Key result
Acoustically induced arousals from sleep increased systolic blood pressure and low-frequency heart rate variability power, which remained above baseline for up to 40 seconds.
Why the study?
How do acoustically induced arousals from sleep affect heart rate and blood pressure variability in normal humans?
Observational (n=16)
How do acoustically induced arousals from sleep affect heart rate and blood pressure variability in normal humans?
Arousal from sleep causes prolonged sympathoexcitation, suggesting repetitive arousals could have cumulative cardiovascular effects.
Answers are grounded in this paper and cite their sources.
Does not support practice changes in sleep or CV care; leaves open clinical relevance of dynamic HRV/BPV measures.
We performed time-varying spectral analyses of heart rate variability (HRV) and blood pressure variability (BPV) recorded from 16 normal humans during acoustically induced arousals from sleep. Time-varying autoregressive modeling was employed to estimate the time courses of high-frequency HRV power, low-frequency HRV power, the ratio between low-frequency and high-frequency HRV power, and low-frequency power of systolic BPV. To delineate the influence of respiration on HRV, we also computed respiratory airflow high-frequency power, the modified ratio of low-frequency to high-frequency HRV power, and the average transfer gain between respiration and heart rate. During cortical arousal, muscle sympathetic nerve activity and heart rate increased and returned rapidly to baseline, but systolic blood pressure, the ratio between low-frequency and high-frequency HRV power, low-frequency HRV power, the modified ratio of low-frequency to high-frequency HRV power, and low-frequency power of systolic BPV displayed increases that remained above baseline up to 40 s after arousal. High-frequency HRV power and airflow high-frequency power showed concommitant decreases to levels below baseline, whereas the average transfer gain between respiration and heart rate remained unchanged. These findings suggest that 1) arousal-induced changes in parasympathetic activity are strongly coupled to respiratory pattern and 2) the sympathoexcitatory cardiovascular effects of arousal are relatively long lasting and may accumulate if repetitive arousals occur in close succession.
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Blasi et al. (2003) conducted an observational in Healthy (n=16). Acoustically induced arousals from sleep vs. Baseline was evaluated on Time courses of heart rate variability and blood pressure variability spectral parameters. Acoustically induced arousals from sleep increased systolic blood pressure and low-frequency heart rate variability power, which remained above baseline for up to 40 seconds.
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