Background & Aims
At chronic neck and shoulder pain, 30 minutes light effort paced arm cycling meant increased pain instead of healthy exercise induced analgesia. Increased pain was also extended in time (Grimby-Ekman et al., 2020).
Chronic musculoskeletal pain (MS) relates to longstanding stress, unfavorable psychosocial conditions (Theorell 1990; Kendall 1991) and non-musculoskeletal symptoms such as sleep problems, heart burn, extra heartbeats/palpitations, dizziness, anxiety, depression, chest pain, stomach discomfort, fatigue (Tschudi-Madsen et al., 2011), Burn out (BO) (Grossi et al., 2009; Armon et al., 2010) and failing analgetic Blood pressure (BP) regulation. Thus, MS frequently occurs in a context of physiological, emotional and cognitive failing functions. The potential significance of various failing physiological, emotional, and cognitive functions regarding origin and manifestations of pain in everyday life with MS could be examined based on a light physical effort/recovery condition.
Methods
Included; patients with neck and shoulder pain (?3 months) (N=25) and 12 healthy controls. Light effort from paced arm cycling (3 levels of load) and recovery could correspond to light physical effort from work tasks (Grimby-Ekman et al., 2020) or structured household shores and therefor be used to examine hypothesized diverse failing functions in everyday life manifestations of pain. Self-reports concerned everyday life (last 3-4 weeks)Pain spread (number of sites), Pain frequency, Burn out (BO) and Exercise habits . Recorded before cycling was blood pressure (BP), also further during cycling; heart rate (HR), self-rated pain and physical exertion (RPE) (Borg, 1982). At baseline and during recovery from cycling low grade proInflammatory (I-) reactions (sickness behavior) measurements were I-Pain, I-Energy and I-Emotion also forming an I-Index. Analysis of data meant correlative links and step wise linear regression. Results from healthy controls clarified the results at chronic pain.
Results
At chronic pain BO, Pain frequency, Pain spread and diastolic (D)BP were increased. Exercise habits were less extensive and not related to baseline HR. BO related to Pain spread r=0.529, p= 0.005 and to (lower)systolic(S)BP and DBP r=-0. 533, p=0.015 and r=0.-542. Also, baseline I-Pain meant lower DBP r=-0.462, p=0.028.
At arm cycling, more RPE related to more Exercise. During cycling RPE was clearly higher and not managed by customized HR. The more customized HR response (increased) the less increase in pain from cycling (r=-0.426 p=0.032) but also less frequent everyday Pain r =-0.417, p=0.043. At all levels of load, pain was associated to everyday pain spread r=0.523-0.608 p=0.00-0.00.
Regressions
Pain spread was best predicted by I-Pain 1 hour after arm cycling and the BO scale Cognitive weariness R2 =0.574.The HR response to cycling (reversely) predicted Pain frequency R2 =0.156. Pain before cycling, the HR response to effort (reversely) and Pain spread predicted Pain directly after arm cycling R2 =0.741. Pain the first evening after cycling was predicted by I-Pain at 1 hour after cycling, reversely by moderate Exercise and by harder Exercise R2 =0.739, p=0.000. Pain the second evening was predicted by I-Index 1 hour after arm cycling and I-Pain this day R2 =0.493.
Conclusions
Besides pain processing disparities, the origin of pain appeared partly due to the functioning of the autonomous nervous system (ANS) being impaired; non appearing gains from exercise in terms of correpondingly lower HR but pronouncedly increased effort during cycling together with non appearing customization of HR. Failing functioning of ANS included BP regulatory disparities. The level of health in terms of BO related to both BP disparities and to Pain spread.
With longer time distance from the ANS related arm cycling condition, the significance for the pain level, of the pain reaction itself, was increased.
References
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