CO₂ - The Gas That Changes the Heart, Brain, and Digestion

Breathing does not only change how much oxygen enters. It also changes the environment in which the heart, blood vessels, brain, and viscera must function.

In the previous blog, we saw that not every breath is the same.

One person may breathe slowly while moving a large volume of air.

Another may breathe faster while moving very little.

One may breathe through the nose.

Another through the mouth.

One may produce a broad, apparently “deep” breath and still ventilate more than metabolism requires.

Now one molecule appears capable of connecting much of this story:

CO₂.

We usually treat it simply as waste.

We inhale oxygen.

We exhale carbon dioxide.

End of story.

But physiologically, that is not how it works.

Carbon dioxide participates in acid-base balance, in the chemoreflexes that regulate ventilation, and, especially important for this series, in the regulation of cerebral blood vessels.

This means that a respiratory change can reach the heart, the brain, and what we record with NIRS without necessarily beginning as a primary change in neuronal activity.

Breathing Too Much Does Not Necessarily Mean Breathing Fast

We need to begin with a fundamental distinction.

Hyperventilation does not simply mean breathing fast.

Hyperventilation means ventilating the alveoli more than is required for the body’s metabolic production of CO₂.

If we eliminate CO₂ faster than the organism produces it:

arterial CO₂ tends to fall.

This is hypocapnia.

So a person may breathe slowly and still hyperventilate if each breath moves an excessively large volume.

Likewise, a relatively high respiratory rate does not necessarily mean hyperventilation if the volume moved is small and appropriate for metabolic demand.

This is why observing respiratory rate alone can be misleading.

We want to know:

**rate

• volume

• airflow

• ETCO₂.**

When CO₂ Falls, the Brain Receives a Different Blood Flow

The brain has a particularly strong relationship with CO₂.

Arterial partial pressure of CO₂ is one of the major modulators of cerebral blood flow.

In general terms:

CO₂ ↓
→ pH tends to rise
→ cerebral vessels tend to constrict
→ vascular resistance increases
→ cerebral blood flow tends to decrease.

In the opposite direction:

CO₂ ↑
→ pH tends to fall
→ cerebral vessels tend to dilate
→ vascular resistance decreases
→ cerebral blood flow tends to increase.

A 2024 review on CO₂ vasomotor reactivity describes exactly this relationship: reduced PaCO₂ is associated with lower cerebral blood flow, while elevated PaCO₂ tends to increase flow through cerebrovascular reactivity.

This helps explain why hyperventilation can produce:

dizziness,

visual changes,

tingling,

unusual bodily sensations,

and changes in subjective experience.

We do not need to begin by assuming that the brain has “entered a higher state.”

First, we need to ask:

how much did CO₂ change?

But 40 mmHg Is Not a Switch

In clinical settings, PaCO₂ values around 35–45 mmHg are often used as an approximate reference range for normocapnia.

But there is no switch:

39 = normal
40 = normal
41 = vasodilation.

The system is continuous.

For our future experiment, it will be much more useful to observe the relative change:

ΔCO₂ from the individual baseline.

One person may begin with an ETCO₂ of 39 mmHg and reach 44.

Another may begin at 35 and reach 40.

The final value looks similar.

The physiological trajectory is not necessarily the same.

That is why CO₂ needs to be followed through time.

NIRS Sees This Change — but It Does Not Know Why It Happened

Here we reach one of the most important issues for our future experiments.

NIRS sends near-infrared light through tissue and estimates relative changes in oxygenated and deoxygenated hemoglobin:

HbO
and
HbR.

When a brain region increases its neural activity, local blood flow may increase through neurovascular coupling.

HbO may rise.

We might then conclude:

HbO ↑ = the brain became more active.

But there is another pathway.

Imagine a breath hold.

CO₂ rises.

Cerebral vessels dilate.

Cerebral blood flow increases.

HbO changes.

So we may have:

CO₂ ↑
→ vasodilation
→ blood flow ↑
→ HbO ↑

without the observed change being explained only by greater neuronal activity.

