This claim has not been demonstrated at this time, and a recent comparative study of buffered creatine against basic creatine monohydrate found no significant differences between the two in 36 resistance trained individuals, in regard to the effects or the accumulation of creatine in muscle tissue.[71] There also were no significant differences in the amount of adverse side-effects reported.
Guanidoacetate (made by AGAT) then receives a methyl donation from S-adenosyl methionine via the enzyme guanidinoacetate methyltransferase (GAMT), which produces S-adenosylhomocysteine (as a byproduct) and creatine. Deficiencies in GAMT are more severe (although equally rare) relative to AGAT, resulting in severe mental retardation and autism-like symptoms.[31]
Creatine ingested through supplementation is transported into the cells exclusively by CreaT1. However, there is another creatine transporter Crea T2, which is primarily active and present in the testes [12]. Creatine uptake is regulated by various mechanisms, namely phosphorylation and glycosylation as well as extracellular and intracellular levels of creatine. Crea T1 has shown to be highly sensitive to the extracellular and intracellular levels being specifically activated when total creatine content inside the cell decreases [12]. It has also been observed that in addition to cytosolic creatine, the existence of a mitochondrial isoform of Crea T1 allows creatine to be transported into the mitochondria. Indicating another intra-mitochondrial pool of creatine, which seems to play an essential role in the phosphate-transport system from the mitochondria to the cytosol [13]. Myopathy patients have demonstrated reduced levels of total creatine and phosphocreatine as well as lower levels of CreaT1 protein, which is thought to be a major contributor to these decreased levels [14].
Creatine is mostly synthesized in the liver via AGAT and GAMT[28][32] (the other locations are neurons,[34] the pancreas, and kidneys[33]) despite it not being stored in high levels in the liver like glycogen or adipose would be. Supplemental creatine is known to suppress AGAT by downregulating transcription,[30] which probably occurs in humans (since the products of AGAT are reduced with creatine supplementation).[38]

Different forms of creatine in combination with other sports supplements as well as varying doses and supplementation methodology should continue to be researched in an attempt to understand further application of creatine to increase sports and exercise performance of varying disciplines. It is important to remain impartial when evaluating the safety of creatine ingested as a natural supplement. The available evidence indicates that creatine consumption is safe. This perception of safety cannot be guaranteed especially that of the long term safety of creatine supplementation and the various forms of creatine which are administered to different populations (athletes, sedentary, patient, active, young or elderly) throughout the globe.
Supplementation of creatine at 5g daily alongside rehabilitation (after limb immobilization for two weeks while taking 20g daily) is associated with a preservation in GLUT4 levels, which were reduced during immobilization. During exercise rehabilitation, it increased to 40% above placebo.[330] This study failed to note an increase in GLUT4 in control, despite exercise normally doing so.[331][332] This effect is thought to be the result of the low frequency of activity. Thus, creatine was thought to augment the increase (insignificant due to low exercise) to significant levels.[330] In other studies, creatine was found to increase GLUT by approximately 30% relative to control, but this effect failed to reach statistical significance. This study did not issue an exercise protocol.[207]

If you’re a beginner, you should train with three full-body workouts per week. In each one, do a compound pushing movement (like a bench press), a compound pulling movement (like a chinup), and a compound lower-body exercise (squat, trap-bar deadlift, for example). If you want to add in 1–2 other exercises like loaded carries or kettlebell swings as a finisher, that’s fine, but three exercises is enough to work the whole body.
Intensive weight training causes micro-tears to the muscles being trained; this is generally known as microtrauma. These micro-tears in the muscle contribute to the soreness felt after exercise, called delayed onset muscle soreness (DOMS). It is the repair of these micro-traumas that results in muscle growth. Normally, this soreness becomes most apparent a day or two after a workout. However, as muscles become adapted to the exercises, soreness tends to decrease.[22]

Creatine is a hydrophilic polar molecule that consists of a negatively charged carboxyl group and a positively charged functional group [64]. The hydrophilic nature of creatine limits its bioavailability [65]. In an attempt to increase creatines bioavailability creatine has been esterified to reduce the hydrophilicity; this product is known as creatine ethyl ester. Manufacturers of creatine ethyl ester promote their product as being able to by-pass the creatine transporter due to improved sarcolemmal permeability toward creatine [65]. Spillane et al [65] analyzed the effects of a 5 days loading protocol (0.30 g/kg lean mass) followed by a 42 days maintenance phase (0.075 g/kg lean mass) of CM or ethyl ester both combined with a resistance training program in 30 novice males with no previous resistance training experience. The results of this study [65] showed that ethyl ester was not as effective as CM to enhance serum and muscle creatine stores. Furthermore creatine ethyl ester offered no additional benefit for improving body composition, muscle mass, strength, and power. This research did not support the claims of the creatine ethyl ester manufacturers.
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