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DISCUSSION

In the present study, following the practice of very rapid yoga breathing, there was an increase in the low frequency power, decrease in the high frequency power and an increase in the low frequency / high frequency power ratio (Table 1). There was no significant change following nadisuddhi pranayama. Also, the mean heart rate did not change following either Practice. There were baseline differences between low and high frequency power values for the two sessions.

The low frequency band (0.05-0.15Hz) of the heart rate variability spectrum is thought to correspond to sympathetic modulation, especially when expressed as normalized as opposed to absolute units (7). The representation of low frequency and high frequency energy values in normalized units expresses the degree of control exerted and the relative balance of the two branches of the autonomic nervous system. The efferent vagal activity is a major contributor to the high frequency band (0.15-0.50Hz). The low frequency / high frequency ratio is correlated with the sympathovagal balance (9).

Hence the present results suggest that the practice of kapalabhati shifts the sympathovagal balance towards sympathetic activation. Following nadisuddhi pranayama, the change is not as clear, though there appears to be an increased activation of both components.

The differences in baseline values could not be explained. Recordings of kapalabhati and nadisuddhi on each subject were made on separate days at the same time of the day. There was no fixed order for the two types of sessions on different days. However, at the start of each session, subjects were told the practice which was to the tested on that day. It is not known whether this influenced their baseline levels of autonomic activity. In order to understand the contribution of the differences in baseline values to the nature of change following either practice, separate calculations were made as described below. The percentage change in the five lowest values of the baseline low frequency (LF) component preceding kapalabhati and the five highest baseline LF values preceding nadisuddhi were calculated. Following kapalabhati, the percentage change was 8.9% for these 5 values. Since the average percentage change for the LF component of the 12 subjects was 43.2%, this suggested that the baseline low values of the LF component preceding kapalabhati did not correlate with the increase in this component following the practice. In contrast, following nadisuddhi for the 5 subjects with highest LF values preceding the practice, the percentage change was 45.3% (decrease). Since the average percentage change for the LF component of the 12 subjects was 15.5% (decrease ), this suggested that the baseline high values of the LF component preceding nadisuddhi was correlated with the decrease in this component following the practice.

While attempting to explain the mechanisms underlying the changes, the respiratory sinus arrhythmia has to be taken into account. At typical respiratory frequencies near 0.20Hz (12 breath cycles per minute), the heart rate increases simultaneously with inspiration (10). Most investigators have found that cardiac vagal efferents are involved in mediating the heart rate fluctuations that occur with respiration at this frequency. It was also observed that the modulation of cardiac sympathetic efferents also plays a role in generating respiratory sinus arrhythmia at lower respiratory frequencies below 0.15Hz (9 breath cycles per min). Separate polygraph recordings of respiration showed that the breath rate values before and after kapalabhati as well as before and after nadisuddhi practice were in the range of 0.20-0.26Hz (11). Within this frequency, the respiratory sinus arrhythmia is correlated with vagal activity. Hence the increase in cardiosympathetic tone following kapalabhati is probably due to other factors. In response to variations in breathing patterns a number of central and autonomic nervous system mechanisms as well as mechanical (heart) and haemodynamic adjustments are triggered, thereby causing both tonic and phasic change in cardiovascular functioning (12).

An association between high frequency breathing and cardiovascular sympathetic activation was demonstrated in an earlier study (2) which reported an increase in heart rate and systolic blood pressure following the practice. However there are two main differences between the present study and the earlier one. In the previous study, there was no change in the frequency components of the heart rate variability spectrum, while the heart rate increased. These changes were reported during the practice, whereas in the present study, the effects reported apply to the period immediately after the practice. The differences may also be related to the fact that subjects of the earlier study practised kapalabhati for three 5 minute periods, whereas in the present study the duration of practice was 1 minute in keeping with yoga texts (8).

The absence of change following nadisuddhi pranayama, compared to the earlier report (3), could be due to the fact that the earlier study described baseline changes after 4 weeks of practice, whereas in the present study, the immediate effect was assessed

This difference between the factors determining the changes in heart rate versus changes in the heart rate variability spectral components is already known (4). Additional factors influence the heart rate compared to the HRV. Since the heart rate variability spectral components are determined by the autonomic nervous system, measurement of the heart rate variability may have greater application in assessing autonomic status than recording of heart rate alone. This application has been highlighted in the present study.

 
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