Temperature, the abiotic masterenvironmental factor, has a profound effect on the abundance and distributionof ectothermal animals on the earth which cannot physiologically regulate theirbody temperature. Predicted increases in ambient water temperature will acts asa leading factor which control the boundary of habitats, locomotion,reproduction, development, immune defense and general performance level offishes and other ectotherms. In northern latitudes, All fishes have to accommodatelarge range of temperature changes between winter and summer. Fish heart iselectrically excitable muscle, i.e. a small voltage change of plasma membrane (actionpotential, AP) sets the rate and rhythm of the heart, initiates contraction andregulates force production of cardiac myocytes. Cardiac AP is generated by a harmoniousco-operation between several ion channels in the cell membrane. Hence, a smalldisturbance in ions distribution could cause cardiac arrhythmias, conductionfailure and compromise force of cardiac contraction.
Electrical excitability offish heart should be sensitive and stable to temperature changes to producetemperature-dependent acceleration and deceleration of heart rate (fH)and parallel changes in the rate of impulse conduction over the heart. Recently,Vornanen (2016) suggests that the mismatch between the temperature-dependent ofoutward K+ and inward Na+ may cause compromise in theelectrical excitability which termed as hypothesis of temperature-dependentdepression of electrical excitation (TDEE). Strongly response of fishes to thewarming makes them as indicator for reporting climate-induced modifications on aquaticecosystems. To this end, the thermal plasticity of electrical excitability infish heart and the TDEE hypotesis were tested by using seasonally acclimatized roach(Rutilus rutilus) as an experimental animal. Responses of roach heart totemperature changes are determined at different levels of biologicalorganization starting from in vivo recordings of heart function inliving animals down to organ, cell and molecule level of in vitroexperiments.Generally, thermaltolerance increases with increasing complexity of biological organization, i.e.,molecular functions have the highest thermal tolerance while the intact fish hasthe lowest one.
Seasonal acclimatization increases heart rate (fH)of roach heart in both seasons to the maximum without compromising thestability of cardiac electrical-excitatability. The upper thermal tolerance of ECGand AP variables are higher in summer than in winter roach. Evidence of cardiacarrhythmias clearly appeared with rising temperature around and above the breakpoint temperature (TBP) in both seasonal groups. Among ioncurrents of roach heart, the inward rectifier K+ current (IK1)has the highest thermal tolerance, while sodium current (INa) is thelowest one in both seasonal groups. In winter roach, the lower thermal toleranceof INa is consistent with the lower thermal tolerance of in vivofH, while the matching between INa and fHis not ideal in summer as winter roach, thus other factors beside INamay be included. Collectively, INa is clearly the mostheat-sensitive ion current, and considering the weakest link which probablylimiting the upper thermal tolerance of electrical excitation in roachcardiomyocytes.
Current findings are consistent with the hypothesis of the TDEEwhich provides a mechanistic explanation for high temperature-inducedarrhythmias and bradycardia and post-exercise depression of fHin fish heart in vivo at cellular and molecular level, and thereforepoor survival of fishes exposed to thermal, exercise and handling stresses.