## 1 Introduction  
Cyclical fluctuations in intensity during the day, called circadian rhythms, are observed in a wide variety of human physiological processes: from behavioral responses, motor activity, and sleep-wake cycle to cycles of hormone secretion, such as melatonin, cortisol, and thyroid-stimulating hormones. Ambient light is a major synchronizer (Zeitgeber) of the circadian system. Daily exposure to natural light corrects the endogenous period of biological rhythms, which is not exactly 24 h, but about 24.2 h [1]. These processes are realized due to neural pathways coming from melanopsin-containing retinal ganglion cells (mRGCs), which are photoreceptors of the human circadian system. mRGCs constitute 1-2% of all retinal ganglion cells, their axons form a retinohypothalamic tract, which monosynaptically connects these cells with the center of circadian regulation, located in the suprachiasmatic nuclei of the hypothalamus (SCN). mRGCs transmit to SCN information about changes in environment illumination, due to which the cyclic change in the activity of molecular and biochemical reactions and, as a consequence, in physiological processes of the organism during the day take place [2]. The maximum sensitivity of circadian retinal photoreceptors lies in the range of the visible light spectrum with a peak wavelength of 480 \(\pm\) 5 nm [3,4]. The SCN of the anterior hypothalamus serves as a central biological clock, synchronizing the peripheral clock presented in almost every tissue and organ system [5]. The evolution of the circadian and stress-realizing systems has contributed to the adaptation of the human body to repeated and spontaneous changes in the environment and to maintaining functional stability. These adaptive systems are interconnected, and the balance of their interaction determines the state of human health. It is known that stress can have a significant impact on the circadian system and can potentially lead to reversible or persistent disturbances in circadian rhythms [6]. Impaired clock gene expression, in turn, causes changes in the functioning of the hypothalamic-pituitary-adrenal axis. For example, a deficiency of BMAL1 and CLOCK proteins in mice with mutations in corresponding circadian genes (Bmal1 and Clock) results in a significant decrease in the overall level and disruption of the rhythmicity of glucocorticoid secretion [7]. In contrast, null mutations in Cryptochrome or Period genes in mice lead to an increase in glucocorticoid secretion against the background of changes in its rhythm [8,9]. A study in healthy volunteers (N = 14, age 20-41) showed that acute total sleep deprivation (for 40 h) significantly increased cortisol levels (\(p<0.0001\)), while chronic circadian shift (during 25 days) significantly reduced the level of this hormone (\(p<0.05\)). Thus, acute and chronic desynchronosis have opposite effects on the level of stress hormones [10]. [PERSON] and colleagues have shown that circadian disturbances, in addition to a number of metabolic changes in animals, cause changes in the cellular morphology of the prefrontal cortex, which plays a key role in the implementation of cognitive functions. The described impairments are similar to those in chronic stress, which confirms the influence of the circadian system on neural networks that regulate cognitive activity [11]. The response of an organism to a circadian shift depends on various factors, such as the timing of experiments, characteristics of the light flux, and the initial functional state of the subject. However, the mechanisms behind the corresponding effects are not yet fully understood [12]. There is a lack of scientific publications dedicated to investigating the impact of blue light stimulation of the retinal circadian photoreceptors on the systemic mechanisms of human cardiac activity regulation, particularly considering individual stress resistance under conditions of cognitive load [13, 14, 15].