This is one reason researchers have proposed systemic physiology augmented fNIRS: heart rate, blood pressure, breathing, and CO₂ should be recorded alongside NIRS when we want to interpret cerebral hemodynamics correctly.

fNIRS experiments can also use CO₂ as a vasoactive stimulus to measure cerebrovascular reactivity, directly showing that HbO and HbR respond to vascular manipulation produced by the gas.

For us, this changes the question.

We will not ask only:

“Did HbO increase?”

We will ask:

“Did HbO increase while CO₂ remained stable, or while the entire vascular system was being modified by CO₂?”

The Same Respiratory Cycle Also Changes the Heart

While CO₂ influences chemoreceptors and cerebral circulation, respiratory phase continuously modulates cardiac intervals.

During inspiration:

heart rate tends to increase
and RR tends to shorten.

During expiration:

heart rate tends to decrease
and RR tends to lengthen.

In 2025, an international expert recommendation including Brazilian researchers Benedito Machado and Davi Moraes proposed calling this phenomenon Respiratory Heart Rate Variability — RespHRV.

The recommendation also makes an important correction:

the amplitude of RespHRV should not automatically be interpreted as a direct measure of “vagal tone.”

Breathing rate, breathing depth, mechanical factors, respiratory brainstem networks, and cardiovagal activity all participate in this oscillation.

This is crucial.

We do not want to build a new simplification:

exhale → vagus increases → body relaxes.

The organism is more complex than that.

Sympathetic and Parasympathetic Are Not Two Buttons Either

Another popular metaphor says:

sympathetic = fight or flight

and

parasympathetic = rest and digest.

It is useful for teaching.

But biologically incomplete.

The autonomic nervous system is made of diverse, specialized circuits capable of producing different responses in different organs.

A 2025 review in Nature Reviews Neuroscience emphasizes precisely this molecular and functional diversity, moving far beyond the idea of two global switches turning the entire organism on and off.

We may have cardiovascular, digestive, respiratory, and vascular changes occurring in different combinations.

The Body-Territory does not need to be entirely in “sympathetic mode” or entirely in “parasympathetic mode.”

It can distribute priorities.

So Where Does Digestion Enter?

The digestive tract has its own highly complex neural system:

the enteric nervous system.

It can organize much of local motility, secretion, and intestinal function.

But it is not isolated.

It receives sympathetic and parasympathetic influences and communicates continuously with the central nervous system.

A broad 2023 review shows that the enteric nervous system regulates digestion and homeostasis through its own circuitry while autonomic signals modulate its activity.

This means we should not write:

long exhalation → HRV rises → parasympathetic activity rises → digestion improves.

That causal chain has not been demonstrated in that form.

We can say something more careful:

breathing, autonomic activity, and gastrointestinal function can interact, but the digestive system has its own mechanisms and its function cannot be inferred from HRV alone.

A 2023 systematic review found associations between HRV alterations and different functional gastrointestinal disorders, but also enough heterogeneity to prevent HRV from being treated as a simple reading of digestive function.

The Diaphragm Offers Another Link to Digestion

There is, however, a very concrete connection that does not depend on autonomic metaphors.

The diaphragm participates mechanically in the region of the gastroesophageal junction.

Clinical studies indicate that diaphragmatic breathing training can modify the pressure of the anti-reflux barrier and reduce some reflux episodes.

A meta-analysis published in 2026 found a modest improvement in reflux symptoms with diaphragmatic exercises, but also substantial heterogeneity and concluded that the evidence still does not justify definitive recommendations for every patient.

This is very different from saying:

“diaphragmatic breathing activates the vagus and improves digestion.”

We may have:

mechanical effects,
autonomic effects,
attentional effects,
postural effects

and perhaps interactions among them.

We need to measure before choosing an explanation.

And What About Stephen Porges?

Here we enter a territory that requires scientific care.

Stephen Porges developed the Polyvagal Theory, proposing a model in which different vagal circuits participate in states related to safety, social engagement, mobilization, and immobilization.

In his 2025 update, Porges continued to defend a hierarchical organization of the autonomic nervous system and concepts such as neuroception, co-regulation, and the ventral vagal complex.

