Augmatine

[AutoKal47]

Alpha y to the rescue!

I most def do not want to run something that could halt fat loss,
f@ck the pumps if that's the case

 

[Sourdough]

I had mentioned Alpha y cause its an Alpha 2 receptor antagonist.... so it will negate the effects of agmatine if such things are true... also would rely on assuming which has better availability, binding affinity etc etc.... I would honestly think that this isnt that huge of an issue...

 

[AutoKal47]

I had mentioned Alpha y cause its an Alpha 2 receptor antagonist.... so it will negate the effects of agmatine if such things are true... also would rely on assuming which has better availability, binding affinity etc etc.... I would honestly think that this isnt that huge of an issue...

Yeah it makes sense, altho' seems silly to take Alpha y to negate the side effects of something
that is not - in the end - a "necessary" sups ya know? Among all things then, fat loss, sh#t halt my penis before that lol

 

[T-Bone]

Yeah it makes sense, altho' seems silly to take Alpha y to negate the side effects of something
that is not - in the end - a "necessary" sups ya know? Among all things then, fat loss, sh#t halt my penis before that lol

Exactly. Just stop taking the Agmatine. If this study has actual validity to it. I'd like to someone with a science/chemistry background come in here and respond to the study posted or break it down for us non nerds.

 

[AutoKal47]

Exactly. Just stop taking the Agmatine. If this study has actual validity to it. I'd like to someone with a science/chemistry background come in here and respond to the study posted or break it down for us non nerds.

Oh I did already lol, as soon as ssbackwards posted that I was "eehh NO"

 

[Whacked]

WHOA

Say what?????

PLease explain T

Thanks

It doesn't cross the blood-brain barrier, so no "nootropic" type effect. However, it may help with vasolation(pumps) but may also halt fat loss. That is what I got from it anyway. Not sure if I'm interpreting it correctly.

 

[T-Bone]

WHOA

Say what?????

PLease explain T



Thanks

It was in the study that ssbackwards posted on post #96. I'm not sure if I'm interpreting the study correctly though. We need the dinnoi guy or whatever his name is to read that study and comment on it. Hopefully I'm wrong, but that is how I understood what I read.

 

[ssbackwards]

It was in the study that ssbackwards posted on post #96. I'm not sure if I'm interpreting the study correctly though. We need the dinnoi guy or whatever his name is to read that study and comment on it. Hopefully I'm wrong, but that is how I understood what I read.

from what i read you are more then correc.

NMDA antagonist (which subclass i dont know), but alpha AGONIST which would be fine if working one alpha ones (which beta agonist tend to stimulate). but its alpha 2s. which is bad for fat loss.

 

[ssbackwards]

"Agmatine also binds to α2-adrenergic receptors, and agonists of α2-adrenergic receptors have been known to inhibit opioid withdrawal. The activation of α2-adrenergic receptors by agonists like clonidine inhibits dependence and withdrawal. While agmatine was discovered because of its ability to bind to α2-adrenergic receptors,[SUP]1[/SUP] several subsequent functional studies reported that agmatine is not an agonist at this site"

Agmatine recognizes alpha 2-adrenoceptor binding sites but neither activates nor inhibits alpha 2-adrenoceptors. Naunyn Schmiedebergs Arch Pharmacol. 1995;351:10-16.

"agmatine, administered intracerebro-ventricular (i.c.v.) or IP, has not been shown to lower arterial pressure,[SUP]53-55[/SUP] thus ruling out the possibility of α2-adrenergic receptor activation in this action of agmatine."

