The effect of a taurine deficiency on the cardiovascular response of brook char (Salvelinus fontinalis) to hypoxia

Abstract

Taurine is a non-proteogenic β-amino acid found in relatively high abundance within the heart of freshwater teleosts. By exhibiting cardioprotective properties through participation in osmoregulation and calcium (Ca2+) homeostasis, taurine has been linked to supporting the cardiovascular physiology under environmental hypoxia. The functional capacity of the heart is defined by cardiac output (Q ), representing the product of heart rate (fh) and stroke volume (SV). A taurine deficiency has been shown to impair the ability to increase SV under hypoxia in vitro and cause a shorter time to loss of equilibrium (LOE) in vivo, indicating cardiovascular disturbances. The knowledge gap addressed in this study is the effect of a taurine deficiency on all three cardiac parameters in vivo under hypoxia. These measurements were paired with metrics of the O2 carrying capacity of the blood and osmotic stress following acute hypoxia and recovery. Brook char (Salvelinus fontinalis) were used as a representative freshwater teleost, for this analysis. A taurine-deficient (TD) model was achieved through 5% dietary β-alanine supplementation, a known competitive inhibitor of taurine transport. fh, SV, and Q in vivo were quantified using electrocardiograms (ECG) and ultrasonic flows. Significance was found in lower resting fh and blunted bradycardia in TD fish. SV was maintained at similar levels to control fish, although TD fish did not elevate SV under hypoxia, likely tied to their lesser bradycardia. Q was similar in both models, along with hematological parameters characterizing the capacity to transport O2 in circulation. TD hearts had decreased lactate levels, an important metabolite to cardiovascular function under a hypoxia stressor. The main finding of this study is that TD fish have a greater sensitivity to environmental hypoxia, attributed to just a 21% reduction in cardiac taurine. With the typical increase in SV seen under hypoxia attributed to a lower fh, regulatory disruption of contractile frequency may explain the observed physiological differences. As an important mechanism to mitigate osmotic disturbances under hypoxia, a limited ability to perform taurine efflux may be the underlying cause of cardiac dysfunction. This may additionally lead to alterations to the Ca2+current (ICa) acting on the heart's pacemaker or autonomic nervous system activation. With the progression of global warming and v associated disturbances to aquatic O2 availability, ensuring sufficient taurine in the diets of freshwater fish could be a method of supporting cardiovascular function.