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    MuscleChemistry Registered Member Board Certified Psy.D

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    Default Cell Tech Creatine?

    I have a jug of cell tech creatine on hand here...
    for the dosage it says for the loading phase you should take 2 scoops in the morning and 2 scoops at night... and for the maintenance phase just take 2 scoops daily... now, all sounds fine, however, each scoop is 50g!

    That make loading phase of 200g a day and maintenance about 100g a day...
    from what Ive read, thats not right... should be around 20-30?
     

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    Thats jsut the dextrose - the creatine is about 10 grams a serving, and as I recall you only need 2-3 grams a day for the same effect! They just want you to use up more stuff quicker so you'll have to buy another jug.
     

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    Just take what it says on the bottle.

    The loading phase is optional. Some people like it. Some don't.


    Some jugs of creatine are pure creatine with no dextrose/flavor. So you will use less. You have to add dextrose etc yourself.

    Some jugs of creatine have dextrose/flavors in them already, so even though it looks like you're scooping more. It's the same amount of creatine.
     

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    I was thinking that too... so I looked to see how much creatine was in each seving and it didnt state it.... only reason I asked is cause the difference is pretty big.. 20g compared to 100-200g, but if its not all creatine then it makes sense!
    Gracias!
     

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    Let us know how you make out with it

    I love using creatine, I always feel like I have and endless amount of energy to lift and I always feel pumped up.
     

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    this better taste good when mixed with my banana protein shake.... banana and lime, ewww
     

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    Lord Odin
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    Cell Tech, I like the creatine, but I have gotten just as good results from generic creatine mixed with grape juice to use as a delivery system....
     

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    If you're using the celltech, I'd just mix that with water.

    I wouldn't recommend it with the protein. Just don't see that sitting right in the stomach.

    Just down the creatine a half hour before your workout or in the morning and drink the protein shakes after your workout.
     

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    are you saying that in general regarding creatine and protein or specifically cell-tech creatine?
     

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    god damn is this stuff sweet... its like eatting razor blades... and its pure sugar, I dont really wana gain fat because of this, kinda regret buying this brand....
    it also made my stomache turn for a good 2 hours
     

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    Personally, I wouldn't mix my creatine/protein. Of any kind.


    You said you had an upset stomach? Did you take it with your protein? Or before or after your workout?

    Try switching when you take it.

    For myself, I always take my creatine on an empty stomach just mixed with water. Once right in the morning works for me.
     

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    I hate cell tech personally. I used it alot when it first came out and got fat, 75g of sugar per serving, YUUCCKKK, now i prefer pure creatin with juice and r-ala, or even better metformin, talk about pumps.
     

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    the bad part is there is more time and effort put into the 124123532443252345 page advertisement in MD than goes into the creation of the supplement. ANYONE ELSE QUIT BUYING THE MAGAZINE?


    Please do not PM for sources or to check a sources legitimacy...I will not return your PM...YOU WILL BE BANNED

    Bignick is a fictional character and therefore all information given by Bignick is for entertainment purposes only. Bignick does not condone nor support the use of Anabolic Steroids or any other controlled substances.

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    I myself like regular creatine, then you can mix it with a juice of your choice. celltech way to much money.
     

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    Just get the cheapest micronised creatine you can find, add sugar source of choice, take an ala cap and save a fortune. You will have designed a much superior product to cellwreck.
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    This is in part a correction to the reply I made above. I had found a study friday but can't find it now that indicated the same information laid out below. This puff piece for a product contains much of the same information the study had.

    I am not endorsing this product in any way.

    Sodium, not insulin is the means for creatine absorbtion.

    https://themuscleshack.com/fsi003.html

    The most popular creatine on the market today is creatine monohydrate. This is simply because it was the first creatine to become popular in the early 1990Õs. As the evolution of creatine began to speed up through the 90Õs, it became apparent that along with creatine monohydrate came a slew of side effects that include all of the following:

    Stomach Distress

    Diarrhea

    Cramping

    Bloating Unwanted weight gain

    Headaches

    Nausea

    In 1997, FSIÕs V.P. of Research, Joe Carnazzo, R.Ph., invented and patented effervescent creatine. This formulation does not use creatine monohydrate, but instead, a proprietary form of creatine citrate. This product revolutionized the creatine industry, as it rid users of all of the side effects listed above due to its increased bioavailability.

