Abstract
Strenuous exercise can result in an inability of the central nervous system to drive skeletal muscle effectively, a phenomenon known as central fatigue. The impact of central fatigue on the oculomotor system is currently unexplored. Fatigue that originates in the central nervous system may be related to perturbations in the synthesis and metabolism of several neurotransmitters. In this study we examine central fatigue in the oculomotor system after prolonged exercise. The involvement of central neurotransmission was explored by administering caffeine during exercise. Within a double-blind, randomized, repeated measures, crossover design, 11 cyclists consumed a placebo or caffeine solution during 180 min of stationary cycling. Saccadic eye movements were measured using infra-red oculography. Exercise decreased saccade velocity by 8% (placebo trial). This effect was reversed by caffeine, whereby velocity was increased by 11% after exercise. A non-oculomotor perceptual task (global motion processing) was unaffected by exercise. The human oculomotor system is impaired by strenuous exercise of the locomotor system. Caffeine exerts a protective effect on oculomotor control, which could be related to up-regulated central neurotransmission. In addition, cortical processes supporting global motion perception appear to be robust to fatigue.
Highlights
Strenuous exercise can result in an inability of the central nervous system to drive skeletal muscle effectively, a phenomenon known as central fatigue
There was an effect of exercise-induced fatigue on saccade velocity that was modulated by intervention and congruency (3-way interaction INTERVENTION ×TIMEPOINT ×CONGRUENCY, F1,10 = 8.076, p < 0.05)
Changes in saccade velocity from baseline were larger in magnitude and less variable for congruent saccades compared to incongruent saccades (Fig. 2, Panel a)
Summary
Strenuous exercise can result in an inability of the central nervous system to drive skeletal muscle effectively, a phenomenon known as central fatigue. Caffeine exerts a protective effect on oculomotor control, which could be related to up-regulated central neurotransmission. Exercise-induced fatigue is associated with temporary reductions in voluntary muscular force production and poor physical performance[1]. These impairments are not entirely due to biochemical processes occurring within skeletal muscle. While central fatigue has been demonstrated in the skeletal motor system[23,24,25], it is unknown whether this is a ubiquitous phenomenon within the brain that affects motor systems which are not directly involved in locomotion and limb movement, such as the oculomotor control of eye movements. Central fatigue-like effects have been observed in the oculomotor system of non-human primates when measuring saccadic eye movements[26]. Microstimulation of the abducens nucleus pre and post fatigue produced identical saccade profiles thereby implicating processes occurring above www.nature.com/scientificreports/
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