Mang Cameron S, Brown Katlyn E, Neva Jason L, Snow Nicholas J, Campbell Kristin L, Boyd Lara A
Graduate Program in Rehabilitation Sciences, Faculty of Medicine, University of British Columbia, Vancouver, BC, Canada V6T 1Z3.
Graduate Program in Rehabilitation Sciences, Faculty of Medicine, University of British Columbia, Vancouver, BC, Canada V6T 1Z3; Graduate Program in Neuroscience, Faculty of Medicine, University of British Columbia, Vancouver, BC, Canada V6T 1Z3.
Neural Plast. 2016;2016:6797928. doi: 10.1155/2016/6797928. Epub 2016 Apr 4.
Acute aerobic exercise facilitated long-term potentiation-like plasticity in the human primary motor cortex (M1). Here, we investigated the effect of acute aerobic exercise on cerebellar circuits, and their potential contribution to altered M1 plasticity in healthy individuals (age: 24.8 ± 4.1 years). In Experiment 1, acute aerobic exercise reduced cerebellar inhibition (CBI) (n = 10, p = 0.01), elicited by dual-coil paired-pulse transcranial magnetic stimulation. In Experiment 2, we evaluated the facilitatory effects of aerobic exercise on responses to paired associative stimulation, delivered with a 25 ms (PAS25) or 21 ms (PAS21) interstimulus interval (n = 16 per group). Increased M1 excitability evoked by PAS25, but not PAS21, relies on trans-cerebellar sensory pathways. The magnitude of the aerobic exercise effect on PAS response was not significantly different between PAS protocols (interaction effect: p = 0.30); however, planned comparisons indicated that, relative to a period of rest, acute aerobic exercise enhanced the excitatory response to PAS25 (p = 0.02), but not PAS21 (p = 0.30). Thus, the results of these planned comparisons indirectly provide modest evidence that modulation of cerebellar circuits may contribute to exercise-induced increases in M1 plasticity. The findings have implications for developing aerobic exercise strategies to "prime" M1 plasticity for enhanced motor skill learning in applied settings.
急性有氧运动促进了人类初级运动皮层(M1)中类似长时程增强的可塑性。在此,我们研究了急性有氧运动对小脑回路的影响,以及它们对健康个体(年龄:24.8±4.1岁)M1可塑性改变的潜在作用。在实验1中,急性有氧运动降低了双线圈配对脉冲经颅磁刺激所诱发的小脑抑制(CBI)(n = 10,p = 0.01)。在实验2中,我们评估了有氧运动对配对联想刺激反应的促进作用,刺激间隔为25毫秒(PAS25)或21毫秒(PAS21)(每组n = 16)。PAS25而非PAS21所诱发的M1兴奋性增加依赖于跨小脑感觉通路。有氧运动对PAS反应的影响程度在两种PAS方案之间无显著差异(交互作用效应:p = 0.30);然而,计划比较表明,相对于休息期,急性有氧运动增强了对PAS25的兴奋性反应(p = 0.02),但对PAS21没有增强作用(p = 0.30)。因此,这些计划比较的结果间接提供了适度证据,表明小脑回路的调节可能有助于运动诱导的M1可塑性增加。这些发现对于制定有氧运动策略以“激发”M1可塑性从而在应用环境中增强运动技能学习具有重要意义。