Department of Neurobiology, Chair of Biological Sciences, Poznan University of Physical Education, 27/39 Królowej Jadwigi St., 61-871 Poznań, Poland.
Neural Plast. 2019 Jun 24;2019:5413067. doi: 10.1155/2019/5413067. eCollection 2019.
This article presents a concept that wide expression of brain-derived neurotrophic factor (BDNF) and its receptors (TrkB) in the nervous tissue, evoked by regular endurance training (ET), can cause numerous motor and metabolic adaptations, which are beneficial for human health. The relationships between the training-evoked increase of endogenous BDNF and molecular and/or physiological adaptations in the nervous structures controlling both motor performance and homeostasis of the whole organism have been presented. Due to a very wide range of plastic changes that ET has exerted on various systems of the body, the improvement of motor skills and counteraction of the development of civilization diseases resulting from the posttraining increase of BDNF/TrkB levels have been discussed, as important for people, who undertake ET. Thus, this report presents the influence of endurance exercises on the (1) transformation of motoneuron properties, which are a final element of the motor pathways, (2) reduction of motor deficits evoked by Parkinson disease, and (3) prevention of the metabolic syndrome (MetS). This review suggests that the increase of posttraining levels of BDNF and its TrkB receptors causes simultaneous changes in the activity of the spinal cord, the substantia nigra, and the hypothalamic nuclei neurons, which are responsible for the alteration of the functional properties of motoneurons innervating the skeletal muscles, for the enhancement of dopamine release in the brain, and for the modulation of hormone levels involved in regulating the metabolic processes, responsively. Finally, training-evoked increase of the BDNF/TrkB leads to a change in a manner of regulation of skeletal muscles, causes a reduction of motor deficits observed in the Parkinson disease, and lowers weight, glucose level, and blood pressure, which accompany the MetS. Therefore, BDNF seems to be the molecular factor of pleiotropic activity, important in the modulation processes, underlying adaptations, which result from ET.
本文提出了一个概念，即规律的耐力训练（ET）会引起神经组织中广泛表达脑源性神经营养因子（BDNF）及其受体（TrkB），从而引起许多运动和代谢适应，这对人类健康有益。本文介绍了训练引起的内源性 BDNF 增加与控制运动表现和整个机体内稳态的神经结构的分子和/或生理适应之间的关系。由于 ET 对身体各个系统产生了非常广泛的可塑性变化，因此讨论了运动技能的提高和由于 BDNF/TrkB 水平升高后训练引起的文明病发展的对抗，这对进行 ET 的人来说很重要。因此，本报告介绍了耐力运动对（1）运动神经元特性的改变，这是运动通路的最终元素，（2）帕金森病引起的运动缺陷的减少，以及（3）代谢综合征（MetS）的预防的影响。本综述表明，训练后 BDNF 及其 TrkB 受体水平的升高会导致脊髓、黑质和下丘脑核神经元的活性同时发生变化，这负责改变支配骨骼肌的运动神经元的功能特性，增强大脑中的多巴胺释放，并调节参与调节代谢过程的激素水平。最后，训练引起的 BDNF/TrkB 增加会改变骨骼肌的调节方式，导致帕金森病中观察到的运动缺陷减少，并降低体重、血糖水平和伴随 MetS 的血压。因此，BDNF 似乎是 ET 引起的适应过程中调节过程的多效性活动的分子因素。
