Thus, postmortem muscle metabolism progresses in an organized manner. This process is initiated by energy substrate shortage and subsequent glycolysis with the stimulation of glycogenolysis , leading to lactate accumulation and pH decline . Postmortem muscle glycolysis largely affects the downstream biochemical changes associated with meat quality , which have been recently unveiled by metabolomics studies. Metabolomics has exerted its power to mine the relevant metabolisms and pathways that are minor in postmortem muscle aging and thereby have never been unveiled so far, other than glycolysis and purine metabolism. For example, pyruvate temporally accumulated by glycolysis is likely mobilized to the citrate cycle to generate NADH, a major reducing metabolite. The changes in metabolites in the citrate cycle, fumarate, citrate, succinate, and malate, during postmortem aging also suggest the contribution of the citrate cycle to NADH regeneration. The resultant reduced cellular conditions are critical for protecting intracellular molecules against an oxidizing environment. In terms of NADH generation, AAs generated by protein degradation are important sources of citrate cycle materials , which may be induced by decrease in energy substrates. Acidification of the intracellular environment by pH decline is thought to result in calpain activation by increased Ca 2+ concentration from the dysregulated sarcoplasmic reticulum and caspase-3 activation, possibly via mitochondrial apoptosis-related pathways , and may release cathepsins from lysosomes. Activated proteases degrade proteins that contribute to AA and peptide production. ATP degradation to ADP and related metabolites, originating from energy demand for cell survival, could be linked with energy generation-related metabolism, including glycolysis and the citrate cycle . This could also be true for postmortem autooxidation, which occurs on lipids and proteins in association with mitochondrial degeneration and NADH depletion .