The role of brain catecholamines in exercise-induced oculomotor fatigue

Abstract

Fatigue during exercise is associated with reductions in voluntary muscular force production and poor physical performance. Central fatigue, a term that refers to the processes occurring within the central nervous system that contribute to these impairments, is associated with widespread alterations in the activity of the central catecholamines. Exercise-induced decreases in the velocity of saccadic eye movements might be a hallmark of central fatigue that is detectable via the oculomotor system - a motor system that is functionally independent of the corticospinal movement system and not directly challenged by prolonged exercise. The objective of this thesis was to investigate the role of central catecholamines in the development of exercise-induced fatigue using measures of eye movement control to index fatigue within the oculomotor system. The first experiment indirectly manipulated central catecholaminergic neurotransmission by administering caffeine to resting, alert participants. Caffeine exerted selective effects on oculomotor control, increasing speed in eye movement types characterised by a high velocity, such as saccades, but not affecting slower velocity, tracking eye movements and visual perception. Without caffeine, eye movement kinematics were stable across repeated measures, and deemed suitable for use in later experiments. The second experiment demonstrated that caffeine confers no benefit on the visuospatial processes of attention that support eye movement control. The third and fourth experiments administered nutritional and pharmacological treatments to upregulate dopaminergic and noradrenergic activity during exercise. Fatigue-related decrements in eye movement kinematics were offset by the individual manipulation of dopamine and norepinephrine via targeted reuptake inhibitors, suggesting that both of these neurochemicals are involved in preserving oculomotor function during fatiguing exercise. The fourth experiment developed this hypothesis showing that direct and indirect manipulation of central catecholamines, via combined norepinephrine-dopamine reuptake inhibition and caffeine respectively, prevents oculomotor system fatigue. This thesis constitutes the first comprehensive investigation into the influence of exercise fatigue on the human visual system. Overall, the findings support the hypothesis that central catecholamines are involved in mediating central fatigue during prolonged exercise. The outcomes of this thesis may inform the practical use of permitted neurostimulants, such as caffeine, in occupational or sporting contexts where visual system fatigue during prolonged physical activity could challenge performance and safety.