Li Guangqi, Shang Liying, Wang Xin, Zhang Lequn, Zhao Yuchu, Ni Weifeng, Bai Xueyuan, Liu Junyi
Northeast Normal University School of Physical Education, Northeast Normal University, Changchun, Jilin, China.
Northeast Asian Institute of Traditional Chinese Medicine, Changchun University of Chinese Medicine, Changchun, Jilin, China.
J Food Sci. 2025 Jul;90(7):e70286. doi: 10.1111/1750-3841.70286.
Whey protein (WP) can improve muscle mass and strength. However, its effects and underlying molecular mechanism in promoting recovery from muscle damage caused by excessive physical exercise remains unknown. Therefore, the present study aimed to investigate the therapeutic effect of WP on skeletal muscle injury caused by exogenous oxidants and excessive physical exercise and the potential underlying mechanism. An oxidative stress injury model of mouse skeletal muscle cells was established using hydrogen peroxide (HO) and excessive physical exercise. The results revealed that WP effectively improved the migration and differentiation of C2C12 cells exposed to HO. Moreover, WP significantly increased the body weight of mice following excessive physical exercise. It also reduced food intake, improved behavioral parameters, enhanced skeletal muscle morphology and function, and promoted protein synthesis, thereby alleviating oxidative stress injury in skeletal muscles. The results further indicated that the mechanism underlying the mitigation of oxidative stress injury in skeletal muscles may involve the silent information regulator sirtuin 1 (SIRT1)/ NF-E2-related factor-2 (Nrf2)/ hemeoxygenase-1 (HO-1) axis. This axis could, in turn, activates the AMP-activated protein kinase (AMPK)/tuberous sclerosis complex subunit 2 (TSC2)/mammalian target of rapamycin (mTOR)/4E-binding protein 1 (4EBP1) pathway, thereby promoting protein synthesis and improving the physiological function of skeletal muscles. This study provides important insights into the role of WP in promoting recovery from muscle damage, offering a basis for future research on WP-based nutritional intervention strategies.
乳清蛋白（WP）可以增加肌肉量并增强力量。然而，其在促进过度体育锻炼所致肌肉损伤恢复方面的作用及潜在分子机制尚不清楚。因此，本研究旨在探究WP对外源性氧化剂和过度体育锻炼所致骨骼肌损伤的治疗作用及其潜在机制。使用过氧化氢（HO）和过度体育锻炼建立小鼠骨骼肌细胞氧化应激损伤模型。结果显示，WP有效改善了暴露于HO的C2C12细胞的迁移和分化。此外，WP显著增加了过度体育锻炼后小鼠的体重。它还减少了食物摄入量，改善了行为参数，增强了骨骼肌形态和功能，并促进了蛋白质合成，从而减轻了骨骼肌的氧化应激损伤。结果进一步表明，减轻骨骼肌氧化应激损伤的机制可能涉及沉默信息调节因子sirtuin 1（SIRT1）/NF-E2相关因子2（Nrf2）/血红素加氧酶-1（HO-1）轴。该轴继而可激活AMP活化蛋白激酶（AMPK）/结节性硬化复合物亚基2（TSC2）/雷帕霉素靶蛋白（mTOR）/4E结合蛋白1（4EBP1）途径，从而促进蛋白质合成并改善骨骼肌的生理功能。本研究为WP在促进肌肉损伤恢复中的作用提供了重要见解，为未来基于WP的营养干预策略研究提供了依据。
