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#26 2012-07-26 01:32

Re: Peptidai lietuviskai

cia biski kalba, bet angliskai hmm

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azuolyno bicas
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#27 2012-07-26 15:55

Re: Peptidai lietuviskai

Why would someone use igf1-lr3 for something other than "site enhancement" if it actually causes hyperplasia?
I'm really sick of people touting this ridiculous bro-science without any shred of evidence, either anecdotal or scientific to back it up! lr3 is an 83 amino acid chain (vs. 70 amino acids in bio-identical igf-1) that was developed to have a longer life for research purposes in a petri dish, not in the human body. Researchers were having trouble testing "regular" igf-1 so this alteration was done to make longer-duration tests possible in the lab. It was never meant to "work better" in the human body, and, it doesn't. Why would it?

Take MGF for example. It's very fast acting, so now PEG-MGF is marketed (often by well-meaning sellers) in its place because it has a longer half-life. But, that half-life comes at a cost. PEGylation, depending on how it's done, can cause the molecules of MGF, that PEG is bound to, to become "too heavy" and not able to be recognized by the body as natural MGF. That's why so many say regular MGF just seems to work better for site-enhancement than PEG-MGF. Why? Because it is bio-identical. It's hit or miss depending on the quality of the peptide purchased, process used etc. Half-life goes out the window when the results just aren't as good. (Quality PEG-MGF is still effective, but when it comes to site-enhancement MGF is still much better- due in part to its short half-life to some extent, but mostly it's molecular weight and "usability" in the body.)

Talk to anyone who's used the original, bio-identical igf-1 and they'll tell you how much better it works for site-enhancement than igf1-lr3. But, you won't find many of them around these days because igf-1, in that form, is increasingly hard to find due to the pority of lr3.

Why is lr3 so por? I think it's because people can "feel" they are getting results from it due to its insulin-like effects. In fact, many who've used lr3 (myself included) know that a good dose of lr3 is equal to an effective (8-10 iu) dose of humalog or humalin-r. So, using it pre or post workout you are going to get noticeable results. Results you can see and feel because it binds to the same receptors insulin does (both igf-1 receptors and insulin receptors). And, judging by anecdotal results, it binds in a similar ratio!

So, you get people using igf1-lr3 touting it's "general" muscle-building properties but saying to use MGF for actual site-enhancement. Again, if igf1-lr3 was doing anything other than what insulin does, why isn't it just as great for site-enhancement as MGF? I'm not trying to promote insulin use here. But, people should realize you can go hypo and have all the same side-effects from lr3 as you do from insulin. There are subtle differences, but, basically, you are just taking another form of insulin when you are taking lr3. It's effective, yes, but in almost the exact same way humalog is. Don't fool yourself and blind yourself with science into thinking anything otherwise until there's any kind of measureable results that state otherwise- and I'm including anecdotal evidence here. Is ANYONE getting site-enhancement or general hyperplasia from igf1-lr3? Anyone? And, if so, how did you come to that conclusion? Think about it. It's not junk, I'm not saying that. I'm just saying it's not what people want it to be, pure and simple. It's just not.

If you are looking for an igf-1 that is actually bio-identical and will give you the type of special results that most are looking for from lr3, look to des (1-3) igf-1. It's a 67 amino acid chain where the last 3 amino acids in the sequence of standard, bio-identical igf-1 have been removed. This results in a substance that is found in the body post-training. During exercise the body produces lactic acid. When exposed to lactic acid in the body igf-1 (whatever hasn't been bound by igf-1 binding proteins) loses those last three amino acids making des (1-3) igf-1. When in this form it is resistant to igf-1 binding proteins and is the most potent form (on paper anyway) of igf-1. In a way it is like the test-suspension of the igf-1 drugs. It is super potent and short acting. But, unlike supsension (and I'm only using this example as an over-simplified metaphor here) it has special properties that make it ideal to binding to the igf-1 receptors in the muscle while not being rendered ineffective by binding proteins!

