In healthy humans blood pressure and heart periods fluctuate at respiratory and other frequencies. The degree of these fluctuations is situation and age dependent. Although literature concurs that the majority of these fluctuations are reflex driven, some insist on an exemption for the respiratory oscillations. In view of the common central nervous activity related to respiration, it is reasoned that in the course of evolution the cardiovascular system has, centrally, become entrained to the respiratory drive. This might, teleologically, improve air uptake by increasing heartrate in the inspiratory phase.
Here I make the case that respiratory sinus arrhythmia is principally a reflex phenomenon, powered by incoming information from baroreceptors. I’ll base this debate on well-established physiological facts and understanding that may be gained from simple computational models. This won’t refute animal tests that show respiration to modulate centrally the blood circulation pressure to heart period reflex. However, I plan to show that in awake humans this phenomenon is insufficient to clarify respiration-to-heart rate relations.
The issue of modeling is the complexity of most models: they require so many variables and mathematical formulas that, to the non-expert reader, any desired end result might be obtained. In this essay I shall make an effort to simplify and limit modeling to the bare minimum; more complex models and reasoning can be found in the literature. Now suppose that in a sequence of beats as depicted in Fig. 1A, instantly the central anxious system decides to control an inspiratory motion and at the same time it inhibits (“gates”) incoming baroreceptor traffic.
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This would, inevitably, lead to a rise of the next diastolic pressure, as shown in Fig. 1B. Than dampened diastolic pressure variability at the respiratory rate of recurrence Rather, one would expect conspicuous respiratory blood circulation pressure oscillations. The jumping between rate of recurrence and time domain should be done with extreme care. Usually the correlation between heart periods and pressure derived parameters is not computed in the time domain by looking at scatterplots but in the frequency domain by looking at phase delays.
I have emphasized the need for baroreflex physiology to comprehend blood pressure-heart rate interactions. Of course, reality is more technical than can be installed into a 1,200-word article. Fig. 1.A: baroreflex-to-heart period schematic. Throughout: systemic pressure, ensuing baroreceptor afferent volley, ECG, evoked vagal efferent activity, and the slowing effect on the sinus node.
B: “central modulation only” schematic. The central nervous system “gates” the inbound baroreceptor afferent activity, no vagal efferent and faster depolarization of the sinus node therefore. Another diastolic pressure is higher than the prior Therefore. C: “baroreflex only” schematic. An increased systemic pressure wave evokes more afferent activity, therefore more vagal efferent activity.