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Author Topic: Creatine constatly  (Read 3351 times)
D-bol
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« on: January 01, 2007, 11:21:29 PM »

Wanted to ask anyone's experience w/ taking creatine constantly for 12 months or so. Any good? Sides?

I don't experience great gains from it but it really boosts muscle endurance, which in my heavily loaded schedule is important. However, I am cautious of taking it continuosly.


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« Reply #1 on: January 02, 2007, 12:46:36 AM »

i take a teaspoon everyday (unless i forget) and havent had any problems.... not sure if it has diminishing returns taking over a long period of time

some people say to cycle it etc

i say don't worry as its in foods and we take a multi everyday on the same criteria

also ive heard that if theres excess then u just excrete it anyways
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« Reply #2 on: January 02, 2007, 06:51:29 AM »

Wanted to ask anyone's experience w/ taking creatine constantly for 12 months or so. Any good? Sides?

I don't experience great gains from it but it really boosts muscle endurance, which in my heavily loaded schedule is important. However, I am cautious of taking it continuosly.




Not a good idea. I'd like to quote myself on this topic and post the scientific proof for my saying again.  Grin Grin

scientific proof:  Grin Grin Grin


 Down-regulation of the creatine transporter after chronic creatine ingestion:

The creatine transporter (CreaT), responsible for the uptake of creatine into a variety of tissues and cells, was detected in rat skeletal and cardiac muscle, cerebellum, forebrain and kidney. Two polypeptides with an apparent Mr of 70 kDa and 55 kDa were always recognized by both of our specific polyclonal antibodies directed against synthetic peptides of either the NH2- or the COOH-terminus of CreaT, indicating a high degree of homology between the two proteins [51]. In contrast to published data obtained by Northern blot analysis, suggesting a complete absence of CreaT mRNA message in liver, we could clearly detect both CreaT polypeptides also in rat liver and hepatocyte lysates. In support of this, cultured hepatocytes show an endogenous CreaT activity which is antagonized by the creatine analogue, b-guanidino propionic acid (b-GPA), a well known inhibitor of CreaT. Glyco-staining of CreaT, enriched by immuno-affinity chromatography, mainly containing both the 70 and 55 kDa bands, showed strong glycosylation of preferentially the upper 70 kDa polypeptide indicating that the latter is a posttranslationally modified form of the 55 kDa core protein. HeLa cells transfected with rat CreaT cDNA showed an increase in [14C]-creatine uptake, when compared to control cells, that was antagonized by b-GPA. In parallel, an increase in the expression of both the 70 and the 55 kDa polypeptides over endogenous CreaT of controls was noticed on Western blots. Furthermore, we have found that chronic creatine supplementation of rats, at very high dosage, down-regulates in vivo the expression and/or accumulation of the CreaT in skeletal muscle, but not in brain and heart [58]. Although the amounts of creatine taken by athletes, 20 grams / day during a 10 days loading phase and 5 grams as a maintenance dose during the following three months (amounting to approximately 0.1 gram of Cr /kg body weight/ day), is significantly lower than the amounts given in the above experiments to the rats (approximately 0.5 grams /kg body weight /day), the finding made with laboratory animals nevertheless may have consequences with respect to creatine supplementation schedules for humans. In the future, however, detailed studies on humans are needed to optimize the creatine supplementation schedules in use with respect to the observed down-regulation of CreaT expression and/or accumulation in animal experiments. According to most recent results, using "normal" Cr supplementation schedules with humans, CreaT seems also to be down-regulated, especially in combination with exercise (Greenhaff et al. unpublished), but, over the time course of this human trial, creatine transporter function did not seem to become a limiting factor for maintaining normal intracellular creatine levels. Nevertheless, as suggested earlier [86], a one month pause, after three months of continuous creatine supplementation, would still seem to be a reasonable thing to do.
With respect to cardiac pathology, a down-regulation of creatine transporter protein expression has recently been shown in experimental animal models of heart disease, as well as in failing human myocardium [91], indicating that the generally lowered PCr and Cr levels measured in failing hearts are related to down-regulated creatine transporter capacity. Thus, creatine supplementation, by improving cellular energetics, may also turn out to be beneficial for certain heart diseases.


http://icbxw.ethz.ch/creatine/creatine_supplementation.html#English
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« Reply #3 on: January 02, 2007, 01:53:08 PM »

phew its too early for my eyes to read lots of small writing in purple  Shocked

anyways i think i basically got "creatine for 3 months then 1 month off"

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« Reply #4 on: January 03, 2007, 02:08:13 PM »

Just for you.  Grin Grin

Down-regulation of the creatine transporter after chronic creatine ingestion:

The creatine transporter (CreaT), responsible for the uptake of creatine into a variety of tissues and cells, was detected in rat skeletal and cardiac muscle, cerebellum, forebrain and kidney. Two polypeptides with an apparent Mr of 70 kDa and 55 kDa were always recognized by both of our specific polyclonal antibodies directed against synthetic peptides of either the NH2- or the COOH-terminus of CreaT, indicating a high degree of homology between the two proteins [51]. In contrast to published data obtained by Northern blot analysis, suggesting a complete absence of CreaT mRNA message in liver, we could clearly detect both CreaT polypeptides also in rat liver and hepatocyte lysates. In support of this, cultured hepatocytes show an endogenous CreaT activity which is antagonized by the creatine analogue, b-guanidino propionic acid (b-GPA), a well known inhibitor of CreaT. Glyco-staining of CreaT, enriched by immuno-affinity chromatography, mainly containing both the 70 and 55 kDa bands, showed strong glycosylation of preferentially the upper 70 kDa polypeptide indicating that the latter is a posttranslationally modified form of the 55 kDa core protein. HeLa cells transfected with rat CreaT cDNA showed an increase in [14C]-creatine uptake, when compared to control cells, that was antagonized by b-GPA. In parallel, an increase in the expression of both the 70 and the 55 kDa polypeptides over endogenous CreaT of controls was noticed on Western blots. Furthermore, we have found that chronic creatine supplementation of rats, at very high dosage, down-regulates in vivo the expression and/or accumulation of the CreaT in skeletal muscle, but not in brain and heart [58]. Although the amounts of creatine taken by athletes, 20 grams / day during a 10 days loading phase and 5 grams as a maintenance dose during the following three months (amounting to approximately 0.1 gram of Cr /kg body weight/ day), is significantly lower than the amounts given in the above experiments to the rats (approximately 0.5 grams /kg body weight /day), the finding made with laboratory animals nevertheless may have consequences with respect to creatine supplementation schedules for humans. In the future, however, detailed studies on humans are needed to optimize the creatine supplementation schedules in use with respect to the observed down-regulation of CreaT expression and/or accumulation in animal experiments. According to most recent results, using "normal" Cr supplementation schedules with humans, CreaT seems also to be down-regulated, especially in combination with exercise (Greenhaff et al. unpublished), but, over the time course of this human trial, creatine transporter function did not seem to become a limiting factor for maintaining normal intracellular creatine levels. Nevertheless, as suggested earlier [86], a one month pause, after three months of continuous creatine supplementation, would still seem to be a reasonable thing to do.
With respect to cardiac pathology, a down-regulation of creatine transporter protein expression has recently been shown in experimental animal models of heart disease, as well as in failing human myocardium [91], indicating that the generally lowered PCr and Cr levels measured in failing hearts are related to down-regulated creatine transporter capacity. Thus, creatine supplementation, by improving cellular energetics, may also turn out to be beneficial for certain heart diseases.

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« Reply #5 on: January 03, 2007, 03:11:03 PM »

Just for you.  Grin Grin

Down-regulation of the creatine transporter after chronic creatine ingestion:

The creatine transporter (CreaT), responsible for the uptake of creatine into a variety of tissues and cells, was detected in rat skeletal and cardiac muscle, cerebellum, forebrain and kidney. Two polypeptides with an apparent Mr of 70 kDa and 55 kDa were always recognized by both of our specific polyclonal antibodies directed against synthetic peptides of either the NH2- or the COOH-terminus of CreaT, indicating a high degree of homology between the two proteins [51]. In contrast to published data obtained by Northern blot analysis, suggesting a complete absence of CreaT mRNA message in liver, we could clearly detect both CreaT polypeptides also in rat liver and hepatocyte lysates. In support of this, cultured hepatocytes show an endogenous CreaT activity which is antagonized by the creatine analogue, b-guanidino propionic acid (b-GPA), a well known inhibitor of CreaT. Glyco-staining of CreaT, enriched by immuno-affinity chromatography, mainly containing both the 70 and 55 kDa bands, showed strong glycosylation of preferentially the upper 70 kDa polypeptide indicating that the latter is a posttranslationally modified form of the 55 kDa core protein. HeLa cells transfected with rat CreaT cDNA showed an increase in [14C]-creatine uptake, when compared to control cells, that was antagonized by b-GPA. In parallel, an increase in the expression of both the 70 and the 55 kDa polypeptides over endogenous CreaT of controls was noticed on Western blots. Furthermore, we have found that chronic creatine supplementation of rats, at very high dosage, down-regulates in vivo the expression and/or accumulation of the CreaT in skeletal muscle, but not in brain and heart [58]. Although the amounts of creatine taken by athletes, 20 grams / day during a 10 days loading phase and 5 grams as a maintenance dose during the following three months (amounting to approximately 0.1 gram of Cr /kg body weight/ day), is significantly lower than the amounts given in the above experiments to the rats (approximately 0.5 grams /kg body weight /day), the finding made with laboratory animals nevertheless may have consequences with respect to creatine supplementation schedules for humans. In the future, however, detailed studies on humans are needed to optimize the creatine supplementation schedules in use with respect to the observed down-regulation of CreaT expression and/or accumulation in animal experiments. According to most recent results, using "normal" Cr supplementation schedules with humans, CreaT seems also to be down-regulated, especially in combination with exercise (Greenhaff et al. unpublished), but, over the time course of this human trial, creatine transporter function did not seem to become a limiting factor for maintaining normal intracellular creatine levels. Nevertheless, as suggested earlier [86], a one month pause, after three months of continuous creatine supplementation, would still seem to be a reasonable thing to do.
With respect to cardiac pathology, a down-regulation of creatine transporter protein expression has recently been shown in experimental animal models of heart disease, as well as in failing human myocardium [91], indicating that the generally lowered PCr and Cr levels measured in failing hearts are related to down-regulated creatine transporter capacity. Thus, creatine supplementation, by improving cellular energetics, may also turn out to be beneficial for certain heart diseases.