It'd be like if there was some kind of super test suspension that not only was fast acting and super potent, but was 10 times as specifically effective as regular test. So, although the half-life is quite short, that doesn't mean it's not effective. I mean, you can take 2 doses of beastdrol per day (half-life around 4.5 hrs or so) and get a lot of growth out of it. Why would this be any different? It's not. Half-life isn't everything- especially when the drug with the longer half-life has been modified to the point where it's nearly totally ineffective when it comes to it's original intended purpose. Lr3 works great in the lab and works like insulin in our bodies. Des would be terrible in the lab due to its short half-life, but makes total sense for our bodybuilding goals.

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ivan
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#28 2012-07-26 22:10

Re: Peptidai lietuviskai

Man tai cia isvis pakaitalas xemijai smile tarpinis variantas tarp papildu ir xemijos. Nafik ta xemija xujarint  pagalvojau, teisingai peptidus pasirinkus ir reguliariai vartojant efektas tikrai neblogas

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HRS
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#29 2012-07-26 22:22

Re: Peptidai lietuviskai

ivan rašė:

Man tai cia isvis pakaitalas xemijai smile tarpinis variantas tarp papildu ir xemijos. Nafik ta xemija xujarint  pagalvojau, teisingai peptidus pasirinkus ir reguliariai vartojant efektas tikrai neblogas

na jo,tas pasirinkimas ir yra didziausia problemele,kai nzn nei ka su kuo,nei kaip ;/

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azuolyno bicas
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#30 2012-07-26 22:41

Re: Peptidai lietuviskai

ivan rašė:

Man tai cia isvis pakaitalas xemijai smile tarpinis variantas tarp papildu ir xemijos. Nafik ta xemija xujarint  pagalvojau, teisingai peptidus pasirinkus ir reguliariai vartojant efektas tikrai neblogas

LABAI TEISINGAI PASAKYTA..

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squat
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#31 2012-07-27 08:31

Re: Peptidai lietuviskai

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rolka78
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#32 2012-07-28 16:48

Re: Peptidai lietuviskai

Cia gan geros info radau.Manau daugeliui bus vertinga paskaitinet.
http://buypeptides.org/combinations.html

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azuolyno bicas
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#33 2012-07-29 21:08

Re: Peptidai lietuviskai

rolka78 rašė:

Cia gan geros info radau.Manau daugeliui bus vertinga paskaitinet.
http://buypeptides.org/combinations.html

big_smile big_smile maladec.. ar dar pats nesusigundei? big_smile

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rolka78
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#34 2012-07-30 09:58

Re: Peptidai lietuviskai

azuolyno bicas rašė:

rolka78 rašė:

Cia gan geros info radau.Manau daugeliui bus vertinga paskaitinet.
http://buypeptides.org/combinations.html

big_smile big_smile maladec.. ar dar pats nesusigundei? big_smile

Net nezinau kaip pasakyt.Kai paskaitai ir pasidomi,tai tokia isvada persasi kad peptidai geriau nei as tik sakyciau dieta turi but zymiai griestesne su peptidais nei su as.Aisku ko nori ar bulkint ar cutint.Ir pinigu atzvilgiu turetu but pigiau.

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azuolyno bicas
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#35 2012-08-16 19:59

Re: Peptidai lietuviskai

na ka bandysim i raumenis shaudyt peptidus, cia patare vienas dede is uk forumo, jis visus peptidus leidzia tik i raumenis, paziesim ar skirtumo jausis..

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rolka78
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#36 2012-08-16 20:23

Re: Peptidai lietuviskai

skaiciau kad jokio skirtumo ar i riebalini audini ar i raumeni smile

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Protecting
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#37 2012-08-23 22:03

Re: Peptidai lietuviskai

O i LT parsisiusti galima? Ant sienos neluztu krovinys? big_smile Tikriausiai lt jie neregistruoti

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azuolyno bicas
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#38 2012-08-23 22:14

Re: Peptidai lietuviskai

siaip neturetu luzti, research purposes big_smile

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azuolyno bicas
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#39 2012-09-04 22:32

Re: Peptidai lietuviskai

nesenai uzsireginau vienam uzsienio forume, kur tik su pakvietimais, ir ten mokslines info labai daug, apie pulsacija ir pan.. pabandysiu pakopint info bet anglu kalba, ten labiau viskas isanalizuota.. is teorines bei praktines puses, jei ryt netingesiu permesiu siek tiek info, gal kas pades pavertejaut, nes man kartais nestovi ant vertimo, bet tikiuosi atsiras entuziastu.. arba kas tikrai gali pavertejaut i pm parasykit

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Knoxville
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#40 2012-09-04 22:34

Re: Peptidai lietuviskai

As parasysiu santrumpas lietuviskai to ka perskaitysiu smile

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Rlyeh
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#41 2012-09-05 18:17

Re: Peptidai lietuviskai

nedaug info apie petpidus .. idomu butu suzinot daugiau jeigu  jie nieko nekenkia ir geresnis efektas uz papildus..

