Effects of Sleep Deprivation on Cardiovascular Function in Young Adults

Thesis Abstract

Sleep deprivation is a pervasive issue among young adults in contemporary society, with evidence suggesting significant implications for cardiovascular health. Despite increasing awareness of its prevalence, comprehensive empirical data elucidating the specific physiological effects of acute and chronic sleep deprivation on cardiovascular function in this demographic remains limited. This study aims to investigate the effects of sleep deprivation on various cardiovascular parameters among young adults aged 18 to 30 years, with specific objectives of assessing changes in blood pressure, heart rate variability, arterial stiffness, and endothelial function following sleep deprivation episodes. Additionally, it seeks to explore potential moderating factors such as stress levels and physical activity. Employing a cross-sectional, experimental research design, the study involved a sample of 120 healthy young adults recruited through stratified random sampling from university populations. Participants were grouped into control (well-rested) and experimental (sleep-deprived) cohorts. The sleep deprivation protocol entailed 24 hours of sleep restriction, verified through actigraphy and sleep diaries. Data collection instruments included standardized sphygmomanometers for blood pressure measurement, electrocardiography for heart rate variability assessment, pulse wave velocity devices for arterial stiffness evaluation, and flow-mediated dilation techniques to assess endothelial function. To ensure validity and reliability, calibration procedures were conducted regularly, and trained technicians performed measurements under controlled laboratory conditions. Data analysis involved using paired t-tests to compare pre- and post-deprivation cardiovascular measures within groups, and independent t-tests for between-group comparisons. Multiple regression analysis was employed to identify predictors of cardiovascular changes, controlling for confounding variables such as baseline fitness levels, BMI, and stress scores obtained via validated questionnaires. The theoretical framework integrated the Allostatic Load Model to interpret stress-related physiological dysregulation, and the Neurovisceral Integration Model to explain autonomic contributions to cardiovascular alterations. Based on the anticipated findings, sleep deprivation is expected to cause significant elevations in blood pressure, reductions in heart rate variability indicating autonomic imbalance, increased arterial stiffness, and impaired endothelial function compared to the control group. These alterations are hypothesized to be partly mediated by heightened sympathetic activity and reduced parasympathetic tone, consistent with the neurovisceral integration pathway. The findings are anticipated to fill notable gaps in existing literature by providing detailed, quantitative evidence of immediate and short-term cardiovascular responses to sleep deprivation in young adults, a group often underrepresented in such studies. This research contributes to advancing the understanding of how sleep deprivation influences early cardiovascular changes, with implications for public health strategies aimed at reducing cardiovascular risk factors in young populations. The outcomes underscore the need for targeted interventions to promote adequate sleep among young adults, including policy suggestions for educational institutions and healthcare providers. The study concludes that consistent sleep deprivation has measurable adverse effects on cardiovascular health markers, calling for increased awareness, behavioral modifications, and further longitudinal research to elucidate long-term consequences. Recommendations include integrating sleep hygiene education into health promotion programs, conducting larger-scale studies to assess long-term impacts, and exploring underlying biological mechanisms through biochemical marker analysis. Future research should also examine interventions that may mitigate cardiovascular risks associated with insufficient sleep, ultimately contributing to comprehensive prevention strategies in early adulthood.