1. Introduction

Sleep has the extraordinary ability to reduce negative effects, restore health, and enhance learning and memory. However, in the modern era, achieving high-quality, timely sleep has become increasingly challenging. According to the World Health Organization, around a third of the global population (27%) suffer from sleep disorders. The prevalence of various sleep disorders is even more pronounced in China, where 38.2 percent of people have them, affecting more than 300 million people - more than the global average.

Numerous studies have shown that sleep deprivation has significant effects on cognitive function and neuroplasticity of the brain. Scientists have clarified that lack of sleep leads to the accumulation of toxic beta-amyloid metabolites in the brain and the phosphorylation of tau protein. These processes adversely affect central nervous system plasticity, activate glial cells, trigger nervous system inflammation, induce neuronal DNA damage, and ultimately increase the risk of Alzheimer’s disease. Sleep, once considered a miracle cure, has become a critical issue in protecting cognitive health.

As the brain functions, it constantly produces metabolic waste. However, it is during sleep that the brain activates its “clearing mode.” Lack of sleep leads to a gradual accumulation of metabolic waste in the brain, which leads to progressive damage. In addition, sleep has various effects on our neuroplasticity. Neuroplasticity refers to the ability of the brain to grow, reorganize, and change the structure and function of neural networks.

Our brains remain neuroplastic throughout our lifespan, even in older adults who experience persistent changes due to environmental influences. Notably, experiments on sleep-deprived mice revealed a worrying finding: synaptic proteins no longer follow the expected cyclical pattern. This striking observation strongly suggests that sleep deprivation disrupts the circadian rhythm of synaptic proteins, leading to significant impairment of neuroplasticity.

These interesting findings from previous experiments raise a whole new set of questions. How exactly does sleep affect neuroplasticity? What substances are involved in this complex process? Also, how does sleep regulation intersect with environmental factors? By synthesizing the broader literature and subsequent synthesis of conclusions, we can shed more light on these issues.

These studies and their summary reveal the profound effects of sleep on neural tissue repair and the rebuilding of synaptic connections, providing valuable insights into the underlying processes. These insights not only open up new avenues for clinical treatment, but also provide a solid theoretical foundation for fields such as neurobiology and psychotherapy, providing new perspectives and possibilities for the development of these disciplines.

2. Macro research on neuroplasticity and sleep

2.1. Sleep deprivation reduces concentration

A considerable decline in cognitive performance is linked to ongoing sleep deprivation. There have been several research on how lack of sleep impacts attention, but four key conclusions have emerged. First, lack of sleep causes a general slowing of reactions. Second, lack of sleep makes people more likely to lapse for extended periods of time (>500 ms) and commit mistakes. Third, lack of sleep makes the time-on-task impact in each test bout stronger. Last but not least, PVT findings during prolonged awake point to the existence of coupled circadian and homeostatic sleep drives[1]. Notably, it causes a notable decline in sustained attention, which is defined by a reduced capacity to focus for lengthy periods of time. Furthermore, alert attention, which involves swift responses to stimuli, also experiences a substantial decline, often resulting in an increased error rate in cognitive tasks. It is worth emphasizing that the adverse effects on attention, reaction speed, and error rates become more pronounced with prolonged periods of sleep deprivation, underscoring the cumulative impact of insufficient sleep on cognitive functioning.

Beyond the cognitive realm, sleep deprivation has far-reaching consequences. Research has shown that it not only impairs behavioral attention but also increases the expenditure of physical energy. This heightened energy expenditure can contribute to feelings of fatigue and lethargy, eroding an individual’s motivation for both learning and daily life activities.

Moreover, chronic sleep deprivation has been linked to a higher likelihood of experiencing mood disturbances, such as depression. The persistent lack of restorative sleep can lead to a sense of despondency and a loss of enthusiasm for life and learning, posing significant challenges to overall well-being and quality of life.

2.2. Sleep deprivation affects memory

The influence of sleep on memory is multifaceted and exhibits variability across individuals. In general, sleep is an important process of memory consolidation and information integration, and plays a key role in learning and remembering new knowledge. Empirical research underscores the substantial impact of obtaining sufficient sleep on enhancing memory quality and effectiveness.

