Sympathetic restraint of respiratory sinus arrhythmia: implications for vagal-cardiac tone assessment in humans

Clinicians and experimentalists routinely estimate vagal-cardiac nerve traffic from respiratory sinus arrhythmia. However, evidence suggests that sympathetic mechanisms may also modulate respiratory sinus arrhythmia. Our study examined modulation of respiratory sinus arrhythmia by sympathetic outflow. We measured R-R interval spectral power in 10 volunteers that breathed sequentially at 13 frequencies, from 15 to 3 breaths/min, before and after β-adrenergic blockade. We fitted changes of respiratory frequency R-R interval spectral power with a damped oscillator model: frequency-dependent oscillations with a resonant frequency, generated by driving forces and modified by damping influences. β-Adrenergic blockade enhanced respiratory sinus arrhythmia at all frequencies (at some, fourfold). The damped oscillator model fit experimental data well (39 of 40 ramps; r = 0.86 ± 0.02). β-Adrenergic blockade increased respiratory sinus arrhythmia by amplifying respiration-related driving forces ( P < 0.05), without altering resonant frequency or damping influences. Both spectral power data and the damped oscillator model indicate that cardiac sympathetic outflow markedly reduces heart period oscillations at all frequencies. This challenges the notion that respiratory sinus arrhythmia is mediated simply by vagal-cardiac nerve activity. These results have important implications for clinical and experimental estimation of human vagal cardiac tone.

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

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00036.2010 ◽

2010 ◽

Vol 298 (5) ◽

pp. H1588-H1599 ◽

Cited By ~ 48

Author(s):

P. Y. W. Sin ◽

D. C. Galletly ◽

Y. C. Tzeng

Keyword(s):

Blood Pressure ◽

Respiratory Sinus Arrhythmia ◽

Pattern Analysis ◽

Time Interval ◽

Adrenergic Blockade ◽

Breathing Frequency ◽

Sinus Arrhythmia ◽

Temporal Relationships ◽

Sympathetic Modulation ◽

Slow Breathing

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 (∼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 ∼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) β1-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.

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Determinants of respiratory sinus arrhythmia in the vagotomized rabbit

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1995.269.3.h909 ◽

1995 ◽

Vol 269 (3) ◽

pp. H909-H915 ◽

Cited By ~ 11

Author(s):

S. Perlini ◽

P. L. Solda ◽

M. Piepoli ◽

G. Sala-Gallini ◽

A. Calciati ◽

...

Keyword(s):

Respiratory Sinus Arrhythmia ◽

Blood Gases ◽

Power Spectral Analysis ◽

Rate Of Change ◽

Right Atrial ◽

Adrenergic Blockade ◽

Sinus Arrhythmia ◽

Beta Adrenergic ◽

Arterial Blood ◽

Ventilatory Mechanics

After cardiac denervation, a small-amplitude respiratory sinus arrhythmia (RSA) has been described in animals and humans. Its mechanical and chemical determinants were investigated in 19 urethan-anesthetized, vagotomized, and mechanically ventilated rabbits. We measured the influence on RSA of arterial blood gases, beta-adrenergic blockade, and phasic and steady changes in right atrial pressure (RAP) induced by changes in tidal volume (VT, 20, 40, 60 ml), respiratory frequency (RF, 10, 20, 30 cycles/min), and dextran-induced RAP increases. Phasic changes in RAP during each recording were quantified as standard deviation of the first derivative of the RAP signal (dRAP) as a measure of magnitude of variations of the rate of change due to respiration. RSA was assessed by combined autoregressive power spectral analysis of R-R interval and respiration on sequences of 256 heart-beats. Despite vagotomy, RSA was present in all recordings in all animals. During room air breathing, RSA changes were dependent on RF and VT (P < 0.025 and P < 0.001, respectively) and correlated with dRAP (P < 0.001) and arterial PO2 (P < 0.001). beta-Adrenergic blockade did not change the amplitude of this residual RSA or its dependence on ventilatory mechanics. Dextran-induced increase in mean RAP from 2.9 to 11.9 mmHg did not modify RSA or dRAP. During 100% O2 inhalation, RSA changes were no longer significantly linked to RF and VT, and also the correlation of RSA with dRAP was reduced (P < 0.05). Changing the arterial PCO2 from 28 to 79 mmHg (induced by increasing dead space at fixed ventilation) did not modify RSA.(ABSTRACT TRUNCATED AT 250 WORDS)

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Respiratory Sinus Arrhythmia During Sleep and Waking

Journal of Psychophysiology ◽

10.1027/0269-8803/a000200 ◽

2019 ◽

Vol 33 (1) ◽

pp. 1-12 ◽

Cited By ~ 2

Author(s):

Elizabeth M. Stoakley ◽

Karen J. Mathewson ◽

Louis A. Schmidt ◽

Kimberly A. Cote

Keyword(s):

Individual Differences ◽

Respiratory Sinus Arrhythmia ◽

Slow Wave Sleep ◽

Self Regulation ◽

Nrem Sleep ◽

Sinus Arrhythmia ◽

Affective Style ◽

Waking State ◽

Optimal Period ◽

The Stability

Abstract. Resting respiratory sinus arrhythmia (RSA) is related to individual differences in waking affective style and self-regulation. However, little is known about the stability of RSA between sleep/wake stages or the relations between RSA during sleep and waking affective style. We examined resting RSA in 25 healthy undergraduates during the waking state and one night of sleep. Stability of cardiac variables across sleep/wake states was highly reliable within participants. As predicted, greater approach behavior and lower impulsivity were associated with higher RSA; these relations were evident in early night Non-REM (NREM) sleep, particularly in slow wave sleep (SWS). The current research extends previous findings by establishing stability of RSA within individuals between wake and sleep states, and by identifying SWS as an optimal period of measurement for relations between waking affective style and RSA.

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Measures of RSA Suppression, Attentional Control, and Negative Affect Predict Self-Ratings of Executive Functions

Journal of Psychophysiology ◽

10.1027/0269-8803/a000053 ◽

2011 ◽

Vol 25 (4) ◽

pp. 164-173 ◽

Cited By ~ 7

Author(s):

Brian Healy ◽

Aaron Treadwell ◽

Mandy Reagan

Keyword(s):

College Students ◽

Heart Rate ◽

Regression Analysis ◽

Individual Differences ◽

Negative Affect ◽

Respiratory Sinus Arrhythmia ◽

Attentional Control ◽

Executive Processes ◽

Sinus Arrhythmia ◽

Low Levels

The current study was an attempt to determine the degree to which the suppression of respiratory sinus arrhythmia (RSA) and attentional control were influential in the ability to engage various executive processes under high and low levels of negative affect. Ninety-four college students completed the Stroop Test while heart rate was being recorded. Estimates of the suppression of RSA were calculated from each participant in response to this test. The participants then completed self-ratings of attentional control, negative affect, and executive functioning. Regression analysis indicated that individual differences in estimates of the suppression of RSA, and ratings of attentional control were associated with the ability to employ executive processes but only when self-ratings of negative affect were low. An increase in negative affect compromised the ability to employ these strategies in the majority of participants. The data also suggest that high attentional control in conjunction with attenuated estimates of RSA suppression may increase the ability to use executive processes as negative affect increases.

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