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Enhanced availability of serotonin increases activation of unfatigued muscle but exacerbates central fatigue during prolonged sustained contractions

Justin J. Kavanagh,Amelia J McFarland,Janet L. Taylor

Published 2018 in Journal of Physiology

ABSTRACT

Animal preparations have revealed that moderate synaptic release of serotonin (5‐HT) onto motoneurones enhances motor activity via activation of 5‐HT2 receptors, whereas intense release of 5‐HT causes spillover of 5‐HT to extrasynaptic 5‐HT1A receptors on the axon initial segment to reduce motoneurone activity. We explored if increasing extracellular concentrations of endogenously released 5‐HT (via the selective serotonin reuptake inhibitor paroxetine) influences the ability to perform unfatigued and fatigued maximal voluntary contractions in humans. Following the ingestion of paroxetine, voluntary muscle activation and torque generation increased during brief unfatigued maximal contractions. In contrast, the ability to generate maximal torque with increased 5‐HT availability was compromised under fatigued conditions, which was consistent with paroxetine‐induced reductions in motoneurone excitability and voluntary muscle activation. This is the first in vivo human study to provide evidence that 5‐HT released onto the motoneurones could play a role in central fatigue.

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