Pain is essential for our survival because it helps to protect us from severe injuries. Nociceptive signals may be exacerbated by continued physical activities but can also be interrupted or overridden by physical movements, a process called movement‐induced hypoalgesia. Several neural mechanisms have been proposed to account for this effect, including the reafference principle, non‐nociceptive interference, and top‐down descending modulation. Given that the hypoalgesic effects of these mechanisms temporally overlap during movement execution, it is unclear whether movement‐induced hypoalgesia results from a single neural mechanism or from the joint action of multiple neural mechanisms. To address this question, we conducted five experiments on 129 healthy humans by assessing the hypoalgesic effect after movement execution. Combining psychophysics and electroencephalographic recordings, we quantified the relationship between the strength of voluntary movement and the hypoalgesic effect, as well as the temporal and spatial characteristics of the hypoalgesic effect. Our findings demonstrated that movement‐induced hypoalgesia results from the joint action of multiple neural mechanisms. This investigation is the first to disentangle the distinct contributions of different neural mechanisms to the hypoalgesic effect of voluntary movement, which extends our understanding of sensory attenuation arising from voluntary movement and may prove instrumental in developing new strategies for pain management.

Pain is essential for our survival by protecting us from severe injuries. Pain signals may be exacerbated by continued physical activities but can also be interrupted or over-ridden by physical movements, a process called movement-induced analgesia. A number of neural mechanisms have been proposed to account for this effect, including the reafference principle, the gate control theory of pain, and the top-down psychological modulation. Given that the analgesic effects of these mechanisms are temporally overlapping, it is unclear whether movement-induced analgesia results from a single neural mechanism or the joint action of multiple neural mechanisms. To address this question, we conducted five experiments on 130 healthy human subjects. First, the frequency of hand shaking was manipulated in order to quantify the relationship between the strength of the voluntary movement and the analgesic effect. Second, the temporal delay (between hand shaking and nociceptive laser stimuli) and the stimulated side (nociceptive laser stimuli were delivered on the hand ipsilateral or contralateral to the shaken one) were manipulated to quantify the temporal and spatial characteristics of the analgesic effect induced by voluntary movement. Combining psychophysics and electroencephalographic recordings, we demonstrated that movement-induced analgesia is a result of the joint action of multiple neural mechanisms. This investigation is the first to disentangle the distinct contributions of different neural mechanisms to the analgesic effect of voluntary movement. These findings extend our understanding of sensory attenuation arising from voluntary movement and may prove instrumental in the development of new strategies in pain management.