How Breathing Regulates the Cardiovascular System and Improves Chemosensitivity

Key Points

• Breathing modulates the cardiovascular system through respiratory sinus arrhythmia

• Slow breathing reduces chemosensitivity to high carbon dioxide and low oxygen

• Controlled breathing could be a beneficial intervention in different pathological states

The Breathing Diabetic Summary

How does breathing affect us physiologically?  Well, the answer to that is complex.  Breathing is felt by various receptors throughout the body, affecting cardiovascular and autonomic variability on many levels. This review study examined these different modulatory effects of breathing through a comprehensive analysis of the peer-reviewed literature.

Breathing and the Cardiovascular System

The cardiovascular system is sensitive to external stimuli. Just picture something scary (like giving a presentation), and your heart rate will likely increase. Consequently, your breathing will also change to match your metabolic needs.

But this is a two-way street. Controlled, rather than reactive, breathing also has profound impacts on the cardiovascular system. This can be temporary, for example, breathing rapidly for one minute, or permanent, for example, developing the behavior/habit of chronic over-breathing.

Knowing that breathing has "direct access" to the cardiovascular system, let's look at how this occurs and how controlled breathing might be beneficial in different pathological states.

Respiratory Sinus Arrhythmia

One way in which breathing permeates the cardiovascular system is through respiratory sinus arrhythmia (RSA). RSA is a measurement of how breathing, heart rate, and blood pressure all interact. In simple terms, RSA refers to the increase in heart rate as you inhale and decrease in your heart rate as you exhale. RSA is thought to be an index of vagal activity and direct measurement of heart rate variability.  

When we breathe so that the length of our inhale matches seamlessly with our heart rate increase and our exhale with our heart rate decrease, we maximize RSA. Typically, this occurs when breathing at around 6 breaths per minute. This coherence among respiration and heart rate leads to the maximization of heart rate variability, improving cardiovascular efficiency.

Breathing and Chemoreflexes

Slow breathing can reduce breathlessness and improve exercise performance in patients with chronic heart failure. These results suggest that slow breathing could be modifying the chemoreflexes, allowing one to tolerate higher concentrations of carbon dioxide and lower concentrations of oxygen.

To test this hypothesis, a study was conducted with yoga trainees and non-yoga trained participants. Both groups performed different breathing protocols to test their response to high carbon dioxide (hypercapnia) and low oxygen (hypoxia). Although none of these participants had heart problems, the goal was to see if slow breathing could reduce chemoreflexes in the controls to the levels seen in yoga practitioners.

As we might expect, the chemoreflexes of the yoga practitioners at baseline were much lower than the non-trained participants.  This means their breathing did not increase as much when exposed to hypercapnia or hypoxia. Interestingly, the chemoreflexes of the controls decreased to levels similar to the yogis when breathing at 6 breaths per minute.  Therefore, the simple act of slow breathing reduced chemosensitivity to carbon dioxide and hypoxia, regardless of previous training.

These results indicate that breathing could represent another way to better coordinate the breathing muscles, improve chemoreflexes, and improve exercise performance in patients with cardiovascular problems. Slow breathing could, therefore, be a practical alternative when other rehabilitation programs are not available.

Breathing Modulates Cardiovascular and Autonomic Control

To summarize, breathing is a potent modulator of cardiovascular and autonomic systems.  Deliberate practice of different breathing patterns (for example, slow breathing) could be beneficial for increasing heart rate variability, improving breathing efficiency, improving chemosensitivity, and enhancing cardio-autonomic control.

Abstract

Respiration is a powerful modulator of heart rate variability, and of baro- and chemoreflex sensitivity. Abnormal respiratory modulation of heart rate is often an early sign of autonomic dysfunction in a number of diseases. In addition, increase in venous return due to respiration may help in maintaining blood pressure during standing in critical situations. This review examines the possibility that manipulation of breathing pattern may provide beneficial effects in terms not only of ventilatory efficiency, but also of cardiovascular and respiratory control in physiologic and pathologic conditions, such as chronic heart failure. This opens a new area of future research in the better management of patients with cardiovascular autonomic dysfunction.

Journal Reference:

L Bernardi, C Porta, A Gabutti, L Spicuzza, P Sleight.  Modulatory Effects of Respiration.  Auton Neurosci. 2001;90(1-2):47-56. doi: 10.1016/S1566-0702(01)00267-3.

Treat & reverse the root cause of diabetic complications (tissue hypoxia) with slow breathing

Key Points

• Type-1 diabetics exhibit lower resting oxygen saturation, lower cardiovascular control, reduced hypoxic chemoreflexes, and enhanced hypercapnic chemoreflexes

• The root cause of these problems is resting tissue hypoxia, which causes over-activation of the sympathetic nervous system and autonomic and cardiovascular dysfunction

• Autonomic imbalance in diabetes is largely functional, and therefore reversible

The Breathing Diabetic Summary

This is a follow-on to our previous paper on cardio-respiratory control in diabetes.  This paper, however, is a clinical study rather than a literature review.

