Physiological disturbances at critically high temperatures: a comparison between stenothermal antarctic and...

The effect of gradually increased water temperature on the metabolism of temperate eelpout from the North Sea (Zoarces viviparus) and Antarctic eelpout (Pachycara brachycephalum) was investigated. Standard metabolic rate (SMR) was similar in cold-adapted P. brachycephalum and cold-acclimated Z. viviparus in the low temperature range. This indicates that Antarctic eelpout show no metabolic cold adaptation (as originally defined by Wohlschlag); however, they do show a compensatory increase of oxygen consumption compared to warm-acclimated eelpout. SMR increased more strongly with rising temperature in P. brachycephalum than in Z. viviparus, which is reflected in a higher Arrhenius activation energy for oxygen consumption (99+/-5 kJ mol(-)(1), versus 55+/-3 kJ mol(-)(1) for cold-acclimated Z. viviparus; means +/- s.d.). The intracellular pH in the white musculature of Z. viviparus follows alphastat regulation over the whole investigated temperature range and dropped at a rate of -0.016 pH units per degrees C between 3 degrees C and 24 degrees C. In Antarctic eelpout white muscle pH declined at a rate of -0.015 pH units per degrees C between 0 degrees C and 3 degrees C, but deviated from alphastat at higher temperatures, indicating that thermal stress leads to acid-base disturbances in this species. The upper critical temperature limit (Tc(II); characterised by a transition to anaerobic metabolism) was found to be between 21 degrees C and 24 degrees C for Z. viviparus and around 9 degrees C for P. brachycephalum. In both species a rise of succinate concentration in the liver tissue turned out to be the most useful indicator of Tc(II). Obviously, liver is more sensitive to heat stress than is white muscle. Accordingly, the energy status of white muscle is not diminished at Tc(II). Heat-induced hyperglycaemia was observed in Antarctic eelpout (at 9 degrees C and 10 degrees C), but not in common eelpout. Based on our results and on literature data, impaired respiration in combination with circulatory failure is suggested as the final cause of heat death. Our data suggest that the southern distribution limit of Zoarces viviparus is correlated with the limit of thermal tolerance. Therefore, it can be anticipated that global warming would cause a shift in the distribution of this species.