Temperature, the abiotic masterenvironmental factor, has a profound effect on the abundance and distributionof animals on the earth, in particular ecotherms. Ectothermic animals (fishes,frogs, reptiles, and invertebrate animals), cannot physiologically regulatetheir body temperature, and are therefore especially vulnerable to temperaturechanges to which they are not adapted but to which they might be exposed on thewarming earth. Indeed, understanding how climate change will affect animal lifeis one of the greatest challenges of the current biological research. Climatewarming is considered to be the most critical environmental threat, inparticular for aquatic ecosystems and their biodiversity. According to thecurrent scenarios, the annual mean temperature in Finland is projected to riseby 2-5°C and 2-7°C by the 2050s and 2080s, respectively.
The duration of icecover in lakes will become shorter, winters will be milder and extremetemperature peaks are likely to be higher and occur more often which inturnwill affect fish populations in Finland. Predicted increases in ambienttemperature will acts as a leading factor which control the boundary ofhabitats, locomotion, reproduction, development, immune defense and generalperformance level of fishes and other ectotherms, and thereby will impact thedistribution and abundance of animal species and possibly distort the precise balanceof the ecosystems to which they belong.Fishesrepresent the most variable and largest group among vertebrates. Acute andchronic temperature changes will be reflected on the cardiac function whichconsiders as a key physiological variable in environmental adaptation andacclimation of aquatic vertebrates via delivery oxygen and nutrients to differenttissues and providing homeostatic balance between body parts. In northernlatitudes, All fishes have to tolerate large seasonal temperature changes:their hearts have to function close to zero in winter, while summertemperatures may be 20-30 degrees higher. Heart muscle is electricallyexcitable, i.
e. a small voltage change of plasma membrane (cardiac actionpotential, AP) sets the rate and rhythm of the heart, initiates contraction andregulates force production of cardiac myocytes. Cardiac AP is generated by a complexinteraction between several ion channels in the cell membrane.
Hence, smalldisturbances in ion channel function may generate cardiac arrhythmias, conductionfailure and compromise force of cardiac contraction. Moreover, thermal plasticity of fish heart is substantialto maintain contractility and to avoid disturbances in the electricalexcitability that should be sensitive and stable to temperature changes toproduce temperature-dependent acceleration and deceleration of heart rate (fH)and parallel changes in the rate of impulse conduction (action potential; AP)over the heart. Strongly response of fishes to the warming makes them asindicator for detecting and documenting climate-induced modifications on aquaticecosystems. To this end, effects of seasonal acclimatzation on the electricalexcitbility of roach (Rutilus rutilus) heart, one of the most abundantfish species in Finnish lakes and coastal waters, is examined. Also, the hypothesisof temperature-dependent depression of electrical excitation (TDEE) is recentlysuggested by Vornanen (2016), the mismatch between the temperature-dependent ofoutward K+ and inward Na+ may cause compromise in theelectrical excitability, is examined in roach cardiomyocytes. Responses of roachheart to temperature 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.The presentstudy revealed that seasonal acclimatization of electrical excitation is crucialfor proper function of roach heart under widely range of water temperatures inwinter and summer seasons.
Seasonal thermal acclimation of electricalexcitability increases pumping capacity of the roach heart by increasing fHin both seasons to the maximum without compromising the stability of cardiacexcitatability. Sensitivity to thermal disturbances increases with increasingcomplexity of biological organization, i.e.
, molecular functions beinggenerally the the most temperature sensitive and the intact organism is themost temperature resistant. The upper thermal tolerance of fHis higher in summer- than in winter-acclimatized roach. Evidence of cardiacarrhythmias clearly appeared with rising temperature around and above the breakpoint temperature (TBP), the temperature after which steadyincrease/decrease of the variables in response to temperature changes reversedinto continuous decrease/increase, respectively, initially as missing QRScomplexes to complete cessation of contractility (asystole) in both seasonal acclimatizedgroups. Interestingly, Action potential (AP) of atrial myocytes in summer roachrecorded by microelectrode technique were characterized by a rapid initialrepolarization where the striking shortening in atrial AP duration at 10% (APD10)and 20% (APD20) repolarization levels in comparison to atrialmyocytes of winter roach. Among ion currents of roach heart, the inwardrectifier K+ current (IK1) has the highest thermaltolerance, while sodium current (INa) is the lowest one in bothseasonal groups. in winter acclimatized roach, the lower thermal tolerance of INais consistent with the lower thermal tolerance of in vivo fH,while the matching between INa and fH is not idealin summer- as winter-acclimatized roach, thus other factors beside INamay be included.
In both seasonal acclimatized groups, molecular composition ofion channels regulates ion currents in temperature-dependend manner andconsistent with the electrophysiological data.Exercise,capture and handling stress can cause remarkable changes in the metabolite andion composition of the extracellular fluid and elevate extracellular K+concentration (K+o) which may cause a significantpost-stress mortality of fishes. In the present study, The combined effects of hightemperature and high K+o on the electrical excitabilityof winter-acclimatized roach ventricular myocytes was examined. Surprisingly,some myocytes completely failed to elicit all-or-none AP in 8 mM K+oat 24°C with reduction in AP amplitude and overshoot by elevation of K+o.Effects of high K+o antagonizes the negative effects ofhigh temperature on excitation threshold, the steepy depression of the rate ofAP upstroke (Vmax) and complete loss of excitability in somemyocytes suggest that the combination of high temperature and high K+owill severely impair ventricular excitability in roach.