DOMS (Delayed Onset Muscle Soreness) is Neural Microdamage Rather Than Muscle Damage

[Aurelius]

For whom it may concern:

https://www.mdpi.com/2076-3921/9/3/212/htm

 

[pattismith]

That's an exciting article.

I thought that my muscle pain and exercice intolerance was possibly related to SFN (damaged unmyelinated nerve fibers C fibers and small Aδ fibers, ), but it may be that these other A sensory nerve fibers (Aβ ) could be the culprit

Group A nerve fiber - Wikipedia

 

[Aurelius]

And would there be a treatment for repairing them again?

 

[Learner1]

You might try these.

 

[Pyrrhus]

And here's some information from Wikipedia about Delayed-Onset Muscle Soreness (DOMS):

Delayed onset muscle soreness (DOMS) is the pain and stiffness felt in muscles several hours to days after unaccustomed or strenuous exercise.

The soreness is felt most strongly 24 to 72 hours after the exercise.[1][2]: 63  It is thought to be caused by eccentric (lengthening) exercise, which causes small-scale damage (microtrauma) to the muscle fibers. After such exercise, the muscle adapts rapidly to prevent muscle damage, and thereby soreness, if the exercise is repeated.[1][2]: 76

Delayed onset muscle soreness is one symptom of exercise-induced muscle damage. The other is acute muscle soreness, which appears during and immediately after exercise.

Source: https://en.wikipedia.org/wiki/Delayed_onset_muscle_soreness

Note that Delayed-Onset Muscle Soreness (DOMS) is different from Acute Muscle Soreness (AMS)!

 

[Pyrrhus]

And here's the abstract:

Have We Looked in the Wrong Direction for More Than 100 Years? Delayed Onset Muscle Soreness Is, in Fact, Neural Microdamage Rather Than Muscle Damage (Sonkodi et al., 2020)

According to our hypothesis, delayed onset muscle soreness (DOMS) is an acute compression axonopathy of the nerve endings in the muscle spindle. It is caused by the superposition of compression when repetitive eccentric contractions are executed under cognitive demand. The acute compression axonopathy could coincide with microinjury of the surrounding tissues and is enhanced by immune-mediated inflammation.

DOMS is masked by sympathetic nervous system activity at initiation, but once it subsides, a safety mode comes into play to prevent further injury. DOMS becomes manifest when the microinjured non-nociceptive sensory fibers of the muscle spindle stop inhibiting the effects of the microinjured, hyperexcited nociceptive sensory fibers, therefore providing the ‘open gate’ in the dorsal horn to hyperalgesia. Reactive oxygen species and nitric oxide play a cross-talking role in the parallel, interlinked degeneration–regeneration mechanisms of these injured tissues.

We propose that the mitochondrial electron transport chain generated free radical involvement in the acute compression axonopathy. ‘Closed gate exercises’ could be of nonpharmacological therapeutic importance, because they reduce neuropathic pain in addition to having an anti-inflammatory effect. Finally, DOMS could have an important ontogenetical role by not just enhancing ability to escape danger to survive in the wild, but also triggering muscle growth.

 

[Pyrrhus]

Here's a related discussion about Acute Muscle Soreness (AMS):

ASICs required for immediate exercise-induced muscle pain
https://forums.phoenixrising.me/thr...immediate-exercise-induced-muscle-pain.80581/

 

[bread.]

And here's the abstract:

Have We Looked in the Wrong Direction for More Than 100 Years? Delayed Onset Muscle Soreness Is, in Fact, Neural Microdamage Rather Than Muscle Damage (Sonkodi et al., 2020)

= likely a mechanism at play or disarray in me/cfs it seems to me

 

[Pyrrhus]

= likely a mechanism at play or disarray in me/cfs it seems to me

Yes, I often wonder what role DOMS might have in PEM, or if PEM is a similar process to DOMS...

 

[pattismith]

Yes, I often wonder what role DOMS might have in PEM, or if PEM is a similar process to DOMS...

this is exactely the question; are they different in nature or intensity only,

Here a recent review article (juanary 2024)

Neurochemical mechanism of muscular pain: Insight from the study on delayed onset muscle soreness​

Abstract​

We reviewed fundamental studies on muscular pain, encompassing the characteristics of primary afferent fibers and neurons, spinal and thalamic projections, several muscular pain models, and possible neurochemical mechanisms of muscle pain. Most parts of this review were based on data obtained from animal experiments, and some researches on humans were also introduced.

We focused on delayed-onset muscle soreness (DOMS) induced by lengthening contractions (LC), suitable for studying myofascial pain syndromes.

The muscular mechanical withdrawal threshold (MMWT) decreased 1–3 days after LC in rats. Changing the speed and range of stretching showed that muscle injury seldom occurred, except in extreme conditions, and that DOMS occurred in parameters without muscle damage.

The B2 bradykinin receptor—nerve growth factor (NGF) route and COX-2—glial cell line-derived neurotrophic factor (GDNF) route were involved in the development of DOMS.

The interactions between these routes occurred at two levels.

A repeated-bout effect was observed in MMWT and NGF upregulation, and this study showed that adaptation possibly occurred before B2 bradykinin receptor activation.

We have also briefly discussed the prevention and treatment of DOMS.

https://link.springer.com/article/10.1186/s12576-023-00896-y