Key Points
- To determine whether low-frequency fluctuations in heart rate and blood pressure originate from a central medullary oscillator, baroreflex mechanisms, or a combination of both.
- Assessed 10 healthy participants (mean age 27 ± 1 years) using spectral analysis of heart rate (R-R interval) and mean blood pressure during breath-holding (apnea).
- Manipulated preapnea entrainment by controlling respiration rate (0.1 or 0.25 Hz) or applying sinusoidal neck suction (0 to -30 mmHg at 0.1 or 0.2 Hz) to stimulate baroreceptors.
- High-frequency respiratory sinus arrhythmia power significantly decreased during apnea from 6.73 ± 0.15 to 3.67 ± 0.10 ln ms² (P < 0.0001) across all preapnea conditions.
- Low-frequency power fell during apnea only when preceded by 0.1-Hz respiration (8.71 ± 0.18 to 6.52 ± 0.11 ln ms², P < 0.001) or 0.1-Hz neck suction (8.31 ± 0.23 to 6.90 ± 0.38 ln ms², P < 0.01).
- Apneic low-frequency rhythm was slower than during 0.25-Hz breathing (0.082 ± 0.01 vs. 0.112 ± 0.001 Hz, P < 0.001) and maintained constant power without modulation by prior entrainment.
Structured PICO
PPopulation10 healthy subjects, mean age 27 +/- 1 yr
IInterventionApnea following different preapnea entrainment stimuli (controlled respiration at 0.1 or 0.25 Hz, or sinusoidal neck suction at 0.1 or 0.2 Hz)
CComparatorPreapnea conditions
OOutcomeSpectral analysis of heart rate (R-R interval) and blood pressuresurrogate
In healthy subjects, a slow rhythm present during apnea suggests that low-frequency oscillations in heart rate may be generated by a central oscillator in addition to the baroreflex.