Recovery and Performance Laboratory, Faculty of Medicine, L.A. Miller Centre, Memorial University of Newfoundland, St John's, Newfoundland, Canada.
J Neurol Phys Ther. 2020 Apr;44(2):132-144. doi: 10.1097/NPT.0000000000000308.
Even a single bout of aerobic exercise (AE) enhances corticospinal excitability (CSE), a biomarker of neuroplasticity. Because neurodegeneration limits capacity for neuroplasticity, it is not clear whether AE would induce CSE changes in people with progressive multiple sclerosis (MS).
People with progressive MS (n = 10) requiring ambulatory assistive devices completed a graded maximal exercise test. Dual-energy x-ray absorptiometry was used to quantify body fat and lean mass. Before and following one 40-minute AE session using body weight-supported (<10% support) treadmill at moderate intensity, CSE was measured using transcranial magnetic stimulation. Variables included resting and active motor thresholds, motor evoked potential (MEP) amplitudes, recruitment curves, and length of the cortical silent period (CSP).
Aerobic exercise reduced inhibition (shorter CSP) and increased excitation (increased MEP amplitude) only in the hemisphere corresponding to the stronger hand. Controlling for age, higher fitness and lower body fat significantly predicted exercise-induced reduction in resting motor threshold (ΔR = +0.458, P = 0.046) and CSP (ΔR = +0.568, P = 0.030), respectively.
Despite high levels of disability, capacity for exercise-induced neuroplasticity was retained among people with progressive MS. The hemisphere contralateral to the weaker hand was resistant to exercise-induced CSE changes, suggesting less neuroplastic potential. Lower fitness and higher body fat were associated with diminished exercise-induced CSE benefits, suggesting that therapists should consider interventions aimed at improving fitness and combating sedentarism to ultimately enhance the benefits of exercise on the brain.Video Abstract available for more insights from the authors (see the Video, Supplemental Digital Content 1, available at: http://links.lww.com/JNPT/A302).
单次有氧运动（AE）即可增强皮质脊髓兴奋性（CSE），这是神经可塑性的生物标志物。由于神经退行性变限制了神经可塑性的能力，因此尚不清楚 AE 是否会引起进展性多发性硬化症（MS）患者的 CSE 变化。
需要助行器辅助行走的进展性 MS 患者（n = 10）完成了分级最大运动测试。双能 X 射线吸收法用于定量体脂和瘦体重。在使用体重支撑（<10%支撑）的跑步机以中等强度进行 40 分钟 AE 疗程之前和之后，使用经颅磁刺激测量 CSE。变量包括静息和主动运动阈值、运动诱发电位（MEP）幅度、募集曲线和皮质静息期（CSP）长度。
有氧运动仅在与较强手相对应的半球中减少抑制（较短的 CSP）并增加兴奋（增加 MEP 幅度）。控制年龄、更高的健康水平和更低的体脂量可显著预测运动引起的静息运动阈值（ΔR = +0.458，P = 0.046）和 CSP（ΔR = +0.568，P = 0.030）降低。
尽管残疾程度较高，但进展性 MS 患者仍保留了运动引起的神经可塑性的能力。与较弱手相对的对侧半球对运动引起的 CSE 变化具有抗性，表明神经可塑性潜力较小。较低的健康水平和较高的体脂量与运动引起的 CSE 益处减少有关，这表明治疗师应考虑干预措施，以提高健康水平并对抗久坐不动，从而最终增强运动对大脑的益处。（参见视频，补充数字内容 1，可在以下网址获得：http://links.lww.com/JNPT/A302）。
