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Enhanced availability of serotonin limits muscle activation during high-intensity, but not low-intensity, fatiguing contractions.

Serotonin (5-HT) modulates motoneuron excitability during muscle contractions, where the release of 5-HT in the central nervous system (CNS) is linked to the intensity of physical activity. Although there is evidence that enhanced availability of 5-HT can exacerbate fatigue, these effects on the development of fatigue during different contraction intensities are largely unknown. The purpose of this study was to investigate how enhanced 5-HT availability affects voluntary muscle activation and corticospinal excitability during fatigue-inducing contractions. Two experiments were performed. In the first experiment (n = 11), twelve isometric elbow flexions at 20% maximal voluntary contractions (MVC) were performed for 2-min each with 40-s rest periods. In the second experiment (n = 14), twelve maximal isometric elbow flexions were held for 10-s each with 40-s rest periods. In both experiments, the selective serotonin reuptake inhibitor (20 mg paroxetine), or a placebo, was administered in a two-way crossover-design. Muscle responses to transcranial magnetic stimulation (TMS) of the motor cortex (both experiments 1 and 2), as well as motor point stimulation of the elbow flexors (experiment 2) were assessed. Paroxetine reduced both motor cortical (p = 0.018) and motor point voluntary activation (p = 0.036) during the maximal contraction protocol. Paroxetine also reduced exercise-induced lengthening of the TMS silent period during the submaximal (p = 0.037) and maximal (p = 0.002) contraction protocols. Activation of inhibitory 5-HT1A receptors on motoneurons likely exacerbated exercise-induced reductions in voluntarily drive to the elbow flexors. However, 5-HT modulation of motor activity also appeared at the supraspinal level.