Introduction Metabolic dysfunction is increasingly recognized as a contributor to cardiac pathology, but its mechanistic links to electromechanical function remain difficult to disentangle from experimental data alone. Existing computational models of the human ventricular myocyte, including the latest T-World framework, do not represent cellular energy metabolism, whereas current cardiac metabolism models either lack some key metabolite pathways or do not incorporate the regulatory role of cytosolic calcium dynamics. The integration of key metabolite pathways into the electromechanical myocyte model offers a route to capture their mutual interactions. Methods We present an integrated metabolism–electromechanical (MEM) model of the human ventricular myocyte, in which a detailed cardiac metabolism module is coupled to the T-World framework so that intracellular energetic state evolves dynamically with electrical and mechanical activity, while metabolic perturbations feed back onto excitation–contraction coupling. Results The MEM model was verified against human ventricular biomarkers, validated across the physiological pacing range, and probed under graded electron transport chain inhibition as a proof-of-concept metabolic perturbation. It reproduced a positive force–frequency relationship, a graded respiratory response to elevated workload, and the expected metabolic adaptation under progressive hypoxic stress, qualitatively consistent with experimental observations. Conclusion The MEM model thereby establishes a baseline framework for future mechanistic investigation of metabolism-related cardiac disease.