The effect of chronic renal failure and the accompanying hyperphosphat
aemia on muscle metabolism at rest and during exercise was examined in
a group of undialysed patients suffering from chronic renal failure.
P-31 magnetic resonance spectroscopy was used to measure intracellular
high-energy phosphates in resting muscle as well as changes in the co
ncentrations of these metabolites during exercise and recovery from ex
ercise. In resting muscle, cell [Pi] rose with plasma [Pi], and free [
ADP] changed such that the phosphorylation potential ([ATP]/([ADP]x[Pi
])), which probably controls mitochondrial oxidation in resting muscle
, was preserved despite a wide variation in cell [Pi]. The maximal oxi
dative capacity of the muscle was calculated from the kinetics of phos
phocreatine recovery after exercise. There was no reduction in uraemic
muscle oxidative capacity compared to control muscle. This contrasts
with our finding of a reduction in the mitochondrial oxidative capacit
y in the muscle of patients established on dialysis, suggesting that a
substance crucial for mitochondrial function or substrate supply to m
itochondria is removed by dialysis.