Science of Slow Diaphragmatic Sine wave Breathing

Before explicating the physiology of slow Diaphragmatic Sine wave Breathing, I must begin from the beginning and explain how our breath works.

Take a Slow Breath. Despite the inherently involuntary nature of breathing, most of us have to learn a lot and improve upon this most basic of the physiological function of our body.

A normal person breathes about 12 breaths a minutes, but most breathe at a fairly quick pace most of the time- anywhere around 15-20 breaths per minute- which is about three times faster than the optimised 5-6 ‘yogic’ breaths per minute. This optimised ‘yogic’ breathing has been proven to be the most effective way to lower stress and improve variety of health pursuits ranging from mood to metabolism.

The Breathing cycle. On an Inhale… 

On the inhale, diaphragm – the dome shaped muscle that separates chest from abdomen, contracts, lowers and flattens. This increases the intra-thoracic space (chest cavity enclosed by the rib cage), which makes the room for the air coming into the lungs by changing the pressure inside the lungs. 

The air travels through your nostrils and into your nasal cavities routed through the bronchi (passageways connecting windpipe to lungs) into the lungs.

In the lungs, the air reaches the alveoli (air sacs), which serve as a place where exchange of O2 and CO2 takes place.

From the alveoli, O2 move into the capillaries (thin-walled blood vessels) and attach to red blood cells, which start making their way to the heart.

The heart, then contracts and pumps O2 rich blood to every single cell in the body via the network of arteries and capillaries.

The Breathing cycle. On an Exhale…

In every cell, Mitochondria (the centre that produces energy) uses oxygen to metabolise sugars, fats, and proteins for energy and releases CO2, a byproduct of this process. 

CO2 travels into the veins that carry CO2-rich blood to the heart. Next, the heart contracts, pushing the CO2-rich blood into the pulmonary artery and back to the lungs.

As the blood enters the alveoli, the CO2 leaves the bloodstream and enters into the lungs. Then the diaphragm relaxes, decreasing the intra-thoracic pressure and initiates an exhalation thereby release CO2 out of the system. 

The Science behind Breathing.

The Diaphragm receives orders to contract from phrenic nerve. The phrenic nerve receives signals from the brainstem indicating when to contract and relax.

The brainstem, part of the brain, contains group of neurons-known as central pattern generators (CPG). (Boron & Boulpaep, 2012). The central pattern generators (CPG) control our normal rhythm of breathing… BUT how to explain the variation in rate, rhythm, and depth that characterises your everyday breathing? 

The Brainstem functioning…

Many external factors influence our breath, but for today’s discussion I will limit our discussion to two Regulatory processes – Central and Peripheral.

“Central” sources originate from the central nervous system (brainstem, limbic system and the prefrontal cortex). “Peripheral” sources are those that originate somewhere outside of the central nervous system.

The two peripheral sources are…

(a) Chemoreceptors
Pulmonary Stretch Receptors (SARs)

(a) Chemoreceptors

Receptors located near the arch of aorta (largest artery of the body) and neck, sends signals and feedback to the respiratory centre to modulate ventilatory output depending on the CO2 (mainly) and O2 concentrations.

For example, during exercise CO2 levels increases significantly. This can stimulate chemoreceptors, which in turn signals respiratory centre to increase the respiratory rate- this is what we actually need during aerobic exercise.

Along with an increase in respiratory rate, low O2 or high CO2 and the subsequent triggering of the chemoreceptors also enhances the sympathetic nervous system output. (Boron & Boulpaep, 2012).

(b) Pulmonary Stretch Receptors (SARs)

Receptors triggered by the expansion of lungs during inhalation. The signals from SARs are then transmitted to brainstem via vagus nerve (10th cranial nerve).

These signals inhibits respiratory centre and inhibits inspiratory drive-thus preventing over-inflation of lungs

Now that we have discussed the physiology of lungs and receptors during breathing, let’s turn to the Heart…

The rate and rhythm of your heartbeat is maintained by the group of cells present in heart called the SA Node. The SA Node receives signals from both sympathetic and parasympathetic nervous system. 

The SNS and PNS represent a sort of body’s internal yin and yang system. Our body always maintains a homeostasis by balancing between these two systems.

In the case of the Heart, the SNS accelerates the heart rate and raises blood pressure, whereas The PSNS slows down the rate of the heart and causes dilation of blood vessels.

Role of baroreceptors in Blood pressure regulation

These are the receptors located at the same position as that of chemoreceptors. An increase in blood pressure stimulates baroreceptors and the signals are then relayed in the brainstem neurons.

Upon activation, these neurons increase PNS activity at the SA node thus slowing the heart rate.

Now let’s examine blood pressure changes during each respiratory cycle.

 As you inhale, your diaphragm flattens and creates a negative pressure within the chest. This negative pressure acts as a vacuum and sucks blood towards the right side of the heart with subsequent lack of blood to the left ventricle (heart’s output center).

Lack of blood to the left ventricle decreases the amount of blood ejected during contraction (stroke volume) of heart and subsequently decreases blood pressure.

