1989American Journal of Physiology-Regulatory, Integrative and Comparative PhysiologyRequires access

Fish muscle energy metabolism measured by in vivo 31P-NMR during anoxia and recovery

Guido van den Thillart, Aren van Waarde, Henk Jan Muller, Cornelis Erkelens, Albert D.F. Addink, Johan Lugtenburg

Open publisher page 82 citations

Abstract

By means of in vivo 31P nuclear magnetic resonance (NMR) we measured energy stores and intracellular pH at 10-min intervals in the myotome of unanesthetized carp and goldfish before, during, and after a period of anoxia (1 h for carp and 4 h for goldfish). The fish were mounted in a modified bioprobe, and their gills were irrigated with a constant flow of aerated or anoxic water. Anoxia caused a steep decline of phosphocreatine and intracellular pH in carp muscle. After the phosphocreatine stores had been exhausted by greater than 85%, [ATP] fell, whereas IMP and phosphodiesters accumulated. In goldfish muscle, initial changes followed the same pattern, but after 20 min a steady state of high-energy phosphates was reached and the development of acidosis was dampened. The resistance of goldfish to anoxia is due to metabolic suppression and a switch from lactate to ethanol and CO2 as the anaerobic end products. In both species, recovery was complete within 3 h. The fast pH recovery seems to be mainly caused by H+ and lactic acid efflux.

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By means of in vivo 31P nuclear magnetic resonance (NMR) we measured energy stores and intracellular pH at 10-min intervals in the myotome of unanesthetized carp and goldfish before, during, and after a period of anoxia (1 h for carp and 4 h for goldfish). The fish were mounted in a modified bioprobe, and their gills were irrigated with a constant flow of aerated or anoxic water. Anoxia caused a steep decline of phosphocreatine and intracellular pH in carp muscle. After the phosphocreatine stores had been exhausted by greater than 85%, [ATP] fell, whereas IMP and phosphodiesters accumulated. In goldfish muscle, initial changes followed the same pattern, but after 20 min a steady state of high-energy phosphates was reached and the development of acidosis was dampened. The resistance of goldfish to anoxia is due to metabolic suppression and a switch from lactate to ethanol and CO2 as the anaerobic end products. In both species, recovery was complete within 3 h. The fast pH recovery seems to be mainly caused by H+ and lactic acid efflux.

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Available abstract

By means of in vivo 31P nuclear magnetic resonance (NMR) we measured energy stores and intracellular pH at 10-min intervals in the myotome of unanesthetized carp and goldfish before, during, and after a period of anoxia (1 h for carp and 4 h for goldfish). The fish were mounted in a modified bioprobe, and their gills were irrigated with a constant flow of aerated or anoxic water. Anoxia caused a steep decline of phosphocreatine and intracellular pH in carp muscle. After the phosphocreatine stores had been exhausted by greater than 85%, [ATP] fell, whereas IMP and phosphodiesters accumulated. In goldfish muscle, initial changes followed the same pattern, but after 20 min a steady state of high-energy phosphates was reached and the development of acidosis was dampened. The resistance of goldfish to anoxia is due to metabolic suppression and a switch from lactate to ethanol and CO2 as the anaerobic end products. In both species, recovery was complete within 3 h. The fast pH recovery seems to be mainly caused by H+ and lactic acid efflux.

Key concepts: Phosphocreatine, Intracellular pH, Carp, Anaerobic exercise, Acidosis, Chemistry, In vivo, Gill

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