Suboptimal sleep patterns can significantly contribute to cognitive impairment, including memory deficits. Typically, these sleep disturbances are associated with irregular dietary habits, disrupted sleep schedules, prolonged wakefulness into late hours, and heightened psychological distress. Sleep, fundamentally, serves as a vital restorative process for the brain, underpinning cognitive functions. Crucially, the process of neuroplasticity, which governs the brain’s capacity to adapt and reorganize, hinges upon the robust delivery of cerebral blood flow. This facilitates the elimination of metabolic waste products while also ensuring the supply of oxygen to active neurons. The cyclical sleep-wake transitions are significantly linked to dynamic changes in cerebral blood flow, and these uncontrollable variations may have a significant impact on the subconscious mechanisms that control neuroplasticity while we sleep [2].

Insufficient amounts of sleep can seriously impede the brain’s ability to repair itself, potentially leading to energy and oxygen deficiencies in the cerebral area. As a consequence, these weaknesses may show up as distractions, slowed intellectual processing, and a noticeable loss in memory performance. The negative effects of sleep deprivation on brain neural activity are the cause of these deficits. Lack of sleep negatively affects the complex web of neural connections and jeopardizes the smooth transfer of information that exists between neurons. As a result, it causes significant cognitive deficits that particularly disrupt memory function.

Lack of sleep additionally has the potential to impact mood stability, heighten stress and anxiety, and hinder the intricate process of memory development and retention. Insufficient sleep for prolonged periods has been associated with impaired cognitive performance and a higher risk of neurodegenerative illnesses like Alzheimer’s. It is important to remember that everyone has different sleep requirements; some people may require less sleep to maintain normal memory function, whilst others may require longer rest several times. Additionally, the quality of sleep has emerged as a significant factor in memory preservation, with continuous deep sleep being essential for memory consolidation.

Therefore, in addition to sleep time, carefully creating a favorable sleep environment and developing healthy sleep habits are crucial to maintaining memory function. If persistent sleep disturbances occur, it is prudent to seek medical guidance for therapeutic interventions such as diazepam and Zopiclone.

In daily life, you should pay attention to your diet, avoid spicy foods, including scallions, ginger, etc., and eat more nutritious foods such as milk and eggs. In addition, proper aerobic exercise before bed, such as yoga or jogging, can be used as an effective way to improve sleep disorders and improve overall sleep quality.

3. Microscopic studies on neuroplasticity and sleep

In previous studies, neuroplasticity can be explained and acted on through these aspects. First, the chronology of the neurophysiological mechanisms implementing neuroplasticity ranges from short-term, transient synaptic strength amendments to longer-term, structural alterations.[3] Second, these components make up the molecular architecture and process of neuroplasticity. Neuroplasticity is facilitated by molecular processes such as synaptogenesis (the establishment of freshly developed synaptic connections), neurogenesis (the proliferation of new neurons), angiogenesis (the formation of new blood vessels), and gliogenesis (the production of non-neuronal glial cells from within the brain).[4] Additionally, the following is a theoretical description of neuroplasticity’s biological structure: Presynaptic changes such as increased neurotransmitter and neurotrophin discharge from the presynaptic neuron, went down neurotransmitter reintroduction and breakdown in the cleft between synaptic neurons, and postsynaptic adaptations that bring about the deposition of extra neurotransmitter receptors on the membrane of the cell are examples of cellular adaptations in response to sensory experience[5].

Table 1. Neurophysiological and molecular measures of neuroplasticity.

BDNF, brain-derived neurotrophic factor; CSP, contralateral silent period; cTBS, continuous theta-burst stimulation; EEG, electroencephalography; ELISA, enzyme-linked immunosorbent assay; ERP, event-related potential; ICF intracortical facilitation; IGF-1, insulin-like growth factor 1; LICI: long-interval intracortical inhibition; M1, primary motor cortex; MEP, motor-evoked potential; PAS, paired-associative stimulation; PNS, peripheral electrical nerve stimulation; RMT, resting motor threshold; rTMS, repetitive TMS; SAI; short-latency afferent inhibition; SICI, short-interval intracortical inhibition; TCD, transcranial doppler, VEGF, vascular endothelial growth factor[6].

