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Supplements and Scientific Studies

dieselbuilder

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to all you guys out there who know your shit (which I know there are a lot of) could anyone spare a minute and pull up any scientific studies that you have done or found for the following ( I am not asking you to research for me, just share research you have bookmarked or saved):

Proven studies that show that as little as 2-3 ius of HGH per day or even every other 3rd day actually increases collagen synthesis....

Whether GABA can actually pass the blood barrier and get to the brain to ensure it helps HGH release....

Whether glutamine actually works for recovery

Whether Beta Alanine works for endurance

Whether taking L-Arginine actually helps raise hgh levels

Thanks and I completely appreciate all the help I can get!
 
Last edited:

gelatine

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What you need is a PhD for yourself and graduate students competing for grants you control. Without that, doing your research for you just isn't as compelling an option.

I will however give you the following hearsay and opinion:

L-Arginine, glutamine - no go
beta alanine - makes my lips tingle, seems to work
GABA - I get some in my trueprotein herbal sleep stuff that gives me some noticeably deeper sleep. probably doesn't hurt, dunno about GH release.
 

dieselbuilder

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What you need is a PhD for yourself and graduate students competing for grants you control. Without that, doing your research for you just isn't as compelling an option.
Yea, well, this is a different situation. Plenty of members already have great studies saved on their computers and all I was asking was for some help. Believe me, I have researched.

And thanks for the heresay, but thats exactly what I dont need, cuase the only reason I use those supplements is mostly heresay, and thats exactly the problem.

Thanks anyway though
 

SacToSD

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to all you guys out there who know your shit (which I know there are a lot of) could anyone spare a minute and pull up any scientific studies that you have done or found for the following ( I am not asking you to research for me, just share research you have bookmarked or saved):

Proven studies that show that as little as 2-3 ius of HGH per day or even every other 3rd day actually increases collagen synthesis....

Whether GABA can actually pass the blood barrier and get to the brain to ensure it helps HGH release....

Whether glutamine actually works for recovery

Whether Beta Alanine works for endurance

Whether taking L-Arginine actually helps raise hgh levels

Thanks and I completely appreciate all the help I can get!
Dude you should've put "ATTN: DatBeTrue" in your title. He's bound to pop up somewhere on this thread, if he hasn't already. I don't know how he does it, but I've seen him pull up studies on just about everything. I've even seen him pull obscure articles from the 80's translated from Swedish, before. Sometimes I wonder if Dat is human, or not.
 

dieselbuilder

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Dude you should've put "ATTN: DatBeTrue" in your title. He's bound to pop up somewhere on this thread, if he hasn't already. I don't know how he does it, but I've seen him pull up studies on just about everything. I've even seen him pull obscure articles from the 80's translated from Swedish, before. Sometimes I wonder if Dat is human, or not.
Yea I actually thought about doing that! hopefully he shows up cause I know he has great studies!
 

anhuka

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maybe i can add any study that proves that L-carnitine burns fat inject or oral, and if the oral suprasses the stomatch
 

DatBtrue

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GH = collagen synthesis

Proven studies that show that as little as 2-3 ius of HGH per day or even every other 3rd day actually increases collagen synthesis....


Growth Hormone (GH) Effects on Bone and Collagen Turnover in Healthy Adults and Its Potential as a Marker of GH Abuse in Sports: A Double Blind, Placebo-Controlled Study, The Journal of Clinical Endocrinology & Metabolism Vol. 85, No. 4 1505-1512 2000

The effects of GH on bone remodeling in healthy adults have not been systematically investigated....The aim of this study was to evaluate the effects of GH administration on biochemical markers of bone and collagen turnover in healthy volunteers. Ninety-nine healthy volunteers of both sexes were enrolled in a multicenter, randomized, double blind, placebo-controlled study and assigned to receive either placebo (40 subjects) or recombinant human GH (0.1 IU/kg·day in 29 subjects and 0.2 IU/kg·day in 30 subjects). The treatment duration was 28 days, followed by a 56-day wash-out period. The biochemical markers evaluated were the bone formation markers osteocalcin and C-terminal propeptide of type I procollagen, the resorption marker type I collagen telopeptide, and the soft tissue marker procollagen type III.

