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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.