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University of Medicine and Dentistry of New Jersey, New Jersey Medical School, Piscataway, NJ University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Piscataway, NJ
Correspondence to: Paul Lehrer, PhD, Department of Psychiatry, D-335, UMDNJ-Robert Wood Johnson Medical School, 671 Hoes Ln, Piscataway, NJ 08854; e-mail: lehrer{at}umdnj.edu
To the Editor:
Yasuma and Hayano (February 2004)1 have theorized that respiratory sinus arrhythmia improves respiratory efficiency by the pairing of increases in heart rate with inhalation, when the concentration of oxygen in the alveoli is maximal. However, this phase relationship only occurs under specific circumstances.
Saul et al2 applied vagal and sympathetic blocking agents, and found that the phase lag from breathing to heart rate is near 0°, but only under pure vagal conditions. Under pure sympathetic conditions, the phase relationship varies from 180° at low frequencies to approximately –180° at high frequencies.
We asked eight healthy subjects to breathe at seven frequencies between 0.04 and 0.5 Hz for 2 min each, matching their strain-gauge respiration record to a computer-generated sine curve3 to ensure a constant respiratory depth and a sinusoidal shape for respiratory curves. Using Fourier filtration,3 we determined that the phase relationship between heart rate and respiration was 0° only at a respiratory frequency of approximately 0.1 Hz, in which the target frequency heart rate variability also was highest (Fig 1 ).
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Thus, the hypothesis of Yasuma and Hayani1 would be specifically relevant for sympathetically medicated heart rate variability, or for respiratory sinus arrhythmia associated with slow breathing at approximately 0.1 Hz.
References
Suzuka National Hospital, Suzuka, Japan Nagoya City University School of Medicine, Nagoya, Japan
Correspondence to: Fumihiko Yasuma, MD, FCCP, Suzuka National Hospital, 3–2-1 Kasado, Suzuka, Japan 513-8501; e-mail: f-yasuma{at}mtb.biglobe.ne.jp
To the Editor:
We appreciate the interest by Drs. Vaschillo and Lehrer in our Opinions/Hypothesis article (February 2004)1 on respiratory sinus arrhythmia (RSA). We agree with their comment that heartbeat synchronizes with respiratory rhythm only under certain conditions, so that the results of the physiologic experiment are only applicable to the model used in the study. In their well-organized investigation,2 Vaschillo and coworkers2 used healthy subjects who were strictly instructed to breathe in synchrony with the extrinsic pacemaker (ie, a metronome) at predetermined respiratory frequencies between 0.04 and 0.5 Hz for 2 min. As was noted in our Opinions/Hypothesis article,1 humans are a species with a weak RSA compared with dogs. Moreover, a paced breathing that is in synchrony with the extrinsic rhythm generator might precipitate mental stress for subjects, and the equilibrium state of CO2/O2 metabolism through the paced breathing could not have been obtained in a very short period of time. Such factors as species, state of the subjects (ie, very alert, alert, relaxed, or asleep), and metabolism should always be considered in clinical/basic experiments on the synchrony of heartbeat with respiratory rhythm. Therefore, for this purpose we used trained dogs to lie down in a relaxed state under spontaneous breathing,345 as dogs are a species with a strong RSA.
The phase relationship between heart rate and respiration shows frequency dependence, but the relationship is known to be nonlinear.6 Eckberg6 has reported that the phase analysis between heart rate and respiration shows a clear hysteresis, and that the prolongation of the R-R interval begins shortly after the onset of expiration independently of respiratory frequency. He has also demonstrated that the shortening of the R-R interval begins progressively earlier in reference to the onset of inspiration as respiratory frequency decreases. As a result, the timing of the maximum instantaneous heart rate occurs instantly after end-inspiration, with the maximal lung volume at least for a respiratory frequency of < 0.25 Hz. Although the phase of the maximum heart rate lags behind the phase of the maximum lung volume as respiratory frequency increases, the amplitude of RSA decreases progressively.7 These facts seem to be consistent with the hypothesis that RSA is a function of physiologic respite for the cardiovascular and respiratory systems in resting animals and humans, because the phase relationship at a reduced respiratory frequency is optimal to cardiac and respiratory energy savings by reducing unnecessary heartbeats during expiration and unnecessary ventilation during the waning phase of the heart beat.18
References
This article has been cited by other articles:
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  P. Lehrer, E. Vaschillo, S.-E. Lu, D. Eckberg, B. Vaschillo, A. Scardella, and R. Habib Heart rate variability biofeedback: effects of age on heart rate variability, baroreflex gain, and asthma. Chest, February 1, 2006; 129(2): 278 - 284. [Abstract] [Full Text] [PDF]
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