Taurine efflux counters the hydrodynamic impact of anaerobic metabolism to protect cardiorespiratory function under acute thermal stress in brook char (Salvelinus fontinalis).

Upper thermal tolerance may be limited by convective oxygen transport in fish, but the mechanisms constraining heart function remain elusive. The activation of anaerobic metabolism imposes an osmotic stress on cardiomyocytes at high temperatures that must be countered to prevent swelling and cardiac dysfunction. We tested the hypothesis that cardiac taurine efflux is required to counter the osmotic impact of anaerobic end product accumulation in brook char, Salvelinus fontinalis. Fish were fed a diet enriched in β-alanine, a competitive inhibitor of the taurine transporter, to induce taurine deficiency and inhibit transporter function. In vivo, stroke volume increased by 60% and cardiac output doubled in control fish during a 2°C h-1 thermal ramp. Stroke volume was temperature insensitive in taurine-deficient (TD) fish, so cardiac output was 30% lower at high temperatures. The thermal sensitivity of aerobic metabolism did not differ, and lactate accumulated to a similar degree in the two diet treatment groups, indicating that taurine deficiency does not impact energy metabolism. Heart taurine efflux was absent and ventricular muscle osmolality was 40 mOsmol kg-1 higher in TD brook char following thermal stress. Swelling and decreased ventricular compliance likely impair diastolic filling to constrain stroke volume in TD fish. The adrenaline sensitivity of cardiac contractility and the regulation of intracellular pH in the brain and liver were also impacted in TD brook char. Taurine efflux appears necessary to counteract the hydrodynamic impact of activating anaerobic metabolism and this process may limit heart function under acute thermal stress.