Abstract
BackgroundOcean acidification and warming are happening fast in the Arctic but little is known about the effects of ocean acidification and warming on the physiological performance and survival of Arctic fish.ResultsIn this study we investigated the metabolic background of performance through analyses of cardiac mitochondrial function in response to control and elevated water temperatures and PCO2 of two gadoid fish species, Polar cod (Boreogadus saida), an endemic Arctic species, and Atlantic cod (Gadus morhua), which is a temperate to cold eurytherm and currently expanding into Arctic waters in the wake of ocean warming. We studied their responses to the above-mentioned drivers and their acclimation potential through analysing the cardiac mitochondrial function in permeabilised cardiac muscle fibres after 4 months of incubation at different temperatures (Polar cod: 0, 3, 6, 8 °C and Atlantic cod: 3, 8, 12, 16 °C), combined with exposure to present (400μatm) and year 2100 (1170μatm) levels of CO2.OXPHOS, proton leak and ATP production efficiency in Polar cod were similar in the groups acclimated at 400μatm and 1170μatm of CO2, while incubation at 8 °C evoked increased proton leak resulting in decreased ATP production efficiency and decreased Complex IV capacity. In contrast, OXPHOS of Atlantic cod increased with temperature without compromising the ATP production efficiency, whereas the combination of high temperature and high PCO2 depressed OXPHOS and ATP production efficiency.ConclusionsPolar cod mitochondrial efficiency decreased at 8 °C while Atlantic cod mitochondria were more resilient to elevated temperature; however, this resilience was constrained by high PCO2. In line with its lower habitat temperature and higher degree of stenothermy, Polar cod has a lower acclimation potential to warming than Atlantic cod.
Highlights
Ocean acidification and warming are happening fast in the Arctic but little is known about the effects of ocean acidification and warming on the physiological performance and survival of Arctic fish
For a deeper understanding of the impact of ocean acidification and warming on the bioenergetics of the two species in relation to thermal tolerance, we further investigated mitochondrial function in the cardiac muscle of animals incubated for 4 months at four different temperatures (Polar cod: 0, 3, 6, 8 °C and Atlantic cod: 3, 8, 12, 16 °C), and two PCO2 (400μatm and 1170μatm) in a cross factorial design
We discuss our results in light of the findings reported by Kunz et al [61], who showed wider thermal windows for growth and standard metabolic rate (SMR) in Northeast Arctic cod (NEAC) than in Polar cod from the same acclimation experiment
Summary
Ocean acidification and warming are happening fast in the Arctic but little is known about the effects of ocean acidification and warming on the physiological performance and survival of Arctic fish. Increasing temperatures can alter the cellular membranes packing order, which can cause changes in membrane-associated processes until a potential complete loss of function [22]. Towards the upper limit of the thermal window, the cellular energetic costs for maintenance rise, increasing baseline energy turnover and allowing only for time-limited periods of passive tolerance. If high temperature persists over this period of passive tolerance, the costs of maintenance can only be covered at the expense of other functions such as growth and reproduction, decreasing the overall animal fitness [17]. In light of ongoing ocean acidification and warming it is important to understand how fish respond to increasing habitat temperatures, their ability to adjust their thermal sensitivity and the role that high PCO2 plays in thermal acclimation [2, 25]
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