Core Viewpoint - The research highlights the mitochondrial origins of sleep pressure, suggesting that sleep is not merely a resting state for the brain but a crucial maintenance process for the body's energy supply system [4][11]. Group 1: Research Findings - A study published in Nature reveals that sleep pressure arises from ATP surplus in specific brain cells, indicating a physical basis for sleep drive [4]. - The research team conducted a comparative analysis of the single-cell transcriptome characteristics of fruit flies under sufficient sleep and sleep deprivation, finding significant gene expression changes related to mitochondrial respiration and ATP synthesis in sleep-deprived flies [6][11]. - Mitochondrial fragmentation and increased mitochondrial-autophagy were observed in affected neurons, which could be reversed by restoring sleep [6][9]. Group 2: Mechanisms of Sleep Regulation - The study found that mitochondrial dynamics (fusion and fission) significantly influence the excitability of sleep-regulating neurons, thereby affecting sleep demand [9][11]. - During wakefulness, especially under sleep deprivation, the activity of these neurons is suppressed, leading to increased ATP concentration due to reduced consumption [9]. - Manipulating mitochondrial dynamics can either enhance or reduce sleep duration, indicating a direct link between mitochondrial function and sleep regulation [9][11]. Group 3: Implications and Future Directions - The findings provide insights into the relationship between metabolism, sleep, and lifespan, suggesting that sleep may be an unavoidable byproduct of aerobic metabolism, similar to aging [10][11]. - The research opens new avenues for understanding sleep disorders and their potential interventions by targeting mitochondrial function in specific neurons [11].