The threat to human health from cold stimulation is increasing due to the frequent occurrence of temperature extremes. It is a challenge for people to resist the negative effects of prolonged cold stimulation on the heart. In this study, we created prolonged cold stimulation pig models to investigate the cardiac energy metabolism and injury during prolonged cold stimulation, and the molecular mechanisms by which dietary supplementation with full-fat rice bran reduces cardiac injury. The results showed that lesions in the morphological structure of the heart were detected under prolonged cold stimulation. At the same time, dystrophin was downregulated under the effect of prolonged cold stimulation. Cardiac fatty acid transport and utilization were promoted, and oxidative stress was increased under prolonged cold stimulation. It also increased MDA content and decreased T-AOC level in the heart, while promoting the mRNA expression of Nrf2 and NQO1, as well as the protein content of Nrf2 and HO-1. Prolonged cold stimulation induced mitochondrial lesions, mitochondrial fusion, and mitophagy in the heart. Prolonged cold stimulation promoted the mRNA expression of PTGS2, TLR4, MyD88, NLRP3, and IL-1β; and protein expression of PTGS2, NLRP3, and mature-IL-1β. GCH1 and FtH inhibited by prolonged cold stimulation caused the activation of heart ferroptosis. In addition, dietary supplementation with full-fat rice bran improved oxidative stress in the heart and inhibited mitophagy, ferroptosis, and pyroptosis. In conclusion, prolonged cold stimulation heightens the risk of cardiac ferroptosis and imbalance of energy metabolism, whereas dietary supplementation with full-fat rice bran mitigates the adverse effects of prolonged cold stimulation on the heart.