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Phosphocreatine (PCr) was reduced to equivalent levels in carp white muscle by high-intensity exhaustive exercise and exposure to hypoxia at 15 degrees C and 25 degrees C in order to assess the influence of intracellular pH (pH(i)), temperature and lactate levels on PCr recovery in vivo. High-intensity exercise resulted in a significantly lower pH(i) compared with hypoxia exposure and the rate of PCr depletion and tissue acidification during hypoxia exposure was significantly higher in carp held at 25 degrees C compared with those at 15 degrees C. During recovery, PCr and pH(i) returned towards normoxia/resting levels at a faster rate following hypoxia exposure than after exercise. The lower pH(i) in exercised carp caused a greater perturbation to cellular energy status (assessed as the free energy of ATP hydrolysis; DeltafG') and resulted in a higher [ATP]/[ADP(free)] ratio, which may limit mitochondrial ATP production and contribute to the slower recovery from exercise compared with recovery from hypoxia exposure. Rates of recovery from exercise and hypoxia exposure were not affected by acclimation temperature (15 and 25 degrees C), suggesting that the processes involved in acclimation compensate for the Q(10) effects of temperature on metabolic processes. Finally, using a dual 31P-NMR and 1H-NMR analysis technique, we demonstrated that the greater tissue acidification observed after high-intensity exercise compared with hypoxia exposure occurred at similar white muscle lactate concentrations.

Differential recovery from exercise and hypoxia exposure measured using 31P- and 1H-NMR in white muscle of the common carp Cyprinus carpio