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Thread: Clinical Pharmacology of Creatine Monohydrate

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    Clinical Pharmacology of Creatine Monohydrate

    Abstract——Creatine is a dietary supplement purported to improve exercise performance and increase fat-free mass. Recent research on creatine has demonstrated positive therapeutic results in various clinical applications. The purpose of this review is to focus on the clinical pharmacology and therapeutic application of creatine supplementation.

    Creatine is a naturally occurring compound obtained in humans from endogenous production and consumption through the diet. When supplemented with exogenous creatine, intramuscular and cerebral stores of creatine and its phosphorylated form, phosphocreatine, become elevated.

    The increase of these stores can offer therapeutic benefits by preventing ATP depletion, stimulating protein synthesis or reducing protein degradation, and stabilizing biological membranes. Evidence from the exercise literature has shown athletes benefit from supplementation by increasing muscular force and power, reducing fatigue in repeated bout activities, and increasing muscle mass. These benefits have been applied to disease models of Huntington’s, Parkinson’s, Duchenne muscular dystrophy, and applied clinically in patients with gyrate atrophy, various neuromuscular disorders, McArdle’s disease, and congestive heart failure.

    This review covers the basics of creatine synthesis and transport, proposed mechanisms of action, pharmacokinetics of exogenous creatine administration, creatine use in disease models, side effects associated with use, and issues on product quality.

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    Re: Clinical Pharmacology of the Dietary Supplement

    Quote Originally Posted by Dr. Solar Wolff
    Someone told me that creatine only increased the ATP storage ability of individual muscle cells. This means that they can just store more energy in the form of glycogen which may be good for strength-endurance but means nothing in terms of absolute strength, has nothing to do with muscle protein itself, and will go away rapidly. Am I wrong?

    Cr exerts various effects upon entering the muscle. It is these effects that elicit improvements in exercise performance and may be responsible for the improvements of muscle function and energy metabolism seen under certain disease conditions.

    Several mechanisms have been proposed to explain the increased exercise performance seen after acute and chronic Cr intake. A. Energy Metabolism Adenosine triphosphate (ATP) concentrations maintain physiological processes and protect tissue from hypoxia-induced damage. Cr is involved in ATP production through its involvement in PCr energy system. This system can serve as a temporal and spatial energy buffer as well as a pH buffer.

    As a spatial energy buffer, Cr and PCr are involved in the shuttling of ATP from the inner mitochondria into the cytosol (Meyer et al., 1984; Bessman and Carpenter, 1985). In the reversible reaction catalyzed by creatine kinase, Cr and ATP form PCr and adenosine diphosphate (ADP) (Fig. 2). It is this reaction that can serve as both a temporal energy buffer and pH buffer. The formation of the polar PCr “locks” Cr in the muscle and maintains the retention of Cr because the charge prevents partitioning through biological membranes (Greenhaff, 1997) (Fig. 2). At times during low pH (viz., during exercise when lactic acid accumulates), the reaction will favor the generation of ATP.

    Conversely, during recovery periods (e.g., periods of rest between exercise sets) where ATP is being generated aerobically, the reaction will proceed toward the right
    and increase PCr levels. This energy and pH buffer is one mechanism by which Cr works to increase exercise performance.

    Finally, Cr is also involved in regulating glycolysis. When humans and animals are depleted of tissue Cr, they adapt by increasing oxidative enzymes such as mitochondrial creatine kinase (O’Gorman et al., 1996), succinate dehydrogenase (Ren et al., 1993; O’Gorman et al., 1996), citrate synthase (Ren et al., 1993), and GLUT-4 glucose transporters (Ren et al., 1993). All of these proteins are involved in aerobic metabolism and can offset the lack of anaerobic energy supplied by the PCr system. Little information is available on whether enzyme activities are affected by increasing intracellular Cr stores.

    One study by Brannon et al. (1997) found citrate synthase activity increased in the soleus but not the plantaris in rodents supplemented with 3.3 mg of Cr per gram of diet. PCr and inorganic phosphate may also regulate energy processes by inhibiting the enzymes glycogen phosphorylase a, phosphofructokinase, pyruvate kinase, and lactate dehydrogenase (Wyss and Kaddurah-Daouk, 2000). However, the control of PCr on these enzymes has come under debate since the PCr used in these studies contained impurities like inorganic pyrophosphate (Wyss and Kaddurah-Daouk, 2000).

    One beneficial effect of Cr supplementation in young, healthy males is enhanced muscle fiber size and increased lean body mass. Typically, Cr loading of 20 g/day
    for 4 to 28 days in humans increases total body mass from 1 to 2 kg (Balsom et al., 1993; Greenhaff et al., 1994; Earnest et al., 1995; Green et al., 1996a; Vandenberghe et al., 1997; Kreider et al., 1998; Maganaris and Maughan, 1998; McNaughton et al., 1998; Snow et al., 1998) with increases coming from fat-free mass (Vandenberghe et al., 1997; Kreider et al., 1998; Volek et al., 1999; Becque et al., 2000; Mihic et al., 2000). Volek et al. (1999) found after 12 weeks of resistance training in men, Cr supplementation increased muscle fiber diameter in both Type 1 and Type 2 muscle fibers by 35%

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