Cardiovascular responses to agmatine, a clonidine-displacing substance, in anesthetized rat. Clin Exp Hypertens. 1995;17:115-128.
PubMed

54. Szabo B, Urban R, Limberger N, Starke K. Cardiovascular effects of agmatine, a “clonidine-displacing substance”, in conscious rabbits. Naunyn Schmiedebergs Arch Pharmacol. 1995;351:268-273.
PubMed DOI: 10.1007/BF00233246


55. Raasch W, Schafer U, Qadri F, Dominiak P. Agmatine, an endogenous ligand at imidazoline binding sites, does not antagonize the clonidine-mediated blood pressure reaction. Br J Pharmacol. 2002;135:663-672.


nothing wqas shown in human models in terms of it binding or not i dont believe. thing is i dont know how it recognizs it with out either activating it or not. could be partial antagonist which could cause issues with it halting fat loss, or partiol agonist which may increase fat loss

Partial meaning it acts like it somewhat therefore essentially blocking the action at the site (so with what i said above it act as oppisite, get it? meaning partial agonist is blocking the site there for overall effects are antagonizing or inhibition of binding.) but i havent seen that in any literature on it.

this study below (well abstract) is saying it can inhibit NA release (which means agonizes Aplha 2).

"Agmatine can regulate vascular function by two opposing actions at sympathetic nerve terminals, with different latencies: a transient inhibition of NA release mediated by prejunctional alpha 2-adrenoceptors and a cocaine-sensitive delayed facilitation the mechanism of which is undetermined at present. 8. The results reveal the existence of a novel endogenous amine modulating NA release in the perivascular sympathetic terminals."
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1915776/

 

[Whacked]

WOW. Had no clue. Good info. Thanks

 

[AutoKal47]

from what i read you are more then correc.

NMDA antagonist (which subclass i dont know), but alpha AGONIST which would be fine if working one alpha ones (which beta agonist tend to stimulate). but its alpha 2s. which is bad for fat loss.

Then agma stays supsended indeed

 

[Sourdough]

Then agma stays supsended indeed

Wait suspended as in not taking it?

I think you misinterpreted what he just posted n what I was basically just about to come into this thread to post...

Many things can attach to the different receptors in the body that don't exert any effect or cause the receptor or whatever it attaches to, not exert its effect, essentially bound/blocked.

A less direct correlation would be aromatase inhibitors and shbg inhibitors (even shbg itself), where something binds to another stopping it from exerting its effect or displacing something else from being bound allowing it to exert its effects elsewhere....

More directly this could be compared to a serm or something like atd where it can bind to the receptor and simply blocks the effects of normal agonists starving the cell of that simulation and exerting the desired effect...

So in plain english, agmatine can create fast loss by stopping alpha2 adrenergic agonists from binding to the sites and halting fat loss.... It would seemingly stack well with most beta agonists which create a negative feedback loop antagonizing alpha receptors and halting the productive fat loss...

This is of course only if the studies translate to humans and more importantly the doses we use in our applications....

Either way with all the other benefits health wise agmatine offers I wouldn't stop dosing especially when it obviously offers positive aesthetic benefits in real world applications.

 

[bigdavid]

I agree with sourdough real world results along with the many other health benefits of the compound should win in this case keep in mind this is one small study on rats. You might even start to stress from taking this compound because of this study which will increase your cortisol and make fat loss harder. So I suggest try not to stress over it lol.

 

[Sourdough]

Lol...here's a study actually showing its a receptor agonist... Not good ...(except this is in the case of seizures not fat loss)

Funny thing is it ALSO shows the use of yohimbe to completely negate its effects on the adrenoreceptor as per my suggestion of using alpha y :thumbsup:

http://www.ncbi.nlm.nih.gov/pubmed/21651904

(1-3):93-9. Epub 2011 Jun 1. Additive anticonvulsant effects of agmatine and lithium chloride on pentylenetetrazole-induced clonic seizure in mice: involvement of ??-adrenoceptor. Bahremand A, Ziai P, Payandemehr B, Rahimian R, Amouzegar A, Khezrian M, Montaser-Kouhsari L, Meibodi MA, Ebrahimi A, Ghasemi A, Ghasemi M, Dehpour AR. Tehran University of Medical Sciences, School of Medicine, Department of Pharmacology, Iran.

