Pergolide Mesylate & Set-Point Manipulation - Part II

Pergolide Mesylate & Set-Point Manipulation – Part II

You did it. You told yourself you weren’t going to, but you did it. I even explicitly told you not you, but “screw me,” you did it anyways. You cashed the paycheck, told the spouse you were heading out because they were having a “2-for-1” sale on sweet potatoes at the local grocer, and instead went and paid a trip to Chino the back-alley Pergolide dealer. After all, you told yourself, the weather is getting warmer, and I should be out and about in it, showing up all my buddies with some new freaky striations on my left latissimus dorsi. I’ve got my DNP-dopaminergic, now I’ll just down a dozen a day, and I’ll be swole in no time…

Reality check: you now have in your possession the most potent pharmaceutical DA receptor-stimulator that modern science has been able to whip out from under its perennial sleeve. Used smartly and properly, Pergolide is one of the best nutrient partitioning-enhancing, signal-augmenting compounds you will ever get your hands on. Abused or misused, Pergolide can nuke your body’s natural hormonal rhythm, sink your testosterone levels, make you feel like utter shit (assuming at that point you still have a good sense of who ‘you’ are), or just send you packing for the hospital. Usually I jest. This however, has officially been deemed a “jest-free” paragraph.

Seriously though, it truly is this potent, and care should really be taken when using Pergolide as an adjunct to your diet, maintenance, or mass plan (although I would counsel against the latter, which I’ll explain in a little more detail below). So without further ado, let’s end all the Pergolide puzzlement and address all the hows, whats, whens and whys, so you can start using Pergolide if you so choose.

Look Ma! I Lived to Tell About it!!!

So everyone knows where I’m coming from, I played around with Pergolide proper from late August of last year to this past March. In other words, I spent roughly half of a calendar year on the stuff, and I am well aware of what it does and what it doesn’t do in terms of the tangible and/or visible effects that can come from use. However, I cannot say the same is true in regards to my knowledge of Pergolide-related contraindications or the effects that can come from long-term use– the research simply isn’t there to work with.

But, because “I love” (or at least would love to morally exonerate my ass so I don’t lose any more sleep over this stuff than I already do…), I’m still going to attempt a thorough treatment of the health issues, risks, and myths that have sprung up around Pergolide.

The first place we obviously want to look is the brain itself and the DA activity that goes on when Pergolide is introduced. Me, I like the brain, and I tend to think it’s fairly important in the scheme of things, which is why I’d first like to establish how using Pergolide– even large amounts of it– isn’t going to further neuro-degeneration, promote oxidative stress, permanently impair cognitive impairment, or damage any key receptor(s), cell(s) or nervous tissue(s).

However, when used for body-composition purposes which I will be elaborating on shortly, Pergolide does seem to induce a varying degree of psychological effects in individuals, which is something that all perspective users should be aware of before they begin use. Still, in my own experience, these effects are all dose-correlated; they will not persist if you lower your dose, and they don’t cause any permanent alteration in cognitive perception or function. Once usage has been titrated down and halted to properly allow the Pergolide to clear from your system, you will only have to deal with your new-found signaling and set-point issues, not with any sort of perpetual, Pergolide-related psychotic episodes (unless you choose to give getting the munchies big time such an unsympathetic designation).

It’s important to remember that Pergolide is a direct receptor-agonist that stimulates D1 & D2 only when it (or if one of its potentially-active metabolites) starts binding to post-synaptic striatal neurons (1). Because of this, using Pergolide allows us to elevate DA signaling WITHOUT elevating extracellular dopamine levels, allowing us to circumvent the host of problems that can come from repetitive, excessive DA-buildup. Remember, all dopamine must eventually undergo oxidative metabolization (via MAO– a process which produces reactive oxygen species, dopamine quinone, and several other metabolite-byproducts which can promote neuro-degeneration, negatively alter protein function, and inhibit brain-mitochondrial respiration (2,3)).

Normally, these free-radicals are scavenged effectively by the non-protein anti-oxidant glutathione (GSH). But GSH can easily be overwhelmed if DA-oxidation becomes unnaturally high (2). Most of us get enough liver toxicity as it is (Keg stand on Methyl-Tren! Who’s game!?), so it’s probably best if we all avoid trying to make it a ‘two-fer’ by pursuing the whole neuro-toxicity thing as well. So, let’s go and score at least one for Pergolide, as it enables us to benefit from a massive amount of receptor-activation while side-stepping the problems associated with excessive DA-catabolism.

