Insufficient sleep, defined as less than 7 hours per night for adults, is associated with a myriad of health-related problems, including cardiovascular and neurodegenerative disease. In this study we are investigating the effects of one night of partial sleep deprivation (2 hours sleep) on cerebrovascular and respiratory function, in healthy adults. The findings from this ‘proof-of-concept’ and mechanistic study will contribute to our understanding of how insufficient sleep can contribute to cerebrovascular and/or neurovascular degenerative disease. Specifically, we are investigating a novel pathway by which insufficient sleep may exacerbate severity of sleep disordered breathing (e.g. obstructive sleep apnea) – through interactions of cerebral blood flow and respiratory control. This study is grounded under the rationale and hypothesis that a single night of short sleep will acutely increase sympathetic nervous activity (SNA), which in turn will decrease the cerebrovascular reactivity (blood flow responses) to changes in CO2 through the tonic vasoconstrictor properties of SNA. The impaired cerebrovascular reactivity will cause a larger ventilatory response to changes in CO2 through increased accumulation of cerebral hydrogen - a phenomenon known as an increased ventilatory loop gain. The heightened ventilatory loop gain is an established factor for sleep disordered breathing severity, which, itself is a known cause of insufficient sleep. This study may therefore unravel the feed-forward sequela of insufficient sleep / sleep disordered breathing, and provide mechanistic insight into novel targets for improving health in conditions of impaired sleep – that is through interventions aimed at improving the cerebral blood flow.