Sleep deprivation affects the ability to regulate emotions and causes cognitive decline by reducing the synaptic plasticity of the prefrontal limbic system. Moreover, the loss of synaptic plasticity is linked to three separate types of structural and molecular dysfunction, including reversible blood-brain barrier malfunction, a functional breakdown of neurotransmitter systems, and uneven electrolyte distribution.[7]

4. Research on other influencing factors

4.1. Exercise

Exercise promotes increased neuronal activity throughout the prefrontal limbic system, especially when undertaken at moderate intensity levels. This increase in brain activity supports improved emotional control as well as cognitive function [7]. In order to deal with sleep loss, aerobic exercise is believed to have neuroprotective impact on the microglia-mediated pruning of synaptic connections that takes place in the sleep-deprived brain [8]. Therefore, incorporating aerobic exercise into your daily routine can serve as a valuable strategy for mitigating the adverse effects of sleep deprivation. The cumulative findings and conclusions of these studies highlight the positive effects of sustained daily physical activity on enhancing cortical neuroplasticity. This means that intelligently engaging in physical activity can serve as a means of enhancing neurogenesis and facilitating the construction and repair of synaptic connections, while keeping sleep quality unaffected.

4.2. Diet

Diet is a lifestyle decision that has been demonstrated that it has an impact on brain chemistry and function, which has the potential to alter how neuroplastic the brain is [9,10]. Nutritional therapies that have an impact on cognition and mood consist of calorie restriction, intermittent fasting, as well food supplementation [10].

This intricate web of dietary-sleep interrelationships is exemplified by a comprehensive graduate study that delved into the ramifications of the ketogenic diet on morbidly obese adolescents. The research within demonstrates an intriguing connection between eating habits and the world of sleep. Unexpectedly, the dietary change that caused significant weight loss also resulted in a notable increase in the duration of rapid eye movement (REM) sleep and a discernible decrease in non-rapid eye movement (non-REM) sleep, thereby successfully reestablishing normal sleep patterns. This remarkable change is linked by scientists to the reduction of airway constriction within the sleep cycle, highlighting the complex interaction between eating habits and sleep dynamics [11].

In summation, it is incontrovertibly apparent that the meticulous curation of a health-conscious dietary regimen can wield a salubrious influence on the qualitative attributes of our sleep, thereby potentiating the brain’s intrinsic capacity for neuroplasticity. Thus, the synergistic confluence of diet and sleep emerges as a profound axis through which we may harness and augment the brain’s innate adaptive prowess.

5. Discussion

Based on previous experimental studies and related literature, this paper summarizes the macro and micro understanding of the impact of sleep on neuroplasticity, 1 combining the single factor of sleep with the influence of multiple factors such as environment and diet on neuroplasticity. This paper summarizes and reflects on some relevant theoretical basis: under macro conditions, especially in the state of sleep deprivation, people’s cerebral blood oxygen is reduced, and neurogenesis and synaptic formation are reduced in the state of depression, which shorten the attention span and reaction speed, and even lead to the occurrence of wrong reactions. At the same time, less sleep was frequently connected with improved memory. The findings of linked studies and tests revealed diminished synaptic plasticity in the prefrontal limbic system, impoverished neurotransmitter system function, unequal electrolyte distribution, and reversible blood-brain barrier malfunction. At the same time, sleep is also related to environmental factors such as diet and exercise. Combined with the three, reasonable and effective physical exercise and healthy and appropriate eating habits can help establish high-quality sleep quality, provide protection for us to form healthy and efficient sleep, and then help promote the occurrence of neuroplasticity.

Under the social reality of poor sleep quality and the general reduction of sleep market, the health problems related to sleep have gradually received everyone’s attention, and caused related social hot issues. Under such a background, this review study has enlightenment and practical value from multiple perspectives.