During exhalation, your diaphragm relaxes and intra-thoracic pressure normalises, which replenishes the relative deficit of blood in the left ventricle. This increases stroke volume and normalises blood pressure.

The relative reduction of blood pressure during inhalation decreases your baroreceptor signalling and releases the PNS hold on the SA node, leading to increase in heart rate.

 The relative increase in blood pressure on exhalation increases baroreceptor signaling and stimulates the brainstem to increase PNS signalling to the SA node, thus decreasing the heart rate

To summarise… Heart rate increases during inhalation and decreases during exhalation.

The brainstem receives input from both higher as well as lower sources. Until now I have discussed about the lower or unconscious half of the equation. Now let’s turn to the higher or subconscious/conscious factors influencing breathing- the limbic system and prefrontal cortex.

During panic attack, the raw data of the fear response is transmitted to your amygdala (part of limbic system) and prefrontal cortex (area of consciousness). This response releases norepinephrine and epinephrine (stress hormones) and stimulates SNS- leading to increase in heart rate and respiratory rate It also begins a domino effects that ends with the release of cortisol by the adrenal glands (located near kidneys)

The intricacies of a Slow Breathing…

Our lung’s total capacity is about 6000c.c. and during normal breathing we use only about 600c.c per breath. Whereas in deep breathing you can, theoretically, inhale up to the total capacity of the lungs, which makes breathing more efficient.

Slow deep breathing also reduces the amount of CO2 you expel during each exhalation, by decreasing number of exhalations per minute. This increase in CO2 levels is only a relative increase and doesn’t reflect a pathological mechanism that stimulates your brainstem to increase respirations.

With continuous practice of slow deep breathing, the increased exposure of chemoreceptors to higher levels of CO2 subsequently decreases their sensitivity, thereby reducing the SNS stimulation to the exposure of higher CO2 levels.

Also, the improved oxygenation of the tissues decreases their Stress, further decreasing the SNS (sympathetic nervous system) stimulation and shifting the balance towards PNS (parasympathetic nervous system) activation (Pal & Velkumary, 2004)

Because of slow and optimised breathing- longer inhalation increases both the signal intensity and duration of the slowly adapting pulmonary stretch receptors (SARs). This enhanced signalling of SARs (mainly inhibitory signals) travels along the vagus nerve to the brainstem.

Inhibitory signals in the brainstem enhance the synchronisation between hypothalamus and brainstem and have shown to enhance overall PNS (parasympathetic nervous system) outflow. ( Jerath, Edry, Barnes, 2006)

Returning to the regulation of heart rate and blood pressure during normal respiration, you have noted that the PNS outflow is more during the expiratory phase of your breathing. (Brown & Gerbarg, 2005)

Thus, the prolongation of exhalation (as done in the slow, deep breathing) results in relative increase of PNS drive.

Along with this, the inhibition and excitation of baroreceptors is also enhanced with slower inhalation and exhalation respectively.

With time, the efficiency of baroreceptors increases and they become more capable of modulating heart rate with the changing blood pressure-thus increasing baroreceptor sensitivity (Kaushik, Kaushik, Mahajan, & Rajesh, 2006)

The increased sensitivity of arterial baroreceptors increases the heart rate variability. And because heart rate variability is mainly determined by vagus nerve and the PNS outflow, the increased sensitivity of baroreceptors reflects a relative increase of PNS activity and vagal tone(Pal & Velkumary, 2004)

To summarise: slow, deep breathing, through a variety of mechanisms, increases PNS activity and decreases SNS activity.

Furthermore, the increase in PSNS drive in the brainstem due to slow deep breathing is transmitted back up to the limbic system and the PFC. The inhibitory nature of the PNS outflow decreases the intensity of fear response of the amygdala and enhances the sense of wellbeing and calmness in the PFC.

These mechanisms are thought to be the reason behind the subjective feeling of relaxation and stress reduction that occurs with the slow, deep breathing (Ankad, Herur, Patil, Shashikala, & Chinagudi, 2011)

Stephen Porges, a psychiatrist at the University of North Carolina has developed the “polyvagal theory”. In this theory he has explained the evolution of vagus nerve and its role in human emotions. High vagal tone and resting PNS tone is associated with happy traits and increased resilience to anxiety and stress.

In a way you are biologically programmed with the capacity to relax or in other words your resting vagal tone is inherently determined. But, with conscious practice of slow deep breathing, you can modulate your basic physiology.

Air is a pasture of life and a greatest ruler of all.


I suppose he knew what western science consider breathing- that it a physiological function integral to survival, while the eastern health sciences approach it as food for body, mind and spirit.

I hope my lengthy discussion has encouraged you to look deep into the most under appreciated function of our body- our breathing – and observe the power of restorative change it contains.

Aashish Nanda

The information provided on this website is intended for general reading purpose ONLY. Please do not use this information to diagnose, treat, prevent or cure any disease or condition. Please consult a professional, in case you need any advice...

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