Lee Mon-Chien, Cheng Ting-Yin, Lin Ping-Jui, Lin Ting-Chun, Chou Chia-Hsuan, Chen Chao-Yuan, Huang Chi-Chang
Graduate Institute of Sports Science, National Taiwan Sport University, Taoyuan City 333325, Taiwan.
Center for General Education, Taipei Medical University, Taipei 110301, Taiwan.
Nutrients. 2025 Aug 7;17(15):2568. doi: 10.3390/nu17152568.
: Exercise-induced fatigue arises primarily from energy substrate depletion and the accumulation of metabolites such as lactate and ammonia, which impair performance and delay recovery. Emerging evidence implicates gut microbiota modulation-particularly via probiotics-as a means to optimize host energy metabolism and accelerate clearance of fatigue-associated by-products. : This study aimed to determine whether live or heat-inactivated NB23 can enhance exercise endurance and attenuate fatigue biomarkers in a murine model. : Forty male Institute of Cancer Research (ICR) mice were randomized into four groups ( = 10 each) receiving daily gavage for six weeks with vehicle, heat-killed NB23 (3 × 10 cells/human/day), low-dose live NB23 (1 × 10 CFUs/human/day), or high-dose live NB23 (3 × 10 CFUs/human/day). Forelimb grip strength and weight-loaded swim-to-exhaustion tests assessed performance. Blood was collected post-exercise to measure serum lactate, ammonia, blood urea nitrogen (BUN), and creatine kinase (CK). Liver and muscle glycogen content was also quantified, and safety was confirmed by clinical-chemistry panels and histological examination. : NB23 treatment produced dose-dependent improvements in grip strength ( < 0.01) and swim endurance ( < 0.001). All NB23 groups exhibited significant reductions in post-exercise lactate ( < 0.0001), ammonia ( < 0.001), BUN ( < 0.001), and CK ( < 0.0001). Hepatic and muscle glycogen stores rose by 41-59% and 65-142%, respectively ( < 0.001). No changes in food or water intake, serum clinical-chemistry parameters, or tissue histology were observed. : Our findings suggest that both live and heat-treated NB23 may contribute to improved endurance performance, increased energy reserves, and faster clearance of fatigue-related metabolites in our experimental model. However, these results should be interpreted cautiously given the exploratory nature and limitations of our study.
运动诱导的疲劳主要源于能量底物的消耗以及乳酸和氨等代谢产物的积累，这些会损害运动表现并延迟恢复。新出现的证据表明，调节肠道微生物群——特别是通过益生菌——是优化宿主能量代谢和加速清除与疲劳相关副产物的一种手段。本研究旨在确定活的或热灭活的NB23是否能增强小鼠模型的运动耐力并减轻疲劳生物标志物。将40只雄性癌症研究所（ICR）小鼠随机分为四组（每组n = 10），每天灌胃六周，分别给予赋形剂、热灭活的NB23（3×10⁹细胞/人/天）、低剂量活的NB23（1×10⁹CFU/人/天）或高剂量活的NB23（3×10⁹CFU/人/天）。通过前肢握力和负重游泳至疲劳测试评估运动表现。运动后采集血液以测量血清乳酸、氨、血尿素氮（BUN）和肌酸激酶（CK）。还对肝脏和肌肉糖原含量进行了定量，并通过临床化学指标和组织学检查确认安全性。NB23治疗使握力（P < 0.01）和游泳耐力（P < 0.001）呈剂量依赖性改善。所有NB23组运动后乳酸（P < 0.0001）、氨（P < 0.001）、BUN（P < 0.001）和CK（P < 0.0001）均显著降低。肝脏和肌肉糖原储备分别增加了41 - 59%和65 - 142%（P < 0.001）。未观察到食物或水摄入量、血清临床化学参数或组织组织学的变化。我们的研究结果表明，在我们的实验模型中，活的和热处理的NB23都可能有助于提高耐力表现、增加能量储备并更快清除与疲劳相关的代谢产物。然而，鉴于我们研究的探索性质和局限性，这些结果应谨慎解释。
