Delayed Onset Muscle Soreness and Critical Neural Microdamage-Derived Neuroinflammation
Piezo2 transmembrane excitatory mechanosensitive ion channels were identified as the principal mechanotransduction channels for proprioception. Recently, it was postulated that Piezo2 channels could be acutely microdamaged on an autologous basis at proprioceptive Type Ia terminals in a cognitive dem...
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| Format: | Article |
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MDPI AG
2022-08-01
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| Series: | Biomolecules |
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| Online Access: | https://www.mdpi.com/2218-273X/12/9/1207 |
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| author | Balázs Sonkodi |
| author_facet | Balázs Sonkodi |
| author_sort | Balázs Sonkodi |
| collection | DOAJ |
| description | Piezo2 transmembrane excitatory mechanosensitive ion channels were identified as the principal mechanotransduction channels for proprioception. Recently, it was postulated that Piezo2 channels could be acutely microdamaged on an autologous basis at proprioceptive Type Ia terminals in a cognitive demand-induced acute stress response time window when unaccustomed or strenuous eccentric contractions are executed. One consequence of this proposed transient Piezo2 microinjury could be a VGLUT1/Ia synaptic disconnection on motoneurons, as we can learn from platinum-analogue chemotherapy. A secondary, harsher injury phase with the involvement of polymodal Aδ and nociceptive C-fibers could follow the primary impairment of proprioception of delayed onset muscle soreness. Repetitive reinjury of these channels in the form of repeated bout effects is proposed to be the tertiary injury phase. Notably, the use of proprioception is associated with motor learning and memory. The impairment of the monosynaptic static phase firing sensory encoding of the affected stretch reflex could be the immediate consequence of the proposed Piezo2 microdamage leading to impaired proprioception, exaggerated contractions and reduced range of motion. These transient Piezo2 channelopathies in the primary afferent terminals could constitute the critical gateway to the pathophysiology of delayed onset muscle soreness. Correspondingly, fatiguing eccentric contraction-based pathological hyperexcitation of the Type Ia afferents induces reactive oxygen species production-associated neuroinflammation and neuronal activation in the spinal cord of delayed onset muscle soreness. |
| first_indexed | 2024-03-10T00:37:16Z |
| format | Article |
| id | doaj.art-5d27503679fb4aae9b1f70864ccd022c |
| institution | Directory Open Access Journal |
| issn | 2218-273X |
| language | English |
| last_indexed | 2024-03-10T00:37:16Z |
| publishDate | 2022-08-01 |
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| series | Biomolecules |
| spelling | doaj.art-5d27503679fb4aae9b1f70864ccd022c2023-11-23T15:14:40ZengMDPI AGBiomolecules2218-273X2022-08-01129120710.3390/biom12091207Delayed Onset Muscle Soreness and Critical Neural Microdamage-Derived NeuroinflammationBalázs Sonkodi0Department of Health Sciences and Sport Medicine, Hungarian University of Sports Science, 1123 Budapest, HungaryPiezo2 transmembrane excitatory mechanosensitive ion channels were identified as the principal mechanotransduction channels for proprioception. Recently, it was postulated that Piezo2 channels could be acutely microdamaged on an autologous basis at proprioceptive Type Ia terminals in a cognitive demand-induced acute stress response time window when unaccustomed or strenuous eccentric contractions are executed. One consequence of this proposed transient Piezo2 microinjury could be a VGLUT1/Ia synaptic disconnection on motoneurons, as we can learn from platinum-analogue chemotherapy. A secondary, harsher injury phase with the involvement of polymodal Aδ and nociceptive C-fibers could follow the primary impairment of proprioception of delayed onset muscle soreness. Repetitive reinjury of these channels in the form of repeated bout effects is proposed to be the tertiary injury phase. Notably, the use of proprioception is associated with motor learning and memory. The impairment of the monosynaptic static phase firing sensory encoding of the affected stretch reflex could be the immediate consequence of the proposed Piezo2 microdamage leading to impaired proprioception, exaggerated contractions and reduced range of motion. These transient Piezo2 channelopathies in the primary afferent terminals could constitute the critical gateway to the pathophysiology of delayed onset muscle soreness. Correspondingly, fatiguing eccentric contraction-based pathological hyperexcitation of the Type Ia afferents induces reactive oxygen species production-associated neuroinflammation and neuronal activation in the spinal cord of delayed onset muscle soreness.https://www.mdpi.com/2218-273X/12/9/1207delayed onset muscle sorenessPiezo2 ion channelproprioceptionneuroinflammationnuclear factor-kappa Bnoncontact injury |
| spellingShingle | Balázs Sonkodi Delayed Onset Muscle Soreness and Critical Neural Microdamage-Derived Neuroinflammation Biomolecules delayed onset muscle soreness Piezo2 ion channel proprioception neuroinflammation nuclear factor-kappa B noncontact injury |
| title | Delayed Onset Muscle Soreness and Critical Neural Microdamage-Derived Neuroinflammation |
| title_full | Delayed Onset Muscle Soreness and Critical Neural Microdamage-Derived Neuroinflammation |
| title_fullStr | Delayed Onset Muscle Soreness and Critical Neural Microdamage-Derived Neuroinflammation |
| title_full_unstemmed | Delayed Onset Muscle Soreness and Critical Neural Microdamage-Derived Neuroinflammation |
| title_short | Delayed Onset Muscle Soreness and Critical Neural Microdamage-Derived Neuroinflammation |
| title_sort | delayed onset muscle soreness and critical neural microdamage derived neuroinflammation |
| topic | delayed onset muscle soreness Piezo2 ion channel proprioception neuroinflammation nuclear factor-kappa B noncontact injury |
| url | https://www.mdpi.com/2218-273X/12/9/1207 |
| work_keys_str_mv | AT balazssonkodi delayedonsetmusclesorenessandcriticalneuralmicrodamagederivedneuroinflammation |