    This invention leaves any other creatine product on the market obsolete. Below is a list of creatine forms currently on the market and the problems in using them.

    Pure Creatine Monohydrate Creatine monohydrate was found to be only 20% in absorbable form after 20 minutes in water, compared to 92% for FSIÕs patented technology. This from a recent university study. DonÕt let the phrases Òmuscle uptakeÓ and ÒassimilationÓ confuse you. The uptake of creatine into muscle can only take place after the creatine has been absorbed through the intestine walls into the bloodstreams. What this study shows is that if you take a 10-gram serving of creatine monohydrate, regardless of what additives are included in the product, only 2 grams will even be available for muscle uptake, or assimilation.

    In addition, because 80% of creatine monohydrate is not in an absorbable form for the body, it simply sits in the stomach drawing water from the bloodstream in an attempt to break it down. This simply doesnÕt work and instead causes the body to become dehydrated, which leads to all of the side effects listed above, most common of which is diarrhea.

    Creatine Monohydrate with High Amounts of Dextrose The creation of these products was based on published research using high amounts (up to 96 grams) of dextrose in order to cause a large insulin spike to increase creatine muscle uptake. The problem with this is three-fold. First, it doesnÕt solve the original problem of creatine bioavailability, which we have already addressed. The intestine must first absorb creatine before the muscle can assimilate it.

    Second, taking sugar in these high amounts leads to both weight gain, attributed to fat gain, and the danger of pancreatic damage associated with long term use.

    Third, this concept is based on outdated research. A more current published study concluded that creatine muscle uptake is dependent on sodium, but not on insulin1. If its not dependent on an insulin spike, why take the sugar in the first place??!!

    Creatine liquids or serums FSI has had virtually every liquid and serum creatine product on the market tested for stability, and to date none have come even close to passing label claims. In fact, the leading serum brand was found to have less than 2% of the 5 grams it claimed to have per serving. The remainder was found to be creatinine, a dangerous by-product of creatine conversion.

    Creatine Gel Caps These products use creatine monohydrate in a gel tablet or capsule. This will not help the bioavailability or absorption rate of creatine monohydrate.

    Creatine Citrate in water This sounds half-way plausible. Unfortunately, it again doesnÕt solve the problem of creatine bioavailability or stability.

    Creatine Citrate has been found to be more soluble, or water dispersible, than creatine monohydrate. However, soluble does not equal bioavailable to the body. The definition of these words are below according to Merriam-WebsterÕs Online Dictionary:

    Soluble - susceptible of being dissolved in or as if in a liquid and especially water.

    Bioavailability - the degree and rate at which a substance (as a drug) is absorbed into a living system or is made available at the site of physiological activity.

    As you can see, because a substance is soluble, that does not make it more available to the body to be absorbed. Many companies in this industry try to confuse you with buzzwords such as ÒsolubleÓ, ÒtransportÓ, and ÒassimilationÓ in order to hide the inferiorities of their creatine products and their fundamental problemÉ.bioavailability.

    Yet another problem with Creatine Citrate lies in its stability. A university study looked at the conversion rates of regular creatine citrate in water and FSIÕs proprietary form of creatine citrate in effervescent form. What this study found was that creatine citrate in water has an exceptionally quick and almost instantaneous conversion to creatinine once it is introduced into water. However, FSIÕs technology is 100% stabile for up to 30 days in solution..

    Furthermore, creatine citrate in water does not afford creatine any protection once it is ingested into the stomach. The acidic environment of the stomach can quickly damage both creatine monohydrate and creatine citrate once ingested, converting it to the dangerous by-product creatinine. These forms of creatine can sit in the stomach for an hour or longer, the whole time being exposed to this volatile environment.