Abstract After 60 years, lithium is still the mainstay in the treatment of mood disorders and widely used in clinic. In addition to its mood stabilizer effects, lithium also shows some anticonvulsant properties. Similar to lithium, agmatine also plays a protective role in the CNS against seizures and has been reported to enhance the effect of different antiepileptic agents. Moreover, both agmatine and lithium have modulatory effects on ?(2)-adrenoceptors. So, we designed this study: 1) to investigate whether agmatine and lithium show an additive effect against clonic seizures induced by pentylenetetrazole; 2) to assess whether this additive effect is mediated through the ?(2)-adrenoceptor or not. In our study, acute administration of a single effective dose of lithium chloride (30 mg/kg, i.p.) increased the seizure threshold. Pre-treatment with low and, per se, non-effective doses of agmatine (1 and 3mg/kg) potentiated a sub-effective dose of lithium (10mg/kg). Interestingly, the anticonvulsant effects of these effective combinations of lithium and agmatine were prevented by pre-treatment with low and non-effective doses of yohimbine [?(2)-adrenoceptor antagonist] (0.1 and 0.5mg/kg). On the other hand, clonidine [?(2)-adrenoceptor agonist] augmented the anticonvulsant effect of a sub-effective combination of lithium (5mg/kg i.p.) and agmatine (1mg/kg) at relatively low doses (0.1 and 0.25mg/kg). In summary, our findings demonstrate that agmatine and lithium chloride exhibit additive anticonvulsant properties which seem to be mediated through ?(2)-adrenoceptor.

Copyright © 2011. Published by Elsevier B.V.

PMID: 21651904 [PubMed - indexed for MEDLINE]

 

[AutoKal47]

Understood, thank you a lot for breaking it down.
In the end tho' is a pretty new sup (to me) of which I know very lil
and I rather sticking to other proven stuff with not possible side effect,
especially on fat loss because, well, BF here is quite low and even lil changes
will show and I don't feel like running the risk, where for "risk" I mean dieting my
ass of this hard and at the same time taking something that MIGHT work against my
purpose.. and Alpha y as you say could easily be the solution, and yet, I don't have it
and it seems silly to get it for this, I already take a lot of stuff lol it gets expensive.

I'll leave the agmatine in its tub till some more study shows up, I don't really care
about the pumps (Pumpbol does the trick better than anything else i tried anyway)

 

[ssbackwards]

its not very cut and dry with agmatine yet.

It can be an agonist due to the effects yohimbine has for blocking its action on A2 adrenos. but still seems fairly new.

I never used it, and i wont until i know exactly what im dealing with. usually the case for most everything i take. including the fat burners. havent even toyed with DAA yet, or nitrates. Even the new AIs.

 

[AutoKal47]

its not very cut and dry with agmatine yet.

It can be an agonist due to the effects yohimbine has for blocking its action on A2 adrenos. but still seems fairly new.

I never used it, and i wont until i know exactly what im dealing with. usually the case for most everything i take. including the fat burners. havent even toyed with DAA yet, or nitrates. Even the new AIs.

I'm with you with this one bro, better be safe than sorry

 

[AutoKal47]

bump for the doc about the fat loss thing & agmatine

 

[T-Bone]

Hey guys I just got recent blood work which included fasting glucose. Before my usual fasting glucose was 112, that was consistent over several tests. This time that I happened to have been using agmatine for about 3 weeks straight, my fasting glucose was 82. I have lost a lot of fat since my last blood work, but still the change is impressive.

 

[Whacked]

congrats on the fat losss T-Bone!

The change in glucos levels could be as easily attributed to your fat loss and new/current insulin sensitivity levels (altered for the positive).

Hey guys I just got recent blood work which included fasting glucose. Before my usual fasting glucose was 112, that was consistent over several tests. This time that I happened to have been using agmatine for about 3 weeks straight, my fasting glucose was 82. I have lost a lot of fat since my last blood work, but still the change is impressive.

 

[Jahcuree]

congrats on the fat losss T-Bone!

The change in glucos levels could be as easily attributed to your fat loss and new/current insulin sensitivity levels (altered for the positive).

