Author Topic: Delayed Onset Muscle Soreness Is, in Fact, Neural Microdamage Rather Than Muscle  (Read 13150 times)

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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


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.

6. Conclusions

According to our hypothesis, DOMS is an acute compression axonopathy of the nerve terminals in the muscle spindle caused by the repetitive superposition of compression with a coinciding cognitive demand, coupled with possible microinjury to the surrounding tissues and enhanced by immune-mediated inflammation. Our theory states that DOMS happens only if the superposition of compression reaches the muscle spindle and microinjures the nerve terminals under cognitive demand. The cornerstones of our hypothesis are as follows:

    DOMS could be an acute compression axonopathy of the nerve endings in the muscle spindle,

    The cause of DOMS could be the repetitive superposition of compression under cognitive demand and a resultant metabolic insult,

    DOMS could be initiated from the muscle spindle,

    The fluid cavity in the muscle spindle could play an important functional role in DOMS,

    Mitochondrial electron transport chain generated free radical involvement is suspected with a TAD-like lesion in the acute axonopathy of the sensory nerve endings in DOMS,

    Unaccustomed or strenuous eccentric exercise-induced SNS activity could be an essential underlying factor in DOMS initiation,

    DOMS could be initiated earlier than it is experienced, but at the beginning, it is suppressed by SNS activity,

    Delayed onset of soreness could be a result of the hypoalgesic state of the ‘closed gate’ caused by the enhanced firing of the microinjured Type Ia sensory fibers in addition to the initial SNS suppression,

    There could be a cross-talk on the PGE2 level between the pain pathways,

    Hyperexcited microinjured Type II sensory fibers in the muscle spindle could override, with the possible help of SNS, the conduction velocity reducing microinjured Type Ia sensory fibers’ inhibition with a delayed onset. The result will be an ‘open gate’ in the dorsal horn and the pathway to hyperalgesia in DOMS,

    Keeping a ‘closed gate’ with concentric exercise could have importance in non-pharmacological disease and neuropathic pain management by simultaneously alleviating pain and enjoying the positive anti-inflammatory characteristics of exercise; therefore, we call it a ‘closed gate exercise’,

    DOMS could cause a transient increase of the blood–spinal cord barrier and selective muscle spindle barrier permeability,

    DOMS could be a safety function in repetitive eccentric contractions as it resolves when the microinjury of the muscle spindle afferent sensory and motoneuron nerve endings are regenerated,

    Finally, we suspect that DOMS could play an important role in ontogenesis by triggering muscle growth and adapting the nervous system in the growth process.

The variability of timelines and symptoms of DOMS, after initiation, will depend on how pervasive the injury is to the surrounding tissues and what tissues are affected. The individual differences could be explained by the complexity of pathways and cross-talking of the microinjured tissues and immune systems. The type and duration of eccentric exercise, trained status, age, genetics, and underlying allergies and low-grade inflammation or diseases could also affect the timelines and the extent of symptoms in DOMS.