Potential Effects of NO-Induced Hypoxia-Inducible Factor-1 on Yak Meat Tenderness during Post-Mortem Aging

The objective of this study was to investigate the mechanism underlying nitric oxide (NO)-induced hypoxia-inducible factor-1 alpha (HIF-1 alpha) and its impact on yak muscle tenderness during post-mortem aging. The Longissimus thoracis et lumborum (LTL) muscle of yak were incubated at 4 degrees C for 0, 3, 6, 9, 12, 24, and 72 h after treatment with 0.9% saline, NO activator, or a combination of the NO activator and an HIF-1 alpha inhibitor. Results indicated that elevated NO levels could increase HIF-1 alpha transcription to achieve stable expression of HIF-1 alpha protein (P < 0.05). Additionally, elevated NO triggered HIF-1 alpha S-nitrosylation, which further upregulated the activity of key glycolytic enzymes, increased glycogen consumption, accelerated lactic acid accumulation, and decreased pH (P < 0.05). These processes eventually improved the tenderness of yak muscle during post-mortem aging (P < 0.05). The results demonstrated that NO-induced activation of HIF-1 alpha S-nitrosylation enhanced glycolysis during post-mortem aging and provided a possible pathway for improving meat tenderness