• Christopher Ring, Louisa Edwards, and Maria Kavussanu.
• International Centre for Health & Exercise Research, University of Birmingham, Birmingham B15 2TT, UK. c.m.ring@bham.ac.uk <c.m.ring@bham.ac.uk>
• Biol Psychol. 2008 Apr 1;78(1):123-8.

AbstractSensitivity to pain is reduced during exercise. The underlying mechanism has yet to be established. One possibility is that a baroreceptor-related mechanism may contribute to this exercise-induced hypoalgesia phenomenon. Accordingly, this study examined whether increases in arterial blood pressure during graded isometric exercise, which activate baroreceptors in the aortic arch and carotid sinus, could account for any effects of exercise on pain in 24 normotensive young men. Electrocutaneous stimuli were delivered to the sural nerve while participants performed isometric handgrip exercise at 1%, 15%, and 25% of their maximum voluntary contraction (MVC). Participants provided a pain intensity rating immediately following the delivery of each stimulus. Nociceptive flexion reflex (NFR) responses and thresholds were also determined to provide objective physiological correlates of pain. Pain ratings were attenuated by graded isometric exercise in a linear fashion, whereas nociceptive flexion reflex responses and thresholds were unchanged by exercise. Blood pressure increased in proportion to the force of the contraction. Mediational analyses using analyses of covariance indicated that the reduction in pain with exercise was substantially accounted for by the magnitude of the blood pressure response. These findings are consistent with an arterial baroreceptor inhibition mechanism for exercise-induced hypoalgesia.

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