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      Influence of exercise on visceral pain: an explorative study in healthy volunteers

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          Abstract

          Background and objectives

          Contradictory results have been found about the effect of different exercise modalities on pain. The aim of this study was to investigate the early effects of aerobic and isometric exercise on different types of experimental pain, including visceral pain, compared to an active control condition.

          Methods

          Fifteen healthy subjects (6 women, mean [standard deviation] age 25 [6.5] years) completed 3 interventions consisting of 20 minutes of aerobic cycling, 12 minutes of isometric knee extension and a deep breathing procedure as active control. At baseline and after each intervention, psychophysical tests were performed, including electrical stimulation of the esophagus, pressure pain thresholds and the cold pressor test as a measure for conditioned pain modulation. Participants completed the Medical Outcome Study Short-Form 36 and State-Trait Anxiety Inventory prior to the experiments. Data were analyzed using two-way repeated measures analysis of variance.

          Results

          No significant differences were found for the psychophysical tests after the interventions, compared to baseline pain tests and the control condition.

          Conclusion

          No hypoalgesic effect of aerobic and isometric exercise was found. The evidence for exercise-induced hypoalgesia appears to be not as consistent as initially thought, and caution is recommended when interpreting the effects of exercise on pain.

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          Most cited references 15

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          Interactions between the cardiovascular and pain regulatory systems: an updated review of mechanisms and possible alterations in chronic pain.

          Endogenous pain regulatory system dysfunction appears to play a role in the maintenance of chronic pain. An important component of the pain regulatory process is the functional interaction between the cardiovascular and pain regulatory systems, which results in an association between elevated resting blood pressure (BP) and diminished acute pain sensitivity. This BP/pain sensitivity relationship is proposed to reflect a homeostatic feedback loop helping restore arousal levels in the presence of painful stimuli. Evidence is emerging that this normally adaptive BP/pain sensitivity relationship is significantly altered in chronic pain conditions, affecting responsiveness to both acute and chronic pain stimuli. Several mechanisms that may underlie this adaptive relationship in healthy individuals are overviewed, including endogenous opioid, noradrenergic, and baroreceptor-related mechanisms. Theoretical models are presented regarding how chronic pain-related alterations in the mechanisms above and increased pain facilatory system activity (central sensitization) may contribute to altered BP/pain sensitivity interactions in chronic pain. Clinical implications are discussed.
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            Dysfunctional endogenous analgesia during exercise in patients with chronic pain: to exercise or not to exercise?

            Exercise is an effective treatment for various chronic pain disorders, including fibromyalgia, chronic neck pain, osteoarthritis, rheumatoid arthritis, and chronic low back pain. Although the clinical benefits of exercise therapy in these populations are well established (i.e. evidence based), it is currently unclear whether exercise has positive effects on the processes involved in chronic pain (e.g. central pain modulation). Reviewing the available evidence addressing the effects of exercise on central pain modulation in patients with chronic pain. Narrative review. Exercise activates endogenous analgesia in healthy individuals. The increased pain threshold following exercise is due to the release of endogenous opioids and activation of (supra)spinal nociceptive inhibitory mechanisms orchestrated by the brain. Exercise triggers the release of beta-endorphins from the pituitary (peripherally) and the hypothalamus (centrally), which in turn enables analgesic effects by activating μ-opioid receptors peripherally and centrally, respectively. The hypothalamus, through its projections on the periaqueductal grey, has the capacity to activate descending nociceptive inhibitory mechanisms. However, several groups have shown dysfunctioning of endogenous analgesia in response to exercise in patients with chronic pain. Muscle contractions activate generalized endogenous analgesia in healthy, pain-free humans and patients with either osteoarthritis or rheumatoid arthritis, but result in increased generalised pain sensitivity in fibromyalgia patients. In patients having local muscular pain (e.g. shoulder myalgia), exercising non-painful muscles activates generalized endogenous analgesia. However, exercising painful muscles does not change pain sensitivity either in the exercising muscle or at distant locations. The reviewed studies examined acute effects of exercise rather than long-term effects of exercise therapy. A dysfunctional response of patients with chronic pain and aberrations in central pain modulation to exercise has been shown, indicating that exercise therapy should be individually tailored with emphasis on prevention of symptom flares. The paper discusses the translation of these findings to rehabilitation practice together with future research avenues.
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              The effects of slow breathing on affective responses to pain stimuli: an experimental study.

              This study examined whether breathing rate affected self-reported pain and emotion following thermal pain stimuli in women with fibromyalgia syndrome (FM: n=27) or age-matched healthy control women (HC: n=25). FM and HC were exposed to low and moderate thermal pain pulses during paced breathing at their normal rate and one-half their normal rate. Thermal pain pulses were presented in four blocks of four trials. Each block included exposure to both mild and moderate pain trials, and periods of both normal and slow paced breathing. Pain intensity and unpleasantness were recorded immediately following each pain trial, and positive and negative affect were assessed at the end of each block of trials. Compared to normal breathing, slow breathing reduced ratings of pain intensity and unpleasantness, particularly for moderately versus mildly painful thermal stimuli. The effects of slow breathing on pain ratings were less reliable for FM patients than for HCs. Slow versus normal breathing decreased negative affect ratings following thermal pain pulses for both groups, and increased positive affect reports, but only for healthy controls with high trait negative affect. Participants who reported higher levels of trait positive affect prior to the experiment showed greater decreases in negative affect as a result of slow versus normal breathing. These experimental findings provide support for prior reports on the benefits of yogic breathing and mindful Zen meditation for pain and depressed affect. However, chronic pain patients may require more guidance to obtain therapeutic benefit from reduced breathing rates. Copyright 2009 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.
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                Author and article information

                Journal
                J Pain Res
                J Pain Res
                Journal of Pain Research
                Journal of Pain Research
                Dove Medical Press
                1178-7090
                2017
                28 December 2016
                : 10
                : 37-46
                Affiliations
                [1 ]Department of Surgery, Radboud University Medical Centre, Nijmegen, the Netherlands
                [2 ]Mech-Sense, Department of Gastroenterology, Aalborg University Hospital, Aalborg
                [3 ]Department of Drug Design and Pharmacology, University of Copenhagen, Copenhagen, Denmark
                [4 ]Department of Anesthesiology, Pain and Palliative Medicine, Radboud University Nijmegen Medical Centre, Nijmegen, the Netherlands
                Author notes
                Correspondence: Laura JGM van Weerdenburg, Department of Surgery (route 618), Radboud University Medical Centre, PO Box 9101, 6500 HB Nijmegen, the Netherlands, Tel +31 6 5790 7591, Email laura.van.weerdenburg@ 123456student.ru.nl
                Article
                jpr-10-037
                10.2147/JPR.S121315
                5207470
                © 2017 van Weerdenburg et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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                Original Research

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