All variables increased on days 21 and 28 in the two active treatment groups vs. levels in both the baseline (P < 0.01) and placebo (P < 0.01) groups. The increment was more pronounced in the 0.2 IU/kg·day group and remained significant on day 84 for procollagen type III (from 0.53 ± 0.13 to 0.61 ± 0.14 kU/L; P < 0.02) and osteocalcin (from 12.2 ± 2.9 to 14.6 ± 3.6 UG/L; P < 0.02), whereas levels of C-terminal propeptide of type I procollagen and type I collagen telopeptide declined after day 42 and were no longer significantly above baseline on day 84 (from 3.9 ± 1.2 to 5.1 ± 1.5 µg/L and from 174 ± 60 to 173 ± 53 µg/L, respectively). Gender-related differences were observed in the study; females were less responsive than males to GH administration with respect to procollagen type III and type I collagen telopeptide (P < 0.001).

In conclusion, exogenous GH administration affects the biochemical parameters of bone and collagen turnover in a dose- and gender-dependent manner. As GH-induced modifications of most markers, in particular procollagen type III and osteocalcin, persist after GH withdrawal, they may be suitable markers for detecting GH abuse.

SEE ALSO:

Stimulation of Collagen Synthesis and Linear Growth by Growth Hormone in Glucocorticoid-Treated Children, David B. Allen MD, PEDIATRICS Vol. 89 No. 3 March 1992, pp. 416-421

Treatment of Glucocorticoid-Induced Growth Suppression with Growth Hormone, David B. Allen, The Journal of Clinical Endocrinology & Metabolism Vol. 83, No. 8 2824-2829

Dose-dependent effects of recombinant human growth hormone on biochemical markers of bone and collagen metabolism in adult growth hormone deficiency, Jens Bollerslev, European Journal of Endocrinology, Vol 135, Issue 6, 666-671 1996​
 

DatBtrue

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GABA & GH release

Whether GABA can actually pass the blood barrier and get to the brain to ensure it helps HGH release....

From: Neuroendocrine Control of Growth Hormone Secretion, Eugenio E. Muller, Physiological Reviews Vol. 79, No. 2, April 1999

These and other findings led to the proposition that GABA and its analogs only affect the PeV brain areas, including the somatostatin elements, when injected centrally, without impinging on more distant brain structures in which the GHRH-secreting neurons are located (see sect. IIIA2). These areas, which have no effective BBB, can be reached by drugs such as systemically injected GABA and its analogs or antagonists, which normally do not cross the BBB.

Biphasic behavior of GABA

The actual role of GABA on GH secretion has been a source of considerable controversy, and both stimulatory and inhibitory influences have been reported.​

Datbtrue Originally Posted elsewhere (Reprise):

Slow Wave Sleep (SWS) enhancers

SWS & GH release

There are two types of sleep, rapid eye movement (REM) and non-rapid eye movement (NREM). Sleep proceeds in cycles composed of four types of stages of NREM and a stage of REM usually ordered as: 1 > 2 > 3 > 4 > 3 > 2 > REM

The cycle lasts on average 90 to 110 minutes, with a greater quantity of stages 3 and 4 experienced early in the night and more REM later in the night.

NREM accounts for 75–80% of total sleep time. Non-REM is comprised of four stages; stages 1 and 2 are considered 'light sleep', and 3 and 4 'deep sleep' or slow-wave sleep (SWS).

It has been shown that sleep, more specifically slow-wave sleep (SWS), does affect growth hormone levels in adult men. During eight hours sleep, it has been demonstrated in several studies that the men with a high percentage of SWS (average 24%) also had high growth hormone secretion, while subjects with a low percentage of SWS (average 9%) had low growth hormone secretion.

In one very complete study referenced by several others, it was demonstrated that “GH secretory rates and peripheral GH concentrations were maximally correlated with sleep stage, with lags of 4.5 and 16 min, respectively, suggesting that maximal GH release occurs within minutes of the onset of stage 3 or 4 sleep”.

Furthermore “sleep-related augmentation of GH secretion… usually occurs around midnight and the GH levels at that time are, as a rule, at their highest during the 24-hour period. Partially, this phenomenon is time-entrained and partially related to sleep itself. It is associated with a slow wave sleep, and the maximal GH levels occur within minutes of the onset of slow wave sleep” -Holl RW, Hartman ML, Veldhuis JD, et al. Thirty-second sampling of plasma growth hormone in man: correlation with sleep stages. J Clin Endocrinol Metab 1991;72:854–61.


The origin of nocturnal GH release in humans is still unknown. Most likely hypothalamic GHRH release is a major contributing component, but an additional role of another factor, presumably augmenting GHRH responsiveness of the somatotrophs, is likely. However the precise explanatory mechanisms are still not fully identified.

