Lactate and Proton Dynamics in the Rainbow Trout (Salmo Gairdneri)

Chronically cannulated rainbow trout were subjected to 6 min of severe burst exercise and monitored over a 12 h recovery period. There were short-lived increases in haematocrit, haemoglobin, plasma protein, Na+ and Cl− levels. Plasma [Cl−] later declined below normal as organic anions accumulated. A much larger and more prolonged elevation in plasma [K+] probably resulted from intracellular acidosis. An intense extracellular acidosis was initially of equal respiratory (i.e. Pa,COa,CO2) a nd metabolic (i.e. ΔH+m) origin. However Pa,COa,CO2 was rapidly corrected while the metabolic component persisted. Plasma ammonia increases had negligible influence on acid-base status. Elevations in blood lactate (ΔLa−) were equal to ΔH+m immediately post-exercise but later rose to twice the latter. Simultaneous white muscle biopsies and blood samples demonstrated that muscle to blood gradients of lactate and pyruvate were maximal immediately post-exercise. As blood levels rose and muscle levels declined, an approximate equilibrium was reached after 4 h of recovery. Intra-arterial infusions of lactic acid in resting trout produced a severe but rapidly corrected metabolic acidosis. The rates of disappearance of ΔH+m and ΔLa− from the blood were equal. Infusions of similar amounts of sodium lactate produced a small, prolonged metabolic alkalosis with a much slower ΔLa− disappearance rate. It is suggested that the excess of ΔLa− over ΔH+m in the blood after exercise is associated with differential release rates of the two species from white muscle rather than differential removal rates from the bloodstream, and that the majority of the lactic acid load in muscle is removed by metabolism in situ.