Maximum heart rate in brown trout (Salmo trutta fario) is not limited by firing rate of pacemaker cells.

Abstract

Temperature-induced changes in cardiac output (Q̇) in fish are largely dependent on thermal modulation of heart rate (fH), and at high temperatures Q̇ collapses due to heat-dependent depression of fH This study tests the hypothesis that firing rate of sinoatrial pacemaker cells sets the upper thermal limit of fH in vivo. To this end, temperature dependence of action potential (AP) frequency of enzymatically isolated pacemaker cells (pacemaker rate, fPM), spontaneous beating rate of isolated sinoatrial preparations (fSA), and in vivo fH of the cold-acclimated (4°C) brown trout (Salmo trutta fario) were compared under acute thermal challenges. With rising temperature, fPM steadily increased because of the acceleration of diastolic depolarization and shortening of AP duration up to the break point temperature (TBP) of 24.0 ± 0.37°C, at which point the electrical activity abruptly ceased. The maximum fPM at TBP was much higher [193 ± 21.0 beats per minute (bpm)] than the peak fSA (94.3 ± 6.0 bpm at 24.1°C) or peak fH (76.7 ± 2.4 at 15.7 ± 0.82°C) (P < 0.05). These findings strongly suggest that the frequency generator of the sinoatrial pacemaker cells does not limit fH at high temperatures in the brown trout in vivo.