The other relevant issue in this regard is Pergolide’s effect on the receptors themselves– especially for those who are determined enough to stay lean that they’re getting ready to declare “Pergolide fo’ life,” and leave it at that. Namely, does Pergolide administration (or the use of any other agonistic, dopaminergic receptor stimulant) lead to any alterations in binding parameters or promote receptor-desensitization (downregulation)? Unfortunately, this is a question that simply cannot be answered at present. For one, you can almost count the number of isolated, well-controlled, double-blind, and randomized DA-agonist studies that have been conducted in the past decade on a single hand.

And, as if that wasn’t bad enough, just about every single one of them uses a test group of Parkinson’s patients. These are individuals who suffer from a severe chronic neuro-degenerative disease that has completely skewed their neural dopamine: acetylcholine balance and whose DA-activity is essentially about as far as it can get from natural DA-function and signaling. You know, you’d think by now that at least once some researcher, probably taking a coffee break in the lounge or something, would have sat there and thought to himself: “hey, this drug has fantastic abuse potential for physique-enhancement-obsessed bodybuilders who have delved into the world of progressively-cutting edge grey-market diet drugs. Maybe I should control for this variable and throw them a bone for all those children and old ladies they always help get out from under trapped cars…” But damn if it ain’t happened yet.

See, it’s clear that Pergolide can be used long term– even up to several years– without any diminishment or alterations in its pharmacodynamics or receptor-stimulating properties (4). The real mind-fuck is that, due to the progressive neurodegeneration Parkinson’s disease inevitably causes during the long-term, it is unclear whether these patients needed to increase their Pergolide dosages over the years to compensate for a.) Eventual receptor-desensitization to the drug’s effects or b.) The continual loss of dopaminergic neurons in the substantial nigra.

In fact, both may play some role in the slow, progressive titration-regimen most DA-agonist treatments use, which is why causally isolating any potential effect(s) Pergolide might be having on receptor sensitivity is simply impossible. If I had to speculate based on just general pharmacokinetic principles and a few rat studies that looked at D2 receptor-binding in the dorsal striatum after long term quinpirole [a D2/D3 receptor ligand] treatment, I would assume that long-term use of Pergolide– even though it operates ‘down-stream’ from presynaptic dopamine stores and DA synthesis– will still likely exert some sort of desensitization effect at D1 and D2 (5).

However, even if we grant that this phenomenon might eventually occur, it would have to be an extremely gradual process that could only manifest itself significantly in instances of chronic activation for months and months at a time, and perhaps even this is too short a time frame. It may even take several years of continual Pergolide use for DA receptors to begin to show signs of less signaling after uptake and binding of the drug. It may never even happen at all. The point is that anyone out there still traumatized by those “this is your brain on drugs” commercials who is concerned that taking Pergolide will ‘fry’ their dopamine receptors can now sleep soundly without being haunted by hallucinations of omelets and eggs done over-easy.

Wow, Since I Started Pergolide, My Weight Loszzzzzzzzzz…

While I can’t say it always felt all that gratifying at the time, I now see that the one good thing about my getting hammered by Pergolide side effects is that I can now share those trials with you in the hopes that you yourself don’t end up having similar experiences. It is likely you will suffer some side effects though; it’s pretty hard to just outright bypass side effects with a drug that boasts this kind of potent pharmacokinetic activity. But hey, at least now you’ll know what to expect, right? So let’s scroll down this laundry-list right-quick so we can get to the fun stuff.

1) Pergolide, since it ends up approximately 90% bound to plasma proteins, boasts a high oral bioavailability and an enduring half-life (the elimination half-life is reportedly as long as 27 hours) (6,7). Thus– and this observation stands in line with my own experiences, as well the experiences and anecdotes of others– generally anyone who has begun Pergolide or upped their dose only to find themselves “miserable” at this new level of DA stimulation should lower their next-day dose and expect to find those newly-emergent sides have dissipated noticeably within about 24 hours of that overdose.

2) The single most prevalent and likely side-effect those of you out there will experience when you attempt to use Pergolide is persistent somnolence prompted by postsynaptic DA-receptor stimulation. Pergolide is a drug that should ALWAYS be titrated, both up and down, and cautiously tweaking your dosing plan “by feel” is far and away the best strategy to keep this effect manageable. Still, for roughly the first month I was on Pergolide, the drug made me develop mild, mid-morning narcolepsy, particularly during the period when plasma levels of the drug peak in your system after ingestion, or roughly two hours after I took it.

