Application of spectral analysis to heart rate data collected from infants with intrauterine exposure to cocaine and normal controls showed a significant sleep state effect on HRV, with greater high frequency power seen during quiet sleep (QS) compared to active sleep (AS) and greater low- and mid-frequency power seen in AS compared to QS. However, in both sleep states, the cocaine-exposed neonates showed enhanced total spectral power that appears to be due to an increase in spectral power across all frequency bands. Absolute values for spectral power in the low- and mid-frequency bands of HRV were significantly higher in the cocaine-exposed group in both sleep states. The absolute value for high frequency power was also higher, but this increase attained statistical significance only in quiet sleep. We found no evidence for respiratory patterning differences between the two groups that might account for these findings. Very little of the total respiratory variability in QS and AS was in the low-to-mid-frequency range, suggesting that periodic breathing contributed little to HRV in that same frequency range. We also computed the fractional distribution of heart rate variation across all frequencies as a means of examining sympathovagal balance. Ratios between low- and mid-frequency power compared to high frequency power showed no differences between the groups, although there was a highly significant increase in AS compared to QS. The present results suggest two possibilities: (1) an increase in parasympathetic control of heart rate in the cocaine-exposed infants; or (2) an increase in both vagal and sympathetic modulation of heart rate in the cocaine-exposed group.
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