Can u just fukin summarize it for us please? Shit!
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CEA999
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« Reply #6 on: January 03, 2007, 03:53:19 PM »

The creatine transporter (CreaT), seems also to be down-regulated, especially in combination with exercise (Greenhaff et al. unpublished).
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« Reply #7 on: January 04, 2007, 12:46:41 AM »

I remember back in high school ( 98 ) it was said that creatine lowered sperm count, or some shit like that.  Here I am almost 10 years later, married, and lots of sex, and still no kids.( not a bad thing ), so there might be some truth to that after all, because I should have fathered my own race by now. 
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« Reply #8 on: January 04, 2007, 03:43:54 AM »

I remember back in high school ( 98 ) it was said that creatine lowered sperm count, or some shit like that.  Here I am almost 10 years later, married, and lots of sex, and still no kids.( not a bad thing ), so there might be some truth to that after all, because I should have fathered my own race by now. 

The opposite is true.



The enzyme creatine kinase (CK), catalyzing the reversible transfer of the N-phosphoryl group from phosphocreatine (PCr) to ADP to regenerate ATP, plays a key role in the energy homeostasis of cells with intermittently high, fluctuating energy requirements, e.g. skeletal and cardiac muscle, neurons, photoreceptors, spermatozoa and electrocytes. Cytosolic CK isoenzyme(s) (MM-, MB- and BB-CK) are always co-expressed in a tissue-specific fashion together with a mitochondrial isoform. Using biochemical fractionation and in situ localization, one was able to show that the CK isoenzymes, earlier considered to be strictly soluble, are in fact compartmentalized subcellularly and coupled functionally and/or structurally either to sites of energy production (glycolysis and mitochondria) or energy consumption (cellular ATPases, such as the acto-myosin ATPase and SR-Ca2+-ATPase). Thus they form an intricate, highly regulated energy distribution network, the so-called PCr-circuit or PCr-shuttle (Figure 1, for review see [1] and the special volumes of Mol. Cell Biochem. 133/134, 1994, and 184, 1998).
This non-equilibrium energy transport model has been challenged, based upon global 31P-NMR experiments, measuring CK-mediated flux in muscles at different work-loads [2,3]. The conclusions reached by these authors were i) that the CK system is in equilibrium with the substrates, behaving like a solution of well-mixed enzymes, ii) that effects of compartmentation were negligible with respect to total cellular bioenergetics and iii) that thermodynamic characteristics of the cytosol could be predicted as if the CK metabolites were freely mixing in solution. However, based on the organizational principles of sarcomeric muscle, as well as on our findings concerning the highly structured subcellular CK-compartments, this interpretation seemed rather unlikely and thus has been questionned [4]. In support of this, 31P-NMR CK-flux measurements with transgenic mice showing graded reductions of MM-CK expression in their muscles, revealed a strikingly unexpected, "anomalous" CK-flux behaviour [5]. These results indicate that some flux through CK, presumably bound CK, and possibly also some PCr and/or ATP, are NMR-invisible or otherwise not amenable to this analysis [4,6]. In the meantime, more evidence from NMR-measurements [7,8,9,10], as well as from recent in vivo 14[C]Cr-tracer studies [11], is accumulating in favour of compartmentation of the CK system and for the existence of different pools of CK substrates. As a matter of fact, it has now become clear that in muscle, Cr and PCr molecules do not tumble freely, but display partial orientational ordering, which is in contrast to what is expected for small molecules dissolved in water [7]. Furthermore, 31P-NMR saturation transfer experiments with sea-urchin spermatozoa show that the CK-flux increases by a factor of 10-20 upon sperm activation [12]. These specialized sperm cells derive their energy for motility entirely from fatty oxidation within the single large mitochondrion located just behind the sperm head, from where PCr is diffusing along the 50 Ám long sperm tail to fuel the dynein/tubulin ATPase. It is obvious that in these polar, elongated cells, the diffusional limitation of ADP is the key limiting factor with respect to high-energy phosphate provision [13]. Also in support of the PCr-shuttle model, the calculated diffusional flux of ADP in these sperm cells is by 2 and 3 orders of magnitude smaller than those of ATP and PCr, respectively [13].
In conclusion, it becomes obvious that calculations of free cellular [ADP] by using global [ATP] and [PCr], determined by in vivo 31P-NMR, together with the CK equilibrium constant, may be valid only in certain limited cases, e.g. in fast twitch glycolytic white muscle fibres, where the buffer function of CK by far prevails the transport function and where the flux through the CK reaction at rest and during high work load are higher by a factor of 100 and 20, respectively, than the total cellular ATPase turnover at these respective states. In cases where the transport function of the CK prevails, e.g. oxidative tissues or in polar cells (sea urchin sperms) with high concentrations of Mi-CK, local [ADP] and [ATP] levels, e.g. in the mitochondrial intermembrane space or near CK-ATPase complexes, may differ by orders of magnitude compared to the bulk concentrations calculated from the CK equilibrium constant. Considering the complications of subcellular compartmentation of CK isoenzymes in a cell, where after activation, some CK will work in the forward and some in the reverse direction, the interpretation of global CK flux measurements may also represent a rather difficult endeavour.
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« Reply #9 on: May 28, 2007, 06:59:09 PM »

