The Musculus longissimus thoracis muscle of twenty crossbred cattle was used to investigate the activity of calcium-regulated protein kinase kinase (CaMKKβ), adenosine monophosphate-activated protein kinase (AMPK), glycolysis pathway, and apoptosis during 7 days postmortem maturation. Results showed that CaCl₂ significantly increased the activity of CaMKKβ and AMPK. Meanwhile, the activation of AMPK increased the activity of rate-limiting enzymes in glycolysis (lactate dehydrogenase and pyruvate kinase), and accelerated the speed of postmortem muscle maturation. Besides, CaCl₂ altered the properties of myofibrillar, affected the intramuscular environment, and induced postmortem apoptosis. Our finds indicate that CaCl₂ activates AMPK, accelerating the glycolysis process and increasing mitochondrial ROS level, which was an upstream event of apoptosis. Muscle samples treated with CaCl₂ had better tenderness, probably due to the degeneration of myofibrillar proteins and the occurrence of apoptosis, which may have contributed to the increased AMPK activity and accelerated glycolysis.

中文翻译：

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腺苷单磷酸激活的蛋白磷酸腺苷活化蛋白激酶，糖酵解，肌肉特征和凋亡之间的关联

使用二十只杂交牛的长肌胸肌来研究死后7天钙调节蛋白激酶激酶（CaMKKβ），单磷酸腺苷激活蛋白激酶（AMPK）的活性，糖酵解途径和细胞凋亡。结果表明，CaCl ₂显着增加了CaMKKβ和AMPK的活性。同时，AMPK的激活增加了糖酵解中限速酶（乳酸脱氢酶和丙酮酸激酶）的活性，并加快了死后肌肉的成熟速度。此外，CaCl ₂改变了肌原纤维的特性，影响了肌内环境，并诱导了死后细胞凋亡。我们的发现表明，CaCl ₂激活AMPK，加速糖酵解过程并增加线粒体ROS水平，这是细胞凋亡的上游事件。用CaCl ₂处理的肌肉样品具有更好的嫩度，这可能是由于肌原纤维蛋白的变性和细胞凋亡的发生，这可能有助于增加AMPK活性和加速糖酵解。