IntroductionOngoing 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.ResultsFor 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.ConclusionThe 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 new metabolic equilibrium to meet the elevated energy demand for acid–base regulation. New set points of acid–base regulation under hypercapnia, visible at the systemic and intracellular level, indicate that N. rossii can at least in part acclimate to ocean warming and acidification. It remains open whether the reduced capacities of mitochondrial energy metabolism are adaptive or would impair population fitness over longer timescales under chronically elevated temperature and PCO2.

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Over the past 15 years, multiple areas in the North Atlantic have been closed to destructive fishing practices to protect vulnerable deep-water coral ecosystems, known to provide habitat for diverse associated fauna. Despite the growing number of conservation measures, longterm studies on the recovery of deep-water coral communities from fisheries impacts remain scarce. In the Gulf of Maine, the Northeast Channel Coral Conservation Area (NECCCA) 2 was established in 2002 to protect dense aggregations of the two numerically dominant octocoral species in the region, Primnoa resedaeformis and Paragorgia arborea. To evaluate the effectiveness of the conservation measures, we monitored shifts in abundance and size of these two coral species in the shallow section (400-700 m) of the NECCCA for 12 years after the fisheries closure. We also evaluated the appropriateness of the location of the deep boundaries of the NECCCA that were placed based on a precautionary approach with limited information on coral distribution at depths > 500 m. Video transects were conducted with

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