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As you read this you are probably well aware of the principal role of phosphocreatine (PCr) in skeletal muscle energy metabolism, namely that of a 'temporal' energy buffer at sites of high energy translocation which operates when the rate of ATP utilisation outstrips the rate of production by mitochondrial respiration. Thus, at the onset of steady-state contraction, or during non-steady-state conditions, PCr maintains ATP homeostasis at specific sites of high energy turnover (e.g. myofibrils; Fig. 1, Function 1), particularly in fast contracting skeletal muscle.
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