A mechanistic investigation of the effects of lactic acidosis on myocardial contractility in the Neotropical fast-swimming freshwater fish Brycon amazonicus

Lactic acidosis commonly impairs myocardial contractility in vertebrates, limiting cardiac performance under metabolic stress. However, the rheophilic Neotropical species matrinxã (Brycon amazonicus) appears to exhibit physiological adaptations that support cardiac resilience. In this study, ventricular muscle strips were exposed to extracellular lactic acidosis (LA, 22 mM lactic acid, pH 6.9) and evaluated for twitch contractility and the roles of calcium handling and pH regulation. Isometric ventricular preparations were utilized to assess: (a) the effects of LA; (b) the combined effects of LA and ryanodine, an inhibitor of sarcoplasmic reticulum (SR) function; (c) the combined effects of LA and amiloride, an inhibitor of the Na⁺/H⁺ exchanger (NHE); (d) the effects of lithium, an inhibitor of the Na⁺/Ca²⁺ exchanger (NCX), and its interaction with LA; and (e) the effects of a Ca²⁺-free solution and its interaction with LA. Acidosis initially reduced contractile force, followed by a complete recovery and accelerated relaxation. Ryanodine and amiloride effectively abolished recovery, whereas Na^+/Ca²⁺ exchanger blockade enhanced force but prolonged relaxation. Compared to other acidosis-resilient fish species, our findings show that B. amazonicus employs a distinct adaptive strategy to maintain cardiac function under lactic acidosis. This strategy involves coordinated sarcoplasmic reticulum (SR) Ca²⁺ release and activation of the NHE to restore myocardial performance. Such physiological adjustments likely support survival during intense anaerobic activity in fluctuating aquatic environments.