with pubertal development in the male rat: evidence for an androgen receptor-independent action.
Kerrigan JR, et al.
Endocrinology.128:1029-1035. (1991)

4. Distribution of estrogen receptorimmunoreactive cells in the preoptic area of the ewe: co-localisation with glutamic acid decarboxylase but not luteinizing hormone-releasing hormone.
Herbison AE, et al.
Neuroendocrinology 1993; 57:751–759.

5. Unmasking the neural progesterone receptor in the preoptic area and hypothalamus of the ewe: no colocalization with gonadotropin-releasing neurons.
Skinner DC, at el.
Endocrinology 2001; 142:573–579.

6. Multimodal influences of estrogen upon gonadotropin releasing
hormone neurons.
Herbison AE.
Endocrine Reviews 1998; 19:302–330.

7. Negative Feedback Regulation of the Secretion and Actions of Gonadotropin-Releasing Hormone in Males
A.J. Tilbrook and I.J. Clarke
Biol Reprod, Mar 2001; 64: 735

8. Steroid Control of Gonadotropin-Releasing Hormone Secretion: Associated Changes in Pro-Opiomelanocortin and Preproenkephalin Messenger RNA Expression in the Ovine Hypothalamus
James A. Taylor, et al.
Biol Reprod, Mar 2007; 76: 524

9. Do gonadotropin-releasing hormone, tyrosine hydroxylase-, and ß-endorphin-immunoreactive neurons contain oestrogen receptors? A double-label immunocytochemical study in the Suffolk ewe
Lehman MN, Karsch FJ.
Endocrinology 1993; 133:887–895

10. -Endorphin blocks luteinizing hormone-releasing hormone release by inhibiting the nitricoxidergic pathway controlling its release
Alicia G. Faletti, et al.
PNAS, Feb 1999; 96: 1722.

11. The frequency of gonadotropin-releasing hormone stimulation determines the number of pituitary gonadotropin-releasing hormone receptors.
Katt JA, et al.
Endocrinology. 116:2113–2115. (1985)

12. Exogenous gonadotrophin-releasing hormone (GnRH) stimulates LH secretion in male monkeys (Macaca fascicularis) treated chronically with high doses of a GnRH-antagonist.
Weinbauer GF, et al.
J Endocrinol. 133:439–445. (1992)

13. Chronic administration of the luteinizing hormone-releasing hormone (LHRH) antagonist cetrorelix decreases gonadotrope responsiveness and pituitary LHRH receptor messenger ribonucleic acid levels in rats.
Pinski J, Lamharzi N, Halmos G, et al. 1996
Endocrinology. 137:3430–3436.

14. Acute effects of testosterone infusion and naloxone on luteinizing hormone secretion in normal men.
GB Kletter, et al.
J. Clin. Endocrinol. Metab., Nov 1992; 75: 1215 - 1219.

15. Naloxone-induced increases in serum luteinizing hormone in the male: mechanisms of action
TJ Cicero, et al.
J. Pharmacol. Exp. Ther., Mar 1980; 212: 573.

16. Endogenous opioids participate in the regulation of the hypothalamic-pituitary-luteinizing hormone axis and testosterone’s negative feedback control of luteinizing hormone.
CICERO, T. J., et al.
Endocrinology 104: 1286-1291, (1979)

17. Opiatergic control of LH secretion is eliminated by gonadectomy.
BHANOT, R. et al.
Endocrinology 112: 399-401, (1983)

18. Role of endogenous opiates in the expression of negative feedback actions of androgens and estrogen on pulsatile properties of luteinizing-hormone secretion in man.
Veldhuis JD, et al..
J Clin Invest. 74:47–55 (1984)

19. Counteraction of gonadal steroid inhibition of luteinizing hormone release by naloxone.
VAN VUGT, et al.
J. Chro- naloxone. Endocrinology 34: 274-278, 1982

20. Unexpected effects of nalmefene, a new opiate antagonist, on the hypothalamic-pituitary-gonadal axis in the male rat.
P Limonta, et al.
Steroids, Dec 1985; 46(6): 955-65.