Previous studies have shown respiratory problems in diabetics.  Previous studies also have shown cardiovascular dysfunction in diabetics.  However, no studies simultaneously examined both of these factors in an integrated fashion.  Thus, the aim of this study was to comprehensively examine cardio-respiratory function in type-1 diabetics.

The key measurements from this paper were resting oxygen saturation, baroreflex sensitivity (BRS; a marker of cardiovascular and autonomic control), and both hypoxic and hypercapnic chemoreflexes (markers of respiratory control). 

Their hypothesis: If the BRS and chemoreflexes were suppressed in diabetics, this would indicate nerve damage was present.  However, if cardiovascular function was suppressed, while chemoreflexes were enhanced, this would indicate autonomic imbalance that has a functional cause.  In this latter case, therapies aimed at restoring cardio-respiratory control (for example, slow breathing) could help prevent diabetic complications.

The study had 46 patients with type-1 diabetes and 103 age-matched control subjects.  The participants went through a variety of tests to evaluate baroreflex functioning and chemoreflexes.  For example, to measure the patients’ hypercapnic chemoreflex, oxygen was kept constant while CO2 was gradually increased.  The chemoreflex can then be measured as the slope of the relationship between minute ventilation and change in CO2 (or oxygen in the case of the hypoxic chemoreflex).  A large change in minute ventilation for a small change in CO2 would represent an enhanced hypercapnic chemoreflex.

Interestingly, the results showed that although diabetics displayed larger breathing volumes than controls, they had slightly higher CO2 levels and reduced oxygen saturation.  However, they did have an enhanced hypercapnic chemoreflex, meaning they could not tolerate changes in CO2 as well as controls.  And, somewhat surprisingly, they had a reduced hypoxic chemoreflex, meaning they could tolerate lower oxygen levels without increasing their breathing as much as controls.

The diabetics also exhibited a lower resting oxygen saturation. This is fascinating because the lower resting oxygen saturation implies a significantly reduced partial pressure of oxygen (due to the oxyhemoglobin dissociation curve). This would result in tissue hypoxia. What’s more, they cite a paper (which is now near the top of my reading list) that shows that a high HbA1c also reduces tissue oxygenation by increasing oxygen’s affinity to hemoglobin (shifting the dissociation curve to the left). 

The authors suggest that their results can be interpreted as follows: Resting tissue hypoxia, combined with a suppressed hypoxic chemoreflex, leads to an enhanced compensatory hypercapnic chemoreflex and chronic activation of the sympathetic nervous system.  This, in turn, leads to a suppression of the cardiovascular system (reduced BRS and reduced heart rate variability).  It’s a vicious cycle.

However, this is actually great news.  Their results suggest that diabetic autonomic imbalance is largely functional and not related to nerve damage.  (Remember, both the cardiovascular reflexes and the chemoreflexes would have been suppressed with nerve damage).  In fact, the authors suggest that this imbalance likely leads to nerve damage rather than being the result of it. Therefore, therapies targeting cardio-respiratory control could help reverse/prevent diabetic complications.

Finally, the authors suggest that breathing control and physical exercise could be two such therapies to restore cardio-respiratory function.  We know that slow breathing has many therapeutic benefits for the cardiovascular, autonomic, and respiratory systems.  And, we know that slow, light breathing increases CO2 and increases tissue oxygenation (due to the Bohr effect).  Now, we know that these positive benefits have the potential to stop or reverse diabetic complications. 

Abstract from Paper

BACKGROUND: Cardiovascular (baroreflex) and respiratory (chemoreflex) control mechanisms were studied separately in diabetes, but their reciprocal interaction (well known for diseases like heart failure) had never been comprehensively assessed. We hypothesized that prevalent autonomic neuropathy would depress both reflexes, whereas prevalent autonomic imbalance through sympathetic activation would depress the baroreflex but enhance the chemoreflexes.

METHODS: In 46 type-1 diabetic subjects (7.0±0.9year duration) and 103 age-matched controls we measured the baroreflex (average of 7 methods), and the chemoreflexes, (hypercapnic: ventilation/carbon dioxide slope during hyperoxic progressive hypercapnia; hypoxic: ventilation/oxygen saturation slope during normocapnic progressive hypoxia). Autonomic dysfunction was evaluated by cardiovascular reflex tests.

RESULTS: Resting oxygen saturation and baroreflex sensitivity were reduced in the diabetic group, whereas the hypercapnic chemoreflex was significantly increased in the entire diabetic group. Despite lower oxygen saturation the hypoxic chemoreflex showed a trend toward a depression in the diabetic group.

CONCLUSION: Cardio-respiratory control imbalance is a common finding in early type 1 diabetes. A reduced sensitivity to hypoxia seems a primary factor leading to reflex sympathetic activation (enhanced hypercapnic chemoreflex and baroreflex depression), hence suggesting a functional origin of cardio-respiratory control imbalance in initial diabetes.

Journal Reference:

Bianchi L, Porta C, Rinaldi A, Gazzaruso C, Fratino P, DeCata P, Protti P, Paltro R, Bernardi L. Integrated cardiovascular/respiratory control in type 1 diabetes evidences functional imbalance: Possible role of hypoxia. Int J Cardiol. 2017;244:254 – 259.