In rainbow trout as well as a variety of other teleosts, increased RBC pH stems from the activation of B-andrenergic  exchange protein (BNHE) on the RBC membrane via circulating catelcholamines. This process causes the internal pH of the RBC to increase through the outwards movement of  and inwards movement of . The net consequence of alkalizing the RBC is an increase in Hb-O affinity via the Bohr effect. The net influx of  ions and the compensatory activation of -ATPase to maintain ionic equilibrium within the RBC results in a steady decline in cellular ATP, also serving to increase Hb-O affinity. As a further result of inward  movement, the osmolarity of the RBC increases causing osmotic influx of water and cell swelling. The dilution of the cell contents causes further spatial separation of hemoglobin from the inorganic phosphates and again serves to increase Hb-O affinity.
Intertidal hypoxia-tolerant triplefin fish (Family Tripterygiidae) species seem to take advantage of intracellular acidosis and appears to "bypasse" the traditional oxidative phosphorylation and directly drives mitochondrial ATP synthesis using the cytosolic pool of protons that likely accumulates in hypoxia (via lactic acidosis and ATP hydrolysis).