It is worth reiterating though that nocturnal release of GH makes up only a fraction of the total daily GH release in women, but the bulk of GH output in men.

Gaba & its derivatives

Gamma-amino butyric acid (GABA) is an amino acid and the chief inhibitory neurotransmitter in the central nervous system and the retinas of humans, which regulates muscle tone and other functions. It is also chiefly an excitatory neurotransmitter in most species.

GABA taken orally has been purported to increase the amount of the Human Growth Hormone. One such study demonstrated that gram amounts “induced clear-cut GH increments in plasma with a peak after 60–90 minutes”. The results of those studies have been seldom replicated, and have recently been in question since it is unknown whether GABA can pass the blood-brain barrier. However GABA derivitives when taken in injected form have been shown to both pass the blood-brain barrier and have a pronounced GH secretory effect.

At various times & in various studies GABA has been found to both inhibit GH release and exacerbate it. This contradiction is explained as… “inhibition of the GH release stimulated by GABA and its ability to raise baseline GH share the same basic mechanism, i.e., an action through dopaminergic (DA) neurons. Continuous stimulation of central nervous system (CNS-DA) receptors by GABA mimetics through DA release would ultimately lead to a state of partial refractoriness to DA-mediated events…”

The key then appears to be the avoidance of continuous stimulation of the central nervous system.

Two derivatives of GABA, gamma-amino-beta-hydroxy butyric acid (GABOB) and gamma- hydroxy butyric acid (GHB) have been shown to increase GH secretion as well.

PGH (aka Tyric-6)

PGH (Tyric-6) is a gaba-derivative injectable growth hormone stimulate that simply contains:

GABA - a neurotransmitter with a stabilizing role in the brain that has a calming effect. GABA also under certain circumstances increases levels of human growth hormone; and

GABOB - This has been used in the treatment of epilepsy, but it is a legal molecule that is very similar to GHB (a now illegal molecule) without GHBs negative effects; and

Magnesium amino-bromohydrate - An essential mineral which enhances the effect of GABA & GABOB.

The key to understanding why pGH (Tyric-6) is an effective GH releaser is recognizing that GHB (and presumably GABOB as well as GABA in certain circumstances) enhances both slow wave sleep and GH release. - Van Cauter E, Plat L, Scharf MB, et al. Simultaneous stimulation of slow-wave sleep and growth hormone secretion by gamma-hydroxybutyrate in normal young men. J Clin Invest 1997;100:745–53.

While GHB is illegal and not a component of PGH, its similarly structured brother GABOB has been shown to enhance slow wave sleep as well as increase GH. “Significant increases of prolactin and GH plasma levels were observed after injection with 100 mg GABOB”. - Gamma-amino-beta-hydroxy butyric acid stimulates prolactin and growth hormone release in normal women, P Fioretti,… Journal of Clinical Endocrinology & Metabolism, Vol 47, 1336-1340

In another study an intrathecal injection of 300 mg of L-GABOB to cerebrovascular patients caused significant increases in plasma GH, prolactin and cortisol levels at 60 min after injection. These results indicate that GABOB may elicit the secretion of GH, prolactin and ACTH via the central nervous system. - Stimulatory Effects of Gamma-Aminohydroxybutyric Acid (GABOB) on Growth Hormone, Prolactin and Cortisol Release in Man, J. Takahara…


Although the data is sparse and GABA studies as they relate to GH release no longer occur it appears that injectable forms of GABA & its derivatives enhance SWS (slow wave sleep) which is the time period GH is secreted. Since the majority of GH release is secreted in the first early round of SWS it seems that administration of PGH (GABA & GABOB) by injection just prior to sleep will enhance restful sleep and increase the GH secretory pulse.

Over the last few years anectdotal feedback from users including myself report both of these occurances. A protocol involving taken periodic breaks from use appears to be sufficient to promote continued effectiveness.

PGH is a simple, safe and effective compound whose ingredients may be purchased easily over the counter. GABA is sold in most supplement stores, while GABOB is harder to source but is available with international sourcing likely being less expensive.

Of course pGH is available from some research chemical facilities and if purchased already assembled need only be reconstituted in Bacteriastatic Water prior to use.
 