You slayin' the hype again bro??? just kidding

 

[Whacked]

haha lol

T-Bone is a hype-slayer too

 

[AutoKal47]

you think agmatine is responsible for that?

 

[dinoiii]

Can someone sum up what I missed since I last posted in this thread...this thing is probably the most posted-in misspelled thread in history? It's hard to look at it with the darned "u."

In any event, just give me the top 5 questions I have left unanswered...I simply don't have time to peruse it all with any degree of significance at this time, so this might help bring it back for me...

Thanks in advance,
D_

 

[AutoKal47]

Can someone sum up what I missed since I last posted in this thread...this thing is probably the most posted-in misspelled thread in history? It's hard to look at it with the darned "u."

In any event, just give me the top 5 questions I have left unanswered...I simply don't have time to peruse it all with any degree of significance at this time, so this might help bring it back for me...

Thanks in advance,
D_

Hey Doc,
the main concern here were some studies posted show Agmatine could potentially halt fat loss being an antagonist for NDMA receptor and agonist for alpha 2.
Would be nice to hear your take on this

here's the studies posted bty ssbackwards and Sourdough

"Agmatine also binds to α2-adrenergic receptors, and agonists of α2-adrenergic receptors have been known to inhibit opioid withdrawal. The activation of α2-adrenergic receptors by agonists like clonidine inhibits dependence and withdrawal. While agmatine was discovered because of its ability to bind to α2-adrenergic receptors,[SUP]1[/SUP] several subsequent functional studies reported that agmatine is not an agonist at this site"

Agmatine recognizes alpha 2-adrenoceptor binding sites but neither activates nor inhibits alpha 2-adrenoceptors. Naunyn Schmiedebergs Arch Pharmacol. 1995;351:10-16.

"agmatine, administered intracerebro-ventricular (i.c.v.) or IP, has not been shown to lower arterial pressure,[SUP]53-55[/SUP] thus ruling out the possibility of α2-adrenergic receptor activation in this action of agmatine."

Cardiovascular responses to agmatine, a clonidine-displacing substance, in anesthetized rat. Clin Exp Hypertens. 1995;17:115-128.
PubMed

54. Szabo B, Urban R, Limberger N, Starke K. Cardiovascular effects of agmatine, a “clonidine-displacing substance”, in conscious rabbits. Naunyn Schmiedebergs Arch Pharmacol. 1995;351:268-273.
PubMed DOI: 10.1007/BF00233246


55. Raasch W, Schafer U, Qadri F, Dominiak P. Agmatine, an endogenous ligand at imidazoline binding sites, does not antagonize the clonidine-mediated blood pressure reaction. Br J Pharmacol. 2002;135:663-672.


nothing wqas shown in human models in terms of it binding or not i dont believe. thing is i dont know how it recognizs it with out either activating it or not. could be partial antagonist which could cause issues with it halting fat loss, or partiol agonist which may increase fat loss

Partial meaning it acts like it somewhat therefore essentially blocking the action at the site (so with what i said above it act as oppisite, get it? meaning partial agonist is blocking the site there for overall effects are antagonizing or inhibition of binding.) but i havent seen that in any literature on it.

this study below (well abstract) is saying it can inhibit NA release (which means agonizes Aplha 2).

"Agmatine can regulate vascular function by two opposing actions at sympathetic nerve terminals, with different latencies: a transient inhibition of NA release mediated by prejunctional alpha 2-adrenoceptors and a cocaine-sensitive delayed facilitation the mechanism of which is undetermined at present. 8. The results reveal the existence of a novel endogenous amine modulating NA release in the perivascular sympathetic terminals."
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1915776/

Lol...here's a study actually showing its a receptor agonist... Not good ...(except this is in the case of seizures not fat loss)

Funny thing is it ALSO shows the use of yohimbe to completely negate its effects on the adrenoreceptor as per my suggestion of using alpha y :thumbsup:

http://www.ncbi.nlm.nih.gov/pubmed/21651904

(1-3):93-9. Epub 2011 Jun 1. Additive anticonvulsant effects of agmatine and lithium chloride on pentylenetetrazole-induced clonic seizure in mice: involvement of ??-adrenoceptor. Bahremand A, Ziai P, Payandemehr B, Rahimian R, Amouzegar A, Khezrian M, Montaser-Kouhsari L, Meibodi MA, Ebrahimi A, Ghasemi A, Ghasemi M, Dehpour AR. Tehran University of Medical Sciences, School of Medicine, Department of Pharmacology, Iran.

