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Autonomic integration: the physiological basis of cardiovascular variability

John M. Karemaker

Blood pressure (BP) and heart rate (HR) are continually varying. The nervous mechanisms behind this variability have been studied extensively in non-human animal models (for reviews, see Eckberg & Sleight, 1992). Since the 1980s, the combined availability of non-invasive blood pressure measurement by the Peñáz-Wesseling Finapres, and more and more powerful computers in the laboratory, have revived research into prevalence and physiological meaning of this variability in humans. When Fourier analysis was applied to analysis of BP variability (BPV) and HR variability (HRV), two frequency peaks stood out: one around the respiratory frequency and one around 0·1 Hz, or one oscillation in 10 s. These frequencies had been observed in blood pressure recordings before, actually over 130 years ago: Traube-Hering waves (coupled to respiration) and Mayer waves, the 0·1 Hz and slower oscillations. In the earlier research it had been established that oscillating sympathetic activity causes the Mayer waves in blood pressure. The respiration-coupled blood pressure oscillations were partly explained by mechanical effects of respiration and possibly by the vagally induced heart period oscillations coupled to respiration, known as respiratory sinus arrhythmia (RSA) (Eckberg & Sleight, 1992).

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