Swimming performance in Atlantic Cod (Gadus morhua) following long-term (4-12 months) acclimation to elevated seawater P sub(C)dO sub(2)

Anthropogenic CO sub(2) emissions lead to chronically elevated seawater CO sub(2) partial pressures (hypercapnia). The induced ocean acidification will very likely be a relevant factor shaping future marine environments. CO sub(2) exposure concomitantly challenges the animal's capacity of acid-base and ionic regulation as well as the ability to maintain energy metabolism and calcification. Under conditions of acute hypercapnia, numerous studies have revealed a broad range of tolerance levels displayed by various marine taxa. Thus, it is well known that, in contrast to many marine invertebrates, most teleost fish are able to fully compensate acid-base disturbances in short-term experiments (hours to several days). In order to determine whether marine fish are able to preserve aerobic scope following long-term incubation to elevated CO sub(2), we exposed two groups of Atlantic Cod for 4 and 12 months to 0.3 and 0.6kPa P sub(C) sub(O) sub(2), respectively. Measurements of standard and active metabolic rates, critical swimming speeds and aerobic scope of long-term incubated cod showed no deviations from control values, indicating that locomotory performance is not compromised by the different levels of chronic hypercapnia. While the maintenance of high activity levels is supported by a 2-fold increased Na super(+)/K super(+)-ATPase protein expression and 2-fold elevated Na super(+)/K super(+)-ATPase activity in the 12 month incubated fish (0.6kPa P sub(C) sub(O) sub(2)), no such elevation in Na super(+)/K super(+)-ATPase activity could be observed in the group treated with 0.3kPa P sub(C) sub(O) sub(2). Owing to the relevance of Na super(+)/K super(+)-ATPase as a general indicator for ion regulatory capacity, these results point at an adjustment of enzymatic activity to cope with the CO sub(2) induced acid-base load at 0.6kPa P sub(C) sub(O) sub(2) while under milder hypercapnic conditions the 'standard' Na super(+)/K super(+)-ATPase capacity might still be sufficient to maintain acid-base status.