DatBtrue

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Glutamine & recovery

Whether glutamine actually works for recovery


Effect of oral glutamine on whole body carbohydrate storage during recovery from exhaustive exercise, J. L. Bowtell, Appl Physiol 86: 1770-1777, 1999

Full study (worth reading): http://jap.physiology.org/cgi/content/full/86/6/1770

ABSTRACT:

The purpose of this study was to determine the efficacy of glutamine in promoting whole body carbohydrate storage and muscle glycogen resynthesis during recovery from exhaustive exercise. Postabsorptive subjects completed a glycogen-depleting exercise protocol, then consumed 330 ml of one of three drinks, 18.5% (wt/vol) glucose polymer solution, 8 g glutamine in 330 ml glucose polymer solution, or 8 g glutamine in 330 ml placebo, and also received a primed constant infusion of [1-13C]glucose for 2 h. Plasma glutamine concentration was increased after consumption of the glutamine drinks (0.7-1.1 mM, P < 0.05). In the second hour of recovery, whole body nonoxidative glucose disposal was increased by 25% after consumption of glutamine in addition to the glucose polymer (4.48 ± 0.61 vs. 3.59 ± 0.18 mmol/kg, P < 0.05). Oral glutamine alone promoted storage of muscle glycogen to an extent similar to oral glucose polymer. Ingestion of glutamine and glucose polymer together promoted the storage of carbohydrate outside of skeletal muscle, the most feasible site being the liver.

CONCLUSION:

In conclusion, ingestion of glutamine alone appeared to promote muscle glycogen resynthesis during recovery from exhaustive exercise, relative to that expected from studies in which no substrate was provided. The promotion of muscle glycogen synthesis by consumption of glucose polymer and of glutamine was not additive. However, the addition of glutamine to the glucose polymer drink resulted in a greater storage of carbohydrate in sites other than skeletal muscle, the most likely candidate being the liver.
 

DatBtrue

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Beta Alanine & endurance

Whether Beta Alanine works for endurance.

Beta-Alanine supplementation augments muscle carnosine content and attenuates fatigue during repeated isokinetic contraction bouts in trained sprinters, Wim Derave, J Appl Physiol 103: 1736-1743, 2007

ABSTRACT:

Carnosine (ß-alanyl-L-histidine) is present in high concentrations in human skeletal muscle. The ingestion of ß-alanine, the rate-limiting precursor of carnosine, has been shown to elevate the muscle carnosine content. We aimed to investigate, using proton magnetic resonance spectroscopy (proton MRS), whether oral supplementation with ß-alanine during 4 wk would elevate the calf muscle carnosine content and affect exercise performance in 400-m sprint-trained competitive athletes. Fifteen male athletes participated in a placebo-controlled, double-blind study and were supplemented orally for 4 wk with either 4.8 g/day ß-alanine or placebo. Muscle carnosine concentration was quantified in soleus and gastrocnemius by proton MRS. Performance was evaluated by isokinetic testing during five bouts of 30 maximal voluntary knee extensions, by endurance during isometric contraction at 45% maximal voluntary contraction, and by the indoor 400-m running time. ß-Alanine supplementation significantly increased the carnosine content in both the soleus (+47%) and gastrocnemius (+37%). In placebo, carnosine remained stable in soleus, while a small and significant increase of +16% occurred in gastrocnemius. Dynamic knee extension torque during the fourth and fifth bout was significantly improved with ß-alanine but not with placebo. Isometric endurance and 400-m race time were not affected by treatment. In conclusion, 1) proton MRS can be used to noninvasively quantify human muscle carnosine content; 2) muscle carnosine is increased by oral Beta-alanine supplementation in sprint-trained athletes; 3) carnosine loading slightly but significantly attenuated fatigue in repeated bouts of exhaustive dynamic contractions; and 4) the increase in muscle carnosine did not improve isometric endurance or 400-m race time.
 

DatBtrue

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Arginine & GH

Whether taking L-Arginine actually helps raise hgh levels

Stuff originally posted by me in a thread on another board.

xxxx said:
I do both at the same time(ghrp-6/pGH), as far as oral gaba...I LOVE it and will always use it prior to sleep. My next experiment is inject arginine with the 2.....(ghrp-6/pgh)
xxxx you'll find this study very interesting on a lot of levels...not just its findings on Arginine but it also touches on many interesting things (by-the-way it studied both young & old)....

Arginine and Growth Hormone-Releasing Hormone Restore the Blunted Growth Hormone-Releasing Activity of Hexarelin in Elderly Subjects, E Arvat, Journal of Clinical Endocrinology & Metabolism, Vol 79, 1440-1443 1994​

Here is the "Discussion" section of the study:

This study demonstrates that, like GHRP-6 (28, 29), hexarelin has an age-related GH-releasing activity. However, although the stimulating effect of the maximally effective dose of hexarelin on somatotrope secretion is reduced in human aging, it releases more GH than the supramaximal effective dose of GHRH even in elderly subjects. Our results also indicate that the combined administration of hexarelin and GHRH has a synergistic effect in elderly subjects, as previously reported in young subjects (30).

