For many ball games, both resistance and endurance training are necessary to improve muscle strength and endurance capacity. Endurance training has been reported to inhibit muscle strength and hypertrophy, but some studies have reported that endurance exercise (EE) does not inhibit the effects of resistance exercise. Here, we examined the effect of short‐ or long‐duration EE on mouse skeletal muscle hypertrophy induced by functional overload (OL) at the molecular level. Plantaris muscle hypertrophy was induced by OL with synergist ablation in mice. Body mass was reduced with endurance training, but EE duration (30 or 90 min) had no effect. The ratio of plantaris muscle weight to body weight was higher in the OL and EE for 30 min (OL+EE30) and OL and EE for 90 min (OL+EE90) groups compared with the OL group. Expression of mechanistic target of rapamycin signaling proteins, which is related to protein synthesis and hypertrophy, was increased in the OL+EE30 group. Expression of Forkhead box‐containing protein O1, which is related to protein breakdown and atrophy, remained unchanged. However, microtubule‐associated protein 1 light chain 3, a known marker of autophagy, and MAFbx, which is related to protein breakdown, were significantly increased in the OL+EE90 group. Furthermore, markers of oxidative stress, ubiquitin and 4‐hydroxynonenal were also significantly increased in the OL+EE90 group compared with other groups. In conclusion, EE duration did not affect body mass and plantaris mass and did not interfere with mechanistic target of rapamycin signaling, but it did increase ubiquitinated proteins and oxidative stress. It is therefore necessary to consider training durations for EE when combining endurance and resistance training.

中文翻译：

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耐力运动时长对功能超负荷所致肌肉肥大的影响

对于许多球类运动来说，阻力和耐力训练都是提高肌肉力量和耐力能力所必需的。据报道，耐力训练可抑制肌肉力量和肥大，但一些研究报告称，耐力运动 (EE) 不会抑制阻力运动的效果。在这里，我们在分子水平上检查了短期或长期 EE 对功能超载 (OL) 诱导的小鼠骨骼肌肥大的影响。OL 与协同消融在小鼠中诱导跖肌肥大。耐力训练减少了体重，但 EE 持续时间（30 或 90 分钟）没有效果。与 OL 组相比，OL 和 EE 30 分钟（OL+EE30）和 OL 和 EE 90 分钟（OL+EE90）组跖肌重量与体重的比值更高。与蛋白质合成和肥大有关的雷帕霉素信号蛋白机制靶点的表达在 OL+EE30 组中增加。与蛋白质分解和萎缩有关的含有叉头盒的蛋白质 O1 的表达保持不变。然而，微管相关蛋白 1 轻链 3（一种已知的自噬标志物）和与蛋白质分解相关的 MAFbx 在 OL+EE90 组中显着增加。此外，与其他组相比，OL+EE90 组的氧化应激标志物、泛素和 4-羟基壬烯醛也显着增加。总之，EE 持续时间不影响体重和足底质量，也不干扰雷帕霉素信号传导的机制靶点，但它确实增加了泛素化蛋白和氧化应激。