LACTATE AND METABOLIC H-TROUT WHITE MUSCLE( TRANSPORT AND DISTRIBUTION AFTER EXERCISE IN RAINBOW)

An isolated-perfused tail-trunk preparation was employed to study the influence of transmembrane pH gradient and membrane potential on the t ransport and distribution of L(+)-lactate (Lac), metabolic H+ (Delta H -m(+)), and related parameters in rainbow trout white muscle after exh austive exercise. One resting [arterial pH (pH(a)) approximate to 7.9] and four postexercise treatments (pH(a) approximate to 7.4, 7.9, 8.4, and, high K+, pH(a) approximate to 7.9, partially depolarized by 15 m M K+) were examined. Variations in HCO3- concentration (2-18 mM) at a constant Pco(2) approximate to 2 Torr were used to alter pH(a). The el evated intracellular Lac (approximate to 50 mM) remained unchanged aft er 60 min of perfusion because of very low rates of lactate efflux and oxidation. H+, HCO3-, and Lac(-) distributions were all well out of e lectrochemical equilibrium. Total CO2 efflux was reduced at high extra cellular pH (pH(e)); alterations in the net driving force on HCO3- may have overshadowed the influence of Pco(2) gradients in driving total CO2 efflux. Lac efflux and Delta H-m(+) flux were completely uncoupled . Delta H-m(+) flux reacted to both acid-base and electrochemical grad ients as Delta H-m(+) efflux dropped and even reversed when pH(e) decr eased, whereas partial depolarization in conjunction with depressed in tracellular pH resulted in elevated Delta H-m(+) efflux. Lac efflux di d not respond to changes in pH(e). Changes in Lac efflux corresponded more closely to changes in the Lac(-) concentration gradient than in t he lactic acid gradient. This study provides circumstantial evidence f or the involvement of electroneutral mechanisms (i.e., Lac(-)-H+ cotra nsport and/or Lac(-)/anion exchange) in lactate efflux, but does not e liminate the possibility of an active transport mechanism contributing to the retention of Lac.