Cycle creatine? I've never heard that before. Does anyone else agree with that? I'm not saying you're wrong bro cuse you seem to know your shit, I've just never heard of anyone cycling creatine.
http://icbxw.ethz.ch/creatine/creatine_supplementation.html#English 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.
