Dataset Information

Slow 0.1 Hz Breathing and Body Posture Induced Perturbations of RRI and Respiratory Signal Complexity and Cardiorespiratory Coupling.

ABSTRACT: Objective: We explored the physiological background of the non-linear operating mode of cardiorespiratory oscillators as the fundamental question of cardiorespiratory homeodynamics and as a prerequisite for the understanding of neurocardiovascular diseases. We investigated 20 healthy human subjects for changes using electrocardiac RR interval (RRI) and respiratory signal (Resp) Detrended Fluctuation Analysis (DFA, ?1RRI, ?2RRI, ?1Resp, ?2Resp), Multiple Scaling Entropy (MSERRI1-4, MSERRI5-10, MSEResp1-4, MSEResp5-10), spectral coherence (CohRRI-Resp), cross DFA (?1 and ?2) and cross MSE (XMSE1-4 and XMSE5-10) indices in four physiological conditions: supine with spontaneous breathing, standing with spontaneous breathing, supine with 0.1 Hz breathing and standing with 0.1 Hz breathing. Main results: Standing is primarily characterized by the change of RRI parameters, insensitivity to change with respiratory parameters, decrease of CohRRI-Resp and insensitivity to change of in ?1, ?2, XMSE1-4, and XMSE5-10. Slow breathing in supine position was characterized by the change of the linear and non-linear parameters of both signals, reflecting the dominant vagal RRI modulation and the impact of slow 0.1 Hz breathing on Resp parameters. CohRRI-Resp did not change with respect to supine position, while ?1 increased. Slow breathing in standing reflected the qualitatively specific state of autonomic regulation with striking impact on both cardiac and respiratory parameters, with specific patterns of cardiorespiratory coupling. Significance: Our results show that cardiac and respiratory short term and long term complexity parameters have different, state dependent patterns. Sympathovagal non-linear interactions are dependent on the pattern of their activation, having different scaling properties when individually activated with respect to the state of their joint activation. All investigated states induced a change of ?1 vs. ?2 relationship, which can be accurately expressed by the proposed measure-inter-fractal angle ?. Short scale (?1 vs. MSE1-4) and long scale (?2 vs. MSE5-10) complexity measures had reciprocal interrelation in standing with 0.1 Hz breathing, with specific cardiorespiratory coupling pattern (?1 vs. XMSE1-4). These results support the hypothesis of hierarchical organization of cardiorespiratory complexity mechanisms and their recruitment in ascendant manner with respect to the increase of behavioral challenge complexity. Specific and comprehensive cardiorespiratory regulation in standing with 0.1 Hz breathing suggests this state as the potentially most beneficial maneuver for cardiorespiratory conditioning.

SUBMITTER: Matic Z

PROVIDER: S-EPMC7040454 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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Slow 0.1 Hz Breathing and Body Posture Induced Perturbations of RRI and Respiratory Signal Complexity and Cardiorespiratory Coupling.

Matić Zoran Z Platiša Mirjana M MM Kalauzi Aleksandar A Bojić Tijana T

Frontiers in physiology 20200214

Objective: We explored the physiological background of the non-linear operating mode of cardiorespiratory oscillators as the fundamental question of cardiorespiratory homeodynamics and as a prerequisite for the understanding of neurocardiovascular diseases. We investigated 20 healthy human subjects for changes using electrocardiac RR interval (RRI) and respiratory signal (Resp) Detrended Fluctuation Analysis (DFA, α1RRI, α2RRI, α1Resp, α2Resp), ...[more]

PMID: 32132926

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Project description:Breathing is maintained and controlled by a network of automatic neurons in the brainstem that generate respiratory rhythm and receive regulatory inputs. Breathing complexity therefore arises from respiratory central pattern generators modulated by peripheral and supra-spinal inputs. Very little is known on the brainstem neural substrates underlying breathing complexity in humans. We used both experimental and theoretical approaches to decipher these mechanisms in healthy humans and patients with chronic obstructive pulmonary disease (COPD). COPD is the most frequent chronic lung disease in the general population mainly due to tobacco smoke. In patients, airflow obstruction associated with hyperinflation and respiratory muscles weakness are key factors contributing to load-capacity imbalance and hence increased respiratory drive. Unexpectedly, we found that the patients breathed with a higher level of complexity during inspiration and expiration than controls. Using functional magnetic resonance imaging (fMRI), we scanned the brain of the participants to analyze the activity of two small regions involved in respiratory rhythmogenesis, the rostral ventro-lateral (VL) medulla (pre-Bötzinger complex) and the caudal VL pons (parafacial group). fMRI revealed in controls higher activity of the VL medulla suggesting active inspiration, while in patients higher activity of the VL pons suggesting active expiration. COPD patients reactivate the parafacial to sustain ventilation. These findings may be involved in the onset of respiratory failure when the neural network becomes overwhelmed by respiratory overload We show that central neural activity correlates with airflow complexity in healthy subjects and COPD patients, at rest and during inspiratory loading. We finally used a theoretical approach of respiratory rhythmogenesis that reproduces the kernel activity of neurons involved in the automatic breathing. The model reveals how a chaotic activity in neurons can contribute to chaos in airflow and reproduces key experimental fMRI findings.

Project description:This research aims to investigate whether slow-paced breathing (SPB) improves adaptation to psychological stress, and specifically inhibition, when it is performed before or after physical exertion (PE). According to the resonance model, SPB is expected to increase cardiac vagal activity (CVA). Further, according to the neurovisceral integration model, CVA is positively linked to executive cognitive performance, and would thus play a role in the adaptation to psychological stress. We hypothesized that SPB, in comparison to a control condition, will induce a better adaptation to psychological stress, measured via better inhibitory performance. Two within-subject experiments were conducted with athletes: in the first experiment (N = 60) SPB (or control - neutral TV documentary) was realized before PE ("relax before PE"), and in the second experiment (N = 60) SPB (or the watching TV control) was realized after PE ("relax after PE"). PE consisted of 5 min Burpees, a physical exercise involving the whole body. In both experiments the adaptation to psychological stress was investigated with a Stroop task, a measure of inhibition, which followed PE. Perceived stress increased during PE (partial ?2 = 0.63) and during the Stroop task (partial ?2 = 0.08), and decreased during relaxation (partial ?2 = 0.15), however, no effect of condition was found. At the physiological level PE significantly increased HR, RF, and decreased CVA [operationalized in this research via the root mean square of successive differences (RMSSD)] in both experiments. Further, the number of errors in the incongruent category (Stroop interference accuracy) was found to be lower in the SPB condition in comparison to the control condition, however, these results were not mediated by RMSSD. Additionally, the Stroop interference [reaction times (RTs)] was found to be lower overall in "relax before PE," however, no effect was found regarding SPB and Stroop interference (RTs). Overall, our results suggest that SPB realized before or after PE has a positive effect regarding adaptation to psychological stress and specifically inhibition, however, the underlying mechanisms require further investigation.

Dataset Information

Slow 0.1 Hz Breathing and Body Posture Induced Perturbations of RRI and Respiratory Signal Complexity and Cardiorespiratory Coupling.

Publications

Slow 0.1 Hz Breathing and Body Posture Induced Perturbations of RRI and Respiratory Signal Complexity and Cardiorespiratory Coupling.

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