Key result
Acute respiratory acidosis increases rat skeletal muscle Pi ~50% while preserving phosphorylation potential.
Why the study?
How does acute respiratory acidosis affect high-energy phosphate concentrations in rat skeletal muscle?
How does acute respiratory acidosis affect high-energy phosphate concentrations in rat skeletal muscle?
In rat skeletal muscle, acute respiratory acidosis leads to increased intracellular inorganic phosphate and decreased ADP, preserving the phosphorylation potential to maintain mitochondrial ATP synthesis.
Suggests maintained muscle energetics in rodent acidosis; leaves open translation to human cardiac or skeletal muscle physiology.
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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Thompson et al. (1992) studied Acute respiratory acidosis. Respiratory acidosis (14 and 20% inspired CO2) vs. Baseline/recovery was evaluated on Changes in phosphorus metabolite concentrations. During acute respiratory acidosis in rat skeletal muscle, intracellular pH fell and [P(i)] increased by up to 50% while phosphocreatine decreased by up to 8%, preserving phosphorylation potential.
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