Abstract After 60 years, lithium is still the mainstay in the treatment of mood disorders and widely used in clinic. In addition to its mood stabilizer effects, lithium also shows some anticonvulsant properties. Similar to lithium, agmatine also plays a protective role in the CNS against seizures and has been reported to enhance the effect of different antiepileptic agents. Moreover, both agmatine and lithium have modulatory effects on ?(2)-adrenoceptors. So, we designed this study: 1) to investigate whether agmatine and lithium show an additive effect against clonic seizures induced by pentylenetetrazole; 2) to assess whether this additive effect is mediated through the ?(2)-adrenoceptor or not. In our study, acute administration of a single effective dose of lithium chloride (30 mg/kg, i.p.) increased the seizure threshold. Pre-treatment with low and, per se, non-effective doses of agmatine (1 and 3mg/kg) potentiated a sub-effective dose of lithium (10mg/kg). Interestingly, the anticonvulsant effects of these effective combinations of lithium and agmatine were prevented by pre-treatment with low and non-effective doses of yohimbine [?(2)-adrenoceptor antagonist] (0.1 and 0.5mg/kg). On the other hand, clonidine [?(2)-adrenoceptor agonist] augmented the anticonvulsant effect of a sub-effective combination of lithium (5mg/kg i.p.) and agmatine (1mg/kg) at relatively low doses (0.1 and 0.25mg/kg). In summary, our findings demonstrate that agmatine and lithium chloride exhibit additive anticonvulsant properties which seem to be mediated through ?(2)-adrenoceptor.

Copyright © 2011. Published by Elsevier B.V.

PMID: 21651904 [PubMed - indexed for MEDLINE]

 

[RipdnTxs]

Does Augmatine have any cortisol lowering ability ????

 

[AutoKal47]

Today I gave agmatine another shot,
out of boredoom really, it was arms/abs + full body depletion workout
long wo with the first part being heavy-ish and the depletion part fast and light
took a day off from Craze so I took 750mg of Agmatine prewo with 100mg caffeine 30 min
before the training.

I can definitely say that Agmatine is NOT for me.
First it puts me to sleep, second it puts me in a very bad mood,
it takes my aggression away, it seems to make muscle contraction less intense
and after the first few sets this last thing was really noticeable.
Mind/muscle connection is just not there and (something I noticed before but today
had confirmation) it makes my eyes way too sensitive to light, which makes my head feel
"heavy"..

Overall I am pretty sure agmatine is the WORST supplement I've ever taken,
I genuinely hate what it does to me, awful.. Remaining 40gr of it are heading in the toilet

 

[Whacked]

I can related to the "puts me to sleep" part. It makes me drowsy too.

T-Bone and I were discussing this recently.

Today I gave agmatine another shot,
out of boredoom really, it was arms/abs + full body depletion workout
long wo with the first part being heavy-ish and the depletion part fast and light
took a day off from Craze so I took 750mg of Agmatine prewo with 100mg caffeine 30 min
before the training.

I can definitely say that Agmatine is NOT for me.
First it puts me to sleep, second it puts me in a very bad mood,
it takes my aggression away, it seems to make muscle contraction less intense
and after the first few sets this last thing was really noticeable.
Mind/muscle connection is just not there and (something I noticed before but today
had confirmation) it makes my eyes way too sensitive to light, which makes my head feel
"heavy"..

Overall I am pretty sure agmatine is the WORST supplement I've ever taken,
I genuinely hate what it does to me, awful.. Remaining 40gr of it are heading in the toilet

 

[AutoKal47]

I can related to the "puts me to sleep" part. It makes me drowsy too.

