Front Loading Dbol and enging with it???

[LATS60]

I've seen a few threads with D-Bol being used for 4 weeks at the end of the cycle up until PCT so you stay anabolic til pct???

My cycle was going to be

1 - 12 test E 500mgs
1 - 4 dbol 25mgs ed

but was thinking of adding in 25 mgs of dbol for weeks 10 -14 right up until i hit my pct (2 weeks after last test inj)

i've only seen it on a few cycles so would this be a good/bad idea? is it not advisable to run two oral cycles inside 3 months?

would there be significant gains to be made from the last 4 weeks?

Also could someone explain or post me a link to some more info on t-bol as i couldn't find it on the steroid profile page? is it just a variation of D-Bol - what are the differences?

Cheers

I do it often, it's not a waste. If youv'e just ran test for 12wks anyway.......
Think about it. Class 1 and class 2 synergy again!!!!!!!

[Reed]

I do it often, it's not a waste. If youv'e just ran test for 12wks anyway.......
Think about it. Class 1 and class 2 synergy again!!!!!!!

Got a question for ya... don't you cruise on TRT doses after a "cycle" then blast with no PCT? I would find it hard for someone to maintain after using dbol at the end of the cycle when they are trying to get back to their normal function then when you cruise above your normal test levels and not going back to "0" I can understand how it would not be a waste

[LATS60]

Got a question for ya... don't you cruise on TRT doses after a "cycle" then blast with no PCT? I would find it hard for someone to maintain after using dbol at the end of the cycle when they are trying to get back to their normal function then when you cruise above your normal test levels and not going back to "0" I can understand how it would not be a waste

Yes i do. Who's talking about maintaining, i didn't mention that was my reason for doing it. If i am as you say going back to cruise dose, then i wouldn't be trying to get back to normal function.
What is your Q mate?

[Reed]

Yes i do. Who's talking about maintaining, i didn't mention that was my reason for doing it. If i am as you say going back to cruise dose, then i wouldn't be trying to get back to normal function.
What is your Q mate?

My Q is how is using dbol at the end of a cycle not a waste?
I would just find it hard for someone to maintain the gains made using dbol at the end of the cycle when going onto PCT. Numerous of reasons being that it takes the body 4 weeks minimum to reach a state of homeostasis in order to adjust to new gains made. Hence the reason competitive bodybuilders can't go from a bulking cycle straight into a contest diet/cycle and why most utilize orals at the beginning of the cycle. So when you place the dbol at the end of the cycle the little LBM gains he made (water weight is not something I care about nor should anymore unless they need their ego stroked) during that time I am more than likely willing to bet that he will not be able to hold on to those gains as the body goes catabolic with the high production of estrogen, cortisol that the body produces to reach that homeostasis. Studies as well....

New findings in post-cycle therapy
THe role of glucocorticoids
posted by Bigcat..cutting edge muscle

The GnRH gene contains a glucocorticoid response element (1), which suggest that glucocorticoids have a direct regulatory function on GnRH expression in the hypothalamus. Chandran et al (2) demonstrated that dexamethasone had a direct supressive effect in GnRH release.

Testosterone and DHT are known to inhibit HPTA by slowing GnRH pulse in the hypothalamus. In a rat study (3) castrated and adrenolectomized rats saw a huge increase in LH and FSH secretion. Simply adding testosterone however did not stop the rise in gonadotrophins. only when corticosterone was added did testosterone resume its inhibitory functions. However testosterone had no effect on glucocorticoid mediated GnRH supression (4), which suggest that corticosteroids are inhibitory at the pituitary level as well, quite possibly by reducing pituitary sensitivity to GnRH.

This was confirmed by Kubajak and Kamel (5) who found that corticosterone had no effect with maximal concentrations of testosterone, but augmented the inhibitory effect on LH release in the presence of lower levels of testosterone. This would also warn those against jumping to conclusions that testosterone might not be supressive if no glucocorticoids are present, since maximal levels of T supressed LH maximally as well.

This all taken together suggest the need for glucocorticoid control in the PCT if we want to achieve maximal recovery. In the first place we can do this by avoiding the use of 17AA steroids near the end of a cycle. It has been shown that several 17AA steroids including stanozolol, danazol and methyltestosterone, but not fluoxymesterone or metribolone, can upregulate GR expression (6). Potent short-acting androgens however may be the best way to finish a cycle. Short-acting, to avoid lingering supression from androgens that won't clear the body fast enough, and potent because it has been demonstrated that AR activation in the adrenocortical cells inhibits their growth and steroidogenisis. (7). Lastly I may have finally found a reason to use those pesky arginine supplements the market was swarmed with just a short while ago, (8,9), since there is evidence that nitric oxide can inhibit glucocorticoid action by reducing binding to the GR. This may actually be a wiser choice than searching for a competitive GR inhibitor, since such inhibitors invariably show some affinity for androgen and progesterone receptors as well.

The conclusion is that some form of glucocorticoid control is necessary during PCT, and that there is some evidence that even Glucocorticoid managemen on-cycle can reduce problems post-cycle, likely the reason oxandrolone for instance tends to allow people to bounce back faster than for example stanozolol or Dbol.

