Effects of Chronic Dietary Creatine Feeding on Cardiac Energy Metabolism and on Creatine Content in Heart, Skeletal Muscle, Brain, Liver and Kidney

Little is known about the regulation of total creatine concentration in heart, skeletal muscle, brain, liver and kidney in response to increased dietary creatine intake. The phosphorylated fraction of intracellular creatine (phosphocreatine) remain relatively constant, and therefore, higher intracellular creatine levels may increase the energy reserve of the heart [phosphocreatine and phosphoryl transfer via creatine kinase (CK)] and of other organs. To test the effect of supplying exogenous creatine on the myocardial energy reserve and on creatine content of various organs, rats were given chow containing 0 (Untreated), 1, 3, 5, or 7% (of diet weight) creatine for 40 days. Thereafter, hearts were perfused and left ventricular developed pressure and heart rate were recorded. High-energy phosphate concentrations were determined with31P-NMR spectroscopy, CK reaction velocity by31P-magnetization transfer. Total creatine was determined in heart, skeletal muscle, brain, liver, kidney and serum by high-performance liquid chromatography (HPLC). Creatine feeding increased serum creatine by 73% (1% creatine), 142% (3%), 166% (5%) and 202% (7%). In the heart, increased serum creatine levels did not affect mechanical function; ATP, phosphocreatine, inorganic phosphate, CK reaction velocity and total creatine were all unchanged. Total creatine also remained constant in brain and skeletal muscle, while creatine content increased 4.6-fold in the liver and 1.9-fold in the kidney. We conclude that myocardial energy reserve via CK cannot be increased by exogenous creatine treatment.