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A Single Bout of High-intensity Interval Exercise Increases Corticospinal Excitability, Brain-derived Neurotrophic Factor, and Uncarboxylated Osteolcalcin in Sedentary, Healthy Males.
Neuroscience ( IF 2.9 ) Pub Date : 2020-06-15 , DOI: 10.1016/j.neuroscience.2020.03.042
Chiara Nicolini 1 , Bernadeta Michalski 2 , Stephen L Toepp 3 , Claudia V Turco 3 , Tarra D'Hoine 3 , Diana Harasym 4 , Martin J Gibala 3 , Margaret Fahnestock 2 , Aimee J Nelson 5
Affiliation  

Exercise induces neuroplasticity in descending motor pathways facilitating motor learning, and as such it could be utilized as an intervention in neurorehabilitation, for example when re-learning motor skills after stroke. To date, however, the neurophysiological and molecular mechanisms underlying exercise-induced neuroplasticity remain largely unknown impeding the potential utilization of exercise protocols as 'motor learning boosters' in clinical and non-clinical settings. Here, we assessed corticospinal excitability, intracortical facilitation (ICF) and short-interval intracortical inhibition (SICI) using transcranial magnetic stimulation (TMS) and serum biochemical markers including brain-derived neurotrophic factor (BDNF), total and precursor cathepsin B (tCTSB, proCTSB), uncarboxylated and carboxylated osteocalcin (unOCN, cOCN) and irisin using ELISA. Measurements were carried out in sedentary, healthy males before and after a single session of high-intensity interval exercise (HIIE) or in individuals who rested and did not perform exercise (No Exercise). We found that HIIE increased corticospinal excitability, BDNF and unOCN, and decreased cOCN. We also determined that greater increases in BDNF were associated with increases in unOCN and irisin and decreases in cOCN only in participants who underwent HIIE, suggesting that unOCN and irisin may contribute to exercise-induced BDNF increases. Conversely, no changes other than a decrease in serum unOCN/tOCN were found in No Exercise participants. The present findings show that a single session of HIIE is sufficient to modulate corticospinal excitability and to increase BDNF and unOCN in sedentary, healthy males.

中文翻译:

单次高强度间歇运动可增加久坐不动的健康男性的皮质脊髓兴奋性、脑源性神经营养因子和非羧化骨钙素。

运动在促进运动学习的下行运动通路中诱导神经可塑性,因此它可以用作神经康复的干预,例如在中风后重新学习运动技能时。然而,迄今为止,运动诱发的神经可塑性背后的神经生理学和分子机制仍然很大程度上未知,这阻碍了运动方案在临床和非临床环境中作为“运动学习助推器”的潜在利用。在这里,我们使用经颅磁刺激 (TMS) 和血清生化标志物,包括脑源性神经营养因子 (BDNF)、总组织蛋白酶和前体组织蛋白酶 B (tCTSB, proCTSB)、未羧化和羧化骨钙素 (unOCN, cOCN) 和鸢尾素使用 ELISA。测量是在单次高强度间歇运动 (HIIE) 之前和之后的久坐、健康男性或在休息且不进行运动(无运动)的个体中进行的。我们发现 HIIE 增加了皮质脊髓兴奋性、BDNF 和 unOCN,并降低了 cOCN。我们还确定,仅在接受 HIIE 的参与者中,BDNF 的更大增加与 unOCN 和 irisin 的增加以及 cOCN 的减少有关,这表明 unOCN 和 irisin 可能有助于运动诱导的 BDNF 增加。相反,在没有运动的参与者中,除了血清 unOCN/tOCN 降低外,没有发现任何变化。目前的研究结果表明,单次 HIIE 足以调节久坐不动的健康男性的皮质脊髓兴奋性并增加 BDNF 和 unOCN。
更新日期:2020-06-09
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