Connell Charlotte J W, Thompson Benjamin, Turuwhenua Jason, Srzich Alexa, Gant Nicholas
1Department of Exercise Sciences, Centre for Brain Research, University of Auckland, Auckland, NEW ZEALAND; 2School of Optometry and Vision Science, University of Waterloo, Ontario, CANADA; and 3Department of Optometry and Vision Science, University of Auckland, Auckland, NEW ZEALAND.
Med Sci Sports Exerc. 2017 Sep;49(9):1778-1788. doi: 10.1249/MSS.0000000000001307.
Fatigue-induced impairments in the control of eye movements are detectable via reduced eye movement velocity after a bout of prolonged, strenuous exercise. Slower eye movements caused by neural fatigue within the oculomotor system can be prevented by caffeine, and the upregulation of central catecholamines may be responsible for this effect. This study explored the individual contribution of dopamine and norepinephrine to fatigue-related impairments in oculomotor control.
The influence of a dopamine reuptake inhibitor (methylphenidate) and a norepinephrine reuptake inhibitor (reboxetine) was assessed in 12 cyclists performing 180 min of stationary cycling within a placebo-controlled crossover design. Eye movement kinematics (saccades, smooth pursuit, and optokinetic nystagmus) were measured using infrared oculography. Visual attention was assessed with overt and covert spatial attention tasks.
Exercise-induced fatigue was associated with a 6% ± 8% reduction in the peak velocity of visually guided, reflexive prosaccades. Importantly, both dopamine reuptake inhibition and norepinephrine reuptake inhibition prevented fatigue-related decrements in the peak velocity of prosaccades. Pursuit eye movements, optokinetic nystagmus, and visual attention tasks were unaffected by exercise or drug treatments.
Overall, our findings suggest that alterations in norepinephrinergic and dopaminergic neurotransmission are linked with the development of fatigue within circuits that control eye movements. Psychiatric medications that target central catecholamines can exert a protective effect on eye movements after prolonged exercise.
长时间剧烈运动后，通过眼动速度降低可检测到疲劳引起的眼动控制障碍。动眼系统内神经疲劳导致的眼动减慢可被咖啡因预防，中枢儿茶酚胺的上调可能是造成这种效应的原因。本研究探讨了多巴胺和去甲肾上腺素对动眼控制中与疲劳相关障碍的个体作用。
在一项安慰剂对照的交叉设计中，对12名骑自行车者进行180分钟的固定骑行，评估多巴胺再摄取抑制剂（哌甲酯）和去甲肾上腺素再摄取抑制剂（瑞波西汀）的影响。使用红外眼动图测量眼动运动学（扫视、平稳跟踪和视动性眼震）。通过显性和隐性空间注意任务评估视觉注意。
运动诱发的疲劳与视觉引导的反射性前扫视峰值速度降低6%±8%有关。重要的是，多巴胺再摄取抑制和去甲肾上腺素再摄取抑制均能预防与疲劳相关的前扫视峰值速度下降。跟踪眼动、视动性眼震和视觉注意任务不受运动或药物治疗的影响。
总体而言，我们的研究结果表明，去甲肾上腺素能和多巴胺能神经传递的改变与控制眼动的回路中疲劳的发展有关。针对中枢儿茶酚胺的精神药物可在长时间运动后对眼动发挥保护作用。
