Hypobaric hypoxia (HH) leads to various adverse effects on skeletal muscles, including atrophy and reduced oxidative work capacity. However, the effects of HH on muscle fatigue resistance and myofiber remodeling are largely unexplored. Therefore, the present study aimed to explore the impact of HH on slow-oxidative fibers and to evaluate the ameliorative potential of exercise preconditioning and nanocurcumin formulation on muscle anti-fatigue ability. C2C12 cells (murine myoblasts) were used to assess the effect of hypoxia (0.5%, 24 h) with and without the nanocurcumin formulation (NCF) on myofiber phenotypic conversion. To further validate this hypothesis, male Sprague Dawley rats were exposed to a simulated HH (7620 m) for 7 days, along with NCF administration and/or exercise training. Both in vitro and in vivo studies revealed a significant reduction in slow-oxidative fibers (p < 0.01, 61% vs. normoxia control) under hypoxia. There was also a marked decrease in exhaustion time (p < 0.01, 65% vs. normoxia) in hypoxia control rats, indicating a reduced work capacity. Exercise preconditioning along with NCF supplementation significantly increased the slow-oxidative fiber proportion and exhaustion time while maintaining mitochondrial homeostasis. These findings suggest that HH leads to an increased transition of slow-oxidative fibers to fast glycolytic fibers and increased muscular fatigue. Administration of NCF in combination with exercise preconditioning restored this myofiber remodeling and improved muscle anti-fatigue ability.

低压缺氧（HH）会对骨骼肌产生各种不利影响，包括萎缩和氧化功能力降低。然而，HH 对肌肉抗疲劳性和肌纤维重塑的影响在很大程度上尚未被探索。因此，本研究旨在探讨HH对慢氧化纤维的影响，并评估运动预处理和纳米姜黄素制剂对肌肉抗疲劳能力的改善潜力。使用 C2C12 细胞（小鼠成肌细胞）评估缺氧（0.5%，24 小时）在有或没有纳米姜黄素制剂 (NCF) 的情况下对肌纤维表型转化的影响。为了进一步验证这一假设，将雄性 Sprague Dawley 大鼠暴露于模拟 HH (7620 m) 中 7 天，同时进行 NCF 给药和/或运动训练。p  < 0.01，相对于常氧对照为 61%）在缺氧条件下。 缺氧对照大鼠的力竭时间也显着减少（p < 0.01，与常氧相比减少 65%），表明工作能力下降。运动预处理和 NCF 补充显着增加了慢氧化纤维的比例和疲劳时间，同时维持了线粒体稳态。这些发现表明，HH 会导致慢氧化纤维向快糖酵解纤维的转变增加，并增加肌肉疲劳。NCF 与运动预处理相结合可恢复肌纤维重塑并提高肌肉抗疲劳能力。