Archive for August 2014

Peptides Usage for Bodybuilding

Peptides Usage for Bodybuilding

 

When used for bodybuilding, peptides:

• Lower the recovery time in between workouts
• Increase lean body mass
• Enhance your overall workout performance
• Do not have a risk of detection
• Fortify joints and ligaments
• Repair damaged muscle tissue

 

Other benefits bodybuilders see from peptide use  include:

• Increase the ability of protein synthesis
• Increases the amount of effective insulin you can use
• Increase the amount of effective anabolic steroids you can use

If you happen to be a bodybuilder and would like to improve your physical appearance via peptide usage the advantages you will enjoy include:
• Healthy weight gain
• Gaining strength
• Losing fat
• Lower muscle loss when not in training
• No side effects

In Conclusion, Bodybuilding peptide use :
• Peptides will increase the number of muscle cells
• The usage of bodybuilding peptides means that you will be able to lesson  weight training to develop the muscle density you want while also having the ability to lose a significant amount of extra body fat
• Peptides will help you reverse generic outlook while allowing you to increase muscle density and definition

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Bodybuilding weight loss peptide Ipamorelin

Bodybuilding peptide 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).

Get your Ipamorelin here
Get your Ipamorelin here

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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Using T3 cytomel for Excellent Weight Loss

T3 (cytomel)

 

Ilosing-weightt has been over 100 years since the discovery by Magnus-Levy that thyroid hormones play a central role in energy homeostasis, and 75 years since the hormones were first used for weight loss. Despite this great length of time, the precise mechanisms by which thyroid hormones exert their calorigenic effect are not completely characterized, and still actively debated. Despite numerous clinical studies having shown that the administration of thyroid hormone induces weight loss, it is not currently indicated as a weight loss agent. This is probably due to the number of side effects observed during thyroid hormone use at the relatively high doses used in the majority of obesity treatment studies. These deleterious effects include cardiac problems such as tachycardia and atrial arrhythmias, loss of muscle mass as well as fat, increased bone resorption and muscle weakness. Nevertheless, thyroid hormones, particularly triiodothyronine (T3) are a mainstay in the arsenal of drugs used by bodybuilders for fat loss. The widespread underground use of T3 warrants an understanding of its mechanism of action, as well as a knowledge of how it is most effectively and safely used, with an eye to minimizing side effects.

Thyroid Function and Physiology

Before jumping right into a discussion of the use of thyroid hormone for fat loss, a little review of thyroid function and physiology might be in order. The thyroid gland secretes two hormones of interest to us, thyroxine (T4) and triiodothyronine (T3). Cytomel is considered the physiologically active hormone, and T4 is converted peripherally into T3 by the action of the enzyme deiodinase. The bulk of the body’s T3 (about 80%) comes from this conversion. The secretion of T4 is under the control of Thyroid Stimulating Hormone (TSH) which is produced by the pituitary gland. TSH secretion is in turn controlled through release of Thyrotropin Releasing Hormone which is produced in the hypothalamus. This is analogous to testosterone production, where GnRH from the hypothalamus causes the pituitary to release LH, which in turn stimulates the testes to produce testosterone.

In addition to Cytomel, it has recently been recognized that there exist two additional active metabolites of T3: 3,5 and 3,3′ diiodothyronines, which we will collectively call T2. Studies have shown that 3,3′-T2 may be more effective in raising resting metabolic rate when hypothyroid subjects are treated with T3, than when normal (euthyroid) subjects are given Cytomel. Therefore in normal subjects 3,5-T2 may be the principal active metabolite of T3 (1)

Like the hypothalamic-pituitary-gonadal axis, the thyroid gland is under negative feedback control. When T3 levels go up, TSH secretion is suppressed. This is the mechanism whereby exogenous thyroid hormone suppresses natural thyroid hormone production. There is a difference though between the way anabolic steroids suppress natural testosterone production and the way T3 suppresses the thyroid. With steroids, the longer and heavier the cycle is, the longer your natural testosterone is suppressed. This is not the case with exogenous thyroid hormone.

