Abstract: This review systematically expounds on the multiple mechanisms by which mitochondrial dysfunction affects lamb tenderization. It exerts a synergistic effect mainly through four interrelated pathways, 1) energy metabolism imbalance: hypoxia leads to the inhibition of oxidative phosphorylation, causing cells to switch to glycolysis, resulting in depletion of adenosine triphosphate (ATP), accumulation of lactic acid and a decrease in pH, thereby activating the calpain system and initiating the degradation of myofibrillar proteins; 2) oxidative stress: dysfunction of the electron transport chain leads to an outbreak of reactive oxygen species (ROS), and the tenderness is regulated by a “double threshold” mechanism, that is, moderate ROS promotes protein hydrolysis, while excessive ROS causes protein oxidative cross-linking; 3) apoptosis is triggered by calcium overload and ROS through the mitochondrial pathway, which involves the opening of the mitochondrial permeability transition pore (MPTP), the release of cytochrome c (Cyt-c), and the activation of the caspase cascade reaction, which directly hydrolyzes the structural proteins of the myofibril; and 4) the imbalance of Ca2+ homeostasis leads to ATP depletion, resulting in an increase in cytoplasmic calcium ion concentration. This not only directly activates calpain but also causes mitochondrial calcium overload, thereby exacerbating apoptosis. These pathways form a complex regulatory network, providing an important theoretical basis for precisely improving the quality of lamb by targeted regulation of mitochondrial function.

Key words: mitochondria; tenderness of lamb; energy metabolism; oxidative stress; apoptosis; Ca2+ homeostasis