Seasonal is between 0 and 4°C, the

Seasonal thermal acclimation of electrical excitation
is vital for convenient heart function under widely range of temperatures between
winter and summer waters. Roach are eurythermic fish with the ultimate upper
lethal temperature of 33.5°C (Cocking 1959). The ultimate upper lethal
temperature of roach acclimated at 4 and 18°C is consistent with recent
findings of TBPs for in vivo fH
(Cocking 1959; Badr et al. 2016). These findings show that the upper thermal
tolerance limit, below which the majority of the fish are able to survive
“indefinitely”, and the temperature above which in vivo fH starts
to decrease almost coincide. Pumping capacity of the roach heart increased by maximizing
fH in both seasonal acclimatization groups without
compromising the stability of cardiac excitation in response to seasonal
acclimatization. Even though fH is seasonally optimized, both
winter and summer roach hearts retain the safety margin of approximately 10°C
for cardiac arrhythmias. Considering that water temperature in winter in
ice-covered lakes is between 0 and 4°C, the upper thermal tolerance limits of fH
and INa of winter roach heart are more than sufficient to allow
active life in winter and there is plenty of rooms for temperature increases without
danger of heat intolerance. The situation is slightly different for summer
roach, since maximum summer temperatures of surface water (25-26°C) in lakes in
northern Europe can be within a few degrees from the TBPs of fH
and arrhythmia (TARR) , but above the TBP
of INa (Badr et al., 2016; Badr et al., 2017b).

Thermal
tolerance of the cardiac IK1, IKr and ICaL are
markedly higher in winter- and summer-acclimatized roach than the lethal
temperatures of the fish and the TBPs of fH.
This suggests that IK1, IKr and ICaL are not
critical factors in thermal tolerance of the heart or the fish. Contrary, INa
is much more sensitive to high temperatures than either fH or
intact fish in both seasonal acclimatized roach. Similar to the brown trout heart,
INa is clearly the most heat-sensitive ionic current of cardiac
myocytes in roach, and therefore the weakest link in cardiac excitation
(Vornanen et al., 2014; Badr et al., 2017b). These present findings are
consistent with the assumptions of the TDEE hypothesis in that a mismatch in
temperature dependence between inward INa and outward K+ currents
(IK1) is causative to high temperature-induced arrhythmias and
bradycardia in fish hearts in vivo (Vornanen, 2016). The match between TBPs
of fH and INa was not quantitatively perfect in
summer-acclimatized roach as in winter-acclimatized fishes suggesting that
other factors may be involved. Densities of INa and IK1 in
vivo are affected by the shifts in intra- and extracellular Na+ and
K+ ion concentrations, which are likely to occur as an outcome from
changes in fH (Kunze 1977; Kline & Morad 1978; Cohen et
al. 1982). Increased fH and shortened diastolic interval at high
temperature may limit recovery of INa from inactivation (Haverinen &
Vornanen 2006). Furthermore, atrial myocytes have an acetylcholine-induced
inward rectifier K+ current, IKACh, which is seasonally
primed, and could therefore antagonize INa together with the
background IK1 (Abramochkin & Vornanen, 2016). High temperature
limitation of fH does not occur at single cell level: beating
rate of isolated pacemaker cells is not limited by high temperatures and
ventricular APs can be triggered much above the TBP of fH
in vivo (Vornanen et al. 2014; Haverinen et al. 2017; Badr et al. 2017a).
Thermal limitation of fH is an emergent property that appears
at tissue level as an outcome of interaction between cardiac myocytes.

We Will Write a Custom Essay Specifically
For You For Only $13.90/page!


order now

Small
changes in K+o have a major impact on electrical
excitability of roach ventricular myocytes. Effects of temperature and high K+o
on excitability of roach ventricular myocytes are partly antagonistic and in
some respects synergistic. High temperature hyperpolarizes RMP, increases Vmax
and elevates excitation threshold, while high K+o
depolarizes RMP, depresses Vmax and reduces excitation threshold.
APD50 is strongly shortened and densities of IK1 and IKr
are increased by both high temperature and high K+o.
However, the depressing effects of high K+o are so
strong that they override the positive effects of high temperature on RMP and Vmax.
Indeed, electrophysiological properties of roach ventricular AP are very
sensitive to small changes in K+o. High concentration
of extracellular K+ is most probably cardiotoxic to roach, since Vmax
is severely depressed and some ventricular myocytes become unexcitable and
cannot generate propagating APs. Because basic features of electrical excitability
are common to all excitable cells, the present findings are probably valid for
neurons and muscle cells. Therefore, future studies should examine the combined
effects of K+o and temperature on muscular and neuronal
excitability. Those studies could reveal the impact of environmental and
physiological stresses on locomotion, sensory function, behavior and fitness of
ectotherms.