An early study that looked at thyroid function and recovery under the influence of exogenous thyroid hormone was undertaken by Greer (2). He looked at patients who were misdiagnosed as being hypothyroid and put on thyroid hormone replacement for as long as 30 years. When the medication was withdrawn, their thyroids quickly returned to normal.

Here is a remark about Greer’s classic paper from a later author:

“In 1951, Greer reported the pattern of recovery of thyroid function after stopping suppressive treatment with thyroid hormone in euthyroid [normal] subjects based on sequential measurements of their thyroidal uptake of radioiodine. He observed that after withdrawal of exogenous thyroid therapy, thyroid function, in terms of radioiodine uptake, returned to normal in most subjects within two weeks. He further observed that thyroid function returned as rapidly in those subjects whose glands had been depressed by several years of thyroid medication as it did in those whose gland had been depressed for only a few days” (3)

These results have been subsequently verified in several studies.(3)(4) So contrary to what has been stated in the bodybuilding literature, there is no evidence that long term thyroid supplementation will somehow damage your thyroid gland. Nevertheless, most bodybuilders will choose to cycle their T3 (or T4 which in most cases works just as well) as part of a cutting strategy, since T3 is catabolic with respect to muscle just as it is with fat. As previously mentioned, long term T3 induced hyperthyroidism is also catabolic to bone as well as muscle.

The proviso about T4 vs T3 for weight loss alluded to above needs some elaboration. There have been a number of studies that have shown that during starvation, or when carbohydrate intake is reduced to approximately 25 to 50 grams per day, levels of deiodinase decline, hindering the conversion of T4 to the physiologically active T3.(5) From an evolutionary standpoint this makes sense: during periods of starvation the body, teleologically speaking, would like to reduce its basal metabolic rate to preserve fat and especially muscle stores. However, a recent study demonstrating the effectiveness and safety of the ketogenic diet for weight loss recorded no change in circulating T3 levels.(6) So this issue not completely settled. Nevertheless, persons contemplating thyroid supplementation during ketogenic dieting might prefer Cytomel over T4 since the bulk of the research does suggest a decline in the peripheral conversion of T4 to T3 during low carb dieting.

Now that we have reviewed a little about thyroid function, let’s consider just how it is that thyroid hormone exerts its fat burning effects.

Increased Oxidative Energy Metabolism while using Cytomel

 

Thyroid hormone has long been recognized as a major regulator of the oxidative metabolism of energy producing substrates (food or stored substrates like fat, muscle, and glycogen) by the mitochondria. The mitochondria are often called the “cell’s powerhouses” because this is where foodstuffs are turned into useful energy in the form of ATP. T3 and T2 increase the flux of nutrients into the mitochondria as well as the rate at which they are oxidized, by increasing the activities of the enzymes involved in the oxidative metabolic pathway. The increased rate of oxidation is reflected by an increase in oxygen consumption by the body.

T3 and T2 appear to act by different mechanisms to produce different results. T2 is believed to act on the mitochondria directly, increasing the rate of mitochondrial respiration, with a consequent increase in ATP production. T3 on the other hand acts at the nuclear level, inducing the transcription of genes controlling energy metabolism, primarily the genes for so-called uncoupling proteins, or UCP (see below). The time course of these two actions is quite different. T2 begins to increase mitochondrial respiration and metabolic rate immediately. T3 on the other hand requires a day or longer to increase RMR since the synthesis of new proteins, the UCP, is required (1).

There are a number of putative mechanisms whereby T2 is believed to increase mitochondrial energy production rates, resulting in increased ATP levels. These include an increased influx of Ca++ into the mitochondria, with a resulting increase in mitochondrial dehydrogenases. This in turn would lead to an increase in reduced substrates available for oxidation. An increase in cytochrome oxidase activity has also been observed. This would hasten the reduction of O2, speeding up respiration. These and a number of other proposed mechanisms for the action of T2 are reviewed by Lannie et al.(7)

What is the fate of the extra ATP produced during hyperthyroidism? There are a number of ways by which the increased ATP promotes an increase in metabolic activity, including the following:

Increased Na+/K+ATPase. This is the enzyme responsible for controlling the Na/K pump, which regulates the relative intracellular and extracellular concentrations of these ions, maintaining the normal transmembrane ion gradient. Sestoft(7) has estimated this effect may account for up to to 10% of the increased ATP usage.

