Metabolic shifts in the Antarctic fish Notothenia rossii in response to rising temperature and PCO2

• Published in: Frontiers in Zoology
• Main Authors: Strobel, Anneli, Bennecke, Swaantje, Leo, Elettra, Mintenbeck, Katja, Pörtner, Hans O, Mark, Felix Christopher
• Format: Article in Journal/Newspaper
• Language: unknown
• Published: BIOMED CENTRAL LTD 2012
• Subjects: Antarctic; Antarctic Peninsula; The Antarctic; Antarc*; Notothenia rossii
• Online Access: https://epic.awi.de/id/eprint/31987/; https://epic.awi.de/id/eprint/31987/1/Strobel2012b.pdf; https://doi.org/10.1186/1742-9994-9-28; https://hdl.handle.net/10013/epic.40675; https://hdl.handle.net/10013/epic.40675.d001

Introduction: Ongoing ocean warming and acidification increasingly affect marine ecosystems, in particular around the Antarctic Peninsula. Yet little is known about the capability of Antarctic notothenioid fish to cope with rising temperature in acidifying seawater. While the whole animal level is expected to be more sensitive towards hypercapnia and temperature, the basis of thermal tolerance is set at the cellular level, with a putative key role for mitochondria. This study therefore investigates the physiological responses of the Antarctic Notothenia rossii after long-term acclimation to increased temperatures (7°C) and elevated PCO2 (0.2 kPa CO2) at different levels of physiological organisation. Results: For an integrated picture, we analysed the acclimation capacities of N. rossii by measuring routine metabolic rate (RMR), mitochondrial capacities (state III respiration) as well as intra- and extracellular acid–base status during acute thermal challenges and after long-term acclimation to changing temperature and hypercapnia. RMR was partially compensated during warm- acclimation (decreased below the rate observed after acute warming), while elevated PCO2 had no effect on cold or warm acclimated RMR. Mitochondrial state III respiration was unaffected by temperature acclimation but depressed in cold and warm hypercapnia-acclimated fish. In both cold- and warm-exposed N. rossii, hypercapnia acclimation resulted in a shift of extracellular pH (pHe) towards more alkaline values. A similar overcompensation was visible in muscle intracellular pH (pHi). pHi in liver displayed a slight acidosis after warm normo- or hypercapnia acclimation, nevertheless, long-term exposure to higher PCO2 was compensated for by intracellular bicarbonate accumulation. Conclusion: The partial warm compensation in whole animal metabolic rate indicates beginning limitations in tissue oxygen supply after warm-acclimation of N. rossii. Compensatory mechanisms of the reduced mitochondrial capacities under chronic hypercapnia may include a ...