Metabolic shifts in the Antarctic fish Notothenia rossii in response to rising temperature and P CO 2

• Published in: Frontiers in Zoology
• Main Authors: Strobel Anneli, Bennecke Swaantje, Leo Elettra, Mintenbeck Katja, Pörtner Hans O, Mark Felix C
• Format: Article in Journal/Newspaper
• Language: English
• Published: BMC 2012
• Subjects: Notothenioid; Oxygen consumption; Routine metabolic rate; Extracellular pH (pH e ); Intracellular pH (pH i ); Mitochondrial respiration; Acclimation; Acid–base; Zoology; QL1-991; Antarctic; Antarctic Peninsula; The Antarctic; Antarc*; Notothenia rossii
• Online Access: https://doi.org/10.1186/1742-9994-9-28; https://doaj.org/article/f1bc4e66404848b2ad09c43aacb293fe

Abstract 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 P CO 2 (0.2 kPa CO 2 ) 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 P CO 2 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 (pH e ) towards more alkaline values. A similar overcompensation was visible in muscle intracellular pH (pH i ). pH i in liver displayed a slight acidosis after warm normo- or hypercapnia acclimation, nevertheless, long-term exposure to higher P CO 2 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 ...