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Muscle soreness can “spread” to other muscle groups via nervous system

PainSci » bibliography » Ayles et al 2011
updated
Tags: etiology, pain, exercise, pro, self-treatment, treatment

Two pages on PainSci cite Ayles 2011: 1. A Deep Dive into Delayed-Onset Muscle Soreness 2. Neurological growing pains: the nature of exercise soreness 

PainSci notes on Ayles 2011:

For this study, young men exercised one leg hard enough to make it good and sore. Pressure pain thresholds and sensitivities were measured a day later in the sore muscles, but also in other muscles that send their sensory information to the same part of the spinal cord — that’s unexercised and non-sore muscles on the sore side, that just happen to be connected to the same area of the spinal cord.

Not surprisingly, pain thresholds were lower in the sore, exercised muscles. But — and this is cool — vibrating the sore muscles caused soreness in other muscles that should not have been sore! So soreness effectively “spread” to other muscle groups, via the central nervous system. This raises interesting questions about how people with brain-regulated pain dysfunction might react to exercise soreness: could the pain spread to unaffected areas by the same mechanism? It seems likely.

original abstract †Abstracts here may not perfectly match originals, for a variety of technical and practical reasons. Some abstacts are truncated for my purposes here, if they are particularly long-winded and unhelpful. I occasionally add clarifying notes. And I make some minor corrections.

Evidence suggests large diameter afferents, presumably in response to centrally mediated changes, augment the mechanical allodynia or hyperalgesia seen in delayed onset muscle soreness (DOMS) conditions. Healthy males aged 18 to 30 (n = 16) performed eccentric exercise eliciting DOMS in the tibialis anterior muscle of a randomly assigned exercised leg. The contralateral leg served as a control. Mechanosensitivity was assessed on the exercised and control legs prior to and 24 hours postexercise via pressure pain thresholds (PPTs). PPTs were assessed at the muscle site, and at a distant segmentally related site, either without vibration or with vibration concurrently applied to the distant muscle, segmentally related, or control extra-segmentally related site. Participants completed a 6-point Likert scale providing a subjective measure of DOMS 5 days postexercise. Baseline mechanosensitivity was not significantly different at any site between the exercised and control legs prior to the exercise. Soreness ratings were higher 24 to 48 hours postexercise (P < .05), and baseline PPTs at the exercised legs muscle site decreased postexercise (P < .001). On day 1 following exercise, segmentally related site PPTs reduced significantly when vibration was applied concurrently to the DOMS affected tibialis anterior muscle (P < .04) compared to baseline mechanosensitivity or extrasegmental control vibration.

PERSPECTIVE: Further evidence is presented by this article indicating that large diameter afferents, presumably via centrally mediated mechanisms, augment the mechanical hyperalgesia seen in DOMS conditions. Future research examining eccentric activity in individuals with likely centrally sensitized conditions may be warranted.

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