Archive for August 2014

Bodybuilding Anti-Estrogens used in steroid cycles

Bodybuilding Anti-Estrogens used in steroid cycles

Most people have heard of Anti-E’s due to their role in a person’s steroid cycle. Anti-Estrogens are used to prevent gynocomastia (the formation of breast tissue) from steroids that aromatize and also reduce water retention. However, Anti-Estrogens can be also used for a host of other reasons, and in our case, fat loss. Estrogen is a fattening hormone, and if it is kept in check while dieting you can receive a hard look without even using anabolic steroids. If you don’t believe me, notice the body fat gain when a girl starts using birth control, this is caused by the increase in estrogen levels.

The best drugs for this effect would be Nolvadex (if you are not using anabolic drugs), or the much more powerful (but also very expensive) Arimidex and Femara. Dosages of Nolvadex are usually between 20mg and 40mg a day, Arimidex is usually 1/2mg to 1mg a day, and for Femara, one 2.5mg tab could be used ED or EOD. These could all be used by them self but you could stack Nolvadex with Arimidex or Femara due to the fact that Nolvadex and Arimidex both effect estrogen in the body differently.

These are very good for the natural dieter due to the fact that they will give you a hard (steroid) look, and they will also allow you to retain more muscle mass while dieting. For someone using Anabolic drugs during a fat loss cycle, they should be used regardless because of steroids aromatizing into estrogen, and also they will keep water down and give you a dry look.

So here they are, but how would you combine them for the best results Lets put together a theoretical cycle using only the drugs mentioned in the article for someone who has used them before, for someone that has not, just taper like stated in the article.

Week 1-2

- 20mg of Nolvadex
- 60mcg of Clenbuterol upon wakening
- 50mcg of Cytomel
- 1 tab of Yohimbine around 30min after the Clen
- 25mcg of Cytomel
- 60mcg of Clenbuterol before 2-4 p.m.
- 1 tab of Yohimbine around 30min after the Clen
- 2000mg of Metformin spread through out the day

Weeks 3-4

* Same as the previous weeks, but switch the Clen with ECA, if you want to you can also increase the Nolvadex to 40mg a day.

Weeks 5-6

* Drop the ECA and the Yohimbine, and taper down the dosage of T-3 by 25mcg each week, you can keep the Metformin the same or drop it if you want.

Weeks 7-10

Stay off all the drugs and keep your calories the same or slightly increase your carb intake (if you are on low carbs) to aid in your metabolism. During these weeks your metabolism will be sluggish, so watch your diet and keep up with your cardio, the diet isn’t over yet.

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Ipamorelin peptide for muscle growth

Ipamorelin is a fascinating new muscle building discovery that is getting a lot of attention in the bodybuilding world. It is a synthetic peptide that has powerful Growth Hormone releasing properties. And these GH releasing properties are what is of interest to athletes and bodybuilders since they can make a tremendous difference in the amount of muscle you can grow and how quickly you burn fat.

Ipamorelin is a penta-peptide. (Aib-His-D-2-Nal-D- Phe-Lys-NH2) And, the strength it displays may very well make regular old Growth Hormone (GH) obsolete. But what athletes and bodybuilders really want to know is what is this wonder peptide capable of doing, how is it used, and how does it compare to the other GHRP peptides?

Athletes are taking Ipamorelin in a 200mcg -300mcg dosage, two or three times daily, using a tiny insulin needle to inject. They usually start with the lower dose since side effects can include headaches or what feels like a head-rush. Ipamorelin can be taken at anytime but taking it about 30-45 minutes before a workout would seem ideal because of the pulse in Growth Hormone (GH) it creates allowing for maximum growth.

Studies on the effects of Ipamorelin on bone growth, body weight, and GH release showed some interesting conclusions.In one experiment, various doses were administered over the course of 15 days to test the group’s reactions.

There was a distinct and dose-dependent effect on body weight gain however, the treatment group did not show a change in total IGF-I levels. Nor did the treatment group produce serum markers of bone development. For example, the number of cells in the wide portion of the tibia (the shinbone) did not change significantly. This is a good thing because it suggests muscle growth with less potential for deformity of bone or cartilage.

The reaction of the pituitary to an aggressive i.v. dose of Ipamorelin showed that plasma GH levels were notably reduced whereas they were unchanged after a comparable dose of GHRH. This is actually a good thing as it suggests that Ipamorelin may not decrease your body’s natural GH production – further demonstrating that Ipamorelin is a selective GH releaser.

Ipamorelin does not induce hunger making it advantageous to those on a restricted calorie diet. And obviously, Ipamorelin’s side-effects are enhanced when combined with anabolic steroids since they too influence Growth Hormone/Insulin Growth Factor release and production.
Another document states that in healthy swine, Ipamorelin released GH with a consistency that is very comparable to GHRP-6. Also noteworthy was that none of the GH releasers tested affected FSH, LH, PRL or TSH blood serum plasma levels.