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azuolyno bicas
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#42 2012-09-09 21:49

Re: Peptidai lietuviskai

[INSERT-> The section Re: What is GH pulsation, how does it occur & how are pulses amplified? (momentarily housed in the first part of this post .................GH pulse as a prelude to understanding what happens inside the cell in response to GH initiating a signal. At the link is a description of how somatotrophs in the pituitary coordinate a GH releasing response, the regulation of blood flow & increase in cellular energy to release GH, the accumulation of GH in vessels awaiting a build up of GH followed by an all at once release from the "staging area" in the vessels.

This accumulation of GH finds its way to receptors on cells primarily in the liver where they bind and bring about intracellular signalling.

<-END INSERT]

Growth hormone brings about many of its physiological (normal) functions by regulating the transcriptions of genes for the making of proteins. These proteins include insulin-like growth factor (IGF-1), transcription factors and metabolic enzymes (partially described so far in GH Pulsation, metabolic enzymes, cancer ). The processes that bring these functions about are referred to as inside-the-cell (intracellular) signalling pathways.

Growth Hormone also brings about physiological (normal) functions that we usually refer to as metabolic actions. GH has both insulin-like and anti-insulin-like effects on cells and tissues. The insulin-like actions are temporary and
include transient increases in glucose and amino acid transport, lipogenesis and protein synthesis. In order for these effects to occur signaling pathways need to be activated. GH and insulin might activate some common signaling pathways.

The anti insulin-like actions of GH are longer lasting and lead to reductions of body fat by decreasing lipogenesis and increasing lipolysis. In order for these effects to occur signalling pathways need to be activated. when you ask the question "how does GH bring about changes in body fat?", the first layer of abstraction is to state that it increases lipolysis (the release of fatty acids from fat cells), increases resting energy expenditure and in the deficient increases the energy expended during exercise and increases lipid oxidation (the use of fatty acids for fuel).

The next layer of abstraction if the question is asked in regard to affecting lipogenesis and lipolysis, "How does it do that?" is the reply "GH appears to inhibit adipocyte differentiation at a step before the induction (or activation) of genes required for differentiation, such as the gene encoding peroxisome proliferator activated receptor y (PPARy)." So GH inhibits a receptor that induces the proliferation of adipocytes.

If one persists in asking "How does that happen?", well the only choice we are left with is to take that microscope and train it into the cell to look at the signalling mechanisms. The answer will be ugly because the language that is used to describe those events are not part of our everyday lexicon. Here is what that answer could be, "one signaling event that might be important in this process is GH activation of the cAMP-specific phosphodiesterase PDE4A5 by a PI 3' kinase-dependent mechanism.1 GH and glucocorticoid stimulation of lipolysis is thought to involve an inhibitory action on the G protein Gi, thereby increasing cAMP accumulation and lipolysis.2 An involvement of STAT5 proteins in the lipolytic action of GH has also been reported.3

Did your eyes just glaze over?

Let's see if we can build up some basic knowledge.

Where does GH signalling begin? GH is drawn to a receptor on the membrane of the cell. The receptor has two binding posts. The initial step is high-affinity binding of GH to one GH receptor binding post. By binding we mean an amino acid on one of the GH-receptor posts being attracted to form a chemical bond with a specific amino acid on the GH molecule. High-affinity means that there is a strong attraction. A different area of GH then contacts the second GH receptor binding post which stabilizes the GH receptor and creates a twist which reverberates along the root of the receptor into the cell which initiates signaling.

