Zhou Lei, Mozaffaritabar Soroosh, Kolonics Attila, Kawamura Takuji, Koike Atsuko, Kéringer Johanna, Gu Yaodong, Karabanov Roman, Radák Zsolt
Research Institute of Molecular Exercise Science, Hungarian University of Sport Science, Budapest, Hungary.
Waseda Institute for Sport Sciences, Waseda University, Saitama, Japan.
Front Nutr. 2024 Jan 15;10:1335187. doi: 10.3389/fnut.2023.1335187. eCollection 2023.
Iron is an essential micronutrient that plays a crucial role in various biological processes. Previous studies have shown that iron supplementation is related to exercise performance and endurance capacity improvements. However, the underlying mechanisms responsible for these effects are not well understood. Recent studies have suggested the beneficial impact of iron supplementation on mitochondrial function and its ability to rescue mitochondrial function under adverse stress and rodents. Based on current knowledge, our study aimed to investigate whether the changes in exercise performance resulting from iron supplementation are associated with its effect on mitochondrial function.
In this study, we orally administered an iron-based supplement to rats for 30 consecutive days at a dosage of 0.66 mg iron/kg body weight and vitamin B6 at a dosage of 0.46 mg/kg.
Our findings reveal that long-term iron supplementation, in combination with vitamin B6, led to less body weight gained and increased VO max in rats. Besides, the treatment substantially increased Complex I- and Complex II-driven ATP production in intact mitochondria isolated from gastrocnemius and cerebellum. However, the treatment did not change basal and succinate-induced ROS production in mitochondria from the cerebellum and skeletal muscle. Furthermore, the iron intervention significantly upregulated several skeletal muscle mitochondrial biogenesis and metabolism-related biomarkers, including PGC-1α, SIRT1, NRF-2, SDHA, HSL, MTOR, and LON-P. However, it did not affect the muscular protein expression of SIRT3, FNDC5, LDH, FIS1, MFN1, eNOS, and nNOS. Interestingly, the iron intervention did not exert similar effects on the hippocampus of rats.
In conclusion, our study demonstrates that long-term iron supplementation, in combination with vitamin B6, increases VO max, possibly through its positive role in regulating skeletal muscle-specific mitochondrial biogenesis and energy production in rats.
铁是一种必需的微量营养素，在各种生物过程中发挥着关键作用。先前的研究表明，补充铁与运动表现和耐力能力的改善有关。然而，这些作用的潜在机制尚不清楚。最近的研究表明，补充铁对线粒体功能具有有益影响，并且在不利应激条件下能够挽救啮齿动物的线粒体功能。基于目前的知识，我们的研究旨在探讨补充铁所导致的运动表现变化是否与其对线粒体功能的影响有关。
在本研究中，我们以0.66毫克铁/千克体重的剂量连续30天给大鼠口服铁基补充剂，并以0.46毫克/千克的剂量口服维生素B6。
我们的研究结果表明，长期补充铁并结合维生素B6，导致大鼠体重增加减少，最大摄氧量增加。此外，该处理显著增加了从腓肠肌和小脑中分离出的完整线粒体中由复合体I和复合体II驱动的ATP生成。然而，该处理并未改变小脑和骨骼肌线粒体中基础和琥珀酸诱导的活性氧生成。此外，铁干预显著上调了几种骨骼肌线粒体生物发生和代谢相关的生物标志物，包括PGC-1α、SIRT1、NRF-2、SDHA、HSL、MTOR和LON-P。然而，它并未影响SIRT3、FNDC5、LDH、FIS1、MFN1、eNOS和nNOS的肌肉蛋白表达。有趣的是，铁干预对大鼠海马体没有产生类似的影响。
总之，我们的研究表明，长期补充铁并结合维生素B6，可能通过其在调节大鼠骨骼肌特异性线粒体生物发生和能量产生中的积极作用，增加最大摄氧量。
