RAPID TRACER LACTATE INFLUX INTO CANINE SKELETAL-MUSCLE

This study evaluated the effects of various lactate transport inhibitors and competitors on rapid tracer lactate influx into the canine gastrocnemius-plantaris muscle (GP). GPs of 25 anesthetized dogs were perfused with red blood cell-free media in situ. At 0.9 mM lactate concentration ([La]), GP oxygen uptake (2.6 +/- 0.1 ml . kg(-1) . min(-1)) and net lactate output (-0.039 +/- 0.007 mmol . kg(-1) . min(-1)) were similar to values during blood perfusion. Rapid tracer lactate influx was inferred by a paired-tracer dilution method at nominal perfusate [La] 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 of 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 was also inhibited by various inhibitors/competitors of lactate transport 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'-diisothiocyanostilbene-2,2'-disulfonic acid (0.3 +/- 1.9%), 0.5 mM p-chloromercuribenzenesulfonic acid (72.9%), 0.5 mM furosemide (+2.8%), 25 mM pyruvate (52.4 +/- 2.9%), and 50 mM DL-lactate (50.2 +/- 4.0%). These experiments support the notion that lactate influx into canine skeletal muscle is a function of both a linear (possible diffusive) component and a Michaelis-Menten (carrier-mediated) component.