Laboratory of Applied Biology, Université Libre de Bruxelles, Brussels, Belgium.
Med Sci Sports Exerc. 2012 Dec;44(12):2299-308. doi: 10.1249/MSS.0b013e318265f356.
Prolonged exhaustive exercise induces a failure of the nervous system to activate the involved muscles maximally (i.e., central fatigue). Part of central fatigue may reflect insufficient output from the motor cortex (i.e., supraspinal fatigue), but the cause is unresolved. To investigate the potential link between supraspinal fatigue and changes in brain concentration of dopamine and noradrenaline in temperate environment, we combined neurophysiological methods and pharmacological manipulation of these two neurotransmitters.
Changes in performance of a cycling exercise (time trial [TT]) were tested after oral administration of placebo (Pla), dopamine, or noradrenaline reuptake inhibitors (methylphenidate and reboxetine [Rebox], respectively) in well-trained male subjects. Changes in voluntary activation, corticospinal excitability, and muscle contractile properties were tested in the knee extensors using transcranial magnetic stimulation and motor nerve electrical stimulation before and after exercise. A psychomotor vigilance task (PVT) was also performed.
Compared with Pla, methylphenidate did not affect exercise performance (P = 0.19), but more time was needed to complete the TT after administration of Rebox (approximately 9%, P < 0.05). For the latter condition, the reduced performance was accompanied by a central/supraspinal fatigue (5%-6%, P < 0.05) and worsened PVT performance (7%, P < 0.05). For the three conditions, corticospinal excitability was unchanged, and peripheral fatigue was similar. Because the ingestion of Rebox induced a greater decrease in voluntary activation and PVT performance after the TT than Pla, with no modification in corticospinal excitability, the noradrenaline reuptake inhibitor likely affected supraspinal circuits located before the motor cortex.
These results suggest that noradrenaline, but not dopamine reuptake inhibition, contributes to the development of central/supraspinal fatigue after a prolonged cycling exercise performed in temperate conditions.
长时间的剧烈运动可导致神经系统无法最大限度地激活相关肌肉（即中枢疲劳）。中枢疲劳的一部分可能反映了运动皮层输出不足（即，脊髓疲劳），但其原因尚未确定。为了研究在温带环境下，中枢疲劳与大脑中多巴胺和去甲肾上腺素浓度变化之间的潜在联系，我们结合了神经生理学方法和这两种神经递质的药理学操作。
在经过训练的男性受试者中，口服安慰剂（Pla）、多巴胺或去甲肾上腺素再摄取抑制剂（哌甲酯和瑞波西汀[Rebox]，分别）后，测试自行车运动（计时赛[TT]）的表现变化。使用经颅磁刺激和运动神经电刺激在膝关节伸肌中测试运动神经元的自愿激活、皮质脊髓兴奋性和肌肉收缩特性，然后在运动前后进行。还进行了一项精神警觉性任务（PVT）。
与 Pla 相比，哌甲酯对运动表现没有影响（P = 0.19），但 Rebox 给药后完成 TT 需要更多时间（约 9%，P < 0.05）。在后一种情况下，运动表现的降低伴随着中枢/脊髓疲劳（5%-6%，P < 0.05）和 PVT 表现的恶化（7%，P < 0.05）。对于这三种情况，皮质脊髓兴奋性没有变化，外周疲劳相似。由于 Rebox 的摄入在 TT 后引起自愿激活和 PVT 表现的降低大于 Pla，而皮质脊髓兴奋性没有改变，因此去甲肾上腺素再摄取抑制剂可能影响了位于运动皮层之前的中枢/脊髓回路。
这些结果表明，在温带条件下进行长时间的自行车运动后，去甲肾上腺素而非多巴胺再摄取抑制有助于中枢/脊髓疲劳的发展。
