Department of Physical Activity and Health, The Swedish School of Sport and Health Sciences, GIH, Stockholm, Sweden; Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden.
Department of Physical Activity and Health, The Swedish School of Sport and Health Sciences, GIH, Stockholm, Sweden.
Behav Brain Res. 2022 Jul 26;430:113926. doi: 10.1016/j.bbr.2022.113926. Epub 2022 May 12.
Brain-derived neurotrophic factor (BDNF) and cortisol are both capable of modulating synaptic plasticity, but it is unknown how physical activity-induced changes in their plasma levels relate to corticospinal plasticity in humans. Sixteen inactive middle-aged men and women participated in three separate interventions consisting of 3 h prolonged sitting (SIT); 3 h sitting interrupted every 30 min with frequent short physical activity breaks (FPA); and 2.5 h prolonged sitting followed by 25 min of moderate intensity exercise (EXE). These 3 h sessions were each followed by a 30 min period of paired associative stimulation over the primary motor cortex (PAS). Blood samples were taken and corticospinal excitability measured at baseline, pre PAS, 5 min and 30 min post PAS. Here we report levels of plasma BDNF and cortisol over three activity conditions and relate these levels to previously published changes in corticospinal excitability of a non-activated thumb muscle. There was no interaction between time and condition in BDNF, but cortisol levels were significantly higher after EXE compared to after SIT and FPA. Higher cortisol levels at pre PAS predicted larger increases in corticospinal excitability from baseline to all subsequent time points in the FPA condition only, while levels of BDNF at pre PAS did not predict such changes in any of the conditions. Neither BDNF nor cortisol modified changes from pre PAS to the subsequent time points, suggesting that the increased corticospinal excitability was not mediated though an augmented effect of the PAS protocol. The relationship between cortisol and plasticity has been suggested to be inverted U-shaped. This is possibly why the moderately high levels of cortisol seen in the FPA condition were positively associated with changes AURC, while the higher cortisol levels seen after EXE were not. A better understanding of the mechanisms for how feasible physical activity breaks affect neuroplasticity can inform the theoretical framework for how work environments and schedules should be designed.
脑源性神经营养因子（BDNF）和皮质醇都能够调节突触可塑性，但尚不清楚运动引起的血浆水平变化与人类皮质脊髓可塑性之间的关系。16 名不活跃的中年男女参加了三项单独的干预措施，包括 3 小时久坐（SIT）；每隔 30 分钟中断 3 小时坐姿，频繁进行短暂的身体活动休息（FPA）；2.5 小时久坐后进行 25 分钟中等强度运动（EXE）。这 3 小时的每个阶段后，都在初级运动皮层（PAS）上进行 30 分钟的配对联想刺激（PAS）。在基线、PAS 前、PAS 后 5 分钟和 30 分钟时采集血样并测量皮质脊髓兴奋性。在这里，我们报告了三种活动条件下的血浆 BDNF 和皮质醇水平，并将这些水平与之前发表的非激活拇指肌肉皮质脊髓兴奋性变化相关联。BDNF 无时间与条件的相互作用，但 EXE 后皮质醇水平明显高于 SIT 和 FPA 后。仅在 FPA 条件下，PAS 前的皮质醇水平较高，预示着从基线到所有后续时间点的皮质脊髓兴奋性增加更大，而 PAS 前的 BDNF 水平并不能预测任何条件下的这种变化。BDNF 和皮质醇都没有改变从 PAS 前到后续时间点的变化，这表明增加的皮质脊髓兴奋性不是通过 PAS 协议的增强作用介导的。皮质醇和可塑性之间的关系呈倒 U 形。这可能就是为什么在 FPA 条件下看到的中等水平的皮质醇与变化 AURC 呈正相关，而在 EXE 后看到的较高皮质醇水平则没有。更好地了解可行的身体活动休息如何影响神经可塑性的机制，可以为如何设计工作环境和时间表提供理论框架。
