Influence of breathing frequency on the pattern of respiratory sinus arrhythmia and blood pressure: old questions revisited

Abstract

Respiratory sinus arrhythmia (RSA) is classically described as a vagally mediated increase and decrease in heart rate concurrent with inspiration and expiration, respectively. However, although breathing frequency is known to alter this temporal relationship, the precise nature of this phase dependency and its relationship to blood pressure remains unclear. In 16 subjects we systematically examined the temporal relationships between respiration, RSA, and blood pressure by graphically portraying cardiac interval (R-R) and systolic blood pressure (SBP) variations as a function of the respiratory cycle (pattern analysis), during incremental stepwise paced breathing. The principal findings were 1) the time interval between R-R maximum and expiration onset remained the same ( approximately 2.5-3.0 s) irrespective of breathing frequency (P = 0.10), whereas R-R minimum progressively shifted from expiratory onset into midinspiration with slower breathing (P < 0.0001); 2) there is a clear qualitative distinction between pre- versus postinspiratory cardiac acceleration during slow (0.10 Hz) but not fast (0.20 Hz) breathing; 3) the time interval from inspiration onset to SBP minimum (P = 0.16) and from expiration onset to SBP maximum (P = 0.26) remained unchanged across breathing frequencies; 4) SBP maximum and R-R maximum maintained an unchanged temporal alignment of approximately 1.1 s irrespective of breathing frequency (P = 0.84), whereas the alignment between SBP minimum and R-R minimum was inconstant (P > 0.0001); and 5) beta(1)-adrenergic blockade did not influence the respiration-RSA relationships or distinct RSA patterns observed during slow breathing, suggesting that temporal dependencies associated with alterations in breathing frequency are unrelated to cardiac sympathetic modulation. Collectively, these results illustrate nonlinear respiration-RSA-blood pressure relationships that may yield new insights to the fundamental mechanism of RSA in humans.

Effects of slow and regular breathing exercise on cardiopulmonary coupling and blood pressure

“…RRI amplitude changed from 47.4 ± 27.6 ms (the SB section) to 113.5 ± 48.0 ms gradually (the 7 BPM section, p < 0.01). The change of amplitude oscillation is consistent with other's study, i.e., amplitude-modulation effect of PB gets more evident when the breathing rate gets lower [37]. PSI, however, did not increase monotonically along with the RRI amplitude when the PB rate got much lower.…”

“…Prior work has documented the effects of slow and deep breathing on cardiovascular system, such as increasing the oscillatory amplitude of HR and BP [37] and reducing BP by cardiovascular reflex [15]. However, the change of phase coupling between cardiovascular and respiratory system during the SPB procedure has rarely been reported.…”

“…It has been demonstrated that PB procedure can lead to increased amplitude oscillations in both HR and BP when breathing rate becomes lower [36,37]. The change of phase dynamics during PB procedure, however, has rarely been explored simultaneously.…”

Depicting Respiratory Characteristics of Blood Pressure Signal by Using Empirical Mode Decomposition

“…The ABP change had a reversal relationship with EtCO 2 concentration in different respiratory patterns [37,38]. The phase delay between EtCO 2 signal and respiratory fluctuation of ABP signal was similar to previous reports [39].…”

Consciously Controlled Breathing Decreases the High-Frequency Component of Heart Rate Variability by Inhibiting Cardiac Parasympathetic Nerve Activity

“…To avoid the respiratory impact on HRV, consciously controlled breathing has been used in experiments and clinical trials to standardize HRV measurements (Grossman et al 1991;Piccirillo et al 2004;Sin et al 2010;DeBeck et al 2010;Schaffer et al 2013). However, it is possible that HRV is influenced by changes in f and V T during the transition from spontaneous to consciously controlled breathing, which might lead to inaccurate estimations that deviate from the true autonomic nervous activity in the heart.…”