Abstract
Fatigue-induced reductions in saccade velocity have been reported following acute, prolonged exercise. Interestingly, the detrimental impact of fatigue on oculomotor control can be prevented by a moderate dose of caffeine. This effect may be related to central catecholamine upregulation via caffeine’s action as an adenosine antagonist. To test this hypothesis, we compared the protective effect of caffeine on oculomotor control post-exercise to that of a norepinephrine-dopamine reuptake inhibitor. Within a placebo-controlled crossover design, 12 cyclists consumed placebo, caffeine or a norepinephrine-dopamine reuptake inhibitor (bupropion) during 180 minutes of stationary cycling. Saccades, smooth pursuit and optokinetic nystagmus were measured using infrared oculography. Exercise fatigue was associated with an 8 ± 11% reduction in the peak velocity of prosaccades, and a 10 ± 11% decrement in antisaccade peak velocity. Optokinetic nystagmus quick phases decreased in velocity by 15 ± 17%. These differences were statistically significant (p < 0.05). Norepinephrine-dopamine reuptake inhibition and caffeine prevented fatigue-related decrements in eye movement velocity. Pursuit eye movements and visual attention were unaffected. These findings show that norepinephrine-dopamine reuptake inhibition protects oculomotor function during exercise fatigue. Caffeine’s fatigue-reversing effects on eye movements appear to be mediated, at least in part, via modulation of central catecholamines.
Highlights
From peripheral factors, subject motivation and learning effects
There was an effect of exercise on peak prosaccade velocity that was modulated by treatment
The findings suggest that caffeine exerts at least part of its protective effects through these neurochemicals
Summary
The remaining participants displayed an increase in peak velocity post-exercise with an average effect size of 0.19 ± 0.13 Caffeine prevented this exercise-induced decrement in prosaccade velocity and increased velocity significantly above pre-exercise levels (6 ± 9%, t23 = −2.96, p < 0.05)(see Fig. 2, panel a). Post-hoc analysis revealed that exercise-induced fatigue significantly reduced the peak velocity of antisaccades in the gap condition compared to pre-exercise by 10 ± 11%. Post-hoc tests revealed a significant decrease in peak velocity post-exercise with placebo (t21 = 3.80, p < 0.01), while there were no differences pre to post-exercise in peak velocity with caffeine and NDRI treatments.
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