Hypoxia stimulates lactate disposal in rainbow trout

Area of Science:

• Physiology
• Biochemistry
• Aquatic Animal Metabolism

Background:

• Lactate metabolism in fish is poorly understood due to reliance on concentration measurements, which don't reflect flux.
• Previous studies could not infer changes in lactate production or disposal rates.

Purpose of the Study:

• Quantify baseline lactate fluxes in rainbow trout under normoxia.
• Determine how lactate appearance and disposal rates change during hypoxia.
• Identify tissues responsible for lactate production.

Main Methods:

• Used continuous infusion of [U-(14)C]lactate in vivo to measure lactate appearance (R(a)) and disposal (R(d)) rates.
• Exposed rainbow trout (Oncorhynchus mykiss) to normoxic and hypoxic (25% O(2) saturation) conditions for 90 minutes.

Main Results:

• In normoxia, lactate R(a) and R(d) were matched, maintaining a stable blood lactate concentration (~0.8 mmol l(-1)).
• Hypoxia significantly increased blood lactate (to 8.9 mmol l(-1)) by elevating R(a) (from 18.4 to 36.5 μmol kg(-1) min(-1)).
• Unexpectedly, hypoxia also increased lactate R(d) by 52% (from 19.9 to 30.3 μmol kg(-1) min(-1)), with white muscle being the main lactate producer.

Conclusions:

• This study provides the first non-steady-state lactate kinetics in fish.
• Increased lactate disposal during hypoxia is a critical compensatory mechanism reducing circulatory lactate load.
• Without enhanced lactate disposal, blood lactate accumulation in hypoxic trout would double.