Just some info. on my first week of Man's Blue-Print at 4caps per day upon waking one hour before my first shake/meal. Some background on me, been training forever, used a bunch of diff. supplements, usually respond well to them. Im 5'5", 155 pounds, %15 BF, 35 years old (but Im told I look 25 )

The things Ive noticed after one week are:

1. No DOMS, usually can really tear myself up after heavy lifting, for instance doing DB shrugs with 110 pound dumbells will usually do the trick, however, on Blue-print I feel the tightness and some minor soreness, but not that full on soreness like usual. This alone makes the supp. worthwhile in my book. We will see if it lasts.

2. Even training heavy and doing HIIT and other cardio daily, I dont feel overtrained as I sometimes do. After my two days off on the weekend I was positively chomping at the bit to get back in the gym I felt so good.

3. I use 30-60 mg.s of oxycodone a day as well, and as some of you may know one of the long term effects of this stuff is you wake up in a serious fog every morning. I mean its the worst thing about it. Well, since Ive been using Blue-print, I wake right up in the morning, and jump right out of bed. This to me is awesome, as Ive been struggling with that mud in your head feeling for a while now. (I know Ive got a problem with this sh/t, im working on it, so please dont lecture me. Thanks.)

We will see if the strength increases Im noticing are from the Blueprint or the RPM/Blue UP combo Ive been on for the last month (two great supps in there own right). The RPM I tried after hearing so much good about it, and the Blue UP to kick me back in gear, along with 7keto after I ran Thermogenic Thyrotabs/Thyro-cuts 2 for the past 6 weeks on a cut, which was very effective as well.


So far after one week, Id say this is some interesting stuff. The price is a little steep, but I found it online for $30 before shipping. I will definetly be picking up another bottle as I cycle off the RPM, then later the Blue up.

Bill, when are you dosing? does it effect your cognition? do yuo take any stims? NMDA antagonists... won't they make you super dumb? I haven't researched those meds yet...

are you trying to get off the oxy?

Dosing according to the label, first thing in the AM, one hour before food, according to the good doc over at Lean Bulk. Im sensitive to stims, so I only use 1 Basic Cuts, which is 100mg. caff, 75mg. PEA, and 2 RPM's which from what Ive been told is about another 100mg.s of caff for both pills also theres some Chocamine in the RPM as well. I use all that pre-workout.

It doesnt make you feel any kind of euphoria or mental effects so far. When I was young and dumb I tried snorting Ketamine once. Good god what a bad idea. I know these are in the same class but its nothing like that. I notice no real mental effects at all.

As far as the oxy not really here to get into that, just threw that in because I hear Agmatine potentiates opiates as well as prevents tolerance.

its cool, I'm not the opiate type myself.

Would love to see some more feedback on this product. A break from DOMS would be really nice.

Ditto, and I've been really curious about this product ever since it came out. Heard nothing but good things so far.

Kimbo, can you tell me what feedback you've heard, as I have seen none.

If anything its an effective pain-killer in its own right. Ive also noticed it potentiates caffiene and my sleep has been more sound with vivid dreams. Im beginning to believe the holy grail comment. LOL. Its very subtle, which is good, no ups and downs, just a nice steady feeling of well being and good energy and recovery in the gym. My for this stuff.

Search on this board,feedback is here and it's pretty positive.

Really? Because I just used Google for this site on blueprint and agmatine and found nothing. Just a bunch of talk of what it might be good for. I'm not interested in abstracts.

Have you noticed any reduction in tolerance or significant potentiation of the oxy? Im intereted in this stuff to help lower my Kratom tolerance among other things

Thanks

That's all I found,besides what you've mentioned.

http://www.mindandmuscle.net/forum/index.p...mp;#entry432545

Thanks. I guess I'll have to resort to other board. Bleh.

NMDA antagonists can boost AMPA receptors.

Too soon to say. Definetly potentiation going on.

So, what are AMPA receptors?

