Abstract
Delayed onset muscle soreness (DOMS) is hypothesized to be caused by glutamate excitotoxicity-induced acute compression axonopathy of the sensory afferents in the muscle spindle. Degeneration of the same sensory afferents is implicated in the disease onset and progression of amyotrophic lateral sclerosis (ALS). A series of “silent” acute compression proprioceptive axonopathies with underlying genetic/environmental factors, damaging eccentric contractions and the non-resolving neuroinflammatory process of aging could lead to ALS disease progression. Since the sensory terminals in the muscle spindle could not regenerate from the micro-damage in ALS, unlike in DOMS, the induced protective microcircuits and their long-term functional plasticity (the equivalent of the repeated bout effect in DOMS) will be dysfunctional. The acute stress invoking osteocalcin, bradykinin, COX1, COX2, GDNF, PGE2, NGF, glutamate and N-methyl-D-aspartate (NMDA) receptors are suggested to be the critical signalers of this theory. The repeated bout effect of DOMS and the dysfunctional microcircuits in ALS are suggested to involve several dimensions of memory and learning, like pain memory, inflammation, working and episodic memory. The spatial encoding of these memory dimensions is compromised in ALS due to blunt position sense from the degenerating proprioceptive axon terminals of the affected muscle spindles. Dysfunctional microcircuits progressively and irreversibly interfere with postural control, with motor command and locomotor circuits, deplete the neuroenergetic system, and ultimately interfere with life-sustaining central pattern generators in ALS. The activated NMDA receptor is suggested to serve the “gate control” function in DOMS and ALS in line with the gate control theory of pain. Circumvention of muscle spindle-loading could be a choice of exercise therapy in muscle spindle-affected neurodegenerative diseases.
Highlights
Delayed onset muscle soreness (DOMS) is defined by delayed onset soreness, muscle stiffness, loss of force-generating capacity, reduced joint range of motion and decreased proprioceptive function [1]
The author of this paper proposes that acute stress response (ASR) could be such a homeostatic driver as well, conducted by the direct sympathetic innervation of the muscle spindles [55]
Acute compression sensory axonopathy, caused by eccentric contractions under ASR, induced microcircuit dysfunction, environmental and genetic factors and an escape from homeostasis mean eventually a point of no return in the case of muscle-spindleaffected neurodegenerative diseases, due to the “silent” detachment of peripheral sensory nerves in the muscle spindle, while regeneration and functional restitution prevail in DOMS
Summary
Delayed onset muscle soreness (DOMS) is defined by delayed onset soreness, muscle stiffness, loss of force-generating capacity, reduced joint range of motion and decreased proprioceptive function [1]. Vaughan et al [10] have noted in animal studies that significant structural changes are present in the sensory terminals of the muscle spindle before the onset of the symptoms of ALS, and these changes happen independently of the degeneration of α-motoneurons (α-MNs). According to a new theory [13], DOMS is an acute compression axonopathy at the proprioceptive sensory terminals in the muscle spindle. The contribution of these large fiber sensory afferents to DOMS was demonstrated in 2001 [14]. Both ALS and DOMS are proposed to have impairment at the proprioceptive sensory terminals in the muscle spindle. The critical path of this ALS dying-back injury mechanism theory points toward the muscle spindle-derived sensory degeneration-induced non-resolving impairment of the proprioceptive circuitry
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