ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2025
Brain-derived neurotrophic factor drives muscle adaptation similar to aerobic training in mice.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Potential Influence of Myokines on Skeletal Muscle Tissue Hypertrophy Signaling Pathways: A Narrative Review.Biomolecules · 2026Review
- Skeletal Muscle as an Auto-, Para- and Endocrine Organ: The Role of Myokines in Muscle Metabolism and Other Metabolic Organs.Physiological research · 2025Review
- Cisplatin-Induced Skeletal Muscle Atrophy: Biomolecular Mechanisms and the Protective Role of Exercise-Induced Myokines.Biomolecules · 2025Review
- Muscle in Endocrinology: From Skeletal Muscle Hormone Regulation to Myokine Secretion and Its Implications in Endocrine-Metabolic Diseases.Journal of clinical medicine · 2025Review
- Brain-derived neurotrophic factor drives muscle adaptation similar to aerobic training in mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- The role and mechanisms of myokines in sarcopenia: new intervention strategies for the challenges of aging.Frontiers in medicine · 2025Review
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Authors and funding
12 authors.
Funding
Abstract
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.
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