Temperature-dependent changes in energy metabolism, intracellular pH and blood oxygen tension in the Atlantic cod

The effect of acute increase in temperature on oxygen partial pressure (Po2) was measured in the gill arches of Atlantic cod Gadus morhua between 10 and 19° C by use of oxygen microoptodes. Oxygen saturation of the gill blood under control conditions varied between 90 and 15% reflecting a variable percentage of arterial or venous blood in accordance with the position of each optode in the gill arch. The data obtained suggested that arterial Po2 remained more or less constant and arterial oxygen uptake did not become limiting during warming. A progressive drop in venous Po2, however, was observed at >10° C indicating that excessive oxygen uptake from the blood is not fully compensated for by circulatory performance, until finally, Po2 levels fully collapse. In a second set of experiments energy and acid–base status of white muscle of Atlantic cod in vivo was measured by magnetic resonance (31P‐NMR) spectroscopy in unanaesthetized and unimmobilized fish in the temperature range between 13 and 21° C. A decrease in white muscle intracellular pH (pHi) with temperature occurred between 10 and 16° C (ΔpH per ° C = −0·025 per ° C). In white muscle temperature changes had no influence on high‐energy phosphates such as phosphocreatine (PCr) or ATP except during exposure to high critical temperatures (>16° C), indicating that white muscle energy status appears to be relatively insensitive to thermal stress if compared to the thermal sensitivity of the whole animal. The data were consistent with the hypothesis of an oxygen limitation of thermal tolerance in animals, which is set by limited capacity of oxygen supply mechanisms. In the case of Atlantic cod circulatory rather than ventilatory performance may be the first process to cause oxygen deficiency during heat stress.