21. In vivo evidence for a direct effect of naloxone on testicular steroidogenesis in the male rat
TJ Cicero, et al.
Endocrinology, Aug 1989; 125: 957

22. Endogenous opioids participate in the regulation of the hypothalamus- pituitary-luteinizing hormone axis and testosterone's negative feedback control of luteinizing hormone
TJ Cicero, et al.
Endocrinology, May 1979; 104: 1286

23. Effect of naloxone on the plasma levels of LH, FSH, prolactin and testosterone in Beetal bucks.
Singh B, et al.
Department of Animal Production Physiology, CCS Haryana Agricultural University, 125004, Hisar, India

24. Endocrinology: The effect of nalmefene on pulsatile secretion of luteinizing hormone and prolactin in men
G.R. Graves, et al.
Hum. Reprod., Oct 1993; 8: 1598 - 1603.

25. Effects of the novel opiate antagonist, SDZ 210-096, on luteinizing hormone secretion in the rat
RA Siegel et al.
J. Pharmacol. Exp. Ther., Apr 1989; 249: 264.

26. Effect of antagonists of dopamine and opiates on the basal and GnRH-induced secretion of luteinizing hormone, follicle stimulating hormone and prolactin during lactational amenorrhoea in breastfeeding women
C.C.K. Tay, et al.
Hum. Reprod., Apr 1993; 8: 532 - 539.

27. Naltrexone administration modulates the neuroendocrine control of luteinizing hormone secretion in hypothalamic amenorrhoea
Alessandro D. et al.
Hum. Reprod., Nov 1995; 10: 2868 - 2871.

28. Heroin and naltrexone effects on pituitary-gonadal hormones in man: interaction of steroid feedback effects, tolerance and supersensitivity
JH Mendelson, et al.
J. Pharmacol. Exp. Ther., Sep 1980; 214: 503.

29. Alcohol effects on luteinizing hormone and testosterone in male macaque monkeys
NK Mello, et al.
J. Pharmacol. Exp. Ther., Jun 1985; 233: 588.

30. Erectile function and naltrexone
Goldstein JA
Ann Intern Med 105:799 (1986)

31. Opiate antagonists in erectile dysfunction: a possible new treatment option? Results of a pilot study with naltrexone
van Ahlen H, et al.
Eur Urol 28:246–250 (1995)

32. The effects of opiates on androgen binding in the forebrain of the rat.
PJ Sheridan and JM Buchanan
Int J Fertil, January 1, 1980; 25(1): 36-43.

33. Morphine exerts testosterone-like effects in the hypothalamus of the castrated
male rat.
CICERO, T. J., et al.
Brain Rae. 202: 151-164, (1980)

34. Studies of gonadotropin-releasing hormone (GnRH) action using GnRH receptor-expressing pituitary cell lines.
Kaiser UB, Conn PM, Chin WW.
Endocr Rev. 18:46–70. (1997)

35. Patterns of LH secretion in castrated bulls during intravenous infusion of androgenic and estrogenic steroids: Pituitary response to exogenous luteinizing hormone-releasing hormone
M.J. D’occhio et al.
Biology of reproduction 26, 249-257 (1982)

36. Demonstration of progesterone receptor mediated gonadotrophin suppression in men.
Brady B, Anderson RA, Kinniburgh D, Baird DT 2002
J Endocrinol 3(Suppl):OC37

37. The direct pituitary effect of testosterone to inhibit gonadotropin secretion in men is partially mediated by aromatization to estradiol.
Bagatell CJ, Dahl KD, Bremner WJ. 1994
J Androl. 15:15–21.

38. Studies on the role of sex steroids in the feedback control of FSH concentrations in men.
Sherins RJ, Loriaux DL. 1973
J Clin Endocrinol Metab. 36:886–893

39. Is aromatization of testosterone to estradiol required for inhibition of luteinizing hormone secretion in men?
Santen RJ. 1975
J Clin Invest. 56:1555–1563

40. Influence of nandrolondecanoate on the pituitary-gonadal axis in males.
JW Bijlsma, et al.
Acta Endocrinol (Copenh), September 1, 1982; 101(1): 108-12.

41. Endocrine approaches to male fertility control.
UA Knuth et al.
Baillieres Clin Endocrinol Metab, February 1, 1987; 1(1): 113-31.

42. Aromatization Mediates Testosterone's Short-Term Feedback Restraint of 24-Hour Endogenously Driven and Acute Exogenous Gonadotropin-Releasing Hormone-Stimulated Luteinizing Hormone and Follicle-Stimulating Hormone Secretion in Young Men
J. A. Schnorr, et al.
J. Clin. Endocrinol. Metab., June 1, 2001; 86(6): 2600 - 2606.

