Sepsis is a life-threatening multi-organ dysfunction syndrome caused by dysregulated host response to infection, posing a significant global healthcare challenge. Sepsis-induced myocardial dysfunction (SIMD) is a common complication of sepsis, significantly increasing mortality due to its high energy demands and low compensatory reserves. The substantial mitochondrial damage rather than cell apoptosis in SIMD suggests disrupted cardiac energy metabolism as a crucial pathophysiological mechanism. Therefore, we systematically reviewed the mechanisms underlying energy metabolism dysfunction in SIMD, including alterations in myocardial cell energy metabolism substrates, excitation-contraction coupling processes, mitochondrial dysfunction, and mitochondrial autophagy and biogenesis, summarizing potential therapeutic targets within them.