To determine whether paced breathing (PB) and respiratory interval of PB modify the relationship between spectral components of heart rate variability (HRV) and cardiac vagal tone, we studied seven healthy young males under the condition of beta-adrenergic blockade by intravenous propranolol (0.2 mg/kg). Compared with spontaneous breathing, PB at the same respiratory interval as that of individual spontaneous breathing showed no significant effect on the amplitude of the high-frequency (HF) component or the mean R-R interval in either the supine or tilt position, whereas the PB decreased the amplitude of the low-frequency (LF; 0.04-0.15 Hz) component in both positions (P = 0.004 and 0.042, respectively). When the respiratory interval was increased from 3 to 6 s, the HF amplitude showed a progressive increase in both positions (P = 0.001 and 0.035, respectively), while the LF amplitude and mean R-R interval remained unchanged. These results indicate that the effects of PB and respiratory interval on the spectral components of HRV are not mediated by the changes in mean cardiac vagal tone and support the hypothesis that increased respiratory interval amplifies the respiratory-related vagal modulation of heart rate.

To examine the hypothesis that the relaxation response is associated with an increase in cardiac parasympathetic tone, the frequency components of heart rate variability during relaxation training were investigated in 16 college students. Electrocardiograms and pneumograms were recorded during a 5-min baseline period followed by three successive 5-min sessions of the autogenic training (relaxation) or by the same periods of quiet rest (control), while subjects breathed synchronously with a visual pacemaker (0.25 Hz). Although neither the magnitude nor the frequency of respiration showed a significant difference between relaxation and control, the amplitude of the high-frequency component of heart rate variability increased only during relaxation (p = .008). There was no significant difference in the ratio of the low-frequency (0.04-0.15 Hz) to the high-frequency amplitudes. The increased high-frequency amplitude without changes in the respiratory parameters indicates enhanced cardiac parasympathetic tone. Thus, our results support the initial hypothesis of this study. Enhanced cardiac parasympathetic tone may explain an important mechanism underlying the beneficial effect of the relaxation response.

The present study was designed to examine the effect of voluntarily slowed respiration on the cardiac parasympathetic response to a threat: the anticipation of an electric shock. Thirty healthy college students were randomly assigned to the slow, fast, and nonpaced breathing groups (10 subjects each). Subjects in the slow and fast paced breathing groups regulated their breathing rate to 8 and 30 cpm, respectively, and those in the nonpaced breathing group breathed spontaneously. Immediately after the period of paced or nonpaced breathing for 5 minutes, the subjects were exposed for 2 minutes to the anticipation of an electric shock during breathing paced at 15 cpm. The amplitude of the high frequency (HF) component of the heart rate variability, an index of cardiac parasympathetic tone, significantly decreased during the threat in the fast and nonpaced breathing groups, whereas it was unchanged in the slow paced breathing group. No significant difference was observed among the three groups in the amplitude of respiration during the threat. Results suggest that a slowed respiration decreases the cardiac parasympathetic withdrawal response to the threat. This study provides a rationale for the therapeutic uses of the slowed respiration maneuver in attenuating the cardiac autonomic responses in patients with anxiety disorder.

The present study was designed to examine the effect of heart rate variability (HRV) biofeedback on the cardiorespiratory resting function during sleep in daily life. Forty-five healthy young adults were randomly assigned to one of three groups: HRV biofeedback, Autogenic Training(AT), and no-treatment control. Participants in the HRV biofeedback were instructed to use a handheld HRV biofeedback device before their habitual bedtime, those in the AT were asked to listen to an audiotaped instruction before bedtime,and those in the control were asked to engage in their habitual activity before bedtime. Pulse wave signal during sleep at their own residences was measured continuously with a wrist watch-type transdermal photoelectric sensor for three time points. Baseline data were collected on the first night of measurements, followed by two successive nights for HRV biofeedback, AT, or control. Cardiorespiratory resting function was assessed quantitatively as the amplitude of high frequency(HF) component of pulse rate variability, a surrogate measure of respiratory sinus arrhythmia. HF component increased during sleep in the HRV biofeedback group,although it remained unchanged in the AT and control groups. These results suggest that HRV biofeedback before sleep may improve cardiorespiratory resting function during sleep.