Fibromyalgia (FM) has been conceptualized as a disorder of the central nervous system, characterized by augmented sensory processing and an inability to effectively modulate pain. We previously reported that physical activity (PA) is related to brain processing of pain, providing evidence for a potential mechanism of pain management. The purpose of this study was to extend our work by manipulating pain modulation and determining relationships to both PA and sustained sedentary behavior. Eleven women with FM completed accelerometer measures of PA and underwent functional magnetic resonance imaging of painful heat, administered alone and during distracting cognitive tasks. Results showed that PA was significantly (P<0.005) and positively related to brain responses during distraction from pain in regions implicated in pain modulation including the dorsolateral prefrontal cortex (DLPFC), the dorsal posterior cingulate and the periaqueducatal grey. A significant negative relationship occurred in the left anterior insula. For sedentary time, significant negative relationships were observed in areas involved in both pain modulation and the sensory-discriminative aspects of pain including the DLPFC, thalamus and superior frontal and pre and postcentral gyri. These results suggest that physical activity and sedentary behaviors are related to central nervous system regulation of pain in FM.

These results provide preliminary evidence that meeting current physical activity recommendations may be beneficial for pain in women. Moreover, participation in vigorous activity seems to account for the decreased pain sensitivity. In our sample, sedentary behavior did not seem to have a deleterious effect on pain. Results from this study have many potential applications including aiding our understanding of why exercise functions as a treatment for those with chronic pain conditions and providing a rationale for including physical activity assessment in pain research.

Pain sensitivity decreases with exercise. The mechanisms that underlie this exercise-induced hypoalgesia (EIH) are unclear. Our purpose was to investigate conditioned pain modulation (CPM) as a potential mechanism of EIH. Sixteen women completed pain testing during three sessions: painful exercise, nonpainful exercise, and quiet rest. Intensity and unpleasantness ratings to noxious heat stimuli were assessed at baseline and during and following each session. Results showed that pain sensitivity decreased significantly during both exercise sessions (p < .05), but not during quiet rest. Effect size calculations showed that the size of the hypoalgesic response was greater following painful exercise than nonpainful exercise. Our results suggest that exercise-induced muscle pain may contribute to the magnitude of EIH. However, as pain sensitivity also decreased following nonpainful exercise, CPM is not likely the primary mechanism of EIH.

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