Warm, but not hypoxic acclimation, prolongs ventricular diastole and decreases the protein level of Na+/Ca2+ exchanger to enhance cardiac thermal tolerance in European sea bass.

One of the physiological mechanisms that can limit the fish's ability to face hypoxia or elevated temperature, is maximal cardiac performance. Yet, few studies have measured how cardiac electrical activity and associated calcium cycling proteins change with acclimation to those environmental stressors. To examine this, we acclimated European sea bass for 6 weeks to three experimental conditions: a seasonal average temperature in normoxia (16 °C; 100% air sat.), an elevated temperature in normoxia (25 °C; 100% air sat.) and a seasonal average temperature in hypoxia (16 °C; 50% air sat.). Following each acclimation, the electrocardiogram was measured to assess how acclimation affected the different phases of cardiac cycle, the maximal heart rate (fHmax) and cardiac thermal performance during an acute increase of temperature. Whereas warm acclimation prolonged especially the diastolic phase of the ventricular contraction, reduced the fHmax and increased the cardiac arrhythmia temperature (TARR), hypoxic acclimation was without effect on these functional indices. We measured the level of two key proteins involved with cellular relaxation of cardiomyocytes, i.e. sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA) and Na+/Ca2+ exchanger (NCX). Warm acclimation reduced protein level of both NCX and SERCA and hypoxic acclimation reduced SERCA protein levels without affecting NCX. The changes in ventricular NCX level correlated with the observed changes in diastole duration and fHmax as well as TARR. Our results shed new light on mechanisms of cardiac plasticity to environmental stressors and suggest that NCX might be involved with the observed functional changes, yet future studies should also measure its electrophysiological activity.

The interactive effects of exercise training and functional feeds on the cardiovascular performance of rainbow trout (Oncorhynchus mykiss) at high temperatures.

The cardiovascular performance of salmonids in aquaculture can be impaired by acute climate warming, posing risks for fish survival. Exercise training and functional feeds have been shown to be cardioprotective in mammals but their action on the fish heart and its upper thermal performance has not been studied. To investigate this, rainbow trout were trained at a moderate water velocity of 1 body length per second (bl s-1) for 6 h per day, either alone or in combination with one of two functional feed-supplements, allicin and fucoidan. After 6 weeks of exercise training and feeding, maximum heart rate and the temperature coefficient of heart rate were significantly higher in the trained fish as compared to untrained ones. There was a slight increase in hematocrit in trained control fish reared on a normal diet (TC group) compared to untrained fish fed with the same diet (CC). This implies that exercise training enhanced oxygen delivery to trout tissues via an increase of cardiac blood flow in warm water. However, cardiac thermal tolerance was not affected by exercise training or feeding, except from the temperature of peak heart rate which was higher in the trained group fed with fucoidan supplement (TF) as compared to the untrained group fed with same diet (CF). Allicin supplement caused a significant reduction in the maximum heart rate and the temperature coefficient of heart rate, especially in trained fish, while fucoidan supplement did not cause any effect on heart rate. No differences were observed in growth performance among groups. However, fish fed with fucoidan-supplemented diet had a slight reduction in feed conversion efficiency. We suggest further investigations to understand the antagonistic effect of allicin supplemental feeding and exercise training on cardiovascular performance. More studies are also required to investigate if other exercise training intensities could increase cardiac thermal tolerance.