These ideas have had enormous influence in psychology, trauma work, education, and body-based practices.

But influence does not mean physiological consensus.

In February 2026, 39 researchers specializing in autonomic physiology, evolution, and vagal neurobiology published a critical evaluation concluding that central premises of Polyvagal Theory were not supported by the available neurophysiology and evolutionary biology.

Among the authors were Brazilian researchers who have already appeared in this series:

Benedito H. Machado
and
Davi J. A. Moraes.

One of the central criticisms concerns the use of RespHRV — formerly RSA — as if it were equivalent to a direct and general measure of vagal activity.

Porges responded in the same year, arguing that his critics had evaluated an inadequate reconstruction of the theory and had confused different levels of analysis, defending Polyvagal Theory as a systemic and pathway-specific model of autonomic organization.

For BrainLatam, we do not need to choose a side.

We can do science.

What Can We Use Without Turning a Theory Into Established Physiology?

Polyvagal Theory raises interesting questions:

How does the organism detect safety and threat?

How do bodily states modify social behavior?

How do people regulate one another?

How can experiences that do not immediately reach conscious perception alter autonomic state?

These questions remain relevant.

But when studying breathing, we do not need to use Polyvagal Theory as the single explanation for the mechanisms involved.

We already have:

chemoreceptors,

respiratory brainstem networks,

baroreflexes,

sympathetic activity,

cardiovagal activity,

the enteric nervous system,

thoracoabdominal mechanics,

CO₂,

blood pressure,

cerebral blood flow.

That physiology is already extraordinarily rich.

An Exhalation Does Not “Turn On the Parasympathetic System”

Return now to your own breathing.

Inhale.

Exhale slowly.

Perhaps RR increases.

Perhaps heart rate decreases.

Perhaps you notice a change in muscle tension.

But we do not need to say:

“the parasympathetic system turned on.”

We can observe something more precise.

Breathing changed:

pressures,

pulmonary afferent signals,

respiratory networks,

cardiovagal modulation,

RR intervals,

alveolar ventilation.

If we continue breathing in a certain way, we may also change CO₂.

And when CO₂ changes:

cerebral vessels respond.

So one breathing technique may simultaneously alter:

**RespHRV

• blood pressure

• CO₂

• cerebral blood flow

• HbO/HbR

• bodily experience.**

That is exactly why studying HRV alone will not be enough.

Jiwasa: No Single Signal Tells the Whole Story

Imagine our future experiment.

A person begins with:

ETCO₂ = 40 mmHg.

They start taking very large breaths.

Respiratory rate decreases.

RespHRV increases.

If we looked only at HRV, we might conclude:

“autonomic regulation improved.”

Then we look at:

ETCO₂: 40 → 32 mmHg.

Now the story changes.

What may be happening is:

excessive ventilation
→ hypocapnia
→ cerebral vasoconstriction
→ altered cerebral blood flow
→ changes in HbO/HbR.

Meanwhile, the person may report:

lightness,

tingling,

changes in perception,

or an intense sense of calm.

Which signal is correct?

They may all be correct.

Each one is observing part of the same Body-Territory.

That is why we want to place in Jiwasa:

**breathing

• CO₂

• ECG/RespHRV

• blood pressure

• SpO₂

• EEG

• NIRS

• first-person experience.**

Not to create one definitive number of “regulation.”

But to observe how an entire organism changes together.

CO₂ may be an excellent teacher for this series.

Because it shows that what we once called “respiratory waste” can reorganize the vessels feeding the brain that perceives the breathing itself.

In the next movement of the series, we can ask something even deeper:

what happens if a Body-Territory repeats a breathing pattern for long enough to keep CO₂ different from its previous equilibrium — how might the kidneys, bicarbonate, and metabolism participate in that adaptation?

This is where our next hypothesis enters:

the RIM Loop.

Main References

MENUET, C. et al. (2025). Redefining respiratory sinus arrhythmia as respiratory heart rate variability: an international Expert Recommendation for terminological clarity. Nature Reviews Cardiology, 22, 978–984.
Proposes RespHRV as a more precise term, describes respiratory modulation of heart rate, and warns that its amplitude should not automatically be treated as a measure of “vagal tone”; the authors include Brazilian researchers Benedito Machado and Davi Moraes.