43. Short-Term Aromatase-Enzyme Blockade Unmasks Impaired Feedback Adaptations in Luteinizing Hormone and Testosterone Secretion in Older Men
Johannes D. Veldhuis et al.
J. Clin. Endocrinol. Metab., Jan 2005; 90: 211 – 218

44. Effects of Aromatase Inhibition in Elderly Men with Low or Borderline-Low Serum Testosterone Levels
Benjamin Z. Leder, et al.
J. Clin. Endocrinol. Metab., Mar 2004; 89: 1174 - 1180.

45. Comparative Assessment in Young and Elderly Men of the Gonadotropin Response to Aromatase Inhibition
Guy G. T’Sjoen, et al
J. Clin. Endocrinol. Metab., Oct 2005; 90: 5717 - 5722.

46. Pharmacokinetics and Dose Finding of a Potent Aromatase Inhibitor, Aromasin (Exemestane), in Young Males
Nelly Mauras, et al.
J. Clin. Endocrinol. Metab., Dec 2003; 88: 5951 - 5956.

47. Differential Regulation of Gonadotropin Secretion by Testosterone in the Human Male: Absence of a Negative Feedback Effect of Testosterone on Follicle-Stimulating Hormone Secretion
Frances J. Hayes, et al
2jz_calgary is offline

 

[dr intensity]

Posted bt Restless on Cuttingedgemuscle



Opioid antagonists and HPTA function
I just heard about the possible effect of opioid antagonists in LH secretion in another board and went to pub med looking for studies on this hoping I could generate some discussion here.

This is the post that started this:

"Now for the most important piece of the post cycle recovery puzzle that you never hear bodybuilders talk about because they usually have no idea. The opioidergic regulation of testosterone. Without going to great lengths in explaining opioids and their effects on hormones and the brain, natural opiates are released in response to the increase in LH by the use of estrogen inhibitors. So you've got increased LH and increased natural opiate levels. Now when the estrogen inhibitors are taken away the LH is greatly reduced and you're back to square one. So your natural opiate levels are still high. LH will not be stimulated until it comes back down. That is in a sense why HCG and estrogen inhibitors are only so affective at stimulating testicular function and restoring the HPT axis. So since opiates suppress gonadotropin secretion i.e. testosterone secretion using opiate antagonists can help bodybuilders completely recover. REVIA is the most popular. Read all you can on the subject because it really is the missing link of post cycle recovery. Later!"

He doesn't provide any references so I went to check it out and did found some stuff (see below). I didn't find anything about the increase in endogenous opioids from LH increases, but I haven't searched yet (anyone knows anything about this?).

Study number found a significant impact on LH levels after naxolone treatment (in goats....).

Second one has this bit that intrigues me:

"Administration of specific opiate antagonists decreases luteinizing hormone (LH) release and increases the frequency and amplitude of the LH pulses"

If I'm not mistaken number 3 shows that naloxone is effective in stimulating LH relese in obese patients, nut not in normal individuals.


Number 4 shows a positive effect in LH and testosterone levels from two different antagonists and some stuff about LH and prolactin pulse sinchrony that is probably meaningless for our purposes.

Number 5 shows a 50% increase in cortisol. Not so good.

Number 6 shows a positive impact in sexual function even without any noticeable changes in hormone levels.


I am not sure this is actually worth trying during PCT, but I'd love to hear people's opinions on this. These drugs have some unpleasant side effects but I think I'm willing to give it a try if I'm convinced there may be something to it.

Thoughts please?



1-Effect of naloxone on the plasma levels of LH, FSH, prolactin and testosterone in Beetal bucks.

Singh B, Dixit VD, Singh P, Georgie GC, Dixit VP.

Department of Animal Production Physiology, CCS Haryana Agricultural University, 125004, Hisar, India

Ten adult male Beetal goats were used for the study to elucidate the modulation of gonadotrophin, prolactin and testosterone secretion by endogenous opioid peptides. An indwelling catheter was placed in the jugular vein of each buck 20h before the onset of the experiment. Bucks were divided randomly into two groups: Group I (n=5) received naloxone at a dose rate of 1mg/kg body weight (BW) and Group II (n=5) received naloxone at a dose rate of 2mg/kg BW intravenous. Blood samplings were done from 2h before treatment until 2h after treatment at 15min intervals. Blood samples were quantified for plasma LH, FSH and prolactin concentration using a heterologous double antibody radioimmunoassay (RIA) and testosterone concentration was quantified by coat-a-count RIA kit. The mean plasma LH levels during pretreatment phase were 0.41+/-0.03ng/ml in Group I and 0.44+/-0.02ng/ml in Group II which significantly (p<0.05) increased to 0.91+/-0.05ng/ml in Group I and 1.53+/-0.07ng/ml in Group II. The mean plasma FSH levels did not show a difference in pre- and post-treatment animals in both groups. A significant (p<0.05) increase in plasma testosterone concentration was observed in both groups after naloxone treatment, whereas, a decrease (p<0.05) was observed in plasma prolactin levels after naloxone treatment. Thus, it can be concluded that endogenous opioids do play an important role in modulating plasma LH, prolactin and testosterone concentrations in male goats.