    FSIÕs technology affords creatine a buffered solution to protect it from this acidic environment once it enters the stomach. In addition, the PH shift caused by the effervescence causes a quick ÒdumpingÓ of the stomach contents to the small intestine. Here, the danger ceases and the absorption process of free creatine ion can begin through the intestinal walls to the bloodstream.

    1 Willot, C.A., Young, M.E., Leighton, B., Kemp, G.J., Boehm, E.A., Radda, G.K., Clarke, K. 1999. Cratine uptake in isolated soleus muscle: kinetics and dependence on sodium, but not on insulinn. Acta Physiol. Scand. 166. 99-104

    University Bioavailability Profile According to the recommendation of the FDA Generic Drugs Advisory Committee, the use of dissolution testing is an in vitro surrogate marker for bioavailability.1

    A recently concluded study at a major, independent university was done comparing the in vitro dissolution profiles of FSI's patented effervescent creatine technology to regular creatine monohydrate. The 2-year study revealed that 92% of FSI's formulation was available in absorbable form after 20 minutes as compared to only 20% in the case of creatine monohydrate.

    Furthermore, regular creatine monohydrate in effervescent form was also profiled in the dissolution testing. There was no significant difference in absorbable form when comparing creatine monohydrate in water and creatine monohydrate in effervescent form. Only FSI's patented technology showed the large increase in bioavailability within 20 minutes.
    Last edited by ColdHeartBear; 11-21-2004 at 04:34 AM.
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    Found the original study which is book length so only a small portion is represented below. Go to the web address for an extended read.



    https://physrev.physiology.org/cgi/co...full/80/3/1107


    B. Regulation of Transport of Cr, PCr, ADP, and ATP Across Biological Membranes

    Transport of intermediary metabolites across biological membranes represents an integral part of Cr metabolism in vertebrates. Arg has to be taken up into mitochondria for guanidinoacetate biosynthesis. Guanidinoacetate is released from pancreas and kidney cells and taken up by the liver. Likewise, Cr is exported from the liver and accumulated in CK-containing tissues. Finally, inside the cells, ATP, ADP, Cr, and PCr have to diffuse or to be transported through intracellular membranes to be able to contribute to high-energy phosphate transport between mitochondria and sites of ATP utilization. Evidently, all these sites of membrane transport are potential targets for the regulation of Cr metabolism.

    In chicken kidney and liver, where AGAT is localized in the mitochondrial matrix, penetration of L-Arg through the inner membrane was found to occur only in respiring mitochondria and in the presence of anions such as acetate or phosphate (301). Consequently, the rate of Arg transport across the mitochondrial membranes might influence Cr biosynthesis.

    Cr uptake into CK-containing tissues, e.g., skeletal muscle, heart, brain, or kidney, is effected by a specific, saturable, Na+- and Cl--dependent Cr transporter (see sect. VIIC). Even though the evidence is not as strong as in the case of AGAT, the expression and/or specific activity of the Cr transporter seems to be influenced by dietary and hormonal factors. A 24-h fast slightly increases [Cr] in the plasma but decreases Cr uptake into tibialis anterior and cardiac muscle of the mouse by ~50% (480). In rats, Cr supplementation of the diet decreases Cr transporter expression (317). Similarly, in rat and human myoblasts and myotubes in cell culture, extracellular Cr downregulates Cr transport in a concentration- and time-dependent manner (571). Na+-dependent Cr uptake is decreased by extracellular [Cr] >1 µM, with 50% inhibition being observed at 20-30 µM, i.e., in the range of the physiological plasma concentration of Cr. In media containing 5 mM Cr, transport of Cr is decreased by 50% within 3-6 h, and maximal inhibition (70-80%) is observed within 24 h. Upregulation of Cr transport upon withdrawal of extracellular Cr seems to occur more slowly. Excessive concentrations (5 mM) of guanidinoacetate and GPA also reduce Cr transport significantly, whereas D- and L-ornithine, Crn, Gly, and PCr are ineffective. Because the downregulation of the Cr transporter activity by extracellular Cr is slowed by cycloheximide, an inhibitor of protein synthesis, it has been hypothesized that Cr transport, like Na+-dependent system A amino acid transport (331), is controlled by regulatory proteins. However, no conclusive evidence for or against this hypothesis is currently available. It also remains to be clarified how extracellular [Cr] is transformed into an intracellular signal. Loike et al. (571) have presented weak evidence suggesting that Cr has to be taken up into the cells to exert its effect on Cr transporter activity. On the other hand, dietary Cr supplementation in humans and animals, despite an at least 3- to 20-fold increase in the serum concentration of Cr, results in only a 10-20% increase in the muscle levels of Cr (see sect. XI). Because, in addition, this latter increase in muscle [Cr] is much lower than the ones observed during physical exercise, it is difficult to envisage that intracellular [Cr] should be a key regulator of Cr uptake.

