Taurine depletion impairs cardiac function and affects tolerance to hypoxia and high temperatures in brook char (Salvelinus fontinalis)

Physiological and environmental stressors can cause osmotic stress in fish
hearts, leading to a reduction in intracellular taurine concentration.
Taurine is a beta amino acid known to regulate cardiac function in other
animal models but its role in fish has not been fully elucidated. We
generated a model of cardiac taurine-deficiency (TD) by feeding brook char
(Salvelinus fontinalis) a diet enriched in β-alanine, which inhibits
cardiomyocyte taurine uptake. Cardiac taurine levels were reduced by 21%,
and stress-induced changes in normal taurine handling were observed in TD
brook char. Responses to exhaustive exercise and acute thermal and hypoxia
tolerance were then assessed using a combination of in vivo, in vitro, and
biochemical approaches. Critical thermal maximum was higher in TD brook
char despite significant reductions in maximum heart rate. In vivo, TD
brook char exhibited a lower resting heart rate, blunted hypoxic
bradycardia, and a severe reduction in time to loss of equilibrium under
hypoxia. In vitro function was similar between control and TD hearts under
oxygenated conditions, but stroke volume and cardiac output were severely
compromised in TD hearts under anoxia. Aspects of mitochondrial structure
and function were also impacted in TD permeabilized cardiomyocytes, but
overall effects were modest. High levels of intracellular taurine are
required to achieve maximum cardiac function in brook char and cardiac
taurine efflux may be necessary to support heart function under stress.
Taurine appears to play a vital, previously unrecognized role in
supporting cardiovascular function and stress tolerance in fish.