2-[Interaction of endogenous opioid peptides with the function of the hypothalamo-hypophyseal-testicular axis]

[Article in Spanish]

Pedron Nuevo N.

Unidad de Investigacion Medica en Biologia de la Reproduccion. Division de Investigacion Biomedica. IMSS, Mexico, D.F.

Since the discovery of endogenous opioid peptides and opioid receptors in the brain, their has been considerable interest in their possible role in a variety of physiological and pharmacological processes. The endogenous opioids and opiate active substances have been clearly implicated in the regulation of male reproductive function. It has been demonstrated that opioid peptides inhibit gonadotropin and TSH secretion and enhance PRL, GH and ACTH. It is believed that opioids elicit their action at the hypothalamic level, most likely by modulating the liberation of hypothalamic releasing or inhibiting factors. In healthy male adults the endogenous opioid peptides (EOP) produce a decrease in serum levels of gonadotropins. Administration of specific opiate antagonists decreases luteinizing hormone (LH) release and increases the frequency and amplitude of the LH pulses. The effects of EOP and specific opiate antagonists are altered in some hypothalamic-hypophysis-testis axis pathologies.

3-Endogenous opioids and hypogonadism in human obesity.

Blank DM, Clark RV, Heymsfield SB, Rudman DR, Blank MS.

Yerkes Regional Primate Research Center, Emory University, Atlanta, GA 30322.

Massively obese males often show symptoms of hypogonadism, but the mechanism for this is unclear. Increased endogenous opioid inhibition of the hypothalamic GnRH pulse generator resulting in insufficient stimulation of the pituitary gonadotroph has been proposed as a possible mechanism. If this hypothesis is correct, obese males should be more sensitive to the LH-elevating effects of the opiate antagonist, naloxone, than men of normal weight and gonadal status. This study investigated the etiology of obesity-related hypogonadism by examining luteinizing hormone (LH) and follicle stimulating hormone (FSH) responses to gonadotropin-releasing hormone (GnRH) and to infusions of saline or naloxone. Subjects were five obese (201 +/- 14% IBW) and five normal weight (control) (97 +/- 4% IBW) males. Before treatment, obese males had significantly (p < 0.05) lower testosterone levels than control subjects (307 +/- 72 vs. 597 +/- 49 ng/dl), whereas estradiol, androstenedione, and dehydroepiandrosterone levels were not different between the two groups. Both groups showed equivalent elevations in LH (fourfold to sixfold) in response to GnRH stimulation, but obese patients had significantly lower basal (p < 0.05) and GnRH-stimulated (p < 0.01) FSH levels. Infusions of naloxone (but not saline) led to significant (p < 0.01) increases in LH above preinfusion baseline levels (20.5 +/- 2.8% in obese and 28.6 +/- 6.3% in controls). In control subjects, integrated LH levels during naloxone infusion were not significantly elevated above those found during saline infusion, while obese subjects exhibited a 43% augmentation of integrated LH (31.0 +/- 5.3 ng/ml during naloxone vs. 21.7 +/- 1.8 ng/ml during saline, p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

4-The effect of nalmefene on pulsatile secretion of luteinizing hormone and prolactin in men.

Graves GR, Kennedy TG, Weick RF, Casper RF.

Division of Reproductive Sciences, University of Toronto, Ontario, Canada.

