Hi, everyone, I found that both respiratory disturbance index (RDI) and micro-arousal index (MI) have significantly positive correlations with nighttime high frequency band power (HFpower) of HRV, and with very low frequency peak. HFpower mainly reflects parasympathetic activation, and very low frequency peak mainly relates to thermoregulation and hormones. What are the possible reasons for these phenomenons? Thank you very much!
Hello Yue chun,
The relationship between breathing/arousal in sleep and HRV is complex. The following thoughts may help you in looking at these associations further.
A neuronal network that coordinates breathing/respiration is located in the medulla, and its neurons are grouped into anterior and posterior respiratory groups. The posterior respiratory group (which modulates respiratory patterns) receives afferent input from the periphery (receptors in lungs). The efferent input from this group coordinate the innervation of the muscles of inspiration. The upper airway is innervated by the vagus n. The anterior respiratory group coordinates both inspiratory and expiratory muscles. At rest and in sleep expiration is passive; forced expiration, requires involvement of the intercostal and the abdominal muscles.
The heart is a muscular organ which receives both sympathetic and parasympathetic input. Sympathetic influence may be increased by the activation of the sympathetic fibers innervating the heart (i.e., under vigorous activity or as a result of apneac events in sleep) or by the secretion of epinephrine/ norepinephrine from the adrenal gland. This influence can manifest as an observed increase in HRV. Conversely, stimulating the parasympathetic nervous system (vagal n) decreases the rate of diastolic depolarization and the heart rate slows.
Numerous studies reported changes in sympathetic and parasympathetic activity from waking rest to sleep, with marked differences between non-REM and REM sleep. These changes were reported to be primarily due to stage-related alterations in vagal tone; however it is also be related to the state of the neuronal network that coordinates breathing/respiration as described above. Nonetheless, REM sleep is characterized by increased sympathetic dominance, due to vagal withdrawal. In persons with respiratory disturbance, RDI and MI are more likely to occur/worsen in REM sleep (when muscle tonus is the lowest). In non-REM sleep, especially in slow wave sleep (SWS), body movements and arousal level both of which can influence HR are minimal. Respiratory patterns are also more regular during SWS than during other stages of sleep. Therefore, it may be reasonable to analyze/discuss frequency band power separately for REM and non-Rem sleep.
Best wishes,
Tatyana
Tatayana provided a very good description of HRV that commonly occurs in sleep during healthy individuals.
But you indicated the variability was associated with the respiratory disturbance index. Sympathetic activation is a common response when the airway opens from a partial or complete obstruction. Was the increased HRV also associated with an apnea/hypopnea index requiring a desaturation > 3% or 4%?
Thank you very much Daniel!
Yes, high frequency band power (HFpower) of HRV and very low frequency peak also significantly related with AHI.
So then its likely the answer to your question is that sleep disordered breathing is the primary source for the increased heart rate variability.
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