New Findings: What is the central question of this study? Influences of types 1 and 2 diabetes on myocardial ischaemic tolerance and cardioprotection are contentious. Opposing outcomes across models may reflect importance of disease duration and onset age. Chronic adult onset diabetes was modelled non‐genetically in C57Bl/6 mice to assess impacts on cardiac ischaemic outcomes and preconditioning. What is the main finding and its importance? The primary finding is that chronic adult‐onset type 2 but not type 1 diabetes significantly impairs myocardial ischaemic tolerance and ischaemic preconditioning. Preconditioning may be detrimental in type 2 diabetes, exaggerating nitrosative stress and apoptotic protein expression. Effects of diabetes on myocardial responses to ischaemia‐reperfusion (I‐R) and cardioprotective stimuli remain contentious, potentially reflecting influences of disease duration and time of onset. Chronic adult‐onset type 1 diabetes (T1D) and 2 diabetes (T2D) were modelled non‐genetically in male C57Bl/6 mice via 5 × 50 mg k−1g daily streptozotocin (STZ) injections + 12 week standard chow; or 1 × 75 mg k−1g STZ injection + 12 weeks obesogenic diet (32% calories as fat, 57% carbohydrate, 11% protein), respectively. Systemic outcomes were assessed and myocardial responses to I‐R ± ischaemic preconditioning (IPC; 3 × 5 min I‐R) determined in Langendorff perfused hearts. Uncontrolled T1D was characterised by pronounced hyperglycaemia (25 mM fasting glucose), glucose intolerance and ∼10% body weight loss, whereas T2D mice exhibited moderate hyperglycaemia (15 mM), hyperinsulinemia, glucose intolerance and 17% weight gain. Circulating ghrelin, resistin and noradrenaline were unchanged with T1D, while leptin increased and noradrenaline declined in T2D mice. Ischaemic tolerance and IPC were preserved in T1D hearts. In contrast, T2D worsened post‐ischaemic function (∼40% greater diastolic and contractile dysfunction) and cell death (100% higher troponin efflux), and abolished IPC protection. Whereas IPC reduced post‐ischaemic nitrotyrosine and pro‐apoptotic Bak and Bax levels in non‐diabetic hearts, these effects were reduced in T1D and IPC augmented Bax and nitrosylation in T2D hearts. Data demonstrate chronic T1D does not inhibit myocardial I‐R tolerance or IPC, whereas metabolic and endocrine disruption in T2D is associated with ischaemic intolerance and inhibition of IPC. Indeed, normally protective IPC may exaggerate damage mechanisms in T2D hearts.