Luteinizing hormone (LH) and prolactin are released in pulses which are relatively synchronous in the luteal phase of the menstrual cycle in women. The concordance of LH and prolactin pulses in normal men has not been reported. The objectives of this study were firstly to determine whether LH and prolactin pulses are synchronous in men, and secondly to examine the effects of naloxone and a new orally active opiate antagonist, nalmefene, on LH and prolactin release in men. Three groups of normal male subjects received saline infusion (control n = 5), naloxone infusion (2 mg/h; n = 5) or nalmefene (10 mg p.o.; n = 6). Blood samples were collected every 15 min for 2 h before and 6 h after study medication for determination of LH, prolactin and testosterone by radioimmunoassay. Both naloxone and nalmefene resulted in a significant increase in LH pulse frequency and in mean serum LH and testosterone concentrations with no change in LH pulse amplitude, prolactin pulse frequency or amplitude. In controls, 61% of LH pulses were synchronous with prolactin pulses. There was a decrease in concomitance of LH and prolactin pulses with naloxone (48%) and nalmefene (24%; P < 0.025) administration. In contrast, 52% of prolactin pulses were concomitant with LH pulses in controls, while naloxone (100%) but not nalmefene (67%) resulted in a significant (P < 0.01) increase in pulse synchrony. The difference observed between naloxone and nalmefene on prolactin--LH pulse synchrony is probably due to differential opioid receptor activity at the pituitary and hypothalamic level.(ABSTRACT TRUNCATED AT 250 WORDS)

5-Different effects of aging on the opioid mechanisms controlling gonadotropin and cortisol secretion in man.

Coiro V, Passeri M, Volpi R, Marchesi M, Bertoni P, Fagnoni F, Schianchi L, Bianconi L, Marcato A, Chiodera P.

Cattedra di Clinica Medica, Universita di Parma, Italia.

The present study was undertaken in order to assess the influence of aging on the endogenous opioid control of gonadotropin and adrenocorticotropin/cortisol secretion in man. For this purpose, the capability of the opioid antagonist naloxone to increase circulating levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH) and cortisol was tested in male subjects of different ages. Thirty normal men were randomly chosen and divided into 3 groups by age: group I = 22-40 years (n = 10); group II = 41-59 years (n = 10); group III = 62-80 years (n = 10). Since the men of group III showed higher basal serum gonadotropin concentrations than the subjects of group I and group II, we selected from a large population a fourth group of elderly men with normal basal LH and FSH levels: group IV = 61-82 years (n = 7). All subjects were tested for 120 min during the intravenous administration of naloxone (4 mg given in an intravenous bolus at time 0, plus 10 mg infused for 2 h). Control tests with normal saline instead of naloxone were performed in all groups. All subjects had similar blood testosterone and cortisol levels, whereas LH and FSH concentrations were significantly higher in group III than in groups I, II and IV. Naloxone increased plasma cortisol concentrations by 50% in all groups. The cortisol secretory response followed a similar pattern regardless of age.(


6-Endorphins in male impotence: evidence for naltrexone stimulation of erectile activity in patient therapy.

Fabbri A, Jannini EA, Gnessi L, Moretti C, Ulisse S, Franzese A, Lazzari R, Fraioli F, Frajese G, Isidori A.

Institute of V Clinica Medica, University of Rome La Sapienza, Italy.

In the present study we evaluated whether naltrexone administration could stimulate sexual function in 30 male patients, ages 25 to 50 years, with idiopathic impotence of at least one year's duration and not of organic etiology. The patients received naltrexone (50 mg/day) or placebo, on a random basis for two weeks. Sexual performance, expressed as the number of full coitus/week, was assessed before (time 0) and during (on days 7 and 15) each treatment. The naltrexone therapy significantly increased the number of successful coitus compared to placebo after 7 and 15 days of treatment: improvement of sexual performance was evident in 11 out of the 15 treated patients. All the patients experienced a significant increase in morning and spontaneous full penile erections/week. No significant side effects were reported. Endocrine studies revealed no significant modification of plasma LH, FSH or testosterone by naltrexone, suggesting that the positive effect of the drug on sexual behavior was exerted at a central level. A two-month follow-up, at which time patients were off treatment, erectile capacity had returned to baseline in 10 patients, while five reported complete recovery of their sexual ability. We hypothesize that an alteration in central opioid tone is present in idiopathic impotence and is involved in the impairment of sexual behavior.

 

[dr intensity]

ok , i found out the DC HPTA upregulation protocol... its something like

Blast week (1 to 4) ; Test + Some anabolic
Blast week (1 to 4) : 0.5mg Arimidex
last 10 days 1000iu HCG/day
Cruise week (5 to 6) 50mg test p eod
Cruise week (5 to 6) 0.5mg Adex
Cruise week (5 to 6) clomid 300mg -day1, 200mg - day2, 150mg-day2, 100mg for rest of the cruise period.

the repeat the blast and the cruise.
then when you completely come off do a full PCT.

try to gain 5 pounds each blast.

 

[dr intensity]

heavyiron recommends;
while on cycle 500iu HCG x 2/week + 10mg Aromasin/day

PCT
2500iu HCG every other day. (You may use less HCG if your testes are normal in size AND you have been using HCG on cycle, i.e. 1,000iu HCG eod.)

