Acid-base disturbances and effects on oxygen uptake rates in Nile tilapia (Oreochromis niloticus) following acute and prolonged CO2 exposure

High levels of dissolved carbon dioxide (CO 2 ) occur nightly in earthen ponds characterized by high respiration rates. Exposure to high CO 2 conditions (hypercapnia) leads to acidosis in fish, which can be compensated by an accumulation of HCO 3 - to recover intra- and extracellular pH levels, with a capacity that appears to be speciesspecific. For Nile tilapia, a freshwater tropical teleost traditionally produced in earthen ponds, little information is available on the tolerance to dissolved levels of CO 2 and associated acid-base disturbances. Here, we investigated first the effects of acute and progressively increasing CO 2 , from normocapnic conditions to 60 mg CO 2 L -1 , on oxygen uptake rates (MO 2 ). This was followed by exposure to three concentrations of CO 2 ; 10, 30, and 60 mg L -1 (equivalent to p CO 2 of 5.4, 16.2, and 32.4 mmHg) against a normocapnic control ( p CO 2 0.3 mmHg), to investigate acute (1 h) or prolonged (24 h) effects on standard (SMR) and maximum metabolic rates (MMR), haematology, and extra- and intracellular acid-base status in adult Nile tilapia (mean BM 435 +/- 16 g +/- SE). Acute exposure to hypercapnia led to concentration-dependent decreases in both SMR and MMR. Fish were able to fully or partially recover MMR and metabolic scope (MS) after 24 h, while depression of SMR persisted at all CO 2 levels. Acute exposure to CO 2 caused intra- and extracellular pH levels to decrease by up to 0.5 units in a concentration-dependent manner. Only the lowest hypercapnic treatment ( p CO 2 5.4 mmHg) was able to fully recover within 24 h. Changes in haematological variables appeared minor, being restricted to increasing haematocrit, haemoglobin concentration, and mean cell volume in the highest CO 2 treatments after 24 h exposure. Although the Nile tilapia is generally considered a species able to tolerate poor water quality, the modest or slow acid-base regulation following hypercapnic exposure suggests sensitivity to hypercapnia.