ok i have a massive headache....what's the condensed version of this? what kind of cycle would you suggest??
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« Reply #10 on: May 29, 2007, 01:00:35 AM »

ok i have a massive headache....what's the condensed version of this? what kind of cycle would you suggest??

6-8weeks on, 4 weeks off.
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« Reply #11 on: May 29, 2007, 04:11:21 AM »

I've been taking creatine since its release years ago....took it for about 9 or 10 years straight....was just part of the routine....went off for about 3 months and had no problems at all....now thats not to say i had no internal problems....just none that i could feel....

my opinion is that its effective and safe at longer intervals ...
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« Reply #12 on: May 30, 2007, 12:31:20 AM »

I've been taking creatine since its release years ago....took it for about 9 or 10 years straight....was just part of the routine....went off for about 3 months and had no problems at all....now thats not to say i had no internal problems....just none that i could feel....

my opinion is that its effective and safe at longer intervals ...

If you would have read the text i posted above you would know now that it is safe but ineffective to take it over longer periods.
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« Reply #13 on: May 30, 2007, 07:41:45 AM »

Exactly, your body will stop producing the little creatine it does naturally and always a good idea to cycle off any supplement other than multi-vits, glutamine, efas.

Stay on 12 months and your toilet will get bigger and stronger!
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« Reply #14 on: May 30, 2007, 10:39:45 AM »

If you would have read the text i posted above you would know now that it is safe but ineffective to take it over longer periods.

with all due respect donkey---next time just summarize the article and provide a link...I didn't have time to read the entire article...bar exam in July!
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« Reply #15 on: May 30, 2007, 11:58:39 AM »

Wanted to ask anyone's experience w/ taking creatine constantly for 12 months or so. Any good? Sides?

I don't experience great gains from it but it really boosts muscle endurance, which in my heavily loaded schedule is important. However, I am cautious of taking it continuosly.


I've used creatine, off and on, since 1996. My first time loading with it was using Phosphagen HP. I ended up with 12 extra lbs. after a period of 21/2 weeks. The astronomical gains that you see in the ads usually come to first-time users.

However, the most consistent used I've had with it has been my use since 2004. For nearly three years, I've been using CELL-TECH. And, it's done right by me. It helped me bulk up to 252 lbs, back in 2005. When trimming down, I used CELL-TECH to regain the strength I lost, while cutting my carbs.

More recently, I've decided to give Size-On a try. The stuff tastes great (at least, the Lemon Ice one does). And, it gives quite a kick. Size-On is taken during the workout; whereas CELL-TECH is designed for consumption after training.

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