I tried stimulants, nootropics– pretty much anything I could think of to try to combat this effect. All of it was to no avail; even an Adderall XR couldn’t keep me from falling asleep in class for a minute or so during the first few days after I had platformed at a higher dosage. Also, these sleep-attacks can be classified as sudden onset. You don’t feel them coming, you won’t even really feel tired– it’ll just kind of hit you, and when I say hit, I’m talking Terry Tate the Office Line-backer style. I’ve case-raced Guinness for craps’ sake, and it still didn’t leave me with a stronger desire to pass out than what I experienced during my first few mornings on Pergolide.

Now, while the exact cause(s) and commonality of sudden-onset sleep attacks in individuals using Pergolide is still a highly contested area of pharmaceutical inquiry, it has been conclusively documented that Pergolide administration enhances inhibition of motor cortex excitability (by decreasing the amount of possible intracortical activity) (8,9,10). In plain English: for those first few hours that it’s active in your system, Pergolide will likely downgrade your motor-skills to the point where they fall somewhere in between drunken trucker and epileptic primate on the “Are-You-Probably-Better-Off-In-a-Padded-Room?” index (with the “E.P.” generally holding up the high end of the scale…). Suffice it to say, I do not recommend trying to do things like a.) Drive a car, b.) Be really productive at work, or c.) Tight-rope walk across the Grand Canyon, within the first three hours of your Pergolide dose. After that, this effect seems to diminish markedly.

3) Finally, according to a recent press release from the Eli Lily Corporation, there have been rare reports of pleuritis, pleural effusion, pleural fibrosis, pericarditis, pericardial effusion, cardiac valvulopathy involving one or more valves, or retroperitoneal fibrosis in patients taking Pergolide (11). I’m not a practicing physician, and I have no clue what half of these conditions entail, but my guess is it’s probably in your best interest if you don’t come down with any of the above. If you were to develop such a condition while using Pergolide, it would be almost impossible to know, which is why I counsel anyone who uses Pergolide that if you ever start feeling “not right” in any way/shape/form, just do yourself a favor and stop using the drug. Please.

Empirically, Pergolide is a very well-tolerated drug. Between 1982 and 1997, clinical data on 1,500 individuals (again, mostly Parkinson’s patients, which means they’re in poorer health than you to begin with) has been collected, which– in sum– has lead researchers to conclude that “adverse reactions are, for the most part, mild and reversible, they mostly include nausea and gastroenteric disturbances” (12). So while I wouldn’t go as far as to say it’s as safe as creatine, I do not think one who is taking the proper precautions and is in good health to begin with has much to worry about. If you experience some of the more common/minor stuff that I described above, I wouldn’t worry. Nonetheless, if you begin to experience tangible, physical pain internally, or notice you are starting to have trouble breathing, STOP THE DRUG. Listen, I don’t care how “hard” you are (or consider yourself to be), because not a soul on Earth is going to be able to see your six-pack once they’ve closed the coffin.

Pergolide & The Ramifications for Your Pimp Game

Pergolide– aside from its use as a Parkinson’s drug– is also commonly used to treat cases of hyperprolactinemia, a condition characterized by atypically elevated serum prolactin levels (13). Prolactin, for those completely unfamiliar with the hormone, is a sex-hormone excreted by the anterior pituitary gland that– in males– binds to receptors in the gonads, one’s lymphoid cells, and also the liver (13). Now, if prolactin levels become unnecessarily elevated for too long a time (such as in persons suffering from hyperprolactinemia), it would essentially create a hormonally-imbalanced milieu where one of our other key sex-hormones, gonadotrophin releasing hormone (GnRH), ends up being suppressed.

If this goes down, your testosterone levels are ultimately going to end up bottoming out harder than Martha Stewart’s stock portfolio, via a related decrease in luteinizing hormone (LH) and follicle-stimulating hormone (FSH) output (14). Aaaaaand if that wasn’t enough of an endocrinological kick-to-the-balls, you end up hypogonadal too. Cheers mate (but good like trying to find a WAY to mate…).

