Uraemic muscle metabolism at rest and during exercise

The effect of chronic renal failure and the accompanying hyperphosphataemiaon muscle metabolism at rest and during exercise was examinedin a group of undialysed patients suffering from chronic renalfailure. ³¹P magnetic resonance spectroscopy was used to measureintracellular high-energy phosphates in resting muscle as wellas changes in the concentrations of these metabolites duringexercise and recovery from exercise. In resting muscle, cell[Pi] rose with plasma [Pi], and free [ADP] changed such thatthe phosphorylation potential ([ATP]/([ADP]x[Pi])), which probablycontrols mitochondrial oxidation in resting muscle, was preserveddespite a wide variation in cell [Pi]. The maximal oxidativecapacity of the muscle was calculated from the kinetics of phosphocreatinerecovery after exercise. There was no reduction in uraemic muscleoxidative capacity compared to control muscle. This contrastswith our finding of a reduction in the mitochondrial oxidativecapacity in the muscle of patients established on dialysis,suggesting that a substance crucial for mitochondrial functionor substrate supply to mitochondria is removed by dialysis.