The Effects of Sleep After Delayed-onset Muscle Soreness, a Comparative Study

Delayed onset muscle soreness (DOMS) represents a phenomenon characterised by a range of symptoms, encompassing varying degrees of muscle stiffness and pain, from mild to severe, with the potential to cause considerable functional impairment. This may be attributed to muscle damage and subsequent inflammation resulting from eccentric contractions or activities of an unusually intense nature. In accordance with these principles, exercise-induced DOMS typically manifests following an abrupt increase in exercise intensity, the execution of unconventional exercise movements, and most notably, following the performance of exercises that necessitate eccentric muscle actions . DOMS frequently results in a reduction in muscle function, including a decline in strength, a narrowing of the range of motion, increased pain sensitivity, and a decrease in the intensity of proprioception sensations within a period of 24 to 72 hours, with the potential for these effects to persist for several days. The processes underlying of DOMS comprise overstretching of sarcomeres, mechanical stresses in muscle structures, overlaps and disruption of filaments, and reactions of biochemical that affect contractile structures of muscle. Furthermore, inflammatory processes linked to oxidative stress and an increased pain receptors sensitivity is additional factors contributing to the development of DOMS .

One of the most significant factors affecting pain is sleep. Those suffering from persistent pain consistently indicate inferior sleep quality in comparison to controls , and a direct correlation has been observed between the quality of sleep and the severity of pain experienced by individuals. It is established in the literature that the sensitisation of pain mechanisms is raised in both intervention models of acute pain and chronic pain. Furthermore, individuals who experience primary insomnia without pain report heightened sensitivity to pain and an increased frequency of spontaneous pain episodes compared to control subjects. The findings of experimental studies indicate that sleep disruption in healthy individuals is linked to a considerable rise in pain sensitivity, potentially associated with elevated serum concentrations of pro-inflammatory biomarkers, even in the absence of tissue damage. This results in a vicious cycle of pain and sleep disorders, with each condition precipitating the other, thereby rendering the problem challenging to comprehend.