Post Orgasmic Illness Syndrome (POIS) and Delayed Onset Muscle Soreness (DOMS): Do They Have Anything in Common?

Abstract

Post orgasmic illness syndrome is a rare, mysterious condition with an unknown pathomechanism and uncertain treatment. The symptoms of post orgasmic illness syndrome last about 2–7 days after an ejaculation. The current hypothesis proposes that the primary injury in post orgasmic illness syndrome is an acute compression proprioceptive axonopathy in the muscle spindle, as is suspected in delayed onset muscle soreness. The terminal arbor degeneration-like lesion of delayed onset muscle soreness is theorized to be an acute stress response energy-depleted dysfunctional mitochondria-induced impairment of Piezo2 channels and glutamate vesicular release. The recurring symptoms of post orgasmic illness syndrome after each ejaculation are suggested to be analogous to the repeated bout effect of delayed onset muscle soreness. However, there are differences in the pathomechanism, mostly attributed to the extent of secondary tissue damage and to the extent of spermidine depletion. The spermidine depletion-induced differences are as follows: modulation of the acute stress response, flu-like symptoms, opioid-like withdrawal and enhanced deregulation of the autonomic nervous system. The longitudinal dimension of delayed onset muscle soreness, in the form of post orgasmic illness syndrome and the repeated bout effect, have cognitive and memory consequences, since the primary injury is learning and memory-related.

Significantly Delayed Medium-Latency Response of the Stretch Reflex in Delayed-Onset Muscle Soreness of the Quadriceps Femoris Muscles Is Indicative of Sensory Neuronal Microdamage

“…However, the exact mechanism of DOMS is still far from entirely explored. Several theories are currently running, such as lactic acid, muscle spasm, inflammation, connective tissue damage, muscle damage, enzyme efflux and, most recently, proprioceptive terminal microdamage or transient Piezo2 channelopathy theory [ 3 , 4 , 5 ], but no single theory or factor has answered the problem entirely. It is notable that DOMS is not the same as pain experienced during or immediately after exercise [ 6 ].…”

“…On the contrary, a newly published acute non-contact compression axonopathy hypothesis of DOMS postulates that the critical cause could be the mechano-energetic microdamage of the proprioceptive neuron terminals in the muscle spindles due to a cognitive-demand-derived acute stress response on top of unaccustomed or strenuous repetitive eccentric contractions [ 4 ]. Later, it was hypothesized that the locus of this causal neuron terminal microdamage is on Piezo2 ion channels, in the form of a transient Piezo2 channelopathy [ 5 ]. Moreover, recent hypotheses suggest that delayed-onset muscle soreness is an analogous bi-phasic non-contact injury mechanism, such as non-contact anterior cruciate ligament (ACL) injury and post-orgasmic illness syndrome (POIS), where the primary microinjury is a proprioceptive Piezo2 channelopathy and the secondary injury is harsher tissue damage due to the loss of proprioception [ 4 , 5 , 11 ].…”

“…Later, it was hypothesized that the locus of this causal neuron terminal microdamage is on Piezo2 ion channels, in the form of a transient Piezo2 channelopathy [ 5 ]. Moreover, recent hypotheses suggest that delayed-onset muscle soreness is an analogous bi-phasic non-contact injury mechanism, such as non-contact anterior cruciate ligament (ACL) injury and post-orgasmic illness syndrome (POIS), where the primary microinjury is a proprioceptive Piezo2 channelopathy and the secondary injury is harsher tissue damage due to the loss of proprioception [ 4 , 5 , 11 ]. Indeed, Piezo2 has been shown to be the principal mechano-transduction channel for proprioception and contributes to vibration sensing and touch discrimination [ 12 , 13 , 14 ].…”

Mechanisms of Peripheral and Central Pain Sensitization: Focus on Ocular Pain

“…Under neuropathic cornea disease, somatosensory PIEZO2 channels could be microinjured mechano-energetically and could alter genetically preprogrammed reflexes with longitudinal central nervous system consequences. The repetitive reinjury of PIEZO2 channels could cause chronic pain even in the absence of secondary harsher tissue injury ( Sonkodi et al, 2021a ; Sonkodi et al, 2021b ).…”

Finishing stationary cycling too early after anterior cruciate ligament reconstruction is likely to lead to higher failure

“…An earlier finding is that long-term or extended, but light to moderate concentric exercise could alleviate the symptoms of the chronic dimension of this type of proprioceptive terminal microdamage or axonal injury [ 4 , 35 ]. These mechano-energetic TAD like lesions seem to be the consequence of an acute stress reaction (ASR) induced mitochondrial energy depletion and mechanical Piezo2 ion channel microdamage, happening in unaccustomed or strenuous eccentric, learning related, exercise moments [ 4 , 12 , 36 ]. Therefore, the proposed strategy is to keep the mitochondrial ‘breathing capacity’ of these impaired proprioceptive axon terminals and axons in good shape or even enhance it with concentric training for at least a year or even longer, otherwise their functional regeneration could be compromised and the longitudinal memory consolidation will be facilitated.…”