The role of IGF-1

More evidence seems to suggest that there is plausible evidence for cycling between androgens and GH/IGF-1. At Least one study (10) demonstrates that IGF-1 plays a key role in regulating GnRH release via a Ras/Raf-1/Mapk induced pathway and an increase in the c-fos factor.

This makes a great case for starting IGF-1 after finishing androgens, both in aiding recovery, as well as keeping gains going. I'm not a big fan of IGF-1 due to the high cost and low returns, but no one can deny its use for athletes that need to maintain mass and keep gaining it while continuous steroid use is not an option.

The role of progesterone

Calogero et al (4) also found a modulating effect of progesterone on corticosterone-related GnRH-inhibition. Though the results of studies cited show differing roles for progesterone, on the one hand protective, on the other hand inhibitory. It was even suggested that progesterone may inhibit corticosterone-related inhibition, but not when higher doses of corticosterone were used. This suggests that we may be able to take the edge off of some really supressive estrogenic drugs, nandrolone and more notably MENT and trenbolone, by reducing glucocorticoid action even a little, as suggested above.

Although it was also suggested that this could be mediated by a progesterone metabolite (progesterone is the base for many neurologically important steroids), which would of course not be plausible with androgenic progestins. So this remains PURE speculation until futher elucidation of the mechanism of progesterone in this regard becomes available, and should not be carried into conversation as saying "hey Big Cat said that progesterone is good for you post-cycle if you lower cortisol".

Role of estrogen

Another study (11) suggests that, at least at the hypothalamic level, estrogen may actually stimulate the HPTA. This data may be consistent with some reports that suggest tamoxifen is estrogenic and not anti-estrogenic at this level. This data does not suggest any different approach, merely explains how it could be possible that nolvadex seems to work better than Clomid, since it acts as an estrogen at the hypothalamus and as an anti-estrogen at the pituitary.


References


(1) Radovick S, Wondisford FE, Nakayama Y, Yamada M, Cutler GB Jr, Weintraub BD.Isolation and characterization of the human gonadotropin-releasing hormone gene in the hypothalamus and placenta.Mol Endocrinol. 1990 Mar;4(3):476-80.

(2)Chandran UR, Attardi B, Friedman R, Zheng Z, Roberts JL, DeFranco DB.Glucocorticoid repression of the mouse gonadotropin-releasing hormone gene is mediated by promoter elements that are recognized by heteromeric complexes containing glucocorticoid receptor.J Biol Chem. 1996 Aug 23;271(34):20412-20.

(3) Vreeburg JT, de Greef WJ, Ooms MP, van Wouw P, Weber RF.
Effects of adrenocorticotropin and corticosterone on the negative feedback action of testosterone in the adult male rat.Endocrinology. 1984 Sep;115(3):977-83.

(4) Calogero AE, Burrello N, Bosboom AM, Garofalo MR, Weber RF, D'Agata R.Glucocorticoids inhibit gonadotropin-releasing hormone by acting directly at the hypothalamic level.J Endocrinol Invest. 1999 Oct;22(9):666-70.

(5)Kamel F, Kubajak CL.Modulation of gonadotropin secretion by corticosterone: interaction with gonadal steroids and mechanism of action.Endocrinology. 1987 Aug;121(2):561-8.

(6)Fernandez L, Boada LD, Luzardo OP, Zumbado M, Lopez A, Diaz-Chico BN, Chirino R.[3H]dexamethasone binding activity in liver microsomes is modulated differently by 17 alpha-alkylated androgens and testosterone in vivo.Pharmacol Toxicol. 1995 Oct;77(4):264-9.

(7)Rossi R, Zatelli MC, Valentini A, Cavazzini P, Fallo F, del Senno L, degli Uberti EC.Evidence for androgen receptor gene expression and growth inhibitory effect of dihydrotestosterone on human adrenocortical cells.J Endocrinol. 1998 Dec;159(3):373-80.

(8) Duma D, Silva-Santos JE, Assreuy J.Inhibition of glucocorticoid receptor binding by nitric oxide in endotoxemic rats.Crit Care Med. 2004 Nov;32(11):2304-10.

(9)Pennisi P, D'Alcamo MA, Leonetti C, Clementi A, Cutuli VM, Riccobene S, Parisi N, Fiore CE.Supplementation of L-arginine prevents glucocorticoid-induced reduction of bone growth and bone turnover abnormalities in a growing rat model.J Bone Miner Metab. 2005;23(2):134-9.

(10)Zhen S, Zakaria M, Wolfe A, Radovick S.Regulation of gonadotropin-releasing hormone (GnRH) gene expression by insulin-like growth factor I in a cultured GnRH-expressing neuronal cell line.Mol Endocrinol. 1997 Jul;11(8):1145-55.

(11)Radovick S, Ticknor CM, Nakayama Y, Notides AC, Rahman A, Weintraub BD, Cutler GB Jr, Wondisford FE.Evidence for direct estrogen regulation of the human gonadotropin-releasing hormone gene.J Clin Invest. 1991 Nov;88(5):1649-55.

So in the end why not just use the prop in order to avoid all that stress but I understand that it would be ok from someone that is cruising and blasting......