AGING AND THE INFLAMMATORY, METABOLIC AND AUTONOMIC RESPONSE TO SLEEP LOSS

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The purpose of this protocol is to investigate the mechanism of increases in inflammation during sleep loss using a 64-hour vigil model because the effects are less influenced by individual differences in resistance to the effects of sleep loss. They hypothesize that sleep loss itself leads to an altered inflammatory homeostasis by placing demands on the autonomic nervous system at a time when the system normally down-regulates, resulting in increased blood pressure, which in turn leads to elevated inflammatory mediators released from both white blood cells, endothelial cells and adipocytes. This study will be a 2x2x2 between groups design with younger (21-40 yrs) and older (50-75 yrs), adipose and lean, sleep versus sleep deprivation. Subjects will be randomly assigned to a sleep or vigilance condition, where they will remain awake for up to 64 hours.