So what are the implications for a male using Pergolide? Will it negatively affect his testosterone levels? Well, as it turns out, the key link in the signaling chain for prolactin happens to be DA activity. DA really dominates prolactin secretion. Prolactin sets the tone for the body’s daily secretion rhythm, since serum prolactin levels fluctuate in line with a pulsatile release pattern that shifts based on levels of sleep, stress, trauma, and a host of other, smaller variables (13,14).

So we have this rhythm, and we also have DA, which can be thought of as the overseer or the ‘break,’ since the lactotrophs in the anterior pituitary that actually produce prolactin have D2 receptors, which– when activated– will inhibit prolactin secretion (15). In fact researchers note that Pergolide “inhibits the secretion of prolactin in humans and causes transient increases in serum growth hormone and decreases in luteinizing hormone. The effects on prolactin secretion persist much longer than antiparkinsonian action” (16). At this point, you’re probably thinking, “wait, huh? If prolactin gets too high, LH goes down, which is bad, but if prolactin gets inhibited, LH goes down too? What’s up with that?” Well, fear not friend, as I shall shortly share with you that:

1.) Pergolide will not adversely affect your testosterone levels if you dose it properly to coincide with your body’s natural hormonal rhythm, and 2.) You can get laid as much as you want (or, at least as much as you can) on Pergolide; it’s not going to nuke your libido in any way shape or form—quite the opposite, actually.

Pergolide and Seeeeeeeeeeeeeexxx… (Hormone levels, that is…)

Pergolide is an ergot D1/D2 agonist which boasts similar binding and stimulation activity at D2 to the D2-only agonist Bromocriptine. Now, in Oseko et. al., the researchers found that chronic Bromocriptine treatment lowered testosterone levels in its male subjects (17). However, they didn’t use Bromo for body-composition augmentation as Lyle McDonald advocates, which is also– as if it’s any surprise– how I’m going to tell you how to use Pergolide. Nor for that matter, the Oseko et. al. study is not the only study to examine the effects of dopaminergic agonists on testosterone levels in males; it just happens to be the only one that actually shows a negative effect, compared to three I was able to find (and I didn’t really look all that hard) that showed those treated demonstrated– on average– no significant decrease in free or total testosterone levels (18,19,20).

Essentially, since Pergolide’s active prolactin-suppressing activity is quite long, if you had a significant amount of the drug active in your system in the early morning hours, then it would suppress your body’s daily morning prolactin pulse. This is a critical component in keeping your body’s testosterone levels in their optimal range, most likely through its inhibitory regulation of aromatase’s enzymatic propensity to convert testosterone into estrogen (21,22,23).

So the answer is pretty simple: take your entire dose of the drug in the morning, between roughly 7am-10am (I could consider the 5am-11am range “safe,” although I STRONGLY urge you to tend more towards the originally proposed 7-10 range) so that you’ll have the least amount of prolactin-suppressing activity in the evening once you go to sleep. It might sound counter-intuitive. It’s not. You will get the metabolic, partitioning, and neuro-protective effects of your dose, and you won’t end up fucking with your body’s natural hormonal rhythm.

Cogito (thy) Ergot, Son

Alright then, I’ve semantically beaten around the bush for long enough; let’s break down how to properly use this puppy. Now, here are preliminary dosage recommendations:

– Level 1 Newbies: individuals who are not ‘bridging’ with Bromocriptine (or Apomorphine), and have no experience with nicotine or any other dopaminergic compound, should begin with a dosage of 125 mcg for at least one week to assess their tolerance/reaction(s).

– Level 2 Newbies: individuals who are not ‘bridging’ with Bromocriptine (or Apomorphine), but do have experience with other dopaminergics, should begin with a dosage of 250 mcg for at least one week to assess their tolerance/reaction(s).

– Level 3 Newbies: individuals who are ‘bridging’ with Bromocriptine (or Apomorphine), and do have experience with dopaminergics, should begin with a dosage of 500 mcg for at least one week to assess their tolerance/reaction(s).

Now, obviously, these dosages are quite low, and– I’m not going to lie– aside from a slight elevation in insulin sensitivity and a mild vasodilatory effect, you’re really not going to see much of anything positive from this initial dose. Conversely, you likely will experience all of the sides, which is why Pergolide is not a quick-fix drug, nor is it one that really provides a great deal of instant gratification.