T-Bone and I were discussing this recently.

Yeah dosing it "solo" I could totally spot that effect, def not nice especially prewo
Are you still running it? Have you noticed any benefit? 'cause aside from some lil more pump
i didn't really see anything altho' I didn't use it long enough tho' but I'm cutting everything that
I'm not 100% sure gives me some improvement, I'm done "guessing" what sups do or are suppose to

 

[Whacked]

No - I stopped as well.

 

[bdcc]

Does Augmatine have any cortisol lowering ability ????

Oh no, the damage of a spelling mistake in the thread title is spreading lol.

"Agmatine" = correct. "Augmatine" = no.

 

[AutoKal47]

No - I stopped as well.

Ja, not worth it imo

Oh no, the damage of a spelling mistake in the thread title is spreading lol.

"Agmatine" = correct. "Augmatine" = no.

lol i tried to point out the wrong title before, it bothers me a lot

 

[T-Bone]

I'm almost done with mine. I'm not throwing it in the toilet though. It is way too expensive and I don't like to waste things no matter what. Mine should be finished up within the next couple days.

 

[StackedCop]

I'm still taking 1.5 grams a day and love it

 

[SuppJunkie]

I'm still taking 1.5 grams a day and love it

Its nice to hear that. I am always looking into new supps for me and adding them to a never ending purchase list. Does this bother your stomach at all in any way. That believe it or not is one of the important things for me. I can deal with feeling sleepy and some other things LOL. Also, how have your results been, ie, pumps, vascualrity, strength etc. And finally, how have your been staked..Sj

 

[AaronJP1]

Personally I have not had any negatives with agmatine.

First day I did notice a mood change, and I shat a lot, but lately nothing...

 

[StackedCop]

Its nice to hear that. I am always looking into new supps for me and adding them to a never ending purchase list. Does this bother your stomach at all in any way. That believe it or not is one of the important things for me. I can deal with feeling sleepy and some other things LOL. Also, how have your results been, ie, pumps, vascualrity, strength etc. And finally, how have your been staked..Sj

I'm good brother how you been man? This product really helps with pumps. Not just workout pumps but I feel fuller all day. Nothing crazy but it is very noticeable for me. Vascularity is ok I'm bulking still so I'm not all that vascular at the moment. No strength gains for me but strength isn't a huge concern for me as long as in pushing body to its limit.

Also no stomach issues. That's a huge factor for me too!! I can't stand a product that makes me sleepy or lose focus and
I can't say I've had any issues with that either. I always gotta be at the ready lol

 

[mr.cooper69]

These agmatine concerns are overblown IMO. The lack of conclusive evidence and transient agonism are likely due to agmatine's halflife.

 

[Bigugly]

These agmatine concerns are overblown IMO. The lack of conclusive evidence and transient agonism are likely due to agmatine's halflife.

How long is the half life for agmatine ???

 

[mr.cooper69]

How long is the half life for agmatine ???

I believe around 10 minutes. However, [some] of its effects are demonstrated to extend beyond that value.

Despite agmatine’s short (<10 min) plasma half-life (Piletz et al., 2003; Raasch et al., 2002; Roberts et al., 2005), its systemic administration consistently affects a wide variety of CNS-mediated processes (Nguyen et al., 2003).

Eur J Pharmacol. 2008 June 10; 587(1-3): 135–140.
Supraspinally-administered agmatine attenuates the development of oral fentanyl self-administration
Carrie L. Wade,2 Daniel J. Schuster,3 Kristine M. Domingo,3 Kelley F. Kitto,2,3 and Carolyn A. Fairbanks1,2,3

 

[AaronJP1]

I believe around 5 minutes. However, [some] of its effects are demonstrated to extend beyond that value.

Some people are also only using 500mg on work out days only right?

 

[mr.cooper69]

Some people are also only using 500mg on work out days only right?

