Eels reared intensively in recirculated water can experience chronic hypercapnia from accumulation of metabolic CO₂, with water CO₂ partial pressures (P_w,CO2) exceeding 30 mmHg, far above that hitherto considered normal for fish (1 to 3 mmHg). The effects on eels of acute and chronic hypercapnia were investigated.

Eels (n = 6) were anaesthetised (0.05 % MS-222 in water), cannulated in the dorsal aorta for withdrawal of blood samples and in the operculum for measurement of gill ventilation rate (f_G) and pressure amplitude (P_OP). A flow cuff placed on the ventral aorta measured cardiac output (CO). Eels were recovered for 48 h in respirometer chambers provided with a flow of normocapnic water. Instantaneous O₂ uptake was measured every 10 min with an automated system. All data are reported as means ± S.E.M., means compared by ANOVA, significance attributed at P < 0.05.

Acute exposure to progressive hypercapnia (20 min at P_w,CO2 values of 10, 20, 40, 60 and 80 mmHg) caused a linear increase in arterial P_CO2 (P_a,CO2) from 3.5 ± 0.4 mmHg in normocapnia to 44.9 ± 2.6 at P_w,CO2 = 80 mmHg, coupled to respective declines in arterial pH (pH_a) from 7.86 ± 0.02 to 7.16 ± 0.04 and in arterial total O₂ content (c_a,O2) from 9.6 ± 0.7 to 2.0 ± 0.5 vol%. There was a significant increase in f_G and P_OP at P_w,CO2 values of 10, 20, 40 mmHg, then a decline in f_G but further increase in P_OP at P_w,CO2 = 60 and 80 mmHg. Despite the severe acidosis and hypoxaemia, there were no significant effects on CO or O₂ uptake.

Eels exposed for 3 months to chronic hypercapnia (P_w,CO2 values of control, 15, 30 or 45 mmHg) were anaesthetised, cannulated and recovered as described above, at the appropriate P_w,CO2. In all groups, P_a,CO2 was about 3 mmHg above P_w,CO2, and hypercapnic eels exhibited a marked accumulation of plasma bicarbonate, from 12.8 ± 1.5 mmol l^-1 in controls (n = 6) to 72.5 ± 4.1 at P_w,CO2 = 45 mmHg (n = 4). The bicarbonate accumulation buffered the effects of hypercapnia on pH_a and c_a,O2, as compared with the acute exposure. Nonetheless, in the eels at P_w,CO2 = 45 mmHg, pH_a was 7.57 ± 0.04 and c_a,O2 5.5 ± 2.2 vol%, significantly lower than in the control animals, where pH_a was 7.89 ± 0.04 and c_a,O2 11.6 ± 1.5 vol%. Exercise performance was studied in a swimming respirometer. Stepwise increases in swimming speed caused similar, exponential increases in O₂ uptake in all groups, with no differences in tailbeat frequencies, aerobic scope or maximum sustainable swimming speed.

The results indicate that the eel is extremely tolerant of hypercapnic acidosis. Acute, severe acidosis and hypoxaemia had no effect on CO or whole animal O₂ uptake; chronic acidosis and hypoxaemia had no effect on the ability to increase O₂ uptake and perform muscular work during exercise.