100/100/100/50 Clomid (50mg taken twice per day weeks 1-3)

20mg/20mg/20mg/10mg Aromasin (20mg daily for 3 weeks, 10mg daily in week 4)

3g Vit C every day split in 3 doses

10g creatine daily


Big A recommends: 5000iu HCG every 4 weeks ( 1000iu HCG/day shots for 5 days) or clomid 50mg everyother day while on then when totally coming off use GAIN KEEPERS FORMULA.

PoWeR PCT protocol

HCG 2500iu eod for day 1 to day 16
Clomid 100mg everyday/form day 1 to day 30
Nolvadex 20mg every day/ from day 1 to day 45

however william L is not worried much about LH levels he says that LH levels are restored to normal within 3 weeks after the cessaton of the drug.
he is more concerned about Testicular Atrophy, therefore he recommends bombarding the testis with a lot of HCG which will lead to rapid restoration of the testicular mass.
However the combined use of 2 antiestrogens which will continue to foster LH release as testosterone levels start to go back up.

he assures that normal hormonal fuctions were achieved in all the pts within 45 days..... as per Anabolics 2009

Dave Palumbo PCT protocol

- HCG: 2000mg every second day for two weeks
- Clomid: (start 2 weeks after conclusion of cycle) 50mg two times per day for two weeks
- Aromatase Inhibitor: Arimidex (.5mg every other day)

 

[trenjin]

i wish there was more info on blast n cruise since it really is the best way to juice

 

[DOGGCRAPP]

ok , i found out the DC HPTA upregulation protocol... its something like

Blast week (1 to 4) ; Test + Some anabolic
Blast week (1 to 4) : 0.5mg Arimidex
last 10 days 1000iu HCG/day
Cruise week (5 to 6) 50mg test p eod
Cruise week (5 to 6) 0.5mg Adex
Cruise week (5 to 6) clomid 300mg -day1, 200mg - day2, 150mg-day2, 100mg for rest of the cruise period.

the repeat the blast and the cruise.
then when you completely come off do a full PCT.

try to gain 5 pounds each blast.

Really thats my protocol? for who exactly? Guys using year round? Guys who do one cycle and done? Where did that come from? Dont tell me.....a cut and paste DC manual (that ive never done) but someone else just took random posts from a decade ago and put together......who was I talking too exactly? a longtime juicer superheavyweight? Anyone else have things they typed to someone (275 pound year round juicers) back in 1999-2000 show up in modern day posts?

 

[PHIL HERNON]

Yea

Really thats my protocol? for who exactly? Guys using year round? Guys who do one cycle and done? Where did that come from? Dont tell me.....a cut and paste DC manual (that ive never done) but someone else just took random posts from a decade ago and put together......who was I talking too exactly? a longtime juicer superheavyweight? Anyone else have things they typed to someone (275 pound year round juicers) back in 1999-2000 show up in modern day posts?

I dont understand why people do this .........

 

[DOGGCRAPP]

Now i have to comment.....on something i dont like to comment about.

I think the worst thing someone can do is be continuously on year round in high amounts......but regardless...a great many of the top competitors and (hell) random Joe Blow gym rats are on year round.

So here is the thing....the decisions you need to make

1) do you want to have kids some day? if the answer is yes, then I would be as sure as hell to send signals to the HPTA at predetermined intervals
2) do you want to be healthy? Im talking hematocrit, kidney health, cardiomyopathy, etc etc etc then you better as sure as hell take being on "year round" into account as it pertains to your health.
3) do you want to suffer muscle/tendon tears (low endo testosterone), low sex drive, lethargy, and disintegrate muscle size wise when you do FINALLY GET OFF......then you better sure as hell send signals to the HPTA at predetermined intervals.

Do you want to do one cycle a year and then be clean the rest of the year? Well that changes everything doesnt it? And my "supposed" 'HPTA upregulation whateverthingamajiggy above really wouldnt make sense now would it? Again it drives me absolutely bonkers when things I say get taken out of a context and I have no idea what that context was.

Do you want to do 2 eight week cycles this year and be off the other 36 weeks? Well that changes the whole equation totally also doesnt it?

This is all about personal choices. And when i comment on this stuff its in regarding the personal choice someone has made concerning their own BEING ON usage.

My opinion?

You tell me.......

Some of you guys hit every show as fans.....YOU TELL ME!

