Mer om hvordan pustefrekvens styrer HRV, eller RSA (Respiratory Sinusoid Arrythmia) som de kaller det i denne studien. Nevner at 0,1 Hz (6 pust i minuttet) gir bedre HRV enn 0,2 Hz (12 pust i minuttet). Den viser også at 0,1 Hz gir høyest CO2 i utpusten. Og den bekrefter at det er vagus som styrer HRV siden blokkade av et hormon ikke påvirket HRV.
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.
Moreover, despite extensive research, it remains unclear as to whether RSA is driven by respiratory synchronous oscillations in blood pressure via the arterial baroreflex or whether RSA and blood pressure are independently related to respiration via nonbaroreflex mechanisms (4, 14, 17, 28, 41, 46). Clarification of these fundamental relationships is important for our understanding of how autonomic neural outflow is coupled with respiratory activity, especially given that RSA is considered a surrogate of cardiac parasympathetic modulation and is widely applied in the calculation of spontaneous baroreflex sensitivity (7, 24, 34, 36, 37, 39).
Following an initial 5-min stabilization period, paced breathing was commenced at 0.20, 0.15, and 0.10 Hz in randomized order for 5 min each, with 2-min rests between trials.
Effect of breathing frequency on baseline variables
|Breathing Frequency, Hz|
|Respiratory sinus arrhythmia amplitude, ms||123 ± 44||167 ± 69∗||227 ± 92∗†||<0.0001|
|R-R interval, ms||954 ± 83||958 ± 85||976 ± 82||0.17|
|Systolic blood pressure amplitude, mmHg||6.6 ± 1.8||8.8 ± 3.4∗||10 ± 3.1∗†||<0.0001|
|Systolic blood pressure, mmHg||120 ± 14||119 ± 13||117 ± 14||0.40|
|Mean arterial blood pressure, mmHg||79 ± 8.2||78 ± 8.0||79 ± 9.6||0.81|
|Diastolic blood pressure, mmHg||62 ± 7.1||62 ± 7.2||61 ± 8.5||0.88|
|End-tidal CO2, %||5.04 ± 0.90||5.11 ± 0.93||5.20 ± 0.94||0.41|
Values are means ± SD. No differences in R-R interval, systolic blood pressure, mean arterial blood pressure, diastolic blood pressure, or end-tidal CO2 were found across the breathing frequencies.
↵* Statistically significant compared with 0.20 Hz;
↵† statistically significant compared with 0.15 Hz.
The present investigation is the first to apply a pattern analysis approach to characterize nonlinearities in the temporal relationships between respiration, RSA, and blood pressure within the boundaries of the respiratory cycle. Under the conditions of this study the five major findings are: 1) the time interval between R-R maximum and expiration onset remained the same irrespective of breathing frequency, whereas R-R minimum progressively shifted from expiratory onset into midinspiration with slower breathing; 2) two qualitatively distinct stages of cardiac acceleration during slow 0.10-Hz breathing were observed in most subjects; 3) both the time intervals between inspiration onset and SBP minimum and between expiration onset and SBP maximum were unchanged by breathing frequency; 4) SBP maximum and R-R maximum maintained a fixed temporal alignment irrespective of breathing frequency, whereas, in contrast, the alignment between SBP minimum and R-R minimum varied according to breathing frequency; and 5) β1-adrenergic blockade did not influence the respiration-RSA relationships or distinct RSA patterns observed during slow breathing.
Finally, consistent with the established literature, we observed a clear relationship between breathing frequency and RSA amplitude (11, 23, 45, 49). In this study 0.10-Hz breathing was associated with a ∼1.8-fold higher RSA amplitude compared with 0.20-Hz breathing. This is most likely due to breathing frequency coinciding with, and thus significantly augmenting, low frequency R-R interval fluctuations. The mechanism(s) behind this resonance phenomenon is unclear, but one proposal is that the augmentation of cardiovascular oscillations associated with slow breathing is due to global enhancement of arterial baroreflex sensitivity (7).
In summary, this study revealed several previously undescribed nonlinearities in respiration-RSA-blood pressure relationships in conscious humans. In contrast to prior studies, we found R-R minimum was not temporally aligned to expiration, beginning in late inspiration with slower breathing. Similarly, the onset of R-R maximum was not fixed to inspiratory onset but occurred in late expiration at slower breathing frequiencies. We also found that R-R maximum consistently occured ∼2.5–3.0 s following expiratory onset irrespective of breathing frequency. We observed two qualitatively distinct stages of cardiac acceleration during slow 0.10-Hz breathing, whereby the rate of cardiac acceleration occurring before inspiration was consistently less than the rate of cardiac acceleration following inspiratory onset, which to the best of our knowledge has not previously been described. Since these temporal dependencies were unaltered by selective β1-adrenergic blockade, they are most likely due to vagally mediated mechanisms. Furthermore, SBP maximum and R-R maximum maintained a temporal alignment of ∼1.1 s irrespective of breathing frequency whereas the delay between SBP minimum and R-R minimum became longer with slower breathing. These results demonstrate that the application of pattern analysis to the study of heart rate and blood pressure variability has potential to yield new insights into fundamental relationships between breathing and autonomic regulation of cardiovascular function.