From Wiki

The alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (also known as AMPA receptor, AMPAR, or quisqualate receptor) is a non-NMDA-type ionotropic transmembrane receptor for glutamate that mediates fast synaptic transmission in the central nervous system (CNS). Its name is derived from its ability to be activated by the artificial glutamate analog, AMPA. AMPARs are found in many parts of the brain and are the most commonly found receptor in the nervous system.

Contents [hide]
1 Structure and function
2 Long Term Plasticity
3 Antagonists
4 References
5 External links



[edit] Structure and function
AMPARs are composed of four types of subunits, designated as GluR1 (GRIA1), GluR2 (GRIA2), GluR3 (GRIA3), and GluR4, alternatively called GluRA-D (GRIA4), which combine to form tetramers.[1][2][3] Most AMPARs are either homo-tetramers of GluR1 or GluR4, or symmetric 'dimer of dimers' of GluR2 and either GluR1, GluR3 or GluR4.

The conformation of the subunit protein in the plasma membrane caused controversy for some time. While the amino acid sequence of the subunit indicated that there were four transmembrane domains (parts of the protein that pass through the plasma membrane), proteins interacting with the subunit indicated that the N-terminus was extracellular while the C-terminus was intracellular. If each of the four transmembrane domains went all the way through the plasma membrane, then the two termini would have to be on the same side of the membrane. Eventually, it was discovered that the second transmembrane domain isn't in fact trans at all, but kinks back on itself within the membrane and returns to the intracellular side.[4] When the four subunits of the tetramer come together, this second membranous domain forms the ion-permeable pore of the receptor.

Each AMPAR has four sites to which a molecule of the agonist (such as glutamate) can bind, one in each subunit. The channel can open when two or more sites are occupied.[5] AMPARs open and close quickly, and are thus responsible for most of the fast excitatory synaptic transmission in the central nervous system.[5]

The AMPAR's permeability to calcium and other cations, such as sodium and potassium, is governed by the GluR2 subunit. If an AMPAR lacks a GluR2 subunit, then it will be permeable to sodium, potassium and calcium. The presence of a GluR2 subunit will almost certainly render the channel impermeable to calcium. This is determined by post-transcriptional modification - RNA editing - of the Q/R editing site of the GluR2 mRNA. Here, editing alters the uncharged amino acid glutamine (Q), to the positively-charged arginine ® in the receptor's ion channel. The positively-charged amino acid at the critical point makes it energetically unfavourable for calcium to enter the cell through the pore. Almost all of the GluR2 subunits in CNS are edited to the GluR2® form. This means that the principal ions gated by AMPARs are sodium and potassium. The prevention of calcium entry into the cell on activation of GluR2-containing AMPARs is proposed to guard against excitotoxicity.[6]

The subunit composition of the AMPAR is also important for the way this receptor is modulated. If an AMPAR lacks GluR2 subunits, then it is susceptible to being blocked in a voltage-dependent manner by a class of molecules called polyamines. Thus when the neuron is at a depolarized membrane potential, polyamines will block the AMPAR channel more strongly, preventing the flux of potassium ions through the channel pore. GluR2-lacking AMPARs are thus said to have an inwardly rectifying I/V curve, which means that they pass less outward current than inward current.

Alongside RNA editing, alternative splicing allows a range of functional AMPA receptor subunits beyond what is encoded in the genome. In other words, although one gene (GRIA1-4) is encoded for each subunit (GluR1-4), splicing after transcription from DNA allows some exons to be translated interchangeably, leading to several functionally different subunits from each gene.

The flip/flop sequence is one such interchangeable exon. A 38-amino acid sequence found prior to (ie towards the C-terminus of) the 4th membranous domain in all four AMPAR subunits, it determines the speed of desensitisation[7] of the receptor and also the speed at which the receptor is resensitised.[8]


