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Abstract
This dissertation quantified the effect of a single bout of exercise on energy and fatigue mood states, and then tested whether histamine binding to the H1 receptor is a mechanism that explains the effect. In a systematic review and meta-analysis of 16 studies, it was concluded that acute exercise can increase energy, and the size of the standardized effect was = 0.47 (95% CI = 0.39, 0.56). The effect on energy was homogeneous and moderate, while the effect on fatigue was small and heterogeneous, = 0.03 (95% CI = -0.08, 0.13). Fatigue was only reduced when light or moderate intensity exercise was performed for at least 20 minutes in people with elevated baseline fatigue. The findings highlighted the usefulness of measuring both energy and fatigue changes after exercise, provided evidence that energy and fatigue are separate but related states, and suggested that changes in these states arise through different mechanisms. A strong inference experiment was conducted next to determine if blocking brain histamine from binding to H1 receptors would prevent expected exercise-induced increases in energy and reductions in fatigue fatigue. Doxepin hydrochloride (6 mg) or placebo was given to 20 women with elevated fatigue and low energy before they completed 30 minutes of light intensity cycling exercise. Changes in mental fatigue, but not mental or physical energy, were blocked with doxepin administration. Doxepin also blocked exercise-induced increases in motivation for cognitive work. The findings suggest that exercise-induced histamine binding to brain H1 receptors has (i) a significant role in reducing mental fatigue and increasing motivation for cognitive work after exercise, and (ii) little effect on mental energy defined as a mood state or inferred from performance on an attention task and related processes requiring visual perceptual processing efficiency and motor speed.