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Acute and Chronic BDNF Responses to Resistance Exercise in Multiple Sclerosis: Links With Neuroplasticity and Symptom Burden | ||
| New Approaches in Exercise Physiology | ||
| دوره 7، شماره 14، اسفند 2025 | ||
| نوع مقاله: Review Article | ||
| شناسه دیجیتال (DOI): 10.22054/nass.2025.90148.1215 | ||
| نویسنده | ||
| Milad piralahi* | ||
| Department of Physical Education and Sport Sciences, Faculty of Humanities, Tarbiat Modares University, Tehran, Iran. | ||
| چکیده | ||
| Multiple sclerosis (MS) is characterized by inflammatory demyelination, neurodegeneration, and a high burden of fatigue, mobility limitation, and cognitive complaints. This narrative review summarizes evidence on acute and chronic BDNF responses to resistance exercise in people with MS and discusses how these responses may relate to symptom burden and functional outcomes. A targeted literature synthesis was conducted by reviewing peer-reviewed studies that assessed circulating BDNF responses to single sessions and/or resistance training programs in MS, alongside related evidence from neuroplasticity-informed outcomes (e.g., fatigue, disability, strength, mobility, and cognition). We also considered methodological features that influence BDNF interpretation, including assay selection, sampling timing, platelet contribution, training intensity/volume, and medication status. Available evidence suggests that a single bout of resistance exercise can transiently elevate circulating BDNF, although findings vary by protocol intensity, baseline fitness, and sampling window. Across weeks of progressive resistance training, several studies report improvements in strength and functional capacity, with mixed but promising indications of sustained BDNF modulation. Importantly, BDNF changes—when observed—tend to align with reductions in fatigue and improvements in mobility and patient-reported outcomes, supporting a plausible link between resistance training, neurotrophic signaling, and symptom burden. Overall, resistance exercise appears capable of eliciting both acute and training-induced BDNF responses in MS, but heterogeneity in study design and biomarker methodology limits firm conclusions. Future trials should standardize BDNF measurement, include neuroplasticity-relevant endpoints, and test dose–response relationships to clarify clinical significance. | ||
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