09/04/2023
Keep moving……
Exercise🏃♂, persistent pain and the brain🧠
👉 Exercise habit is associated with a lower prevalence of persistent pain and lower pain intensity, as shown in previous epidemiological studies. (https://pubmed.ncbi.nlm.nih.gov/21601986/, https://pubmed.ncbi.nlm.nih.gov/24147114/, https://pubmed.ncbi.nlm.nih.gov/23776464/)
👉The association between pain and sedentary behavior through fear of movement and negative affect is represented in the Fear-Avoidance Model (https://pubmed.ncbi.nlm.nih.gov/22321917/), suggesting that low physical activity is a risk of persistent pain. On the other hand, exercise is widely prescribed for individuals with musculoskeletal and neuropsychiatric disorders as a rehabilitation strategy to improve mechanical and muscular conditions and/or central nervous system processes (https://pubmed.ncbi.nlm.nih.gov/23253613/, https://pubmed.ncbi.nlm.nih.gov/26064521/, https://pubmed.ncbi.nlm.nih.gov/15924510/). Thus exercise shows clear evidence for increased pain thresholds (https://pubmed.ncbi.nlm.nih.gov/23141188/).
❓But it is quite unclear whether brain function is involved in increase of pain threshold due to exercise.
📎 Wakaizumi and colleagues examined the effect of self-reported physical activity in forty-five people with low back pain (mean pain intensity = 59.6/100 and mean duration = 9.9 weeks) via brain imaging data using a resting-state functional MRI and performed mediation analyses to identify brain regions mediating the exercise effect on pain. (https://www.sciencedirect.com/science/article/pii/S2452073X23000120)
📊 Participants with an exercise habit (n = 29) showed significant less pain compared to those without an exercise habit (-14 points (100), n = 16). Mediation analysis using resting-state functional connectivity identified the left thalamus (TH), right amygdala (Amy), and medial prefrontal cortex (MPFC) as statistical mediators of the exercise effect on pain (indirect effect = −0.460, 95% confidence interval = −0.767 to −0.153).
🧠 The identified brain regions are involved in some aspects of nociceptive processing (s. figure): TH is a central nucleus of sensory pathways (https://pubmed.ncbi.nlm.nih.gov/23719569/), Amy is a primary region of emotional responses including anxiety and fear (https://pubmed.ncbi.nlm.nih.gov/20525501/), and MPFC plays a role in the inhibitory regulation of the amygdala (https://pubmed.ncbi.nlm.nih.gov/24673881/).
🧠All these regions are included in a brain network of nociceptive modulation due to exercise through a mesocorticolimbic system (https://www.sciencedirect.com/science/article/abs/pii/S1755296609000039), that has been shown to play a key role in the development, modulation, and maintenance of pain following injury in humans (https://pubmed.ncbi.nlm.nih.gov/21146929/, https://pubmed.ncbi.nlm.nih.gov/26247858/) and animal models (https://pubmed.ncbi.nlm.nih.gov/26691834/)
⭕Limitations: cross-sectional study, no detailed parameters with regard to exercise, small sample size.
Figure: https://link.springer.com/chapter/10.1007/978-3-030-80411-4_5
Nociceptive processing and modulation pathways (ACC anterior cingulate cortex, DRG dorsal
root ganglion, PAG periaqueductal grey, PFC prefrontal cortex, RVM rostral-ventromedial medulla,
S1 primary somatosensory cortex, S2 secondary somatosensory cortex)