Ipamorelin in theory may increase Acetylchloine or Cortisol when used in higher dosages. However, and increase in Acetylchloine or Cortisol is even more likely with GHRP-2 and GHRP-6. In fact, in the case of Ipamorelin, there was little to no rise in Acetylcholine and Cortisol blood plasma levels even at injections more than 200 times higher than the effective dosage for comparable GH release.

This clearly proves that Ipamorelin is the first successful GHRP receptor agonist or chemical that binds to a receptor of a cell and triggers a response by that cell with a specific selectivity for the promotion of GH release by itself.

Another advantage to Ipamorelin is that it doesn’t cause sudden spikes in prolactin or cortisol as does GHRP-2 and GHRP-6. Ipamorelin is slower in its delivery unlike GHRP’s which spike GH levels at a more rapid rate. The slower release is more natural and has a more sustained effect.

All in all it looks as if Ipamorelin is the new wave in GH releasing peptides. It appear to be more potent, longer lasting and potentially safer to use in the long run. More studies are being conducted all the time but as it stands, Ipamorelin looks like a serious contender in the arsenal of anabolic advancement.

Biological Activity of Ipamorelin

Ipamorelin is a selective growth hormone secretagogue and agonist of the ghrelin receptor. In pentobarbital anaesthetised rats, ipamorelin released GH with a potency and efficacy comparable to GHRP-6 (ED50 = 80±42 nmol/kg and Emax = 1545±250 ng GH/ml vs 115±36nmol/kg and 1167±120ng GH/ml). In conscious swine, ipamorelin released GH with an ED50 = 2.3±0.03 nmol/kg and an Emax = 65±0.2 ng GH/ml plasma. Again, this was very similar to GHRP-6 (ED50 = 3.9±1.4 nmol/kg and Emax = 74±7ng GH/ml plasma). GHRP-2 displayed higher potency but lower efficacy (ED50 = 0.6 nmol/kg and Emax = 56±6 ng GH/ml plasma). The specificity for GH release was studied in swine.
References on Ipamorelin:
[1] Venkova K et al. J Pharmacol Exp Ther. 2009 Jun;329(3):1110-6

Ipamorelin, the first selective growth hormone secretagogue

Kirsten Raun, Birgit Sehested Hansen, Nils Langeland Johansen, Henning Thøgersen, Kjeld Madsen, Michael Ankersen and Peter Høngaard Andersen
(Departments of GH Biology, Assay and Cell Technology, Medical Chemistry Research, Health Care Discovery, Novo Nordisk A/S, Novo Nordisk Park,
DK-2760 Ma°løv, Denmark)

The development and pharmacology of a new potent growth hormone (GH) secretagogue, ipamorelin,
is described. Ipamorelin is a pentapeptide (Aib-His-D-2-Nal-D-Phe-Lys-NH2), which displays high GH
releasing potency and efficacy in vitro and in vivo. As an outcome of a major chemistry programme,
ipamorelin was identified within a series of compounds lacking the central dipeptide Ala-Trp of growth
hormone-releasing peptide (GHRP)-1.

In vitro, ipamorelin released GH from primary rat pituitary cells with a potency and efficacy similar
to GHRP-6 (EC50 ¼ 1.360.4 nmol/l and Emax ¼ 8565% vs 2.260.3 nmol/l and 100%). A
pharmacological profiling using GHRP and growth hormone-releasing hormone (GHRH) antagonists
clearly demonstrated that ipamorelin, like GHRP-6, stimulates GH release via a GHRP-like receptor.
In pentobarbital anaesthetised rats, ipamorelin released GH with a potency and efficacy comparable
to GHRP-6 (ED50 ¼ 80642 nmol/kg and Emax ¼ 15456250 ng GH/ml vs 115636 nmol/kg and
11676120 ng GH/ml).

In conscious swine, Ipamorelin released GH with an ED50 ¼ 2.360.03 nmol/kg and an Emax ¼
6560.2 ng GH/ml plasma. Again, this was very similar to GHRP-6 (ED50 ¼ 3.961.4 nmol/kg and
Emax ¼ 7467 ng GH/ml plasma). GHRP-2 displayed higher potency but lower efficacy (ED50 ¼
0.6 nmol/kg and Emax ¼ 5666 ng GH/ml plasma).

The specificity for GH release was studied in swine. None of the GH secretagogues tested affected
FSH, LH, PRL or TSH plasma levels. Administration of both GHRP-6 and GHRP-2 resulted in increased
plasma levels of ACTH and cortisol. Very surprisingly, Ipamorelin did not release ACTH or cortisol in
levels significantly different from those observed following GHRH stimulation. This lack of effect on
ACTH and cortisol plasma levels was evident even at doses more than 200-fold higher than the ED50
for GH release.

In conclusion, ipamorelin is the first GHRP-receptor agonist with a selectivity for GH release similar
to that displayed by GHRH. The specificity of ipamorelin makes this compound a very interesting
candidate for future clinical development.

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