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. Recent studies have shown that mediators of inflammation, useful in predicting risk of developing cardiovascular disease in healthy asymptomatic individuals, are also increased by experimental sleep deprivation. Low basal increases in inflammatory markers are also seen in 'metabolic syndrome' and the researchers hypothesize that inadequate or insufficient sleep may be a pivotal contributing factor in the development of metabolic syndrome. The researchers hypothesize that basal changes in inflammation are actually secondary to cardiovascular factors associated with shear stress, using a placebo controlled study where the increase of blood pressure that is known to ensue during sleep deprivation is experimentally clamped, through the use of a beta blocker. They expect that blocking sleep deprivation associated increase in blood pressure will prevent the rise of inflammatory markers. They will also test the hypothesis that moderately adipose individuals are at greater risk to suffer the inflammatory and autonomic consequences of acute sleep deprivation. In screening date from this study, the relationship between adiposity, cardiovascular fitness, C-reactive protein, and habitual sleep duration and quality will be loo
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