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

Temperature-induced changes in cardiac output (Q) in fish are largely dependent on thermal modulation of heart rate (fH) and at high temperatures Q collapses due to heat-dependent depression of f This study tests the hypothesis that firing rate of sinoatrial pacemaker cells sets the upper thermal limit of f in vivo. To this end temperature-dependence of action potential (AP) frequency of enzymatically isolated pacemaker cells (pacemaker rate, f), spontaneous beating rate of isolated sinoatrial preparations (f) and in vivo heart rate (f) of the cold-acclimated (4°C) brown trout (Salmo trutta fario) were compared under acute thermal challenges. With rising temperature, f steadily increased due to the acceleration of diastolic depolarization and shortening of AP duration up to the break point temperature (T) of 24.0±0.37°C where the electrical activity abruptly ceased. The maximum f at T was much higher (193±21.0 beats per minute (bpm)) than the peak f (94.3±6.0 bpm at 24.1°C) or peak f (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 f at high temperatures in the brown trout in vivo.