Impact of Sleep Quality on Cardiovascular Responses to Simulated Hemorrhage in Humans




Hua, Vincent
Barnes, Haley J.
Rosenberg, Alexander
Anderson, Garen K.
Luu, My-Loan
Rickards, Caroline


Journal Title

Journal ISSN

Volume Title



Poor sleep quality may limit cardiovascular responsiveness to physiological stress. We hypothesized that subjects with poor sleep quality would be less tolerant to simulated hemorrhage, which would be associated with lower arterial pressure and cerebral blood flow, and higher heart rates compared to subjects with good sleep quality. Hemorrhage was simulated in 20 human subjects with lower body negative pressure (LBNP). Sleep quality was classified as POOR in 5 subjects (Global Pittsburgh Sleep Quality Index (PSQI) score ≥5), and GOOD in 15 subjects (Global PSQI score < 5). Markers of cardiovascular function were measured continuously throughout the LBNP protocol. Sleep quality had no effect on LBNP tolerance (POOR: 1453±223 s vs. GOOD: 1535±88 s; P=0.34), and there were no differences in the magnitude of central hypovolemia at presyncope (%Δ stroke volume, POOR: -53±8 % vs. GOOD: -49±4 %; P=0.32). However, there were differences in the magnitude of hypotension (%Δ mean arterial pressure, POOR: -18±3 % vs. GOOD: -22±2 %; P=0.08), cerebral blood flow reduction (%Δ MCAv, POOR: -19±6 % vs. GOOD: -28±2 %; P=0.03), and reflex tachycardia (% Δ heart rate, POOR: 103±30 % vs. GOOD: 72±9 %; P=0.09). There was a moderate association between sleep quality and the magnitude of MCAv reduction at presyncope (r=0.53; P=0.02). Sleep quality did not affect tolerance to simulated hemorrhage in healthy human subjects. While there were differences in hemodynamic responses, this may be related to premature termination of the protocol due to early onset of subjective presyncopal symptoms.