Exercise therapy in the application of sleep disorders

Abstract

Sleep disorders often accompany neurological injuries, significantly impacting patient recovery and quality of life.The efficacy and adherence of traditional treatment methods have certain limitations. Exercise has been found to be a highly beneficial treatment method, capable of preventing and alleviating neurological injuries and sleep disorders. This article reviews relevant research findings from both domestic and international sources over the past few decades, systematically summarizing and analyzing the application of exercise therapy in sleep disorders,strategy of exercise intervention program and the potential molecular mechanisms by which exercise therapy improves sleep disorders. Shortcomings in current research and suggestions are presented, providing a reference for future in-depth studies on exercise interventions for sleep disorders.

Keywords: exercise therapy; molecular mechanisms; neurological injuries; sleep disorders; sleep–wake regulation.

Figure 1

The three-factor model of sleep disorders (32): predisposing factors: these refer to an individual’s vulnerability or predisposition to developing insomnia. They include age, sex, heightened arousal, an anxious personality type, familial or personal history of sleep disorders, and genetic factors such as the presence of the short allele of the serotonin transporter gene. Precipitating factors: these are the specific triggers that lead to the onset of insomnia. Research has identified stress as one of the key risk factors in the development of sleep disorders (51, 52). Individuals are more likely to experience sleep disorders when faced with life stressors and strains, such as illness, separation, or prolonged occupational pressures. Perpetuating factors: these are the psychological and behavioral elements that allow the symptoms of insomnia to persist or even exacerbate. Factors such as irregular sleep habits (like extended time in bed) and fears regarding insomnia play a role in maintaining and prolonging the existence of sleep disorders over time. Threshold: equivalent to a dividing line for each of the 3 factors in this, varies from person to person and from time to time, but any time one of them exceeds the threshold, it can lead to sleep disorders. Acute insomnia: a form ofnon-organic insomnia that lasts less than a month. Early insomnia: difficulty falling asleep or easy awakening in the context of shorter, poorer quality sleep, usually of shorter duration and with less impact on daily life. Chronic insomnia: sleep disorders need to occur at least 3 nights per week for at least 3 months.

Figure 2

The brain’s circadian rhythm regulator is located within the Suprachiasmatic Nucleus (SCN) and is greatly influenced by light and external environments. The intrinsically photosensitive retinal ganglion cells (ipRGCs) are responsible for receiving signals and sending them to the SCN. The SCN integrates and coordinates external input rhythms (such as sleep–wake cycles, eating-feeding cycles, and activity-rest cycles) to control the balance of bodily states, including heart rate, body temperature, and hormone levels. Melatonin is a light signaling hormone secreted by the pineal gland, and its biosynthesis is closely linked to the photoperiod. Melatonin mainly regulates the sleep phase, and the level of melatonin at night directly affects the quality of sleep. Reduced melatonin levels are one of the most important signs of sleep disorders and a series of dysfunctions.