Metabolomics has been applied to postmortem meat aging studies to account for the impacts of postmortem aging, mainly on meat quality in terms of metabolites. In pork, postmortem changes in the longissimus lumborum (LL) and vastus intermedius (VI) muscles were investigated using a CE-MS approach . In this study, the levels of numerous muscle metabolites were altered, suggesting that postmortem muscle metabolism was drastically altered, especially within 24 h of slaughter. The PCA and HCA results explicitly show marked differences in the metabolite distribution of samples between postmortem aging times and muscle types (Fig. ).Intermediate glycolytic products, glucose 6-phosphate (G-6P) and fructose 6-phosphate (F-6P), increased in the LL samples until 24 h postmortem, while downstream compounds such as fructose 1,6-bisphosphate (F-1,6P) and phosphoenolpyruvate decreased with exhaustion at 24 h postmortem, indicating the rate-determining activity of phosphofructokinase (F-6P → F-1,6P) in postmortem LL muscle glycolysis. Additionally, in the LL muscle, most of the AAs and identified dipeptides increased after day 1 of aging, suggesting that protein degradation began to be dominant after day 1. In ATP degradation, changes in the product levels were observed along the ADP → AMP → IMP → inosine → hypoxanthine pathway, with a time lag between the products. Similar results were also observed in early postmortem , during 14 days of aging , and in long-term aging of beef . In these studies, metabolism associated with purine, pyrimidine, glutathione, nicotinate, glycerophospholipid, pentose phosphate, and AAs was found to be a prominent biological pathway in postmortem muscle aging . Moreover, other metabolisms related to nutrients, such as choline, nicotinamide, and thiamine, also begin to occur in pork and beef . Most of these pathways were commonly observed in pig and bovine muscles in these studies, indicating that these metabolic pathways are essential for postmortem muscle metabolism. In addition, several citrate cycle metabolites and enzyme cofactors decreased within 24 h postmortem, accompanied by alterations in glycolytic and purine metabolite levels . This may be due to mitochondrial damage during post-mortem muscle aging. Studies focusing on mitochondria have suggested the involvement of reactive oxygen species (ROS) from dysregulated mitochondria in early postmortem muscle aging . According to these results, ROS-induced postmortem mitochondrial degeneration leads to increased drip loss in beef meat. Such mitochondrial damage in early postmortem may induce muscle cell apoptosis, which potentially affects the conversion of muscle to meat , and thereby the meat quality, such as meat discoloration by the oxidation of FAs and lipids .