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Control of heart rate through guided high-rate breathing.

ABSTRACT: Understanding the complex dynamics of cardio-respiratory coupling sheds light on the underlying mechanisms governing the communication between these two physiological systems. Previous research has predominantly considered the coupling at respiratory rates slower than the heart rate and shown that respiratory oscillations lead to modulation and/or synchronization of the heart rate. Whereas the mechanisms of cardio-respiratory communication are still under discussion, peripheral nervous regulation is considered to be the predominant factor. This work offers a novel experimental design and applies the concept of instantaneous phase to detect cardio-respiratory entrainment at elevated respiration rates, close to the resting heart rate. If such 1:1 entrainment exists, it would suggest direct neuronal communication between the respiration and heart centres in the brain. We have observed 1:1 entrainment in all volunteers, with consistently longer synchronization episodes seen in physically fitter people, and demonstrated that cardio-respiratory synchronization at both low and high respiration rates is associated with a common underlying communication mechanism.

SUBMITTER: Perry S

PROVIDER: S-EPMC6367452 | biostudies-literature | 2019 Feb

REPOSITORIES: biostudies-literature

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Control of heart rate through guided high-rate breathing.

Perry Sean S Khovanova Natasha A NA Khovanov Igor A IA

Scientific reports 20190207 1

Understanding the complex dynamics of cardio-respiratory coupling sheds light on the underlying mechanisms governing the communication between these two physiological systems. Previous research has predominantly considered the coupling at respiratory rates slower than the heart rate and shown that respiratory oscillations lead to modulation and/or synchronization of the heart rate. Whereas the mechanisms of cardio-respiratory communication are still under discussion, peripheral nervous regulatio ...[more]

PMID: 30733480

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Project description:BackgroundMaternal sleep-disordered breathing is associated with adverse pregnancy outcomes and is considered to be deleterious to the developing fetus. Maternal obesity potentiates sleep-disordered breathing, which, in turn, may contribute to the effect of maternal obesity on adverse fetal outcomes. However, only a few empirical studies have evaluated the contemporaneous effects of maternal sleep-disordered breathing events on fetal well-being. These events include apnea and hypopnea with accompanying desaturations in oxyhemoglobin.ObjectiveThis study aimed to reconcile contradictory findings on the associations between maternal apnea or hypopnea events and clinical indicators of fetal compromise. It also sought to broaden the knowledge base by examining the fetal heart rate and heart rate variability before, during, and after episodes of maternal apnea or hypopnea. To accomplish this, we employed overnight polysomnography, the gold standard for ascertaining maternal sleep-disordered breathing, and synchronized it with continuous fetal electrocardiography.Study designA total of 84 pregnant women with obesity (body mass index >30 kg/m2) participated in laboratory-based polysomnography with digitized fetal electrocardiography recordings during or near 36 weeks of gestation. Sleep was recorded, on average, for 7 hours. Decelerations in fetal heart rate were identified. Fetal heart rate and heart rate variability were quantified before, during, and after each apnea or hypopnea event. Event-level intensity (desaturation magnitude, duration, and nadir O2 saturation level) and person-level characteristics based on the full overnight recording (apnea-hypopnea index, mean O2 saturation, and O2 saturation variability) were analyzed as potential moderators using linear mixed effects models.ResultsA total of 2936 sleep-disordered breathing events were identified, distributed among all but 2 participants. On average, participants exhibited 8.7 episodes of apnea or hypopnea per hour (mean desaturation duration, 19.1 seconds; mean O2 saturation nadir, 86.6% per episode); nearly half (n=39) of the participants met the criteria for obstructive sleep apnea. Only 45 of 2936 apnea or hypopnea events were followed by decelerations (1.5%). Conversely, most (n=333, 88%) of the 378 observed decelerations, including the prolonged ones, did not follow an apnea or a hypopnea event. Maternal sleep-disordered breathing burden, body mass index, and fetal sex were unrelated to the number of decelerations. Fetal heart rate variability increased during events of maternal apnea or hypopnea but returned to initial levels soon thereafter. There was a dose-response association between the size of the increase in fetal heart rate variability and the maternal apnea-hypopnea index, event duration, and desaturation depth. Longer desaturations were associated with a decreased likelihood of the variability returning to baseline levels after the event. The mean fetal heart rate did not change during episodes of maternal apnea or hypopnea.ConclusionEpisodes of maternal sleep apnea and hypopnea did not evoke decelerations in the fetal heart rate despite the predisposing risk factors that accompany maternal obesity. The significance of the modest transitory increase in fetal heart rate variability in response to apnea and hypopnea episodes is not clear but may reflect compensatory, delimited autonomic responses to momentarily adverse conditions. This study found no evidence that episodes of maternal sleep-disordered breathing pose an immediate threat, as reflected in fetal heart rate responses, to the near-term fetus.

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Control of heart rate through guided high-rate breathing.

Publications

Control of heart rate through guided high-rate breathing.

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