    In a thorough investigation of the Cr transporter activity in cultured mouse G8 myoblasts, Odoom et al. (711) showed that Cr uptake is stimulated by isoproterenol, norepinephrine, the cAMP analog N6,2'-O-dibutyryladenosine 3',5'-cyclic monophosphate, and the beta 2-agonist clenbuterol, but not by the alpha 1-adrenergic receptor agonist methoxamine. Likewise, the stimulatory action of norepinephrine is not affected by alpha -adrenergic receptor antagonists but is inhibited by beta -antagonists, with the beta 2-antagonist butoxamine being more effective than the beta 1-antagonist atenolol. Thus the Cr transporter activity may be controlled predominantly by beta 2-adrenergic receptors that have cAMP as their intracellular signal. In fact, analysis of the Cr transporter cDNA sequence revealed consensus phosphorylation sites for cAMP-dependent protein kinase (PKA) and for protein kinase C (PKC) (691, 927). However, in transiently transfected cells expressing the human Cr transporter, phorbol 12-myristate 13-acetate, an activator of PKC, displayed a small inhibitory effect on Cr uptake, whereas forskolin (an activator of adenylyl cyclase), okadaic acid (a phosphatase inhibitor), A23187 (a calcium ionophore), and insulin were ineffective. The last finding, in turn, contrasts with experiments on rat skeletal muscle where insulin significantly increased Cr uptake, whereas alloxan-induced diabetes had no effect on Cr accumulation (see Ref. 349). Insulin and insulin-like growth factor I also stimulated Cr uptake in mouse G8 myoblasts (711), and insulin at physiologically high or supraphysiological concentrations enhanced muscle Cr accumulation in humans (943). Insulin increases Na+-K+-ATPase activity which, indirectly, may stimulate Cr transporter activity (see Ref. 943). In this context, it seems noteworthy that guanidinoacetate, and to a lower extent Arg and Cr, were seen to stimulate insulin secretion in the isolated perfused rat pancreas (15). Despite using G8 myoblasts and myotubes as Odoom et al. (711; see above), and despite other indications that clenbuterol may exert some of its anabolic effects on muscle by stimulating Cr uptake, Thorpe et al. (1003) failed to detect an effect of clenbuterol on Cr transport.

    The contents of Cr, PCr, and total Cr are decreased in hyperthyroid rat cardiac muscle by 13, 62, and 42%, respectively, with these changes being paralleled by an increased sensitivity of the heart to ischemic damage (874). Although this finding might be explained by a direct action of thyroid hormones on the Cr transporter, experiments with colloidal lanthanum suggest that it is due instead to an increased (reversible) leakiness of the sarcolemma. Kurahashi and Kuroshima (519) suggested that the 3,3',5-triiodothyronine-induced creatinuria and decrease in muscle Cr contents is due both to decreased uptake and increased release of Cr by the muscles. On the other hand, Cr uptake into mouse G8 myoblasts was shown to be stimulated by 3,3',5-triiodothyronine and by amylin which, in muscle, is known to bind to the calcitonin gene-related peptide receptor (711).

