Lack of peripheral modulation of cardiovascular central oscillatory autonomic activity during apnea in humans

Respiratory sinus arrhythmia (RSA) high-frequency oscillations (HF) and slow fluctuations in heart rate (LF) are thought to result from entrainment of a medullary oscillator, from the baroreflex, or from a combination of both central and baroreflex mechanisms. We sought to distinguish between the alternatives by examining with spectral analysis the behavior of heart rate (R-R interval) and blood pressure in 10 healthy subjects (mean age 27 ± 1 yr) during apnea, altering the rate of preapnea entrainment stimuli by changing the frequency either of respiration (controlled at 0.1 or 0.25 Hz) or of baroreceptor stimulation by sinusoidal neck suction (0 to -30 mmHg, 0.1 or 0.2 Hz). During apnea the RSA-HF power decreased (from 6.73 ± 0.15 to 3.67 ± 0.10 ln ms²; P <0.0001), regardless of preapnea conditions, whereas LF power was reduced only if preceded by 0.1-Hz respiration or neck suction [from 8.71 ± 0.18 to 6.52 ± 0.11 ln ms² (P <0.001) and from 8.31 ± 0.23 to 6.90 ± 0.38 ln ms² (P <0.01), respectively]. The LF frequency seen in the R-R interval during apnea was slower than the spontaneous LF during 0.25- Hz breathing (0.082 ± 0.01 vs. 0.112 ± 0.001 Hz, P <0.001), but the maneuvers during preapnea had no influence on the observed frequency or other characteristics of the slow oscillations during apnea. Moreover, we found no evidence of a progressive decrease in the power of the oscillation during apnea. The same behavior was observed on the mean blood pressure signal. In conclusion, a slow rhythm is present during apnea. In healthy subjects at rest the characteristics of this oscillation indicate that it could be generated by a central oscillator; this may thus contribute to the origin of LF present during normal respiration, in addition to the baroreflex.