Do air-breathing fish suffer branchial oxygen loss in hypoxic water?

In hypoxia, air-breathing fish obtain O2 from the air but continue to excrete CO2 into the water. Consequently, it is believed that some O2 obtained by air-breathing is lost at the gills in hypoxic water. Pangasionodon hypophthalmus is an air-breathing catfish with very large gills from the Mekong River basin where it is cultured in hypoxic ponds. To understand how P. hypophthalmus can maintain high growth in hypoxia with the presumed O2 loss, we quantified respiratory gas exchange in air and water. In severe hypoxia (PO2: ≈ 1.5 mmHg), it lost a mere 4.9% of its aerial O2 uptake, while maintaining aquatic CO2 excretion at 91% of the total. Further, even small elevations in water PO2 rapidly reduced this minor loss. Charting the cardiovascular bauplan across the branchial basket showed four ventral aortas leaving the bulbus arteriosus, with the first and second gill arches draining into the dorsal aorta while the third and fourth gill arches drain into the coeliacomesenteric artery supplying the gut and the highly trabeculated respiratory swim-bladder. Substantial flow changes across these two arterial systems from normoxic to hypoxic water were not found. We conclude that the proposed branchial oxygen loss in air-breathing fish is likely only a minor inefficiency.

Arapaima gigas maintains gas exchange separation in severe aquatic hypoxia but does not suffer branchial oxygen loss.

One of the most air-reliant obligate air-breathing fish is the South American Arapaima gigas, with substantially reduced gills impeding gas diffusion, thought to be a result of recurring aquatic hypoxia in its habitat. In normoxic water, A. gigas is reported to satisfy 70-80% of its O2 requirement from the air while excreting 60-90% of its CO2 to the water. If this pattern of gas exchange were to continue in severely hypoxic water, O2 loss at the gills would be expected. We hypothesized therefore that partitioning of CO2 would shift to the air phase in severe aquatic hypoxia, eliminating the risk of branchial O2 loss. By adapting a respirometer designed to measure aquatic MO2/MCO2, we were able to run intermittent closed respirometry on both water and air phase for both of these gasses as well as sample water for N-waste measurements (ammonia-N, urea-N) so as to calculate metabolic fuel utilization. In contrast to our prediction, we found that partitioning of CO2 excretion changed little between normoxia and severe hypoxia (83% versus 77% aquatic excretion, respectively) and at the same time there was no evidence of branchial O2 loss in hypoxia. This indicates that A. gigas can utilize distinct transfer pathways for O2 and CO2. Routine and standard MO2, N-waste excretion and metabolic fuel utilization did not change with water oxygenation. Metabolism was fuelled mostly by protein oxidation (53%), while carbohydrates and lipids accounted for 27% and 20%, respectively.