PURPOSE: Exercise-induced hypoalgesia is frequently documented in the literature. However, the underlying neural mechanism of this phenomenon remains unclear. Here, we explored the effects of different intensities of isometric exercise on pain perception with a randomized controlled design and investigated its neural mechanisms through tracing the dynamic changes of heat-evoked brain responses. METHODS: Forty-eight participants were randomly assigned to one of the three groups with different exercise intensities (i.e., high, low, and control). Their subjective pain reports and brain responses elicited by heat stimuli before and after exercise were assessed. RESULTS: We observed 1) the increased pressure pain thresholds and heat pain thresholds on the dorsal surface of the hand and the biceps brachii muscle of the exercised limb (closed to the contracting muscle), and the decreased pressure pain ratings at the indexed finger of the unexercised limb; 2) more reduction of pain sensitivity on both the biceps brachii muscle and the dorsal surface of the hand induced by the high-intensity isometric exercise than the low-intensity isometric exercise; and 3) both the high-intensity and the low-intensity isometric exercise induced the reduction of N2 amplitudes and N2-P2 peak-to-peak amplitudes, as well as the reduction of event-related potential magnitudes elicited by the heat stimuli on the exercised limb. CONCLUSIONS: The hypoalgesic effects induced by the isometric exercise were not only localized to the moving part of the body but also can be extended to the distal part of the body. The exercise intensities play a vital role in modulating these effects. Exercise-induced hypoalgesia could be related to the modulation of nociceptive information transmission via a spinal gating mechanism and also rely on a top-down descending pain inhibitory mechanism.
PURPOSE: Exercise-induced hypoalgesia is frequently documented in the literature. However, the underlying neural mechanism of this phenomenon remains unclear. Here, we explored the effects of different intensities of isometric exercise on pain perception with a randomized controlled design and investigated its neural mechanisms through tracing the dynamic changes of heat-evoked brain responses. METHODS: Forty-eight participants were randomly assigned to one of the three groups with different exercise intensities (i.e., high, low, and control). Their subjective pain reports and brain responses elicited by heat stimuli before and after exercise were assessed. RESULTS: We observed 1) the increased pressure pain thresholds and heat pain thresholds on the dorsal surface of the hand and the biceps brachii muscle of the exercised limb (closed to the contracting muscle), and the decreased pressure pain ratings at the indexed finger of the unexercised limb; 2) more reduction of pain sensitivity on both the biceps brachii muscle and the dorsal surface of the hand induced by the high-intensity isometric exercise than the low-intensity isometric exercise; and 3) both the high-intensity and the low-intensity isometric exercise induced the reduction of N2 amplitudes and N2-P2 peak-to-peak amplitudes, as well as the reduction of event-related potential magnitudes elicited by the heat stimuli on the exercised limb. CONCLUSIONS: The hypoalgesic effects induced by the isometric exercise were not only localized to the moving part of the body but also can be extended to the distal part of the body. The exercise intensities play a vital role in modulating these effects. Exercise-induced hypoalgesia could be related to the modulation of nociceptive information transmission via a spinal gating mechanism and also rely on a top-down descending pain inhibitory mechanism.