Background and hypothesisPhysical activity (PA) is an important behavioral factor associated with the quality of life and healthy longevity. We hypothesize that extremely low and extremely high levels of daily PA (including occupational PA) may have a negative impact on sleep quality and psychological well-being.ObjectiveThe aim of the study is to investigate the association between the level and type of PA and sleep problems in adult population.Materials and methodsThe sample of the study consisted of the participants from the population-based cohort of The Epidemiology of Cardiovascular Risk Factors and Diseases in Regions of the Russian Federation Study (ESSE-RF). The data of three regions (Saint Petersburg, Samara, Orenburg), varying in geographic, climatic, socioeconomic characteristics, was included into analysis. The total sample consisted of 4,800 participants (1,600 from each region; 1,926 males, 2,874 females), aged 25–64. The level of PA was evaluated using three parameters: the type of PA at work, the frequency of an intensive/high PA including sport (times a week), the mean duration of leisure-time walking (minutes a day). The measures of sleep quality were sleep duration and the frequency of difficulty falling asleep, difficulty maintaining sleep, daytime sleepiness, and sleep medication use. PA and sleep characteristics were assessed by interview carried by the trained medical staff.ResultsWhen controlling for gender, age and socioeconomic status (SES) extremely high occupational PA was a significant risk factor for difficulty falling asleep three or more times a week [OR(CI95%) = 1.9(1.2–3.0), p = 0.003] while working in a sitting position or having moderate physical load at work were not associated with sleep characteristics. Having a high physical load six or more times a week was a risk factor for difficulty falling asleep controlling for gender, age and SES [OR(CI95%) = 1.9(1.4–3.4), p = 0.001]. The association between leisure-time walking and sleep characteristics was insignificant. Walking less than an hour a day was associated with increased depression scores (46.5 vs. 41.9%, p = 0.006).ConclusionHigh physical load at work and excessively frequent intensive PA are associated with difficulties initiating sleep and may represent a risk factor for insomnia.

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The interaction between cardiovascular and respiratory systems is a reciprocal one mediated by mechanical factors, autonomic nervous system, and baroreflex regulation and manifested in the changes in heart rate, blood pressure and ventilation. These changes can be rather easily registered and measured, which opens the opportunity for clinical use (both in diagnostics and therapy). In the paper we briefly review the potential role and implementation of cardiorespiratory biofeedback in treating patients with neurological diseases, in particular, stroke survivors. The available evidence suggests that this method based on the existing cardiorespiratory coupling mechanisms may prove its efficacy in treating a range of medical conditions including cerebrovascular disorders. The prospects of cardiorespiratory biofeedback application in improving a stroke patient's quality of life (including physical, emotional, and cognitive levels) and clinical status require further investigation. The topicality of determining the long-term effect of novel non-pharmacological interventions as an adjunct to conventional therapies is defined by their limitations and significant pharmacological load.

The authors describe two approaches to the classification of insomnia - one was presented in earlier works, the other is currently accepted in the medical scientific community. The following three models of the etiopathogenesis of insomnia are considered: a 3-P model that identifies predisposing, precipitating, and perpetuating factors as the key ones in the development and chronicity of insomnia; a hyperarousal model that defines psychological and neurobiological hyperarousal as a factor contributing to the development of insomnia; and a sleep reactivity to stress model, according to which the pronounced premorbid sleep reactivity to stress increases the risk of developing insomnia. Hyperarousal and sleep reactivity to stress are supposed to be autonomous yet equally predisposing factors of insomnia which act reciprocally and can simultaneously contribute to the development of stress-induced insomnia. It is noteworthy that the clinical usefulness of the sleep reactivity to stress model can extend beyond the preliminary assessment of the risk of insomnia development and be used for screening patients in remission who may be at increased risk of recurrence in future and should receive supportive treatment to minimise this risk. At present, it remains unclear whether hyperarousal is the core of the disorder, its cause, risk factor, or epiphenomenon. Further investigations are required to clarify the psychological and biological basis of chronic insomnia and confirm its current theoretical and conceptual models.