This twisting of the receptor is referred to as a conformational change and from this initial change we have not only a triggering of energenetic behavior that we call signaling inside the cell but also at various times a bringing together or association of the GH-GH-Receptor with the EGF-receptor (epidermal growth factor) and/or the IGF-1 receptor. This association yields a complex where the receptors support each other. In the instance of the IGF-1 receptor associating with the GH receptor we find that if IGF-1 binds to its receptor at the same time as GH does to its receptor, GH stays bound to its receptor longer. This means more GH initiated signalling will take place. It should be noted that IGF-1 is created because of GH binding to its receptor and initiating a signaling cascade involving STAT5b. This results in the delayed emergence of IGF-1. So how can IGF-1 be present when GH binds to a receptor? From a previous pulse of GH. The result is one wave supports the next. We see this concept frequently in the human body and in nature. To effect significant change in the body such as tissue remodeling requires the expenditure of significant resources. The body is thrifty and will often wait for confirmation of a particular status before it commits to expending those resources. This was demonstrated in an interesting study 4 which examined the cellular signaling responses to resistance exercise followed by various rest intervals before another bout of resistance exercise involving the same muscles. They found that in order to prolong the elevation of the mitogenic pathway ERK2, to sustain release of MGF & IGF-1 mRNAs and to show an accumulation of cyclin D1 (a marker which indicates cells entering the cell cycle for proliferation) required a follow on bout of exercise 48 hours later. A bout of exercise only 8 hours later blunted response. The theory is that signalling mechanisms enter a refractory period following resistance exercise which blunts the response to a second immediate bout of exercise. However the magnitude of cellular and molecular response is enhanced when a follow on bout occurs 48 hours later. This is a summation of the signalling such that the body waits before some threshold is crossed in order to prevent the body from entering a costly process of adaptation to a novel stimuli that is not repeated 4.

A few definitions:

Phosphorylation is simply a process that turns protein enzyme action on and off. It is the transfer of a phosphate group whereby the proteins to which they become attached become regulated.

Kinases are a type of enzyme that transfers phosphate groups from high-energy donor molecules, such as ATP, to specific substrates, a process referred to as phosphorylation.

Tyrosines are amino acids which in the area of signalling, function as receivers of phosphate groups that are transferred by way of kinases.

At the root of the GH-receptor resides non-receptor tyrosine kinase JAK2 (Janus kinase 2). When GH binds to the receptor and twists it the JAK2 kinases near each binding post within the cell are pushed, rapidly associate with the GH receptor and because the two JAK2 kinases move closer together they are able to phosphorylate the activating tyrosine amino acid of the other JAK2 molecule. Once this occurs each JAK2 is capable of phosphorylating itself. They then turn around and transfer that phosphate group to the tyrosine residues residing on the GH receptor posts within the cytoplasm.

This is important because the now activated tyrosine residue at the base of the receptor becomes a port. It faces into the sea of cytoplasm and waits for ships to come dock with it. These ships are the signaling proteins that will carry the signals within the cell usually to the nucleus where they will initiate gene transcription. These signaling proteins have phosphotyrosine binding elements which can receive the transfer of high-energy phosphate groups from the tyrosine port. This port becomes an energizing port and the signaling proteins such as STAT5b will continually revisit it for activation until everything is turned off.


Name: GH-R.jpg Views: 684 Size: 148.5 KB

Signalling Pathways through which GH regulates gene transcription

STATs

GH activatesJAK2 through the process described above and ends up phosphorylating at least four members of the signal transducers and activators of transcription (STAT) family. After phophorylation they undock and form dimers in cytoplasm, localize in the nuclear, where they initiate DNA binding and activation of transcription5. Targeted disruption of the Stat5a and Stat5b genes in mice produces defects in liver gene expression and body growth, consistent with an important role of these STATs in GH action6,7.

ERk/MAPk

A second pathway that is important for GH regulation of gene transcription is the Ras–MAP (mitogen-activated protein) kinase pathway. GH activates this pathway through JAK2 phosphorylation of the protein SHC.
[Note: LARGE DISCUSSION to Follow]

IRS PI 3′-kinase

GH stimulates phosphorylation of the insulin receptor substrates 1, 2 and 3 (IRS-1, -2 and -3). Tyrosine phosphorylation of IRS proteins by JAK2 provides a binding site for the SH2 domain of the regulatory subunit of phosphatidylinositol (PI) 3'-kinase 8. Although PI 3'-kinase is required for insulin-stimulated glucose transport, GH-induced glucose transport has been reported not to require PI 3'-kinase9. However, inhibition of PI 3'-kinase blocks GH-stimulated lipid synthesis10 and the anti-lipolytic action of GH 11, suggesting that PI 3'-kinase activity is important for the insulin-like action of GH.

