Lactate utilization was studied in an in situ perfused trout heart preparation that was capable of performing at levels similar to in vivo maximum cardiac performance. Hearts were perfused with modified Cortland saline containing 0.5 mmol l−1 iodoacetic acid (to block endogenous glycolysis) and varying amounts of lactate (1 or 10 mmoll−1). We confirmed previous observations that lactate utilization is limited by substrate availability. However, contrary to previous observations, exogenous fuel availability did not limit cardiac performance, even at the high workload. Furthermore, when plentiful (i.e. 10 mmol l−1), exogenous lactate was preferred over endogenous fuel and was able to supply the heart's energy requirements at both the low and high workloads. Pyruvate at 10- fold greater concentration, had no apparent effect on lactate utilization at the high workload. α-Cyano-4-hydroxycinnamate (α-CIN) (2.5 mmoll−1) proved to be an unsuitable probe of lactate transport in the trout heart as it caused a reduction in both lactate utilization and cardiac performance. However, addition of 20 μmol l−1 isobutyl carbonyl lactyl anhydride or 100 μmol l−1 4-acetamido-4′-isothiocyanostilbene-2,2′-disulphonic acid (putative lactate transport blockers) to the perfusate virtually abolished lactate oxidation at the high workload without affecting cardiac performance. These observations suggest that lactate uptake by the in situ perfused trout heart is carrier-mediated.

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