    As to be expected from the Na+ dependence of the Cr transporter (see sect. VIIC), Cr uptake is diminished in deenergized cells and is also depressed by the Na+-K+-ATPase inhibitors ouabain and digoxin (58, 293, 515, 570, 711). When, however, L6 rat myoblasts are preincubated with ouabain or digoxin, and Cr uptake subsequently is analyzed in the absence of these inhibitors, it is even higher than in untreated control cells (58). Finally, in erythrocytes from uremic patients, the Na+-dependent component of Cr influx is 3.3 times higher than in normal human erythrocytes. This finding may be due, by analogy, to the known occurrence of inhibitors of Na+-K+-ATPase in uremic plasma (950, 984). Obviously, cells may respond to decreased Na+-K+-ATPase activity, which in turn likely decreases Cr transporter activity, by compensatory upregulation of Na+-K+-ATPase (382) and/or Cr transporter expression.

    After incubation of L6 rat myoblasts for 20 h under control conditions, replacement of the conditioned medium by fresh control medium decreases Cr uptake by 32-45% (58). This may indicate that conditioned medium from L6 myoblasts contains a modulator of Cr transport.

    Despite all these investigations on the regulation of Cr uptake, it cannot be decided yet whether regulation of Cr uptake is effected directly by modulating the expression and/or activity of the Cr transporter or indirectly via alterations of the transmembrane electrochemical gradient of Na+ which depends primarily on the Na+-K+-ATPase activity. Accordingly, it is still unclear whether Cr uptake via the Cr transporter is under kinetic or thermodynamic control. The findings that Cr uptake is inhibited by ouabain and digoxin and that 3,3',5-triiodothyronine, isoproterenol, and amylin not only stimulate Cr uptake but also increase the Na+-K+-ATPase activity and, thus, the membrane potential would favor indirect regulation of the Cr transporter by the electrochemical gradient of Na+. However, with the assumption of a Na+ to Cr stoichiometry of the Cr transporter of 1 or 2, the theoretical concentration ratio of intracellular versus extracellular Cr should be between 900 and 3,000 (286, 711). If the chloride dependence of the Cr transporter were also taken into account, this theoretical ratio would be even higher. In sharp contrast to these values, the actual concentration ratio in resting muscle is around 80. Because, in addition, dietary Cr supplementation over several days or weeks considerably increases [Cr] in human and animal serum, but only slightly enhances the Cr levels in muscle (see sect. XI), and because in rats fed GPA and cyclocreatine, these Cr analogs compete efficiently with Cr uptake into muscle and thereby largely deplete the intracellular pools of Cr and PCr, the hypothesis that the Cr transporter is kinetically controlled seems at present more plausible. Clearly, the question of how Cr uptake is regulated in detail is of importance for a deeper understanding of Cr metabolism in health and disease. In particular, it will be crucial to determine the exact Na+ and Cl- stoichiometries of the Cr transporter.

    Because part of the Cr that is accumulated in CK-containing tissues is converted to PCr, it might be anticipated that Cr uptake and phosphate uptake influence each other. In fact, in mouse myoblasts that are exposed to extracellular Cr, Pi uptake is transiently stimulated (773). This finding is probably not due to concerted regulation of the Cr and Pi transporters but may rely on a local decrease in Pi concentration due to phosphorylation of intracellularly accumulated Cr. In Langendorff-perfused rabbit hearts, the intracellular concentrations of Cr and of Cr plus PCr remain significantly higher when the perfusion medium is devoid of phosphate than when it contains 1 mM Pi (286). This effect was attributed to decreased Cr efflux during phosphate-free perfusion.