500mg is sufficient for many, yes. Despite agmatine's halflife, some of its system effects, most notably vasodilation, persist to a significant degree:

[h=1]Agmatine: A novel endogenous vasodilator substance[/h]

• Yuqi Gao[SUP]1[/SUP],
• Bulent Gumusel[SUP]1[/SUP],
• Gabor Koves[SUP]1[/SUP],
• Anand Prasad[SUP]2[/SUP],
• Qingzhong Hao[SUP]1[/SUP],
• Albert Hyman[SUP]1[/SUP][SUP], [/SUP][SUP]3[/SUP],
• Howard Lipptonhttp://anabolicminds.com/forum/#COR1

"The purpose of the study was to investigate the effects of agmatine, an endogenous clonidine-displacing substance (CDS), on systemic hemodynamics in the anesthetized rat. Bolus intravenous (i.v.) injections of agmatine decreased systemic arterial pressure (SAP) and systemic vascular resistance in a dose-dependent manner. The development of acute tachyphylaxis to the systemic vasodepressor response to agmatine did not induce cross-tachyphylaxis to the systemic vasodepressor responses to bradykinin, isoproterenol and nitroglycerin. The present data demonstrate agmatine, as a CDS and agonist for imidazoline (I) receptors, possesses marked systemic vasodilator activity in the rat. The present data suggest that activation of I receptors may represent a novel mechanism of vasodilation in vivo."

 

[mattrag]

Thanks mr Cooper! Good info here.

 

[hsk]

Since it takes time for the amount of agmatine to build up in the body, would there be any benefit to do a loading phase when starting agmatine use in order to build up the level of agmatine in the body faster? If so, what sort of dosage could beused in a loading period?

 

[dinoiii]

I am unsure why all the references to supraspinal and IV admin.

There is an attenuation of total body agmatine stores as we age (pointed out in an article I did for Joey - then, CEO of MAN back with the launch of Blue Print). It may very well come down to younger individuals not benefiting as much as old. As for pre-workout administration; way back with the original launch for MAN Sports I did back in 2007/2008 and the product Blue Print...I have NEVER suggested this to be the time to dose it. I am uncertain how we have come to this really - possibly a lot of "me too" companies promoting it in this fashion (unsure); just as arginine and any other polyamine has shown - pre-workout is NOT the way to go and I maintain this position, now 5 years later!

Post-workout, on the other hand in combination with GABA might be exceedingly interesting.


D_

 

[dinoiii]

Since it takes time for the amount of agmatine to build up in the body, would there be any benefit to do a loading phase when starting agmatine use in order to build up the level of agmatine in the body faster? If so, what sort of dosage could beused in a loading period?

Outside of sheer pontification; I can say, with confidence, that we simply don't know.


D_

 

[dinoiii]

Some people are also only using 500mg on work out days only right?

Volume of distribution estimates wouldn't support oral dosing this low; we'll chalk that dosing protocol up to a hint of placebo.


D_

 

[dinoiii]

Hey Doc,
the main concern here were some studies posted show Agmatine could potentially halt fat loss being an antagonist for NDMA receptor and agonist for alpha 2.
Would be nice to hear your take on this

here's the studies posted bty ssbackwards and Sourdough

Read last line 1 of paragraph 1 of the first quote ("several subsequent functional studies reported that agmatine is not an agonist at this site")...studies have been mixed in this regard and it is just that we know of about 13 receptors that are affected by agmatine; in order to even claim substantial impact to a significant degree in this respect, you'd probably need to take it by the bucket-full from an ORAL standpoint which lends credence to the study discrepency with IV dosing parameters.

I think boys will be boys stirring up a bit of controversy on an ingredient (can't say as I have heard that before at all - obviously a hint / or a landslide of sarcasm).


D_

 

[dinoiii]

Does Augmatine have any cortisol lowering ability ????

Just as arginine before it; all polyamines (arginine, citrulline, ornithine, putrescine, spermine, spermidine, et al...) do to some effect. To suggest that means we know what to do with it in this regard, I would be lying to you.


D_

 

[dinoiii]

Can I suggest a thread title change again?

I agree with those who have said it before me...the thread title disturbs me.

D_