Apoptosis in postmortem muscle is a potential factor affecting meat quality. This study aimed to investigate the changes in apoptotic genes and proteins, reactive oxygen species (ROS), caspase-3 activity and their underlying relationship with meat tenderization. As postmortem time extended, there was a significant increase in myofibril fragmentation index (MFI) and destruction of muscle fibers. Oxidative stress deepened alongside the onset of apoptosis. Mitochondrial membrane potential (MMP) decreased, and caspase-3 activity increased during the first 24 h postmortem. Forty apoptotic genes displayed significant differences, involving DNA damage, autophagy, the death receptor pathway, the mitochondrial pathway, the Bcl-2 family, and the caspases family. The expression of most apoptotic genes was abundant in the early postmortem stage, enhancing the potential for early apoptosis. Apoptotic proteins of apoptosis-inducing factor, mitochondrion-associated 1 (AIFM1) and endonuclease G (ENDOG) showed the damage of apoptosis to DNA. Also, the decreasing expression of Bcl2 and increasing expression of Bak1 with time demonstrated the effects of mitochondrial apoptosis on postmortem muscle. These findings suggest that postmortem muscle apoptosis is a physiological process co-regulated by multiple genes, and potentially contributes to meat tenderization and quality.