The present study was undertaken to examine cardiac responses to some of the temperature challenges that eels encounter in their natural environment. The contractile properties of ventricular muscle was studied on electrically paced tissue strips after long term acclimation at 0 °C, 10 °C, or 20 °C, and following acute ± 10 °C temperature changes. The time-course of contraction, and thus maximal attainable heart rates, was greatly influenced by working temperature, but was independent of acclimation history. The absolute force of contraction and power production (i.e. the product of force and stimulation frequency) was significantly influenced by acute temperature decrease from 20 °C to 10 °C. The role of adrenaline as a modulator of contraction force, power production, rates of contraction and relaxation, and minimum time in contraction was assessed. Increased adrenergic tonus elicited a positive inotropic, temperature-dependent response, but did not influence twitch duration. This suggests that adrenaline acts as an agent in maintaining an adequate contractile force following temperature challenges. A significant increased relative ventricular mass was observed in 0 °C and 10 °C-acclimated eels compared to 20 °C-acclimated, which suggests that at low temperatures, eels secure cardiac output by heart enlargement. Inhibition of specific sarcolemmal Ca(2+) channels by selective drug treatment revealed that, depending on temperature, L-type channels is the major entry site, but also that reverse-mode Na(+)/Ca(2+)-exchange and store operated calcium entry contribute to the pool of activator Ca(2+).