How fisheries will be impacted by climate change is far from understood. While some fish populations may be able to escape global warming via range shifts, they cannot escape ocean acidification (OA), an inevitable consequence of the dissolution of anthropogenic carbon dioxide (CO2) emissions in marine waters. How ocean acidification affects population dynamics of commercially important fish species is critical for adapting management practices of exploited fish populations. Ocean acidification has been shown to impair fish larvae’s sensory abilities, affect the morphology of otoliths, cause tissue damage and cause behavioural changes. Here, we obtain first experimental mortality estimates for Atlantic cod larvae under OA and incorporate these effects into recruitment models. End-of-century levels of ocean acidification (~1100 μatm according to the IPCC RCP 8.5) resulted in a doubling of daily mortality rates compared to present-day CO2 concentrations during the first 25 days post hatching (dph), a critical phase for population recruitment. These results were consistent under different feeding regimes, stocking densities and in two cod populations (Western Baltic and Barents Sea stock). When mortality data were included into Ricker-type stock-recruitment models, recruitment was reduced to an average of 8 and 24% of current recruitment for the two populations, respectively. Our results highlight the importance of including vulnerable early life stages when addressing effects of climate change on fish stocks.
Food intake (FI), feeding activity (FA), and body mass (BM) were recorded continuously throughout a 13-mo period in Svalbard rock ptarmigan kept under natural conditions of light and ambient temperature at Svalbard (79 degrees N). FI was persistently high from March until August, including the period when daylight is continuous, whereas it was low from November until January, when it is permanently dark. From August until November, BM doubled, while FI dropped to one-third. BM fell rapidly from mid-November until April despite a doubling of FI from February until March. From August until mid-November and from February until mid-April FA occurred mainly during the light period of the day. From late November until February and from mid-April until August intermittent FA occurred continuously. It is suggested that the seasonal changes in BM are not determined by FI alone but depend heavily on seasonal changes in locomotor activity as reflected in FA.
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