February = Ironman Pro bodybuilding championships
Did any pro's or top ams you saw at this show look alot smaller or soft to you?
March = Arnold classic
Did any pro's or top ams you saw at this show look alot smaller or soft to you?
May = NY pro show
Did any pro's or top ams you saw at this show look alot smaller or soft to you?
July = USA championships
Did any pro's or top ams you saw at this show look alot smaller or soft to you?
September = Olympia
Did any pro's or top ams you saw at this show look alot smaller or soft to you?
November = Nationals
Did any pro's or top ams you saw at this show look alot smaller or soft to you?

Throw in the Europa, Houston pro, all the guest posings year round, all the appearances, all the photo shoots, all the boothwork at expos!!!!!
Did any pro's or top ams you saw at this appearance look alot smaller or soft to you?

They aint getting off.

So you want my opinion....I'll give it to you below

Whats better?

Stay on year round and drive your HPTA into dormancy so fargone that you destroy any chances of having kids, drive your endo testosterone levels so low that you go into andropause at 32 years of age (when you TRY to maybe clean out for a little bit but panic because you feel so g'damn shitty so you go back on)......and if you do get off you disintegrate and muscle mass falls off you like its dead skin?!?!?!

or

(and ive caught more shit for this over the last decade than anything Ive ever talked about.....but ohhhhh I kind of proved my points over time and it actually DID WORK DIDN'T IT!).....Yes I will be the first to tell you I have a bug up my ass at the arguments i used to get into with this stuff with people telling me I was full of shit below

(sorry rant there) or

Is it better to send intermittent signals to the HPTA so there isnt a gigantic dormancy period?

Trust me on this......intermittent signals is the way to go. Every single one of my former trainee's can, will and/or have kids......including myself. My wife got pregnant in our 2nd month of trying when we decided to have kids and i have yet another one on the way in 2 months.

Now i had these huge huge huge arguments with people online many years back saying sending signals to the HPTA while on or having any tiny bit of outside source of testosterone in your body would do absolutely nothing.

I knew better. And I couldnt prove it until.....

---------------------------------------------------------------

The effects of aging in normal men on bioavailable testosterone and luteinizing hormone secretion: response to clomiphene citrate.

Tenover JS, Matsumoto AM, Plymate SR, Bremner WJ.

Geriatric Research, Education, and Clinical Center, Veterans Administration Medical Center, Seattle, Washington.

Serum testosterone (T) levels in men decline with age while serum LH levels, as measured by RIA, increase. To assess if the decline in serum T levels in healthy aging men is paralleled by an age-related decline in the bioavailable non-sex hormone-binding globulin (SHBG)-bound fraction of T and to determine whether there are age-related changes in LH secretion or LH control of T production, we studied 29 young (aged 22-35 yr) and 26 elderly (aged 65-84 yr) healthy men. All men had single random blood samples drawn, and 14 men in each age group underwent frequent blood sampling for 24 h, both before and after 7 days of clomiphene citrate (CC) administration. Both mean 24-h serum total T levels and non-SHBG-bound T were reduced in elderly men compared to those in young men (P less than 0.05), while estradiol and SHBG levels were similar in the 2 age groups. Serum FSH determined by RIA and LH by RIA and bioassay were higher in the elderly men compared to those in young men (P less than 0.05), but the ratios of LH bioactivity to immunoreactivity and the LH pulse frequency and amplitude were similar. After CC administration, mean serum total T and non-SHBG-bound levels in young men increased by 100% and 304%, respectively, while in older men these values increased by only 32% and 8%, respectively. However, CC-stimulated LH pulse characteristics and serum levels of estradiol, SHBG, FSH, and bioactive and immunoreactive LH were similar in the 2 groups. Thus, both at baseline and after CC stimulation, elderly men had significantly lower serum total T and non-SHBG-bound (bioavailable) T levels than did young men, despite similar or increased levels of bioactive LH and similar bioactive to immunoreactive LH ratios and LH pulse characteristics. These results suggest that major age-related changes in the hypothalamic-pituitary-testicular axis occur at the level of the testes and are manifested by decreased responsiveness to bioactive LH. Administration of CC to young and elderly men resulted in similar changes in LH pulse characteristics and LH bioactivity and immunoreactivity, suggesting preserved hypothalamic-pituitary responsiveness in the elderly.

--------------------------------------------------------------------

Look at the bold=normal healthy men with normal testosterone levels. So there isnt a need for an increase in total T and non-SHBG-bound levels but it happens anyway with the administration of clomid. That told me alot....and I knew i was on the right path with this stuff years ago. So all those people for all these years who have argued vociferously with me that PCT does absolutely nothing if testosterone is present whether endogenous or exogenous, got a big foot in the mouth with this study.

