Hypoxia stimulates lactate disposal in rainbow trout.

Current understanding of lactate metabolism in fish is based almost entirely on the interpretation of concentration measurements that cannot be used to infer changes in flux. The goals of this investigation were: (1) to quantify baseline lactate fluxes in rainbow trout (Oncorhynchus mykiss) under normoxic conditions; (2) to establish how changes in rates of lactate appearance (R(a)) and disposal (R(d)) account for the increase in blood lactate elicited by hypoxia; and (3) to identify the tissues responsible for lactate production. R(a) and R(d) lactate of rainbow trout were measured in vivo by continuous infusion of [U-(14)C]lactate in trout exposed to 25% O(2) saturation or maintained in normoxia for 90 min. In normoxic fish, R(a) lactate decreased from 18.2 to 13.1 μmol kg(-1) min(-1) and R(d) lactate from 19.0 to 12.8. R(a) and R(d) were always matched, thereby maintaining a steady baseline blood lactate concentration of ∼0.8 mmol l(-1). By contrast, the hypoxic fish increased blood lactate to 8.9 mmol l(-1) and R(a) lactate from 18.4 to 36.5 μmol kg(-1) min(-1). This stimulation of anaerobic glycolysis was unexpectedly accompanied by a 52% increase in R(d) lactate from 19.9 to 30.3 μmol kg(-1) min(-1). White muscle was the main producer of lactate, which accumulated to 19.2 μmol g(-1) in this tissue. This first study of non-steady-state lactate kinetics in fish shows that the increase in lactate disposal elicited by hypoxia plays a strategic role in reducing the lactate load on the circulation. Without this crucial response, blood lactate accumulation would double.