This study also shows that in human aging, the GH releasable pool is markedly larger than previously thought. This observation is supported by previous animal (6) and human (3, 4) studies. In addition, our results indicate that hexarelin, like other GHRPs, has a different mechanism of action from that of GHRH in stimulating somatotrope secretion. GHRPs and GHRH have different receptor sites on the pituitary (16, 17, 18), and GHRP receptor activation does not increase intracellular CAMP levels, contrary to GHRH (19). The GH-releasing activity of GHRPs and their synergistic effect with GHRH are greater in viva than in vitro (17, 20), thus suggesting that GHRPs also act at the hypothalamic level, where specific receptors have been identified (21). Normal GHRH activity is needed before GHRPs can exert their GH- releasing effect (20, 31). Therefore, the reduced activity of hexarelin, either alone or combined with GHRH in human aging, may be explained by a decrease in the activity of GHRH-secreting neurons or by changes in GHRH receptors, as shown by other studies conducted in animals (7, 11, 32) and man (5, 33).

We found that arginine, an amino acid that probably acts by suppressing endogenous somatostatin release (9, lo), counteracts the age-related decrease in the GH-releasing effect of hexarelin in elderly subjects. Both animal (6, 8) and human (3, 4) studies suggest that there is a pronounced somatostatinergic hyperactivity in human aging. This could explain the age-related decline in both spontaneous and stimulated GH secretion and the effectiveness of arginine in restoring the response to hexarelin in the elderly. Arginine’s failure to increase the GH response to hexarelin in young subjects, however, remains to be clarified. It may be that GHRPs act at the pituitary level by antagonizing the effect of somatostatin. In fact, GHRPs counteract the hyperpolarizing effect of somatostatin on rat somatotrope cell membrane (18). In man, the GH-releasing effect of hexarelin is blunted, but not abolished, by a high dose of exogenous somatostatin (30), which abolishes the somatotrope response to all known GH secretagogues, including GHRH (30, 34). Thus, it could be hypothesized that hexarelin’s antagonism of somatostatin at the pituitary level is partially overridden in aging by a pronounced hypothalamic somatostatinergic activity.

In conclusion, this study shows that the maximally effective dose of hexarelin releases more GH than the maximally effective dose of GHRH in both normal young and elderly subjects. The effect of hexarelin on GH secretion is age dependent, and the GH response to the combined administration of the two drugs was significantly higher in young subjects compared to elderly subjects. Arginine does not potentiate the GH response to hexarelin in young subjects, whereas it significantly enhances it in elderly subjects. These findings suggest that hexarelin acts, at least partially, independently from GHRH and/or somatostatin. These results also support the presence of a somatostatinergic hyperactivity in aging, which is probably related to a concomitant reduction in the activity of GHRH-secreting neurons.

---

Here's another interesting study Arginine Counteracts the Inhibitory Effect of Recombinant Human Insulin-Like Growth Factor I on the Somatotroph Responsiveness to Growth Hormone-Releasing Hormone in Humans, Laura Gianotti, The Journal of Clinical Endocrinology & Metabolism Vol. 85, No. 10 3604-3608 2000

Cutting to the meat of the study "...In agreement with other studies (6, 14), the GH response to the maximal effective dose of GHRH was significantly inhibited by rhIGF-I. By contrast, no inhibitory effect of rhIGF-I on the somatotroph responsiveness to GHRH was recorded when the neurohormone was administered in combination with ARG, which strikingly potentiated its GH-releasing effect."

In conclusion "...In conclusion, this study shows that ARG overrides the inhibitory effect of rhIGF-I on somatotroph responsiveness to GHRH in humans. These findings indicate that the acute inhibitory effect of acute rhIGF-I administration on somatotroph secretion takes place on the hypothalamus, where concomitant triggering of SS release and inhibition of GHRH-secreting neurons might play a major role."​

---
Post on the oral bioavailability of L-Arginine. The important part is highlighted in dark red.

xxxx said:
...I would go with AAKG or A Ethyl Ester since straight L-Arginine is not as bioavailable orally....
Good, better, best ...is it really THAT important? I don't know...

