RAPID TRACER LACTATE INFLUX INTO CANINE SKELETAL-MUSCLE

This study evaluated the effects of various lactate transport inhibito rs and competitors on rapid tracer lactate influx into the canine gast rocnemius-plantaris muscle (GP). GPs of 25 anesthetized dogs were perf used with red blood cell-free media in situ. At 0.9 mM lactate concent ration ([La]), GP oxygen uptake (2.6 +/- 0.1 ml . kg(-1) . min(-1)) an d net lactate output (-0.039 +/- 0.007 mmol . kg(-1) . min(-1)) were s imilar to values during blood perfusion. Rapid tracer lactate influx w as inferred by a paired-tracer dilution method at nominal perfusate [L a] values of 1, 5, 10, 25, and 50 mM. The maximal tracer influx rate ( U-max) decreased significantly with each increase in unlabeled [La]. A saturation effect was suggested by the fact that percent inhibition o f U-max began to reach a plateau at the higher unlabeled [La] values. The inhibition of U-max was 20.5 +/- 2.9% at 5 mM, 34.1 +/- 3.3% at 10 mM, 47.3 +/- 2.7% at 25 mM, and 56.1 +/- 2.8% at 50 mM [La]. U-max wa s also inhibited by various inhibitors/competitors of lactate transpor t as follows (%inhibition): 50 mM alpha-cyano-4-hydroxy-cinnamate (69. 2 +/- 4.9%), 1.5 mM phloretin (25.4 +/- 5.5%), 0.1 mM 4,4'-diisothiocy anostilbene-2,2'-disulfonic acid (0.3 +/- 1.9%), 0.5 mM p-chloromercur ibenzenesulfonic acid (72.9%), 0.5 mM furosemide (+2.8%), 25 mM pyruva te (52.4 +/- 2.9%), and 50 mM DL-lactate (50.2 +/- 4.0%). These experi ments support the notion that lactate influx into canine skeletal musc le is a function of both a linear (possible diffusive) component and a Michaelis-Menten (carrier-mediated) component.