Chronically elevated GH is anti-insulin-like, promoting insulin resistance and diabetes. GH is thought to have this effect at least in part by interfering with the ability of insulin to stimulate carbohydrate metabolism. How? Decreased insulin receptor, IRS-1 and IRS-2 tyrosyl phosphorylation in response to insulin have been reported in rodent models of chronic GH excess[sup12,13[/sup[/sup]

In contrast, GH excess can lead to chronic activation of the IRS.PI 3'-kinase pathway in liver, reducing the degree of insulin-induced activation14.

In addition, GH inhibits the expression of the gene encoding glucose transporter 1 (GLUT1)15.

Name: GH-R2.jpg Views: 696 Size: 197.1 KB

Signaling pathways involved in GH stimulation of protein synthesis

GH stimulates the activity of p70 S6 kinase, an enzyme regulates translational activity

[Note: Further examination]




References:

1 - MacKenzie, S.J.(1998) Stimulation of p70S6 kinase via a growth hormone-controlled phosphatidylinositol 3-kinase pathway leads to the activation of a PDE4A cyclic AMPspecific phosphodiesterase in 3T3-F442A preadipocytes. Proc. Natl. Acad. Sci. U. S. A. 95, 3549–3554

2 - Yip, R.G. (1999) Growth hormone and dexamethasone stimulate lipolysis and activate adenylyl cyclase in rat adipocytes by selectively shifting Giá2 to lower density membrane fractions. Endocrinology 140, 1219–1227

3 - Fain, J.N.(1999) Stimulation of lipolysis but not of leptin release by growth hormone is abolished in adipose tissue from Stat5a and b knockout mice. Biochem. Biophys. Res. Commun. 263, 201–205

4 - Haddad F. (2002), Exercise Effects on Muscle Insulin Signaling and Action Selected Contribution: Acute cellular and molecular responses to resistance exercise, J Appl Physiol 93: 394–403

5 - Herrington, J. (2000) The role of STAT proteins in growth hormone signaling, Oncogene 19, 2585–2597

6 - Udy, G.B. (1997) Requirement of STAT5b for sexual dimorphism of body growth rates and liver gene expression, Proc. Natl. Acad. Sci. U. S. A. 94, 7239–7244

7 - Teglund, S. (1998) Stat5a and Stat5b proteins have essential and nonessential, or redundant, roles in cytokine responses, Cell 93, 841–850

8 - Smit, L.S. (1999) Molecular events in growth hormone–receptor interaction and signaling. In Handbook of Physiology (Vol. V) (Kostyo, J.L., ed.), pp. 445–480, Oxford University Press

9 - Sakaue, H. (1997) Phosphoinositide 3-kinase is required for insulin-induced but not for growth hormone- or hyperosmolarity-induced glucose uptake in 3T3-L1 adipocytes, Mol. Endocrinol. 11, 1552–1562

10 - Ridderstrale, M. (1994) PI-3-kinase inhibitor wortmannin blocks the insulinlike effects of growth hormone in isolated rat adipocytes, Biochem. Biophys. Res. Commun. 203, 306–310

11 - Yamauchi, T. (1998) Growth hormone and prolactin stimulate tyrosine phosphorylation of insulin receptor substrate-1, -2, and -3, their association with p85 phosphatidylinositol 3-kinase (P13-kinase), and concomitantly P13-kinase activation via JAK2 kinase, J. Biol. Chem. 273, 15719–15726

12 - Smith, T.R. (1997), Growth hormone-induced insulin resistance: role of the insulin receptor, IRS-1, GLUT-1, and GLUT-4, Am. J. Physiol. 272, E1071–E1079

13 - Dominici, F.P. (1999), Alterations in the early steps of the insulin-signaling system in skeletal muscle of GH-transgenic mice, Am. J. Physiol. 277, E447–E454

14 - Dominici, F.P. (1999), Loss of sensitivity to insulin at early events of the insulin signaling pathway in the liver of growth hormonetransgenic mice, J. Endocrinol. 161, 383–392

