Respiratory sinus arrhythmia (RSA) is a naturally occurring variation in heart rate that occurs during a breathing cycle. Heart rate increases during inspiration and decreases during expiration. Heart rate is normally controlled by centers in the medulla oblongata. One of these centers, the nucleus ambiguus, increases parasympathetic nervous system input to the heart via the vagus nerve. The vagus nerve decreases heart rate by decreasing the rate of SA node firing. Upon expiration the cells in the nucleus ambiguus are activated and heart rate is slowed down. In contrast, inspiration triggers inhibitory signals to the nucleus ambiguus and consequently the vagus nerve remains unstimulated.
On an electrocardiogram this phenomenon is seen as subtle changes in the R-R interval synchronized with respiration. The R-R interval on an ECG is shortened during inspiration and prolonged during expiration. In humans, the magnitude of the RSA increases with physical conditioning and self-induced, relaxed breathing. RSA becomes less prominent with age, diabetes and cardiovascular disease.
Previous studies have shown that the efficiency of pulmonary gas exchange is improved by RSA, suggesting that RSA may play an active physiologic role. The matched timing of alveolar ventilation and its perfusion with RSA within each respiratory cycle could save energy expenditure by suppressing unnecessary heartbeats during expiration and ineffective ventilation during the ebb of perfusion. Furthermore, evidence has accumulated of a possible dissociation between RSA and vagal control of that heart rate, suggesting differential controls between the respiratory modulation of cardiac vagal outflow and cardiac vagal tone. RSA or heart rate variability in synchrony with respiration is a biological phenomenon, which may have a positive influence on gas exchange at the level of the lung via efficient ventilation/perfusion matching.
To the contrary, in HRM, we see that heart rate decreases during inhalation and increases during exhalation. To prove this to yourself, plug in your Heart Rate Variability monitor and try holding your inhale and then holding your exhale. Notice that there is a delay of 2 to 3 seconds between your breath and what is shown on the monitor. Nevertheless, if you hold your breath, the heartrate will be relatively flat, so you can easily see which part of the breath cycle you're in.
Here's a HRV graph Puran made:
Notice that the heartrate curve is flat during the second "Hold Inhale" period, and nearly flat during the first such period. During the "Hold Exhale" period, the heart rate climbs steadily, indicating the stress of being without breath.
This efffect was repeated by Dr. Steve Baumann at the Rhine Research Center in Durham, NC in 2006. He used a much more sophisticated instrument with electrodes on the chest to pick up the heart rate electrically, and a tension belt to pick up the movement of breathing. The graph he produced is the following:
This is a graph of three measurements on the same time scale. The top graph is an EKG showing individual heartbeats. The middle graph shows the tension in the belt so that a rise indicates an expansion of the abdomen during an inhalation. The bottom graph is calculated from the EKG and shows Beats Per Minute (BPM).
At the left of the image, the dotted box around breath #1 shows a relationship between the green graph of breath volume and the blue graph of heart rate that is typical of RSA. They are both going up together, so the inhalation (maximum breath volume) creates a rise in the heart rate. Therefor, as it says in the Wikipedia reference, "Heart rate increases during inspiration."
By the end of breath #3, the exhalation is causing a rise in heart rate. From then on, the maximum breath volume, the top of the inhalation, roughly lines up with the lowest heart rate.
Breath #7, for example, is showing a clear case of the opposite-from-RSA relationship between breathing and heart rate. Dr. Baumann was so surprised at this that he said, "This is going to get me an NSF grant." He said this phenomena was completely unknown. He asked the head of cardiology at Duke University, a friend of his, and the cardiologist was skeptical - no reverse-RSA effect has ever been published.
Once again, our lineage was helpful. My teacher, Pir Vilayat, described this relationship between breath and heart rate from self-observation, without any measurement. He explained it thus: "The inhalation fills the lungs, putting pressure on the heart which lies between them. This squuezes the heart and slows its beating. Then the exhalation releases the pressure from the lungs and the heart speeds up again."
What shall we name the Reverse-RSA effect? How about "Lung Pressure Arrhythmia"?
Written by Puran and Susanna Bair
© Copyright 2009 by The Institute for Applied Meditation, Inc.