Nitrite oxidizes haemoglobin (Hb) to methaemoglobin (MetHb), which is unable to bind oxygen. Nitrite exposure can therefore be used as a tool to manipulate the oxygen-carrying capacity of the blood without changing haematocrit. The objective of this study is to examine the relationship between the critical swimming velocity (Ucrit) and the functional haemoglobin concentration ([Hb]) of the blood in adult chinook salmon. Functional [Hb] was reduced by increasing MetHb levels through intraperitoneal administration of a mass-dependent volume of sodium nitrite. In resting fish, MetHb levels were found to stabilize at 25 % of total [Hb] 3 h after the injection of 30 mg kg-1 sodium nitrite. Methaemoglobin levels increased in proportion to the amount of sodium nitrite injected and reached a maximum (following the injection of 90 mg kg-1 sodium nitrite) of 51.8 % in resting fish and 72 % in fish forced to swim to Ucrit. At 60 and 90 mg kg-1 sodium nitrite, MetHb formation was greater in exercised than in resting fish. A second-order regression revealed that Ucrit was virtually independent of functional [Hb] between 51 and 100 % of control functional [Hb], but was positively correlated with functional [Hb] below 51 % of total [Hb] (4.5 g dl-1). The insensitivity of Ucrit to a functional [Hb] greater than 51 % may be partly due to the exponential increase in aerobic metabolism required to provide the power to overcome hydrodynamic drag at higher water velocities. There were no significant changes in intraerythrocytic organic phosphate (adenylates and guanylates) concentrations standardized to [Hb] in swimming or resting fish over the range of MetHb levels induced in this study. Fish may encounter nitrite naturally; if MetHb levels become severely elevated as a result, swimming ability will be significantly impaired.

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