Comprehensive metabolomics and flavoromics analysis reveal the changes in muscle flavor quality of turbot (Scophthalmus maximus) during low-temperature waterless live transport.

Low-temperature waterless live transport impairs turbot muscle flavor, but the metabolic mechanism remains unclear. This study integrated untargeted metabolomics, electronic tongue, and gas chromatography-ion mobility spectrometry to monitor flavor and metabolite changes during transport. Results show transport stress triggers energy depletion (ATP to inosine and hypoxanthine), membrane phospholipid degradation (glycerophosphocholine, glycerophosphoethanolamine), and protein catabolism (decreased umami amino acids), accompanied by elevated alanine aminotransferase, aspartate aminotransferase, and acid phosphatase. Sixteen key metabolites were identified, including anserine, acylcarnitines, betaine, and formic acid. Correlation analysis reveals that umami and richness negatively correlate with anserine, while acylcarnitines negatively correlate with sourness. Volatile oxidation products (hexanal, heptanal) accumulated, and benzaldehyde increased. After 24 h recovery, key metabolites remained below pre-transport levels, indicating that recovery was incomplete. These findings reveal a cascade of energy depletion, membrane damage, oxidative stress, and protein degradation driving flavor deterioration, providing a basis for optimizing waterless live transport.