Muscle (phosphocreatine) dynamics during exercise: implication for understanding the regulation of muscle oxidative metabolism

摘要

In contracting skeletal muscle, phosphocreatine (PCr) is one of the reactants linking mitochondrial respiration with the rate of muscle ATP usage through feedback activation. In contrast to what happens in heart in which [PCr] is stable, in skeletal muscle 31P-MR spectroscopy shows marked changes in [PCr] in response to skeletal muscle activity. The observation of stable [PCr] in working heart over a wide range of contraction levels leads several authors to suggest that there exists a perfectly balanced direct parallel activation of energy supply and demand in heart, but much less intense direct parallel activation, or even no parallel activation, in skeletal muscle (Korzeniewski, 2007), resulting in a weaker homeostasis of the intermediates in the latter tissue during transition from low to high metabolic rate. Interestingly, the intensity of the parallel activation in skeletal muscle may depend on: (i) experimental conditions (muscle stimulated neurally versus electrically); (ii) the context of perfusion (perfused ex vivo where the influence of some factors, e.g. hormones, are absent versus physiologically perfused by the blood stream in vivo); and (iii) the typology of muscle fibres involved in contraction (oxidative versus glycolytic). Keeping in mind points (i) and (ii), therefore only studies carried out in vivo, have the capacity to evaluate the integrated complexity of the regulation of oxidative phosphorylation in contracting skeletal muscle.