    Only few and inconclusive data are available on Cr efflux from cells. Although in L6 rat myoblasts at 37°C, Cr efflux amounted to 2.8-3.6% of intracellular Cr per hour (571), the respective value for G8 mouse myoblasts at 37°C was 5%/day (711). The latter value is comparable to the fractional conversion rate of Cr to Crn and may indicate that the plasma membrane is largely impermeable for Cr once it is intracellularly trapped. Because the liver is the main site of Cr biosynthesis in the body, the plasma membrane of hepatocytes is expected to be more permeable for Cr than that of muscle cells. This finding agrees with the fact that upon administration of Cr, liver, kidney, and viscera constitute a rapidly expansible pool for Cr, whereas muscle and nervous tissues constitute a slowly expansible pool of Cr plus PCr (480; see also Ref. 1077). On the other hand, when transgenic mice expressing CK in liver were fed 10% Cr in the diet for 5 days, Cr efflux from the liver proved to be insignificant (606). Because high dietary intake of Cr makes de novo biosynthesis of Cr superfluous, a putative transport protein responsible for Cr export from the liver may simply have been downregulated in this experimental set-up. In any case, this finding should not be taken as evidence against a significant contribution of the liver to de novo biosynthesis of Cr in vertebrates. Finally, cultured Sertoli cells from the seminiferous epithelium of rats were shown to secrete Cr into the medium (665). Cr secretion was stimulated by physiological and toxicological modulators of Sertoli cell function like follicle-stimulating hormone, dibutyryl cAMP, mono-(2-ethylhexyl)phthalate, or cadmium.

    The permeability itself as well as changes in permeability of the outer mitochondrial membrane may be critical for the stimulation of mitochondrial respiration and high-energy phosphate synthesis, as well as for the transport of these high-energy phosphates between sites of ATP production and ATP utilization within the cell (for reviews, see Refs. 94, 280, 838, 1124). Changes in permeability of the outer mitochondrial membrane pore protein (voltage-dependent anion-selective channel; VDAC) may be accomplished 1) by "capacitive coupling" to the membrane potential of the inner membrane, leading to a voltage-dependent "closure" of the pore, or 2) by a VDAC modulator protein which increases the rate of voltage-dependent channel closure by ~10-fold. To what extent these mechanisms operate in vivo and retard the diffusion of ADP, ATP, Pi, Cr, and PCr remains to be established.

    To conclude, the most critical determinant for the regulation of Cr metabolism seems to be the serum concentration of Cr. An elevation of serum [Cr] over an extended period of time would point to excess de novo biosynthesis or dietary intake of Cr and, in addition, would indicate that the tissue pools of Cr and PCr are replenished. The observed or suspected effects of an elevated serum [Cr], namely, to downregulate the expression and/or activity of AGAT and possibly also the Cr transporter, would therefore help to spare precursors of Cr (Arg, Gly, Met) and to maintain normal, steady levels of Cr and PCr in CK-containing tissues. As a consequence, the rate of Cr biosynthesis is highest in young, healthy, fast-growing vertebrates under anabolic conditions on a balanced, Cr-free diet (1077).
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    MuscleChemistry Registered Member Board Certified Psy.D

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    JESUS Clodheart you know your shit
    1 month supply of roids $300,
    1 month supply of protien $70,
    1 month gym membersip $50,
    not being able to fit through the door cos your too f%&kin wide PRICELESS

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    ColdHeartBear's Avatar
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    Brutal1: I missed clodheart's reply.

    But I can put forth a little extra effort when it comes to critiquing such a typical ripoff the unwary type company as musclewreck.
    Not only do you pay ridiculous prices for their sugar, the evidence is in that the sugar is not the factor in utilization of the creatine.
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    I'd have to disagree with your statement coldheart about getting the cheapest creatine. There is another creatine which is in ester form (they tried to make it illegal before being sold OTC) it is all absorbed into the muscles without waste and sides. Only 1/2 a tsp is taken too which means it lasts forever and is actually more cost effective dose per dose.

    I'm with mask on taking it with R-ala though b/c studies have recently shown that b/c it is an insulin mimicker it helps push it into muscles without having to take more sugar (carbs) with it. I know VPX has the product called CEX and I'm sure there are other brands/makers too unless VPX owns a patent on it which I doubt.

    As for celltech...Yuck, I tried a friends stuff once.I hate the company and their annoying 6 page ads in magazines. I'll never buy that crap. Down with MuscleTech!!!
     

  21. #21
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    Oh yeah...don't do the loading phase. They're trying to get you to waste as much as you can so you'll need more, buy more.
     

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    Actually proud, at the time I made my first reply I knew nothing regarding the new creatine esters. Please accept this as a rethinking of my position subject to time actually supporting the hype in process now.
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    No problem this post was probably up here for awhile but I haven't been as regular as I once was. My fault not yours...
     

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