A Pergolide cycle should take several months really, and should be pyramided in the same manner as one would generally cycle Clenbuterol (begin by titrating up; end by titrating back down). The main difference is time and rate of dosage-increase. Put succinctly, a Clen cycle is like a comic book compared to Pergolide’s “War and Peace” of a titration regimen. So if you actually want to reap the fruits of Pergolide, you need to be ready for a long haul.

If you’re committed to doing this, then there are really two strategies that can be utilized. The first is to use Pergolide at a low dose (500mcg – 1mg) continually for a.) slightly enhancing nutrient partitioning & insulin sensitivity, b.) appetite suppression, c.) and a re-normalization of a lot of the physiological processes that tend to down-regulate as a result of long-term dieting, especially once you start to dip below your set-point. You can also use this latter dose as a mass-gain adjunct (with or without androgens), with the goal being to limit fat gain by distributing a higher percentage of your calories into building new muscle tissue in lieu of new fat tissue.

In my personal opinion, I think this latter manner of using Pergolide (on a mass phase) is basically a waste of your time. It’s not that it doesn’t work; it will work for some, especially if you are very lean. But the fact of the matter is, 5mg of Bromo is much cheaper, and—at this dosage level—can duplicate most of Pergolide’s really important signaling effects.

What I personally recommend—and it’s not easy, so bear with me—is using Pergolide for a big-time cut by using a shoot-the-moon dosage scheme. As we all know, dopamine/DA directly and indirectly exerts effects on nutrient and energy metabolism in humans. When humans receive low-dose, exogenous DA via infusion (specifically at a rate of 5 micrograms min-1 kg-1), circulating noradrenalin (NA[/NE]) levels also rise in direct correlation, leading to an increase in resting metabolism (24).

At higher infusion concentrations, researchers note that DA “increases energy expenditure and circulating free fatty acid and glycerol levels… presumably due to stimulation of lipolysis” (24). At this point, I think we’re probably on the same page. I realize I’m speculating, but after using Pergolide myself, there seems to be a dosage threshold that you can hit with where the drug stops just working as a partitioner and signaling corrector and starts mimicking these same effects.

In other words, it starts seriously promoting lipolysis on its own. In fact, at the temporary peak dosage of 4mg/ED we’re shooting for, Pergolide seems to promote fat loss that I can only term as radical. It helps that you can’t even bring yourself to eat at 50% of maintenance calories at such a high dosage, but in my experience that’s obviously not the only thing going on. As Ensinger et. al. have noted, “administration of… dopamine results in persistent increases in VO2 in volunteers,” and Ruttimann et al. have found similarly that “dopamine infusion produces a dose-dependent thermogenic effect” (25,26).

Although it’s an apples to oranges comparison, in my own personal experience, 4mg of Pergolide seems to be at least the lipolytic equivalent of 800mg of DNP in a cross-comparison over the same 24-hour period. The difference is that instead of carb-cravings that have you staking out the nearest highway with the hopes of knocking off a Ho-Ho truck, your appetite is so strongly regulated you might as well be suffering from English-muffin phobia and a slew of other ridiculous dietary-preference disorders.

Editor’s Note: Due to the gravity, breadth, and sheer volume of this article (the fact that Loki pontificates like a MoFo didn’t help either) it has been halved. The conclusion to this piece will appear in M&M Issue 20, slated for release in early to mid-June.

Works Cited

1. Ammar S, Martin,P. Modelisation des effets des agonistes dopaminergiques en psychopharmacologie: vers une homothetie clinique et experimentale. Psychologie Francaise 1991, 36, 221-232.

2. Grima G, Benz B, Parpura V, Cuenod M, Do KQ. Dopamine-induced oxidative stress in neurons with glutathione deficit: implication for schizophrenia. Schizophr Res. 2003 Aug 1;62(3):213-24.

3. Berman SB, Hastings TG. Dopamine oxidation alters mitochondrial respiration and induces permeability transition in brain mitochondria: implications for Parkinson’s disease. J Neurochem. 1999 Sep;73(3):1127-37.

4. Hubble, J. P. (2002). “Long-term studies of dopamine agonists.” Neurology 58(4 Suppl 1): S42-50.

5. Gurevich EV, Joyce JN. Distribution of dopamine D3 receptor expressing neurons in the human forebrain: comparison with D2 receptor expressing neurons. Neuropsychopharmacology. 1999 Jan;20(1):60-80.
6. Permax– Pergolide Mesylate. Eli Lilly & Co. 5.0 PV 2271 UCP_v2

7. Clarke C E, Speller J M. Pergolide for levodopa-induced complications in Parkinson’s disease (Cochrane Review). The Cochrane Library, Issue 1, 2004. Chichester, UK: John Wiley & Sons, Ltd.