[edit] Long Term Plasticity
AMPA receptors (AMPAR) are both glutamate receptors and cation channels that are integral to plasticity and synaptic transmission at many postsynaptic membranes. One of the most widely and thoroughly investigated forms of plasticity in the nervous system is known as long-term potentiation, or LTP. There are two necessary components of LTP: presynaptic glutamate release, and postsynaptic depolarization. Therefore, LTP can be induced experimentally in a paired electrophysiological recording when a presynaptic cell is stimulated to release glutamate on a postsynaptic cell that is depolarized. The typical LTP induction protocol involves a “tetanus” stimulation, which is a 100Hz stimulation for 1 second. When one applies this protocol to a pair of cells, one will see a sustained increase of the amplitude of the excitatory postsynaptic potential (EPSP) following tetanus. This response is very intriguing because it is thought to be the physiological correlate for learning and memory in the cell. In fact, it was recently shown that following a single paired-avoidance paradigm in mice, LTP could be recorded in some hippocampal synapses in vivo.[9]

The molecular basis for LTP has been extensively studied, and AMPARs have been shown to play an integral role in the process. Both GluR1 and GluR2 play an important role in synaptic plasticity. It is now known that the underlying physiological correlate for the increase in EPSP size is a postsynaptic upregulation of AMPARs at the membrane, which is accomplished through the interactions of AMPARs with many cellular proteins.

The simplest explanation for LTP is as follows (see the long-term potentiation article for a much more detailed account). Glutamate binds to postsynaptic AMPARs and another glutamate receptor, the NMDA receptor (NMDAR). Ligand binding causes the AMPARs to open, and Na+ flows into the postsynaptic cell, resulting in a depolarization. NMDARs, on the other hand, do not open directly because their pores are occluded at resting membrane potential by Mg2+ ions. NMDARs can only open when a depolarization from the AMPAR activation leads to repulsion of the Mg2+ cation out into the extracellular space, allowing the pore to pass current. Unlike AMPARs, though, NMDARs are permeable to both Na+ and Ca2+. The Ca2+ that passes into the cell triggers the upregulation of AMPARs to the membrane, which results in a long-lasting increase in EPSP size underlying LTP.

I've found BluePrint and cissus to be superb for tendonitis and joint pain. Far, far more efficacious than cissus alone.

Can you offer up a medical diagnosis regarding your joint pain i.e. is to the point of having seen a doctor or just persistent aches,DOMS and what not?

Colin did you have any luck finding a bulk source for this stuff? Personally, I'd rather not have the R-ALA that comes with it in Blue Print.

Yes,it is readily available via Alibaba.com and I found several sources-prices qouted for a kilo ranged from $400 to $800.

Alibaba has a "Gold Seller" program which I would think denotes which vendor woudn't be selling me grounded up Pez.I need to verify just how much weight this certification carries.I was offeed a kilo from a gold seller at $400 BTW and if I can be assured that the goods are what they say they are I will certainly pick up a kilo in a few weeks.

I blew a signifigant wad on RU58841 and several AAS powders this past month so I can't afford anything else drug/suppp wise for a few weeks.

I obviously won't need an entire kilogram of the stuff so I'd be fine with splitting an order.I also intend on getting a bunch of CLA around the same time.

if agmatine were coke, and blue print were blue magic, this is like supplement American Gangster.

Diagnosed as chronic tendonitis in both knees.

Ah,only true if I were buying illicits/reselling them and agmatine sulfate is perfectly legal

Seriously,supplements are taxed and if you can buy in bulk and thereby save 80% or so,you're a tool if you choose not to do so.I'm not about to ghetto rig my own SyntheSIZE concoctions,I'm only after a single chemical so no mad scientist action is going down.




Good,confirmation that it attenuates not only DOMS and general aches.

BillCutting, any updates on agmatines effect on your opiate tolerance? this could be gold if it actually works like we've seen in the rat studies

I havent been able to take myself completely off (go figure) but I have noticed when tapering down the usually mild withdrawl symptoms (sweating, runny nose, sneezing, headaches) arent there. Maybe the placebo effect, I dont know. I would like to get it in bulk and then try coming off fast to see how that goes.

I havent been able to take myself completely off (go figure) but I have noticed when tapering down the usually mild withdrawl symptoms (sweating, runny nose, sneezing, headaches) arent there. Maybe the placebo effect, I dont know. I would like to get it in bulk and then try coming off fast to see how that goes.