15 - Tai, P-K.K. (1990), Differential regulation of two glucose transporters by chronic growth hormone treatment of cultured 3T3-F442A adipose cells, J. Biol. Chem. 265, 21828–21834

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metanis
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#43 2012-09-09 22:55

Re: Peptidai lietuviskai

Cia radau azuolynobicas raso, kad ghrp reiktu saudytis 3 kartus per diena? o rolkos linke radau, kad pataria tik 1 karta per diena leistis ant tuscio skrandzio, ir 3 valandas pries leidimasi nevalgyti riebaus maisto, ir 2h iki leidimo angliu nevalgyti. Tai visdelto 1 ar 3 kartus reikia leistis ?
Ir ghrp-2, ghrp-6 ir Ipamorelin yra kaip ir vienas ir tas pats, atliekantis ta pacia funkcija?
ghrp-2 turetu eit kartu su cjc1295 kad butu didziausias efektas, kokius +/- pastebejot vartojant toki derini?

Paskutinį kartą taisė metanis (2012-09-09 23:08)

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MAZIUKAS
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#44 2012-09-10 00:24

Re: Peptidai lietuviskai

Nezmoniskas alkis,tai nezinau ar cia + ar -:)Spresk pats!

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rolka78
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#45 2012-09-10 08:45

Re: Peptidai lietuviskai

metanis rašė:

Cia radau azuolynobicas raso, kad ghrp reiktu saudytis 3 kartus per diena? o rolkos linke radau, kad pataria tik 1 karta per diena leistis ant tuscio skrandzio, ir 3 valandas pries leidimasi nevalgyti riebaus maisto, ir 2h iki leidimo angliu nevalgyti. Tai visdelto 1 ar 3 kartus reikia leistis ?
Ir ghrp-2, ghrp-6 ir Ipamorelin yra kaip ir vienas ir tas pats, atliekantis ta pacia funkcija?
ghrp-2 turetu eit kartu su cjc1295 kad butu didziausias efektas, kokius +/- pastebejot vartojant toki derini?

Jaigu pradedantysis,tai 1 kart sauni.Kai prasuksi kursa su peptidais,tada didini doze iki 2 kartu,paskui iki 3 kartu per diena.
Ten tam link jug raso,atydziau paskaityk smile

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metanis
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#46 2012-09-10 10:19

Re: Peptidai lietuviskai

MAZIUKAS rašė:

Nezmoniskas alkis,tai nezinau ar cia + ar -:)Spresk pats!

Man tai cia pliusas. Bet nejaugi tik del to ir vartojamas sis derinys butu.

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Staffordshire
Get big or die trying
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#47 2012-09-10 11:06

Re: Peptidai lietuviskai

as kiek skaitinejau tai atrodo kad toki cjc galima leisti kasdien arba reciau (priklausomai nuo dozes) o ghrp kada suleidi tada jis tik isskiria hormona tai cia nuo taves pacio priklauso kiek nori tiek leidi,tik leidimai turi buti bent jau kas 3val, del to ir iseina iki 3 suviu per diena. 30min pries maista. beja dar buvo straipsnis kazkur kur pvz jei 30min pries kardio suleisi tai daugiau riebalas degs,jei po sales suleisi tai raumuo biski geriau augs.

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rolka78
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#48 2012-09-10 12:09

Re: Peptidai lietuviskai

As kiek skaiciau tai cjc sauna nuo 1 iki 3 kart per diena po 100mg.Cjc dac karta i savaite vieni 1000mg kiti 2000mg.O ghrp tai irgi pradeda nuo 1 ir iki 3 suviu po 200mg/ed.

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GediminasJ
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#49 2012-09-10 13:23

Re: Peptidai lietuviskai

Kas lt stumdo peptidus? Kokios kainos +-?

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MAZIUKAS
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#50 2012-09-10 14:59

Re: Peptidai lietuviskai

rolka78 rašė:

As kiek skaiciau tai cjc sauna nuo 1 iki 3 kart per diena po 100mg.Cjc dac karta i savaite vieni 1000mg kiti 2000mg.O ghrp tai irgi pradeda nuo 1 ir iki 3 suviu po 200mg/ed.

Rolka ne 100mg,o 100mcg.As suprantu,kad sunku persikvalifikuoti nuo mg prie mcg:D

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