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I most def do not want to run something that could halt fat loss,Alpha y to the rescue!
f@ck the pumps if that's the case
I most def do not want to run something that could halt fat loss,Alpha y to the rescue!
Yeah it makes sense, altho' seems silly to take Alpha y to negate the side effects of somethingI 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...
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.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
Oh I did already lol, as soon as ssbackwards posted that I was "eehh NO"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.
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.
WHOA
Say what?????
PLease explain T
Thanks
from what i read you are more then correc.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.
Then agma stays supsended indeedfrom 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.
Wait suspended as in not taking it?Then agma stays supsended indeed
I'm with you with this one bro, better be safe than sorryits 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.
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.
You slayin' the hype again bro??? just kiddingcongrats 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 Doc,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_
"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]
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
Yeah dosing it "solo" I could totally spot that effect, def not nice especially prewoI can related to the "puts me to sleep" part. It makes me drowsy too.
T-Bone and I were discussing this recently.
Oh no, the damage of a spelling mistake in the thread title is spreading lol.Does Augmatine have any cortisol lowering ability ????
Ja, not worth it imoNo - I stopped as well.
lol i tried to point out the wrong title before, it bothers me a lotOh no, the damage of a spelling mistake in the thread title is spreading lol.
"Agmatine" = correct. "Augmatine" = no.
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..SjI'm still taking 1.5 grams a day and love it
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.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
How long is the half life for agmatine ???These agmatine concerns are overblown IMO. The lack of conclusive evidence and transient agonism are likely due to agmatine's halflife.
I believe around 10 minutes. However, [some] of its effects are demonstrated to extend beyond that value.How long is the half life for agmatine ???
Some people are also only using 500mg on work out days only right?I believe around 5 minutes. However, [some] of its effects are demonstrated to extend beyond that value.
500mg is sufficient for many, yes. Despite agmatine's halflife, some of its system effects, most notably vasodilation, persist to a significant degree:Some people are also only using 500mg on work out days only right?
Outside of sheer pontification; I can say, with confidence, that we simply don't know.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?
Volume of distribution estimates wouldn't support oral dosing this low; we'll chalk that dosing protocol up to a hint of placebo.Some people are also only using 500mg on work out days only right?
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.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
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.Does Augmatine have any cortisol lowering ability ????