Delayed Onset Muscle Soreness Is, in Fact, Neural Microdamage Rather Than Muscle Damage (2020) Sonkodi et al

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

Abstract

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.
Broken into paragraphs for easier reading.
 
DOMS's is one of my symptoms, it feels exactly the same as the DOM's I get after weight training. When it happens I wake up with my legs feeling sore, as if I was squating or sprinting intensively the previous day.

I always thought it is due to the muscles not getting enough energy or lactic acid build up. But maybe it is just due to problem with the nerves after all.
 
When it happens I wake up with my legs feeling sore, as if I was squating or sprinting intensively the previous day.
Could it be due to contracting or flexing your muscles during the night. I believe that is what is happening to me. I sometimes wake up with sore and tight muscles and feels like I had been flexing them all night. I can replicate or intensify the feeling by temporarily flexing the muscles for a bit. I have no idea why i'd be so tense while I'm sleeping.
 
Could it be due to contracting or flexing your muscles during the night. I believe that is what is happening to me. I sometimes wake up with sore and tight muscles and feels like I had been flexing them all night. I can replicate or intensify the feeling by temporarily flexing the muscles for a bit. I have no idea why i'd be so tense while I'm sleeping.
I know my muscles do badly with static stress. That is when they have to supply constant low level contraction for long periods of time. Stress on muscles from postural factors, including when sleeping, can lead to unending pain for me. So can voluntary static muscle load.
 
Some interesting ideas, and definitely worth studying, but I'm not convinced the issue of pain sensation is just in the muscle spindles themselves.
For example, pain thresholds in muscle fascia have been shown to be increased due to DOMS, https://pubmed.ncbi.nlm.nih.gov/25519953/
Type II sensory fibers are focused on proprioception, rather than pain per se.

The authors propose a curious gating/feedback mechanism to explain how both could be true, but this remains to be seen.

I also suggest the associated sense of muscle stiffness can be due to an alteration of gamma motor drive, and thus gamma tone (which usually occurs as a central compensation when there are increased propropceptive prediction errors), or the gamma motor units are injured or fatigued and not responding as well as usual.

There are also feedback loops between antagonistic muscles and resulting muscle spindle sensitivity. https://www.jneurosci.org/content/34/41/13644
This balance could presumably be disturbed due to the hypothesised mechanical damage too.
 
Some interesting ideas, and definitely worth studying, but I'm not convinced the issue of pain sensation is just in the muscle spindles themselves.
For example, pain thresholds in muscle fascia have been shown to be increased due to DOMS, https://pubmed.ncbi.nlm.nih.gov/25519953/
Type II sensory fibers are focused on proprioception, rather than pain per se.

The authors propose a curious gating/feedback mechanism to explain how both could be true, but this remains to be seen.

I also suggest the associated sense of muscle stiffness can be due to an alteration of gamma motor drive, and thus gamma tone (which usually occurs as a central compensation when there are increased propropceptive prediction errors), or the gamma motor units are injured or fatigued and not responding as well as usual.

There are also feedback loops between antagonistic muscles and resulting muscle spindle sensitivity. https://www.jneurosci.org/content/34/41/13644
This balance could presumably be disturbed due to the hypothesised mechanical damage too.

I have a friend who is struggling with back pain. He tells me that it may not be damage but perception. So your body sets the amplitude of the output (pain level) rather that it being solely related to damage muscles etc.

Having skimmed the abstract for maybe 60 seconds, I recall Jaime Seltzer's (ME Action) advice (re GET) is there a testable hypothesis? Can any of this be measured?

Ron Tompkins's group (OMF Harvard) were due to start working on muscle biopsy's (with UK researchers). Any of this related to Ron's proposed work on muscle biopsy's?

Any of this tested via the genetics (GWAS) study? E.g. is there anything organic which would link to a particular gene?
 
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