Effects of Acute Partial Sleep Deprivation and High-Intensity Interval Exercise on Postprandial Network Interactions

Introduction: High-intensity interval exercise (HIIE) is deemed effective for cardiovascular and autonomic nervous system (ANS) health-related benefits, while ANS disturbance increases the risk for cardiovascular disease (CVD). Postprandial lipemia and acute-partial sleep deprivation (APSD) are considered as CVD risk factors due to their respective changes in ANS. Exercising in the morning hours after APSD and have a high-fat breakfast afterwards may alter the interactions of the cardiovascular, autonomic regulation, and postprandial lipemic systems threatening individuals’ health. This study examined postprandial network interactions between autonomic regulation through heart rate variability (HRV) and lipemia via low-density lipoprotein (LDL) cholesterol in response to APSD and HIIE. Methods: Fifteen apparently healthy and habitually good sleepers (age 31 ± 5.2 SD yrs) completed an acute bout of an isocaloric HIIE (in form of 3:2 work-to-rest ratio at 90 and 40% of VO(2) reserve) after both a reference sleep (RSX) and 3–3.5 h of acute-partial sleep deprivation (SSX) conditions. HRV time and frequency domains and LDL were evaluated in six and seven time points surrounding sleep and exercise, respectively. To identify postprandial network interactions, we constructed one correlation analysis and one physiological network for each experimental condition. To quantify the interactions within the physiological networks, we also computed the number of links (i.e., number of significant correlations). Results: We observed an irruption of negative links (i.e., negative correlations) between HRV and LDL in the SSX physiological network compared to RSX. Discussion: We recognize that a correlation analysis does not constitute a true network analysis due to the absence of analysis of a time series of the original examined physiological variables. Nonetheless, the presence of negative links in SSX reflected the impact of sleep deprivation on the autonomic regulation and lipemia and, thus, revealed the inability of HIIE to remain cardioprotective under APSD. These findings underlie the need to further investigate the effects of APSD and HIIE on the interactions among physiological systems.