Brown Alexander D, Marko Alexander D, Marko Daniel M, Baranowski Bradley J, Silvera Sebastian, Finch Michael S, Yang Alex J, Dhaliwal Roopan, Ryan Chantal R, Roy Brian D, Fajardo Val A, MacPherson Rebecca E K
Department of Health Sciences, Faculty of Applied Health Sciences, Brock University, St. Catharines, Ontario, Canada.
Department of Kinesiology, Faculty of Applied Health Sciences, Brock University, St. Catharines, Ontario, Canada.
FASEB J. 2025 Jan 31;39(2):e70321. doi: 10.1096/fj.202402421R.
This study, in vivo and in vitro, investigated the role of brain-derived neurotrophic factor (BDNF) in skeletal muscle adaptations to aerobic exercise. BDNF is a contraction-induced protein that may play a role in muscle adaptations to aerobic exercise. BDNF is involved in muscle repair, increased fat oxidation, and mitochondrial biogenesis, all of which are adaptations observed with aerobic training. The purpose of this study was two-pronged and investigated the skeletal muscle BDNF response to (1) acute and (2) chronic exercise in male C57BL/6J mice. It also examined if chronic BDNF treatment resulted in similar adaptations to chronic exercise. In aim 1, mice underwent a 2 hr. treadmill exercise bout. In aim 2, mice were assigned to one of four groups: (1) control (CON); (2) endurance training (ET; treadmill running 1 h/day, 5 days/wk); (3) BDNF (BDNF; 0.5 mg/kg·bw, 5 days/wk); (4) endurance training and BDNF (ET + BDNF) for 8 weeks. Results demonstrated that the soleus (SOL) had higher BDNF content compared with the extensor digitorum longus (EDL) and that SOL BDNF increased with acute exercise. After chronic exercise and BDNF treatment, treadmill testing to exhaustion demonstrated a main effect of BDNF and ET on increasing exercise capacity. In vitro contractile assessment of the EDL revealed BDNF treatment resulted in similar increases in the max rate of relaxation as ET. EDL force-frequency analysis showed ET + BDNF produced higher force than CON and BDNF, indicating an additive effect. BDNF increased EDL mitochondrial proteins, COXIV, and CS. These results demonstrate that BDNF contributes to muscle adaptations observed with ET.
本研究通过体内和体外实验，探究了脑源性神经营养因子（BDNF）在骨骼肌适应有氧运动过程中的作用。BDNF是一种由收缩诱导产生的蛋白质，可能在肌肉适应有氧运动中发挥作用。BDNF参与肌肉修复、增加脂肪氧化以及线粒体生物合成，而这些都是有氧运动训练所带来的适应性变化。本研究具有双重目的，旨在探究雄性C57BL/6J小鼠骨骼肌BDNF对（1）急性运动和（2）慢性运动的反应。同时，研究还考察了慢性BDNF治疗是否会产生与慢性运动相似的适应性变化。在目标1中，小鼠进行了2小时的跑步机运动试验。在目标2中，小鼠被分为四组之一：（1）对照组（CON）；（2）耐力训练组（ET；每天跑步机跑步1小时，每周5天）；（3）BDNF组（BDNF；0.5毫克/千克体重，每周5天）；（4）耐力训练加BDNF组（ET + BDNF），持续8周。结果表明，比目鱼肌（SOL）的BDNF含量高于趾长伸肌（EDL），且急性运动后SOL的BDNF含量增加。经过慢性运动和BDNF治疗后，进行力竭跑步机测试发现，BDNF和ET对提高运动能力有主要作用。对EDL进行的体外收缩评估显示，BDNF治疗导致的最大舒张速率增加与ET相似。EDL的力-频率分析表明，ET + BDNF产生的力量高于CON组和BDNF组，显示出相加效应。BDNF增加了EDL的线粒体蛋白、细胞色素c氧化酶亚基IV（COXIV）和柠檬酸合酶（CS）。这些结果表明，BDNF有助于产生耐力训练所带来的肌肉适应性变化。