8. Homann CN, Wenzel K, Suppan K, Ivanic G, Kriechbaum N, Crevenna R, Ott E.BMJ. Sleep attacks in patients taking dopamine agonists: review. 2002 Jun 22; 324(7352): 1483-1487.

9. Soares BGO, Lima MS, Reisser AAP, Farrell M. Dopamine agonists for cocaine dependence (Cochrane Review). In: The Cochrane Library, Issue 1, 2004. Chichester, UK: John Wiley & Sons, Ltd.

10. Ziemann U, Tergau F, Bruns D, Baudewig J, Paulus W. Changes in human motor cortex excitability induced by dopaminergic and anti-dopaminergic drugs.
Journal of Physiology (2002), 542.3, pp. 951-961.

11. Valerie E. Simmons, MD, FFPM. 2003 Safety Alert – Permax, Worldwide Pharmacovigilance and Epidemiology; Eli Lilly and Company. 2003

12. Pezzoli G, Canesi M, Pesenti A, Mariani CB. Pergolide mesylate in Parkinson’s disease treatment. Neural Transm Suppl. 1995;45:203-12.

13. Balint Kacsoh. Endocrine Physiology. McGraw Hill Publishing, 2000.

14. Lackritz, RM and A. Bartke. The effect of prolactin on androgen response to human chorionic gonadotropin in normal men. Fertil Steril (1980) 34: 140-143.

15. Nakagawa K et. al. Relationship of changes in serum concentrations of prolactin and testosterone during dopaminergic modulation in males. Clin Endocrinol (Oxf) 1982 17:345-52.

16. DL Kleinberg, A Lieberman, J Todd, J Greising, A Neophytides and M Kupersmith. Pergolide mesylate: a potent day-long inhibitor of prolactin in rhesus monkeys and patients with Parkinson’s disease. Journal of Clinical Endocrinology & Metabolism, Vol 51, 152-154

17. Oseko, F. et. al. Effects of chronic bromocriptine-induced hypoprolactinemia on plasma testosterone responses to human chorionic gonadotropin stimulation in normal men. Fertil Steril (1991) 55: 355-357.

18. Kleinberg DL, Boyd AE 3rd, Wardlaw S, Frantz AG, George A, Bryan N, Hilal S, Greising J, Hamilton D, Seltzer T, Sommers CJ. Pergolide for the treatment of pituitary tumors secreting prolactin or growth hormone. N Engl J Med. 1983 Sep 22;309(12):704-9.

19. Lackritz, RM and A. Bartke. The effect of prolactin on androgen response to human chorionic gonadotropin in normal men. Fertil Steril (1980) 34: 140-143.

20. Nakagawa K et. al. Relationship of changes in serum concentrations of prolactin and testosterone during dopaminergic modulation in males. Clin Endocrinol (Oxf) 1982 17:345-52.

21. Pierrepoint, CG. et. al. Prolactin and testosterone levels in the plasma of fertile and infertile men. J Endocrinology (1978) 76: 171-172.

22. Rubin, RT. et. al. Prolactin-related testosterone secretion in normal adult men. J Clin Endocrinol Metab (1976) 42: 112-116.

23. Martikainen H. and R. Vihko. hCG-stimulaton of testicular steroidogenesis during induced hyper- and hypoprolactinemia in man. Clinical Endocrinology (1982) 16: 227-234.

24. Regan CJ, Duckworth R, Fairhurst JA, Maycock PF, Frayn KN, Campbell IT. Metabolic effects of low-dose dopamine infusion in normal volunteers. Clin Sci (Lond). 1990 Dec;79(6):605-11.

25. Ensinger H, Weichel T, Lindner KH, Grunert A, Georgieff M. Are the effects of noradrenaline, adrenaline and dopamine infusions on VO2 and metabolism transient? Intensive Care Med. 1995 Jan;21(1):50-6.

26. Ruttimann Y, Schutz Y, Jequier E, Lemarchand T, Chiolero R. Thermogenic and metabolic effects of dopamine in healthy men. Crit Care Med. 1991 Aug;19(8):1030-6.

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