Atlantic salmon (Salmo salar) presmolts, smolts, and postsmolts compensate for a respiratory acidosis associated with 96 h of exposure to hyperoxia (100% O2; hO2), hypercapnia (2% CO2 and 98% air; hCO2), and combined hO2/hCO2 in freshwater (FW) by increasing strong ion difference, predominantly through a reduction in plasma [Cl-] (presumably via branchial Cl-/HCO3- exchange). In smolts, compensation during hO2 or hCO2 occurred within 24 h, whereas that in combined hO2/hCO2 was much slower, resulting in 33% mortality by 96 h. FW hO2 and combined hO2/hCO2 appeared to impair gill function, likely through oxidative cell damage. This resulted in reduced hypoosmoregulatory ability following subsequent transfer to seawater (SW), as indicated by changes in plasma ion levels, osmolality, and muscle water content, resulting in considerable mortalities. Interestingly, FW hCO2 appeared to enhance hypoosmoregulatory ability during subsequent SW transfer. Smolts are often transported from FW to a subsequent SW release ...