Post-exercise recovery is essential to resolve metabolic perturbations and promote long-term cellular remodeling in response to exercise. Here, we report that muscle-generated brain-derived neurotrophic factor (BDNF) elicits post-exercise recovery and metabolic reprogramming in skeletal muscle. BDNF increased the post-exercise expression of the gene encoding PPARδ (peroxisome proliferator–activated receptor δ), a transcription factor that is a master regulator of lipid metabolism. After exercise, mice with muscle-specific Bdnf knockout (MBKO) exhibited impairments in PPARδ-regulated metabolic gene expression, decreased intramuscular lipid content, reduced β-oxidation, and dysregulated mitochondrial dynamics. Moreover, MBKO mice required a longer period to recover from a bout of exercise and did not show increases in exercise-induced endurance capacity. Feeding naïve mice with the bioavailable BDNF mimetic 7,8-dihydroxyflavone resulted in effects that mimicked exercise-induced adaptations, including improved exercise capacity. Together, our findings reveal that BDNF is an essential myokine for exercise-induced metabolic recovery and remodeling in skeletal muscle.

中文翻译：

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运动诱导的 BDNF 促进运动恢复期间骨骼肌中 PPARδ 依赖性脂质代谢重编程

运动后恢复对于解决代谢紊乱和促进长期细胞重塑以应对运动至关重要。在这里，我们报告肌肉产生的脑源性神经营养因子（BDNF）可引起骨骼肌运动后恢复和代谢重编程。 BDNF 增加了编码 PPARδ（过氧化物酶体增殖物激活受体 δ）基因的运动后表达，PPARδ 是一种转录因子，是脂质代谢的主要调节因子。运动后，肌肉特异性Bdnf敲除 ( MBKO ) 的小鼠表现出 PPARδ 调节的代谢基因表达受损、肌内脂质含量降低、β-氧化减少和线粒体动力学失调。此外，MBKO小鼠需要更长的时间才能从一轮运动中恢复，并且没有表现出运动引起的耐力能力的增加。用生物可利用的 BDNF 模拟物 7,8-二羟基黄酮喂养幼鼠，会产生模仿运动引起的适应的效果，包括提高运动能力。总之，我们的研究结果表明，BDNF 是运动引起的骨骼肌代谢恢复和重塑的重要肌因子。