LACTATE TRANSPORT BY RAINBOW-TROUT WHITE MUSCLE - KINETIC CHARACTERISTICS AND SENSITIVITY TO INHIBITORS

Citation
Yx. Wang et al., LACTATE TRANSPORT BY RAINBOW-TROUT WHITE MUSCLE - KINETIC CHARACTERISTICS AND SENSITIVITY TO INHIBITORS, American journal of physiology. Regulatory, integrative and comparative physiology, 41(5), 1997, pp. 1577-1587
Citations number
37
Categorie Soggetti
Physiology
ISSN journal
03636119
Volume
41
Issue
5
Year of publication
1997
Pages
1577 - 1587
Database
ISI
SICI code
0363-6119(1997)41:5<1577:LTBRWM>2.0.ZU;2-7
Abstract
This study used an isolated-perfused tail-trunk preparation of rainbow trout to examine the uptake and release of lactate (Lac) and metaboli c protons (Delta H-m(+)) in resting and exercised fish white muscle. I n exercised muscle, L(+)-Lac efflux was inhibited (similar to 40%) by 5 mM alpha-cyano-4-hydroxycinnamate (CIN), but not by 0.5 mM -acetamid o-4'-isothiocyanostilbene-2,2'-disulfonic acid (SITS) or 0.1 mM amilor ide. These results suggest that Lac release occurs through a Lac(-)-H symport and the free diffusion of lactic acid (HLac) or Lac(-), but n ot via the Lac(-)/HCO3-Cl- antiporter. Lac efflux was accompanied by 3 Delta H-m(+) influx in all treatments, and increased Delta H-m(+) inf lux occurred after SITS treatment. In resting muscle, Lac uptake rates were greater than Lac efflux rates in the postexercise preparation. L -Lac influx exhibited partial saturation kinetics, whereas D(-)-Lac in flux was linearly related to its extracellular concentration (0-32 mM) . At 16 mM extracellular L-Lac, with a negligible transmembrane L-HLac gradient and an outwardly directed net driving force on L-Lac(-), CIN , and SITS reduced net L-Lac uptake by 75 and 45%, respectively. At 16 mM extracellular concentration, D-Lac influx was 64% of the net L-Lac influx. These results suggest that in trout muscle at 16 mM extracell ular L-Lac, the Lac(-)-H+ symport accounts for 30-36%, the Lac(-)/HCO3 --Cl- antiport for 39-45%, and diffusion for 19-25% of uptake, althoug h the latter is probably overestimated and the former underestimated f or methodological reasons. Net L-Lac efflux was not affected by extrac ellular D-Lac concentration and/or D-Lac influx, implying the existenc e of a concurrent L-Lac efflux during L-Lac influx. The D-Lac influx k inetics data indicated that the Lac(-)/HCO3- antiport was not saturabl e in the extracellular D-Lac concentration range of 0-32 mM. This stud y clearly demonstrates the involvement of carrier-mediated transport i n transmembrane Lac movement in fish muscle and supports the ''active lactate retention'' mechanism proposed by Turner and Wood.