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ABSTRACT The thermal sensitivity of heart rate (fH) in fishes has fascinated comparative physiologists for well over a century. We now know that elevating fH is the primary mechanism through which fishes increase convective oxygen delivery during warming to meet the concomitant rise in tissue oxygen consumption. Thus, limits on fH can constrain whole-animal aerobic metabolism. In this Review, we discuss an increasingly popular methodology to study these limits, the measurement of pharmacologically induced maximum fH (fH,max) during acute warming of an anaesthetized fish. During acute warming, fH,max increases exponentially over moderate temperatures (Q10∼2–3), but this response is blunted with further warming (Q10∼1–2), with fH,max ultimately reaching a peak (Q10≤1) and the heartbeat becoming arrhythmic. Because the temperatures at which these transitions occur commonly align with whole-animal optimum and critical temperatures (e.g. aerobic scope and the critical thermal maximum), they can be valuable indicators of thermal performance. The method can be performed simultaneously on multiple individuals over a few hours and across a broad size range (<1 to >6000 g) with compact equipment. This simplicity and high throughput make it tractable in lab and field settings and enable large experimental designs that would otherwise be impractical. As with all reductionist approaches, the method does have limitations. Namely, it requires anaesthesia and pharmacological removal of extrinsic cardiac regulation. Nonetheless, the method has proven particularly effective in the study of patterns and limits of thermal plasticity and holds promise for helping to predict and mitigate outcomes of environmental change.