L-arginine-induced vasodilation in healthy humans: pharmacokinetic-pharmacodynamic relationship, Bode-Böger,, British Journal of Clinical Pharmacology, Volume 46, Number 5, November 1998 , pp. 489-497(9)

Abstract:

Aims Administration of l-arginine by intravenous infusion or via oral absorption has been shown to induce peripheral vasodilation in humans, and to improve endothelium-dependent vasodilation. We investigated the pharmacokinetics and pharmacokinetic-pharmacodynamic relationship of l-arginine after a single intravenous infusion of 30 g or 6 g, or after a single oral application of 6 g, as compared with the respective placebo, in eight healthy male human subjects.

Methods l-arginine levels were determined by h.p.l.c. The vasodilator effects of l-arginine were assessed non-invasively by blood pressure monitoring and impedance cardiography. Urinary nitrate and cyclic GMP excretion rates were measured as non-invasive indicators of endogenous NO production.

Results Plasma l-arginine levels increased to (mean±s.e.mean) 6223±407 (range, 5100-7680) and 822±59 (527-955) μmol l−1 after intravenous infusion of 30 g and 6 g l-arginine, respectively, and to 310±152 (118-1219) μmol l−1 after oral ingestion of 6 g l-arginine. Oral bioavailability of l-arginine was 68±9 (51-87)%. Clearance was 544±24 (440-620), 894±164 (470-1190), and 1018±230 (710-2130) ml min−1, and elimination half-life was calculated as 41.6±2.3 (34-55), 59.6±9.1 (24-98), and 79.5±9.3 (50-121) min, respectively, for 30 g i.v., 6 g i.v., and 6 g p.o. of l-arginine. Blood pressure and total peripheral resistance were significantly decreased after intravenous infusion of 30 g l-arginine by 4.4±1.4% and 10.4±3.6%, respectively, but were not significantly changed after oral or intravenous administration of 6 g l-arginine. l-arginine (30 g) also significantly increased urinary nitrate and cyclic GMP excretion rates by 97±28 and 66±20%, respectively. After infusion of 6 g l-arginine, urinary nitrate excretion also significantly increased, (nitrate by 47±12% [P<0.05], cyclic GMP by 67±47% [P=ns]), although to a lesser and more variable extent than after 30 g of l-arginine. The onset and the duration of the vasodilator effect of l-arginine and its effects on endogenous NO production closely corresponded to the plasma concentration half-life of l-arginine, as indicated by an equilibration half-life of 6±2 (3.7-8.4) min between plasma concentration and effect in pharmacokinetic-pharmacodynamic analysis, and the lack of hysteresis in the plasma concentration-versus-effect plot.

Conclusions The vascular effects of l-arginine are closely correlated with its plasma concentrations. These data may provide a basis for the utilization of l-arginine in cardiovascular diseases.

----

So again how does Arginine potentiate GH?

The following reference to Arginine as a GH potentiator from a section of

Neuroendocrine Control of Growth Hormone Secretion, EUGENIO E. MULLER, VITTORIO LOCATELLI, AND DANIELA COCCHI, PHYSIOLOGICAL REVIEWS Vol. 79, No. 2, April 1999

Amino acids are a potent stimulus for GH secretion, either as selected nutrients or when included in a proteinrich meal (99, 283, 516). Parenteral administration of an amino acid solution raises GH secretion by acting on pulsatility and pulse amplitude, an effect presumably mediated by increased GHRH secretion (791).

Arginine is the most striking stimulant, although lysine, ornithine, tyrosine, glycine, and tryptophan are all effective GH releasers (564). An oral mixture of arginine and lysine evokes a sevenfold increase of plasma GH levels (516), and a similar effect is observed after arginine aspartate (99, 163). Arginine-induced GH secretion in humans is blocked by antagonists of a-adrenergic and cholinergic neurotransmission (153, 178), a carbohydrate-rich diet (710), hyperglycemia (711) and NEFA, anti-E2 (878). Estrogens enhance arginine-induced GH secretion in men or women (711).

The effect of arginine on GH secretion appears to be exerted through suppression of hypothalamic SS release, as suggested by neuropharmacological studies (22, 413, 414). Alternatively, the effect of arginine on GH and other pituitary hormones (56, 366) may depend on its conversion to NO, a gaseous neurotransmitter (734). Arginine is in fact a more effective GH releaser than muscarinic cholinergic agonists (414) which inhibit SS release (629). ...L-arginine is a potent GH secretagogue in humans (711); however, its effect does not appear to be linked to NO production...