One is multi-factor and realistic treatment intervention. Studies of influencing factors such as exercise and diet highlight the importance of taking a holistic approach to health and the complexity of multiple environmental factors in reality. It recognizes that sleep is not isolated from other aspects of health, but rather interlinked with lifestyle choices. This holistic viewpoint is in line with contemporary medical practice, which seeks to deal with the underlying causes of health issues while also acknowledging that people differ in their sleep needs as well as responses to lifestyle factors. This perspective also allows for a more thorough comprehension of the mechanisms by which exercise and diet affect sleep, as well as a recognition that neuroplasticity may have potential applications in enhancing general health. For example, individuals, healthcare professionals, and public health policymakers can use this knowledge to develop interventions and recommendations tailored to the individual level. Healthcare providers can work with patients to create customized plans to meet their unique sleep, exercise, and dietary requirements, promoting better sleep and cognitive function and optimizing their cognitive and health levels.

The second is prevention and recovery of health. The findings provide insights into preventative measures for cognitive decline and neurodegenerative diseases. Individuals may decrease their chance of contracting illnesses like Alzheimer’s by encouraging regular physical activity and a balanced diet. This proactive strategy may result in more affordable long-term healthcare expenses and enhanced the long-term health outcomes. At the same time, in addition to preventing cognitive decline, this study suggests that lifestyle factors can positively enhance cognitive function. Individuals seeking to improve attention, memory, and overall cognitive performance can incorporate evidence-based practices into their daily lives, potentially improving productivity and quality of life.

Third, promote disciplinary cooperation and public health policies. Research into the interactions between sleep, exercise, diet, and neuroplasticity encourages interdisciplinary collaboration between fields such as neuroscience, nutrition, psychology, and public health. This collaboration could lead to a more complete understanding of the complex relationship between lifestyle choices and brain health. Governments and healthcare organizations can use this knowledge to develop policies that promote healthier living environments, which could include increasing access to exercise facilities, promoting healthier dietary choices, and raising awareness about the importance of sleep.

In conclusion, the study of influencing factors such as exercise and diet provide valuable insights into how individuals can optimize their cognitive health through lifestyle choices. It provides practical strategies for preventing cognitive decline and enhancing cognitive function, which can benefit individuals, healthcare systems, and society as a whole. By recognizing the interconnections between sleep and other aspects of health, this research paves the way for a more comprehensive and proactive approach to health promotion and disease prevention.

6. Conclusion

This paper summarizes the macro and micro understanding of the influence of sleep on neuroplasticity, and also combines the single factor of sleep with the influence of multiple factors such as exercise and diet. There are three conclusions: First, sleep loss will cause a decline in attention and memory, and even lead to the occurrence of wrong reactions. The second is that sleep deprivation impairs neurotransmitter system performance, causes uneven electrolyte distribution, and causes reversible blood-brain barrier malfunction, all of which diminish the prefrontal limbic system’s synaptic plasticity. Third, sleep is closely related to environmental factors such as diet and exercise. Reasonable physical exercise and healthy eating habits can help establish high-quality sleep quality and help promote the occurrence of neuroplasticity.

However, it is worth noting that this paper still has some limitations. First, the article does not describe each mechanism in detail, but ties each study together to summarize cognition from a larger perspective. This form lacks detailed scrutiny and can be a bit jumpy and difficult to understand. Secondly, this paper lacks its own experimental data and relevant clinical data, and does not provide detailed examples and treatment perspectives to verify whether some conclusions can be completely correlated, which may lead to certain errors or one-sidedness of the conclusions. Third, this article only deals with exercise and eating habits, which is incomplete, and looking at more environmental factors may provide more novel perspectives on the relationship between neuroplasticity and sleep.

In future research, there are two possible expectations: one is to add more clinical data or experimental tests on primates to explore more microscopic brain structures, which can deepen the understanding of the correlation between sleep and neuroplasticity, and provide more molecular biological mechanisms and theories. The second is to find more research angles, not only in terms of exercise and diet, but also in terms of psychological states or environmental atmosphere, such as sleep music, white noise and so on.

In summary, this paper summarizes the mechanism of sleep on neuroplasticity and the correlation between the two from macro and micro perspectives, combining the effects of exercise and diet on sleep and neuroplasticity. The interactions between the organism and its environment have gained greater recognition thanks to these summaries. This can provide a neurobiological basis for the study of brain physiological structure and sleep research, and even provide new therapeutic ideas for the clinical treatment of some neurological diseases, and influence the government or relevant institutions to formulate sleep guidance policies to improve the quality of life and health of contemporary people.