Abstract
We used 31P magnetic resonance spectroscopy to study changes in phosphorus metabolite concentrations in rat skeletal muscle during respiratory acidosis (14 and 20% inspired CO2) and recovery. As intracellular pH fell (from 7.05 to 6.75 after 20 min of 20% CO2), intracellular [P(i)] increased by up to 50% while phosphocreatine concentration decreased by up to 8%. The sum of all intracellular phosphates remained constant. [ADP] decreased by up to 40% in accordance with the creatine kinase equilibrium but the phosphorylation potential [ATP]/([ADP][P(i)]) was preserved as a result of increased [P(i)]. This adjustment may be a mechanism for maintaining mitochondrial ATP synthesis despite low pH. Eventually this increase in cellular [P(i)] could lead to slow efflux of P(i) from the skeletal muscle cell contributing to the hyperphosphataemia of acute respiratory acidosis.
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