Molecular biomarkers of dysphagia targeted exercise induced neuroplasticity: A review of mechanistic processes and preliminary data on detraining effects

While molecular adaptations accompanying neuroplasticity during physical exercises are well-established, little is known about adaptations during dysphagia-targeted exercises. This research article has two primary purposes. First, we aim to review the existing literature on the intersection between resistance (strength) training, molecular markers of neuroplasticity, and dysphagia rehabilitation. Specifically, we discuss the molecular mechanisms of two potential molecular markers: brain-derived neurotrophic factor (BDNF) and insulin-like growth factor-1 (IGF-1) in exercise-induced neuroplasticity. Second, we present preliminary data on the effects of two weeks of detraining on circulating serum BDNF, IGF-1 levels, and expiratory muscle strength. This subset is a part of our more extensive studies related to dysphagia-targeted resistance exercise and neuroplasticity. Five young adult males underwent four weeks of expiratory muscle strength training, followed by two weeks of detraining. We measured expiratory strength, circulating levels of BDNF, and IGF-1 at post-training and detraining conditions. Our results show that expiratory muscle strength, serum BDNF, and IGF-1 levels decreased after detraining; however, this effect was statistically significant only for serum BDNF levels. Oropharyngeal and upper airway musculature involved in swallowing undergoes similar adaptation patterns to skeletal muscles during physical exercise. To fully comprehend the mechanisms underlying the potential neuroplastic benefits of targeted exercise on swallowing functions, mechanistic studies (models) investigating neuroplasticity induced by exercises addressing dysphagia are critical. Such models would ensure that interventions effectively and efficiently achieve neuroplastic benefits and improve patient outcomes, ultimately advancing our understanding of dysphagia-targeted exercise-induced neuroplasticity.