Potential mechanisms of cold-induced myocardial ischaemia are sympathetically mediated coronary vasoconstriction and/or catecholamine-induced increases in cardiac work. To examine these parameters, 11 human volunteers were each studied on one day with, and on another day without, β-adrenoceptor blockade. On each day, warm (37 °C) saline (control) and cold (4 °C) saline (hypothermia) were given intravenously. Myocardial perfusion was assessed by positron emission tomography using H 2 15 O, and coronary vascular resistance was calculated. Plasma catecholamines were measured to assess sympathoadrenal activation. The core temperature decreased by 1.0 ± 0.2 °C with the cold saline, and was unchanged with warm saline. Myocardial perfusion increased by 20% ( P = 0.01) and the rate–pressure product by 33% ( P = 0.0004) with cold saline compared with warm saline. β-Blockade eliminated these increases. Coronary vascular resistance was similar with warm and cold saline, and was unaffected by β-blockade. Plasma adrenaline increased by 120% and noradrenaline by 251% during cold saline, but were unchanged during warm saline. In conclusion, core hypothermia triggers β-adrenoceptor-mediated increased cardiac work, sympathoadrenal activation and increased myocardial perfusion. There is no evidence for hypothermia-induced coronary vasoconstriction.