ELECTRICAL remains elevated for several hours after exercise

ELECTRICAL EXCITATION of sarcolemma triggers contraction of cardiac
myocytes. Excitation originates from a small group of pacemaker cells, which in
fish heart comprise a ring-liked structure at the border between sinus venosus and atrium(25, 44). From there the excitation spreads via
interconnected cardiac myocytes throughout the heart, first into the atrium and
then along a specialized nodal tissues into the ventricle(30, 32). The orderly sequence of electrical
excitation is based on awell-balanced interaction between several Na+,
K+ and Ca2+ specific ion channels of the myocyte
sarcolemma, which generate a fast propagating cardiac action potential (AP).In
each functionally specialized cardiac tissue, AP has a characteristicshapegenerated
bychamber-specificion currents and ion channel compositions(38).However, the shape of the chamber-specificAP
is far from constant, since neuronal inputs, hormones, local tissue factors,temperature
changes and stretching modify it so that the pump function of the heart is optimally
adjusted to the circulatory demands(16, 24, 28, 29, 38). The delicate and complex balance
between interacting cardiac ion channels is affected, and sometimes severely disturbed,
by acute temperature changes and stresses that alterion concentrationsof the
external fluid around cardiac myocytes(21, 41).

Capture-related exercise, air exposure and handling stress
cause significant changes in metabolite and ion composition of the extracellular
fluid and may result in significant post-stress mortality of fishes(12, 20, 33). In particular,increases in externalK+
concentration (K+o) are often marked and detrimental
for post-exercise recovery and survival of the fish (9, 36, 42). For example, in capture-stressed marine
gamefish, including both teleost and elasmobranch species, K+o
ranged from 7 to 20 mM, which markedly exceed the K+ovalues
of non-stressed fishes (usually 3-4 mM) (42). Notably, K+o
remains elevated for several hours after exercise and handling stress(33, 43). Furthermore, the exercise-related
increase in K+oand mortality of the fish are dependent
on temperature and thermal history of the animal(9, 12, 19): e.g. theexercise-induced increase in K+ois
much higher in warm-acclimated rainbow (18.9°C)  trout than in cold-acclimated (4.9°C) trout (19). Indeed, the post-exercise mortality is
much more frequent at high than low temperatures(1, 7, 20).

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Exercise-induced increase in K+ois
mainly due to K+ leakage from the heavily working skeletal muscle
fibers (23). In addition, K+oin
the immediate microenvironment of the cardiac myocyte is altered by heart’s own
activity. In the intact heart, cardiac myocytes are tightly backed leaving only
asmall and diffusion-restricted”paracellular” space around cells,where K+otends
to accumulate at high heart rates. In frog (Rana
pipiens, R.catesbeina, R.ridibunda) hearts, the magnitude of K+
accumulation depends not only on thefrequency of stimulation but also on
temperature (21, 27). In R.
pipiensventricleat 22°C,the paracellularK+ocan rise
from about 3 mM to9-12 mM,when contraction frequency increases from 30 to 60
beats per minute (21).Since heart rate in fishes is strongly dependent
on temperature,it is possible that temperature-dependent increases in heart
rate are associated with increases in paracellularK+ o,similar
to the frog hearts. This could have significant impact on electrical
excitability, since changes in K+odirectly affect
membrane potential of excitable cells. Hyperkalemia is potentially cardiotoxic
by depolarizing the resting membrane potential (RMP), depressing cardiac
contractility and inducing arrhythmias(13, 14, 18).

It is obvious that K+o, temperature
and heart rate are closely interconnected factors in stress responses,which may
exert synergistic or antagonistic effects on cardiacexcitabilityin ectotherms. Although
the importance of K+o on electrical excitability of the
vertebrate heart is well realized, only few studies have been conducted on fish
hearts (18, 26) and nothing is known about the effects
of K+oon cellular excitability. Therefore, the aim of
the current study was to examine how these factors affect electrical
excitability of the fish (roach,Rutilus
rutilus) heart. Based on the existing knowledge from mammalian literature,
it was hypothesized that high K+owill depress
excitability of fish cardiac myocytes(13), possibly on frequency and
temperature-dependent manner. To this end,patch-clamp experiments were
conducted on enzymatically isolated ventricular myocytes of the roach heart in
3 different K+o, at 3 different temperatures and at 4
different pacing rates.