Creatine phosphate is a nitrogenous acid that accumulates in tissues and acts as a buffer against ATP depletion. As ATP is used to provide energy, the creatine phosphate releases phosphate to resynthesise ATP from ADP. Creatine is synthesised naturally in the body from the amino acids glycine and arginine. However the understanding that dietary intakes of creatine can increase whole body stores of creatine and modulate endogenous synthesis rates has been know for nearly 100 years. Within the last 2 decades, creatine monohydrate supplements have been shown to increase skeletal muscle stores of creatine phosphate significantly, and this has been shown to provide ergogenic benefits by allowing maximal force output duration to be extended. While much has been written about the benefits of creatine monohydrate supplements for ergogenic performance gains, less is reported regarding the effects of diet on creatine phosphate storage. In this regard a number of studies have investigated the effects of diet on creatine metabolism.
Dietary creatine is found only in foods of animal origin including the flesh of meat fowl and fish. This makes sense because the skeletal muscle of animals contains a large store of creatine phosphate to provide energy for muscular contraction. Some care should be taken when analysing the effects of dietary creatine ingestion on endogenous synthesis of creatine because low levels of protein in some studies may have caused catabolism of skeletal muscle. Under these conditions the creatine body pools would not be under a steady state and the effects of creatine supplementation through the diet could be exaggerated. Creatinine, the breakdown product of creatine phosphate, has an excretion rate that is directly proportional to the amount of creatine in the body pool, and so measurements of creatinine can give an estimate of the total body size under steady state conditions. Changing protein intake in the diet can therefore allow estimates of this effect on total body creatine stores.
Some studies have fed healthy males high animal meat diets and then changed to feeding vegetarian diets containing similar protein levels but no creatine. When meat is added to the diet urinary creatinine levels increase gradually and then reach a threshold above which they will not increase further. When meat is removed from the diet, creatinine levels decrease gradually, and then reach a lower threshold. Therefore changing the meat content of the diet can alter the creatine pools between two set points, beyond which levels cannot advance. Even modest changes in the amount of ingested creatine of around 1 gram can cause a 25 % change in urinary creatinine urinary over a two week period, despite no changes in lean body mass or protein intake. Evidence suggests that there is a feedback system that alters endogenous creatine synthesis based on dietary intake, but that this system has a time delay, and this delay must be taken into account when assessing the effects of dietary creatine on creatine metabolism.
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