肌发生
心肌细胞
骨骼肌
肌球蛋白
细胞生物学
生物
下调和上调
代谢途径
生物化学
体内
化学
新陈代谢
内分泌学
生物技术
基因
作者
Yu Zhou,Xi Liu,Zhen Qi,Caihua Huang,Longhe Yang,Donghai Lin
摘要
Abstract Lactate can serve as both an energy substrate and a signaling molecule, exerting diverse effects on skeletal muscle physiology. Due to the apparently positive effects, it would be interesting to consider it as a sports supplement. However, the mechanism behind these effects are yet to be comprehensively understood. In this study, we observed that lactate administration could improve the ability of antifatigue, and we further found that lactate upregulated the expression of myosin heavy chain (MYHC I) and MYHC IIa, while downregulating the expression of MYHC IIb. Besides, transcriptomics and metabolomics revealed significant changes in the metabolic profile of gastrocnemius muscle following lactate administration. Furthermore, lactate enhanced the activities of metabolic enzymes, including HK, LDHB, IDH, SDM, and MDH, and promoted the expression of lactate transport‐related proteins MCT1 and CD147, thereby improving the transport and utilization of lactate in both vivo and vitro. More importantly, lactate administration increased cellular Ca 2+ concentration and facilitated nuclear translocation of nuclear factor of activated T cells (NFATC1) in myotubes, whereas inhibition of NFATC1 significantly attenuated the effects of lactate treatment on NFATC1 nuclear translocation and MyHC expression. Our results elucidate the ability of lactate to induce metabolic remodeling in skeletal muscle and promote myofiber‐type transitions by activating the Ca 2+ ‐NFATC1 signaling pathway. This study is useful in exploring the potential of lactate as a nutritional supplement for skeletal muscle adaptation and contributing to a mechanistic understanding of the central role of lactate in exercise physiology.
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