The Regulation and Expression of the Creatine Transporter: A Brief Review of Creatine Supplementation in Humans and Animals

Abstract

Creatine monohydrate has become one of the most popular ergogenic sport supplements used today. It is a nonessential dietary compound that is both endogenously synthesized and naturally ingested through diet. Creatine ingested through supplementation has been observed to be absorbed into the muscle exclusively by means of a creatine transporter, CreaT1. The major rationale of creatine supplementation is to maximize the increase within the intracellular pool of total creatine (creatine + phosphocreatine). There is much evidence indicating that creatine supplementation can improve athletic performance and cellular bioenergetics, although variability does exist. It is hypothesized that this variability is due to the process that controls both the influx and efflux of creatine across the cell membrane, and is likely due to a decrease in activity of the creatine transporter from various compounding factors. Furthermore, additional data suggests that an individual's initial biological profile may partially determine the efficacy of a creatine supplementation protocol. This brief review will examine both animal and human research in relation to the regulation and expression of the creatine transporter (CreaT). The current literature is very preliminary in regards to examining how creatine supplementation affects CreaT expression while concomitantly following a resistance training regimen. In conclusion, it is prudent that future research begin to examine CreaT expression due to creatine supplementation in humans in much the same way as in animal models.

Evaluation of dietary creatine and guanidinoacetic acid supplementation in juvenile red drumSciaenops ocellatus

“…glycine amidino transferase (AGAT), which produces guanidinoacetate TA B L E 7 Muscle, liver and plasma creatine concentrations of juvenile red drum fed diets containing different levels of creatine and guanidinoacetic acid (GDA) in trial 2 acid (GAA), and guanidinoacetate methyltransferase (GAMT), which methylates GDA to produce creatine. In mammals, creatine is endogenously produced in the kidney and liver and then transported to muscle tissue by a creatine transporter through blood circulation (Braissant, Henry, Béard, & Uldry, 2011;da Silva, Nissim, Brosnan, & Brosnan, 2009;Schoch, Willoughby, & Greenwood, 2006). In rainbow trout, creatine synthases are found in muscle tissue, and higher densitometric intensities of CKM and CKB were found in muscle (Borchel et al, 2014).…”

Creatine, L-Carnitine, andω3 Polyunsaturated Fatty Acid Supplementation from Healthy to Diseased Skeletal Muscle

“…It is accepted that the dosing regimen that significantly increase the intracellular phosphocreatine is a loading phase of approximately 20 g/d for 5–7 days followed by a maintenance phase of 5 g/d for several weeks [15, 16]. …”

The effects of creatine supplementation on thermoregulation and physical (cognitive) performance: a review and future prospects

“…These findings seem to mirror the responder/nonresponder issue seen in the Cr supplementation literature in terms of response to resistance training and effects on exercise performance. Some of this variability in response will be due to the process that controls both the influx and efflux of Cr across the cell membrane (see Schoch et al 2006 for review). For example, Tarnopolsky et al (2000) assessed the Cr transport protein (CreaT) and mitochondrial Cr kinase protein (mtCK) in patients with numerous myopathies (i.e., inflammatory, mitochondrial, muscular dystrophy and congenital myopathies).…”