MUSCULOSKELETAL PAIN AND EXERCISE— CHALLENGING EXISTING PARADIGMS AND INTRODUCING NEW

Review written by Ben Cormack info

BACKGROUND & OBJECTIVE

This paper was a narrative review looking at new concepts for understanding the interaction between pain and exercise. Traditional models of pain that focus on a linear transmission of nociception and a simplistic corresponding representation of what is happening within the tissue are inadequate to explain both pain itself and the responses to therapeutic exercise.

Pain can often be seen as something to avoid during exercise as it maybe a sign that the tissue is sustaining more injury. This assumption has been challenged recently by research indicating that exercise that allows some pain has a small statistical benefit in the short term and does not provide worse outcomes in the medium and longer terms.

The aim of the review was to explore mechanisms that might underpin the effect of exercise on pain and how these then fit into the concept of allowing painful exercise. Hopefully this can help optimise the way therapeutic exercise is prescribed.

METHODS

Firstly the authors looked at pain mechanisms such as central sensitisation, affective (emotional) aspects of pain, and the role of the immune system, with many of the mechanisms discussed have a large amount of overlap.

Central sensitisation can be split into hyperalgesia, allodynia, temporal summation of pain (TSP) and diffuse noxious inhibitory control (DNIC). The mechanisms that underpin sensitivity levels such as endogenous opioid activation or inhibition have been shown to be affected by exercise leading to both increased and decreased pain. The role of negative emotional states such as kinesiophobia, catastrophising, low self-efficacy, anxiety and depression are being seen as prognostic factors for recovery from many MSK conditions and share the activation of the same modulatory mechanisms. The role of glial cells and toll-like receptors and other immune system responses also can increase or decrease the experience of pain.

RESULTS

The authors highlight the function of exercise-induced hypoalgesia (EIH) in the role of central pain modulation. Painful exercise often allows greater dosages of exercise so may also increase the amount of EIH. The authors also discuss diffuse noxious inhibitory control

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