First, we used isolated hearts from three teleost species with very different values for maximum heart rate (fHMax: zebrafish, ~300 bpm; Atlantic salmon, ~120 bpm and lumpfish, ~80 bpm) to examine the response of intrinsic fH and atrioventricular delay (AVd) to acute changes in temperature. Heart rate increased linearly with temperature (Q10s of 1.91, 1.50 and 2.67 for zebrafish 16–28℃, salmon 8–20℃ and lumpfish 8–14℃, respectively), whereas AVd decreased (Q10 0.56–0.69). However, the absolute values for AVd showed considerable inter-specific variation. For example, the AVd at 16℃ for 28℃-acclimated zebrafish was ~2 and 3x shorter than that of 8℃-acclimated salmon and lumpfish, respectively. Further, we extrinsically paced their hearts (i.e., at 50, 100 and 150 bpm for zebrafish and 50, 70 and 90 bpm for lumpfish and salmon), and AVd decreased with temperature independent of pacing frequency (i.e., temperature had a direct effect on AV function). Next, we compared 8- vs. 15℃-acclimated salmon, and found that 8℃ fish: 1) exhibited cardiac resetting (i.e., had a higher fH from 12–20℃); 2) experienced 2:1 AV block ~1.7℃ earlier than warm-acclimated fish; and 3) had an ~20% shorter AVd at all test temperatures and pacing frequencies. Finally, we found that although conduction velocity (CV) was consistently ~100–300x faster across the ventricle and atrium than the AV funnel, it also exhibited a plastic thermal response. These data highlight the acclimation capacity of AVd and CV, and suggest that they are key contributors to cardiac thermal compensation and phenotypic plasticity.