You dont need a total test level of 75 to 180 ng for clomiphene to work....it works regardless....and increased normal testosterone levels above by 100 to 304%.........signals to the HPTA Work!

So let me run thru some of my opinions here on all this and again this all comes down to choices.

1) I believe in 250-500IUS of HCG done 2x a week, done on the day before shots.....and believe this is one of the most important things any bodybuilder can do for himself to keep himself as "normalized as possible"....this is Swales recommendation and kudo's go to his work.....dont credit me in the least on this...because its 100% Swale
2)Clomid is a very hard compound for people to take, it makes alot of guys depressed, anxious and absolutely irritable....want to know what its like for your girlfriend/wife on her period? Thats clomid by 5x. It also works very well if you can hack it (alot of people cant)
3)This is just personal opinion and nothing more than that. I believe Letrozole is just too powerful. You need some estrogen for health reasons. Always remember homeostatis......if you drive your estrogen levels down to nothing, guess where your endo testosterone is going to go. And there is nothing more dangerous in my opinion than having seriously low testosterone levels, especially for endothelial/cardiac health. I would probably pick something like exemestane and use the least amount you can of it for an anti arom.
4) Nolvadex/tamoxifen i go back and forth on opinionwise as an anti est. Ive kind of soured on it again....
a) raises HDL
b) can raise LH, FSH and testosterone in some/most
c) can cause blood clots
d) can cause some retinal damage maybe in some (thats for you killerstack)
e) can potentially reduce IGF liberation

(yes Ive started to get to the opinion that steroids and testosterone are pretty safe but its all the ancillary stuff that people are using in large amounts that they think is like pez candy (but are in actuality pretty darn powerful) might be a big culprit in alot of the side effects (especially cardiovascular/lipid/clot wise) we are seeing.

so my opinions would be the following

while on, use the lowest amount of juice you can to make gains so you can always have something to go up to later. Ive seen LATS say this, Ive seen Evan C say this, and ive said this alot of the years......if you do 2 grams of test now when you are 205 pounds......what the hell are you going to have to use when you are 225 pounds and stuck? 4000-5000mg of test a week? What?!?!, till you get past your plateau or have a cardiovascular event?

while on

1) HCG 2x a week
2) if you must use an anti arom...then use exemestane at its lowest dose you can and maybe every 2nd or 3rd day.

always go 4 to 8 (maybe 12 weeks tops if you are still gaining) and then send signals to the HPTA.

Signals-

If i was someone who rarely or sporadically was on.....as I got off i would keep using HCG and exemestane (in the lowest dose possible).....along with clomid if i could hack it either cycled back and forth 2-3 weeks at a time with DAA (very excited by this compound, I think its going to be the one FINALLY EVERYONE HAS BEEN WAITING FOR) or with DAA concurrently (I dont know on that one...DAA is so new).....until the point I felt somewhat normalized....that might mean 1 month, 2 months, maybe even 3 months....depends on the individual......I would also use the lowest dose of clomid I could in that case also. Its all about getting back to normal endogenous testosterone wise. Getting back to normal solves everything....including longterm muscle mass retainment.
(If more people thought in the terms of "how can i get back to normal as quickly as possible after this cycle to keep all this muscle mass" instead of "how can i get get huge during this cycle, fuck what happens after"......there would be so many more happy and content bodybuilders around.....I digress

If I was someone who used year round, I would do everything in my power to keep my endo test levels as normalized as possible.

Every 4-12 weeks, I would try my best to either get completely off or very low dose testosterone (again depending on the individual and his own personal choices)......and use HCG, clom, exemestane and DAA to the best of my ability for 10 days to 3 weeks before getting back on again or raising the low dose testosterone back up...(but hey my opinion on low dose testosterone seems to be alot different than alot of people in this forum).....I am talking either completely off or pyramiding downward during the 10 days to 21 days or using a very low dose amount (25mg to 50mg every 4th day or so) during the 10 to 21 days......before going back up. Again my opinion of going back up means 500-750mg (maybe 1000mg for the big boys) and not the 2000mg and upwards of testosterone that it seems alot of 220 pounders use in this forum. Thats what I would do if I was using year round.

There I commented on something I didnt want to comment on because I felt I had to....LOL

 

[b-boy]

^^^ dayyyuuuummmmm!!!! Good post.