REFERENCES:

22. ALBA-ROTH, J., A. O. MULLER, J. SCHOPOL, AND K. VON WERDER. Arginine: stimulates growth hormone secretion by suppressing endogenous somatostatin secretion. J. Clin. Endocrinol. Metab. 67: 1186–1189, 1988.

56. ASSAN, R., G. ROSSELIN, AND J. DOLAIS. Effects sur la glucagonemie des perfusions et ingestions d’acides amines. J. Ann. Diabetol. Hotel Dieu. Ed. Medicales 7: 25–41, 1967

99. BESSET, A., A. BONARDET, G. RAUDONIN, B. DESCOMPS, AND P. PASSNANT. Increase in sleep-related GH and Prl secretion after chronic arginine aspartate administration in man. Acta Endocrinol. 99: 18–23, 1982.

153. BUCKLER, J. H. M., A. M. BOLD, M. TABERNER, AND D. R. LONDON. Modification of hormonal responses to arginine by adrenergic blockade. Br. Med. J. 3: 153–154, 1969.

163. CAMPISTRON, G. Approache Pharmacologique de l’Arginine et de l’Acide Aspartique. Etude Pharmacocinetique e Pharmacodinamique (PhD thesis). Toulouse, France: Faculte` des Sciences Pharmacocinetique, 1980, no. 112.

178. CASANUEVA, F. F., L. VILLANUEVA, J. A. CABRANES, J. CABEZAS- CERRATO, AND A. FERNANDO-CRUZ. Cholinergic mediation of growth hormone secretion elicited by arginine, clonidine and physical exercise in man. J. Clin. Endocrinol. Metab. 59: 526–530, 1984.

283. DAUGHADAY, W. H. Growth hormone: normal synthesis, secretion, control and mechanisms of action. In: Endocrinology, edited by L. J. De Groot. Philadelphia, PA: Saunders, 1989, vol. 1, p. 318–329.

366. FLOYD, J. C., JR., S. S. FAJANS, J. W. CONN, R. F. KNOPF, AND J. A. RULL. Stimulation of insulin secretion by amino acids. J. Clin. Invest. 45: 1487–1502, 1966.

413. GHIGO, E., S. GOFFI, E. ARVAT, M. NICOLOSI, M. PROCOPIO, J. BELLONE, E. IMPERIALE, E. MAZZA, G. BARACCHI, AND F. CAMANNI. Pyridostigmine partially restores the GH responsiveness to GHRH in normal aging. Acta Endocrinol. 123: 169–174, 1990.

414. GHIGO, E., S. GOFFI, M. NICOLOSI, E. ARVAT, J. BELLONE, M. PROCOPIO, F. VALENTE, E. MAZZA, M. C. GHIGO, AND F. CAMANNI. Growth hormone responsiveness to combined administration of arginine and GH-releasing hormone does not vary with age in man. J. Clin. Endocrinol. Metab. 71: 1481–1485, 1990

564. KNOPF, R. F., J. W. CONN, S. S. FAJANS, J. A. RULL, E. M. GUNTSCHE, AND C. A. THIFFAULT. The normal endocrine response to ingestion of protein and infusion of amino acids. Sequential secretion of insulin and growth hormone. Trans. Assoc. Am. Phys. 79: 312–321, 1966.

516. ISIDORI, A., A. LOMONACO, AND M. CAPPA. A study of growth hormone release in man after oral administration of amino acids. Curr. Med. Res. Opin. 7: 475–481, 1981.

629. LOCATELLI, V., A. TORSELLO, M. REDAELLI, E. GHIGO, F. MASSARA, AND E. E. MU¨ LLER. Cholinergic agonist and antagonist drugs modulate the growth hormone response to growth hormone- releasing hormone in the rat: evidence for mediation by somatostatin. J. Endocrinol. 111: 271–278, 1986.

710. MERIMEE, T. J. Growth hormone: secretion and action. In: Endocrinology, edited by L. De Groot. New York: Grune & Stratton, 1980, p. 123–132.

711. MERIMEE, T. J., D. RABINOWITZ, AND S. E. FINEBERG. Arginine initiated release of human growth hormone: factors modifying the response in normal man. N. Engl. J. Med. 280: 1434–1438, 1969.

734. MONCADA, S., R. M. J. PALMER, AND E. A. HIGGS. Nitric oxide: physiology, pathophysiology and pharmacology. Pharmacol. Rev. 43: 109–142, 1991.