Increased Ca++-dependent ATPase. The intracellular concentration of calcium must be kept lower than the extracellular concentration to maintain normal cellular function. ATP is required to pump out excess calcium. It has been estimated that 10% of a cell’s energy expenditure is used just to maintain Ca++ homeostasis. (1)

Substrate cycling. Hyperthyroidism induces a futile cycle of lipogenesis/lipolysis in fat cells. The stored triglycerides are broken down into free fatty acids and glycerol, then reformed back into triglycerides again. This is an energy dependent process that utilizes some of the excess ATP produced in the hyperthyroid state (8). Futile cycling has been estimated to use approximately 15% of the excess ATP created during hyperthyroidism (8)

Increased Heart Work. This puts perhaps the greatest single demand on ATP usage, with increased heart rate and force of contraction accounting for up to 30% to 40% of ATP usage in hyperthyroidism (9)

Mitochondrial Uncoupling shown from T3

 

As mentioned, the mitochondria are often characterized as the cell’s powerhouse. They convert foodstuffs into ATP, which is used to fuel all the body’s metabolic processes. Much research suggests that T3, like another much more potent agent DNP, has the ability to uncouple oxidation of substrates from ATP production. T3 is believed to increase the production of so called uncoupling proteins. Uncoupling protein (UCP) is a transporter family that is present in the mitochondrial inner membrane, and as its name suggests, it uncouples respiration from ATP synthesis by dissipating the transmembrane proton gradient as heat. Instead of useful ATP being produced from energy substrates, heat is generated instead. There are conflicting studies about the importance of T3 induced uncoupling. Animal studies have demonstrated an actual increase in ATP production commensurate with increased oxygen consumption as we discussed above. Other studies in humans have shown that in fact uncoupling in skeletal muscle does occur. This would contribute to T3 induced thermogenesis, with a resulting increase in basal metabolic rate.(10)

To make up for the deficit in ATP production (as well as provide fuel for the extra ATP production discussed above) more substrates must be burned for fuel, resulting in fat loss. Unfortunately, along with the fat that is burned, some protein from muscle is also catabolized for energy. This is the downside of T3 use, and the reason many people choose to use an anabolic steroid or prohormone during a T3 cycle to help preserve muscle mass. Studies have shown this to be an effective strategy (11). (Muscle glycogen is also more rapidly depleted, and less efficiently stored during hyperthyroidism. This may account for some of the muscle weakness generally associated with T3 use.)

ayurvedic-weight-lossCountering T3 induced muscle loss with anabolic steroids or prohormones makes sense from a physiological viewpoint as well. Thyroid hormone muscle protein breakdown is mainly mediated via the so-called ubiquitin-proteasome pathway. (12). (There are several independent metabolic pathways of protein breakdown in the body. For instance, another pathway, the lysosomal pathway, is responsible for the accelerated rate of muscle protein breakdown during and after exercise.) Testosterone administration has been shown to decrease ubiquitin-proteasome activity. (13) So anabolic steroids specifically target the muscle protein breakdown process stimulated by T3.

What may not be an effective strategy to maintain muscle mass during a T3 cycle is the use of exogenous growth hormone (GH). Studies have shown that when GH and T3 are administered concurrently, the increased nitrogen retention normally associated with GH use is abolished. This has been attributed to the observation that T3 increases levels of insulin like growth factor binding protein, reducing the bioavailability of igf-1 (14). Nevertheless, GH has fat burning properties independent of igf-1, so using GH with T3 would act additively to speed fat burning, but with little if any preservation of lean body mass. So again, if GH is used in conjunction with T3, anabolic steroid/prohormone use would be indicated.

You can fins these weight loss products as well as others by clicking here

 

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