In the phosphorylated form, creatine serves as an energy substrate that contributes to the resynthesis of adenosine triphosphate (ATP) during maximal exercise. Phosphocreatine has been implicated as a causative factor in the development of muscular fatigue based on data demonstrating correlations between phosphocreatine depletion and reduced force production. In 1992, investigators<sup>29 Harris R.C., Söderlund K., Hultman E. Elevation of creatine in resting and exercised muscle of normal subjects by creatine supplementation Clin Sci 1992 ;  83 : 367-374

Cliquez ici pour aller à la section Références</sup> found that several days of creatine supplementation significantly enhances accumulation of both free creatine and phosphocreatine in skeletal muscle. Subsequently, numerous studies<sup>29 Harris R.C., Söderlund K., Hultman E. Elevation of creatine in resting and exercised muscle of normal subjects by creatine supplementation Clin Sci 1992 ;  83 : 367-374

Cliquez ici pour aller à la section Références</sup> have examined the acute effects of creatine supplementation on exercise performance. These studies indicate ingestion of 20 to 25 g/d creatine per day for 5 to 7 days attenuates the normal decrease in force or power production during short-duration, maximal bouts of exercise, especially intermittent protocols. Creatine supplementation has not been shown to improve longer-duration, aerobic exercise. Elevated muscle creatine enhances exercise performance via an increased ability to match ATP supply to ATP demand. An increase in the rate of phosphocreatine resynthesis during recovery between bouts of exercise, and thus higher phosphocreatine levels at the start of the subsequent exercise bout, is believed to be the primary mechanism explaining the ergogenic effects of creatine supplementation during intense, intermittent protocols. These beneficial effects are related to the extent of creatine loading in muscle. An increase in body mass ranging from 1 to 3 kg is common after 1 week of creatine supplementation attributable to an increase in total body water. Limited data describe the effects of long-term creatine supplementation. New data indicate that creatine supplementation may enhance the physiologic adaptations to resistance training in men and women, most likely a result of being able to train more intensely. No adverse side effects associated with creatine supplementation in healthy individuals have been documented in the scientific literature. Athletes most likely to gain from creatine supplementation are those who participate in sports or activities which challenge the phosphagen energy system. Nearly all of the research examining creatine supplementation has been obtained in laboratories. Field studies documenting the beneficial effects of creatine supplementation during specific sports and competitions are limited.

Understanding the effects of creatine supplementation has at times been confounded by information of an anecdotal nature. To date, posturing of fears and cautions about creatine supplementation have many times been mediated by the lack of controlled experimental data and ease of making anecdotal observations from uncontrolled field environments. The fact that creatine has been shown to improve performance under certain physiologic conditions has brought a spotlight upon this supplement with an intensity that is nothing short of a phenomenon in sports nutrition. The insatiable need for answers to many questions by athletes, parents, coaches, trainers, and physicians has at times pushed the available evidence to the limits of interpretation of facts generated by laboratory science. Thus, we are left with many unanswered questions, and we must be patient while an unprecedented number of laboratories around the world continue the study of this supplement. This article presents an overview of the current understanding of creatine supplementation and how it may mediate any changes in human performance.

Creatine is a naturally occurring, energy-producing substance in the human body synthesized from amino acids primarily in the liver, pancreas, and kidney.<sup>65 Walker J.B. Metabolic control of creatine biosynthesis: Restoration of transamidinase activity following creatine repression J Biol Chem 1961 ;  236 : 493-498

Cliquez ici pour aller à la section Références</sup> Figure 1 shows the typical synthesis pathway for creatine from three amino acids. Creatine is also consumed in the diet from the ingestion of animal products. Because our bodies have all of the enzymes required for creatine biosynthesis, dietary sources are not an absolute requirement. Thus, creatine is not considered an essential nutrient in the diet.

In the human body, creatine exists in both the free and the phosphorylated forms, and approximately 95% of all the creatine is contained within skeletal muscle. This makes skeletal muscle the primary target tissue for loading with supplementation. The normal concentration in muscle is 120 mmol/kg dry mass but ranges from approximately 100 to 140 mmol/kg dry mass in the population. Muscle creatine stores break down at a relatively constant rate (approximately 2 g/d) into creatinine. Creatine is filtered in the kidney by simple diffusion and excreted in the urine 1(Figure 2). Excess creatine is also excreted in the urine. In a person who consumes a typical Western diet, the 2 g lost daily is replaced equally from endogenous synthesis and dietary sources. How endogenous production is affected by supplementation remains unclear; however, after one ceases to use creatine, normal creatine concentrations are found in muscle per presupplement concentrations, supporting the hypothesis that creatine supplementation may not alter endogenous mechanisms of production. Once in the bloodstream, uptake of creatine into muscle occurs against a concentration gradient via a specific transporter protein on the sarcolemma.<sup>27 Guerrero-Ontiveros M.L., Wallimann T. Creatine supplementation in health and disease: Effects of chronic creatine ingestion in vivo. Down-regulation of the expression of creatine transporter isoforms in skeletal muscle Mol Cell Biochem 1998 ;  184 : 427-437  [cross-ref]

Cliquez ici pour aller à la section Références, 38 Loike J.D., Zalutsky D.L., Kaback E. , et al. Extracellular creatine regulates creatine transport in rat and human muscle cells Proc Natl Acad Sci USA 1988 ;  85 : 807-811  [cross-ref]

Cliquez ici pour aller à la section Références</sup> Interestingly, preliminary research indicates that chronic creatine ingestion results in down-regulation of the expression of specific creatine receptor protein isomers on skeletal muscle.<sup>27 Guerrero-Ontiveros M.L., Wallimann T. Creatine supplementation in health and disease: Effects of chronic creatine ingestion in vivo. Down-regulation of the expression of creatine transporter isoforms in skeletal muscle Mol Cell Biochem 1998 ;  184 : 427-437  [cross-ref]

Cliquez ici pour aller à la section Références</sup> Furthermore, the rate of creatine transport may be more important than the amount of receptor protein, and futher research is needed. Figure 3 overviews the basic dynamics of the metabolism of creatine in muscle under unloaded and loaded conditions.