791. OKADA, K., H. SUGIHARA, S. MINAMI, AND I. WAKABAYASHI. Effect of parenteral administration of selected nutrients and central injection of g-globulin from antiserum to neuropeptide Y on growth hormone secretory pattern in food-deprived rats. Neuroendocrinology 57: 678–686, 1993.

878. REFETOFF, S., P. H. FRANK, C. ROUBEBUSH, AND L. J. DE GROOT. Evaluation of pituitary function. In: Endocrinology, edited by L. J. De Groot. New York: Grune & Stratton, 1979, p. 175–190.​

---

What is the lowest effective dose?

Low doses of either intravenously or orally administered arginine are able to enhance growth hormone response to growth hormone releasing hormone in elderly subjects, Ghigo E, Ceda J Endocrinol Invest. 1994 Feb;17(2):113-7

...

These results show that the GH response to GHRH in elderly subjects is enhanced even by low iv doses of arginine and by the orally administered amino acid, the lowest effective dose being 8 g. Moreover, they imply that the combined administration of GHRH and arginine may be a useful approach to restore the impaired function of the GH-IGF axis in aging.​

----

Eight (8) grams per day might end up being the lowest effective dose. From the following published in 1993 by THE ENDOCRINE SOCIETY in ENDOCRINE REVIEWS we see that six (6) grams even w/ Lysine wasn't effective.

Human Growth Hormone and Human Aging, EMILIANO CORPAS, S. MITCHELL HARMAN, AND MARC R. BLACKMAN

...
The acute GH response to an iv arginine infusion has been found to be similar in young and old men (139, 147, 148), while an arginine infusion potentiates GH responsivity to GHRH in old men (148). We have recently found that administration of an oral arginine/lysine preparation (6 g of each amino acid /day) for 2 weeks does not increase either spontaneous GH release (as assessed by overnight frequent sampling), plasma IGF-I levels, or GHRH-stimulated GH secretion in old men (148a).
...
NOTES:

148 - Ghigo C, Camanni F 1990 Growth hormone (GH) responsiveness to combined administration of arginine and GH-releasing hormone does not varv with ace in man. J Clin Endocrinol Metab 71: 1481-1485

148a - Corpas, E, Blackman MR. Roberson R. Scholfield DS, Harman SM, bra1 arginine-lysine does not increase growth hormone and insulin-like growth factor-I in old men. J. Gerontol, in press


.. so now we have established a baseline for L-Arginine at 8 grams per day. Now we can take into consideration what xxxx was pointing out about bioavailabiltiy in other forms of Arginine being greater than L-Arginine and use smaller amounts of those types if we want.
 
Last edited:

Chrysler

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Dude you should've put "ATTN: DatBeTrue" in your title. He's bound to pop up somewhere on this thread, if he hasn't already. I don't know how he does it, but I've seen him pull up studies on just about everything. I've even seen him pull obscure articles from the 80's translated from Swedish, before. Sometimes I wonder if Dat is human, or not.
ROFL!!!!!!!! You called it.
 

Phidias

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Thanks for taking the time to post those very informative studies, datbrue. :)

Anhuka, L-Carnitine is not supposed to burn fat, but rather to TRANSPORT it more efficiently into the mitonchondrias once released in the bloodstream (as a direct effect of diet, exercise and thermogenics). It's in the mitonchondrias that fat will be burnt... L-Carnitine just helps supplying those "burning cell" with more energy coming from the body fat other tools make you release from your adipocytes. And it's very efficient at doing the job (from experience, as I have no study to post... ;)).
 

dropshot001

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Newman

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Awesome thread!!! I just had to bump it again.

Does anyone here know whether PGH can be taken orally, or will the stomach & liver kill it?
 

dieselbuilder

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Awesome thread!!! I just had to bump it again.

Does anyone here know whether PGH can be taken orally, or will the stomach & liver kill it?
Yea, DatBrute is a frickin genius.
 

rollerghost

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Hi,

I'm new here and my mother language isn't english so sorry about possible mistakes.

I have a question about pyridostigmine and clonidine. Some studies I've read shows that they should work. I haven't got those studies in my hand now but have anyone here used those drugs and had some benefits from them? I suppose it is difficult to achieve anything noticeable from those kind of drugs because of the feedback systems etc. But at least they are cheap options.

Thanks!
 

The BB Monad

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DatBTrue - I mean this in a good way:

You are a FREAK of knowledge man!!!

Thanks for all your continuous posts and information - they really teach us all so much! :)
 

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