FISHER, J. P.; ZERA, T.; PATON, J. F. R. (2022). Respiratory–cardiovascular interactions. Handbook of Clinical Neurology, 188, 279–308.
Shows that breathing, sympathetic activity, cardiovagal activity, blood pressure, and circulation form coupled physiological oscillators, providing a basis for avoiding simplistic autonomic explanations.

PATON, J. F. R.; MACHADO, B. H.; MORAES, D. J. A.; ZOCCAL, D. B. et al. (2022). Advancing respiratory-cardiovascular physiology with the working heart-brainstem preparation over 25 years. The Journal of Physiology, 600, 2049–2075.
Brings together research, with strong Brazilian participation, on how brainstem networks integrate respiratory and cardiovascular control.

Intracranial and extracranial CO₂ vasomotor reactivity: assessment, approaches and clinical applications (2024). Medical Gas Research.
Reviews vascular reactivity to CO₂ and supports the central relationship of this blog: lower PaCO₂ tends to reduce cerebral blood flow, while relative increases favor vasodilation and greater flow.

SCHOLKMANN, F.; TACHTSIDIS, I.; WOLF, M.; WOLF, U. (2022). Systemic physiology augmented functional near-infrared spectroscopy: a powerful approach to study the embodied human brain. Neurophotonics, 9(3), 030801.
Shows why fNIRS signals should be interpreted alongside CO₂, breathing, heart rate, blood pressure, and extracerebral circulation, making it a central reference for our experimental design.

Cerebrovascular Reactivity Measurement with Functional Near Infrared Spectroscopy (2022).
Demonstrates that fNIRS can record HbO and HbR changes during controlled CO₂ challenges, directly showing that hemodynamic changes in NIRS are not automatically equivalent to neural activation.

WANG, T. et al. (2025). Molecular and functional diversity of the autonomic nervous system. Nature Reviews Neuroscience, 26, 607–622.
Shows the molecular and functional diversity of autonomic circuits and helps replace the overly simple metaphor of sympathetic and parasympathetic systems as two global switches.

SPENCER, N. J.; HUI, X.; TRAVAGLI, R. A. et al. (2023). The enteric nervous system. Physiological Reviews.
Presents the enteric nervous system as a highly autonomous network that is nevertheless modulated by sympathetic, parasympathetic, and brain-gut pathways, preventing digestion from being reduced to a simple consequence of HRV.

ALI, M. K.; CHEN, J. D. Z. (2023). Roles of Heart Rate Variability in Assessing Autonomic Nervous System in Functional Gastrointestinal Disorders: A Systematic Review. Diagnostics, 13(2), 293.
Finds relationships between HRV and several functional gastrointestinal disorders, but also substantial heterogeneity, supporting caution against treating HRV as a direct reading of digestive function.

Efficacy and Safety of Diaphragmatic Breathing Exercises for Gastroesophageal Reflux Disease: A Systematic Review and Meta-Analysis (2026). Journal of Clinical Medicine, 15(9), 3406.
Finds modest benefits of diaphragmatic breathing for reflux symptoms but substantial heterogeneity, reinforcing that digestive effects may involve diaphragm mechanics and should not automatically be attributed to “increased vagal activity.”

PORGES, S. W. (2025). Polyvagal Theory: Current Status, Clinical Applications, and Future Directions. Clinical Neuropsychiatry, 22(3), 169–184.
Presents Porges’s contemporary formulation of Polyvagal Theory, including neuroception, co-regulation, hierarchical autonomic organization, and his interpretation of vagal function.

GROSSMAN, P. et al. (2026). Why the Polyvagal Theory Is Untenable: An international expert evaluation of the polyvagal theory. Clinical Neuropsychiatry, 23(1), 100–112.
Brings together 39 specialists who challenge neuroanatomical, evolutionary, and physiological premises of Polyvagal Theory, including the use of RespHRV/RSA as equivalent to general vagal activity; Brazilian researchers Benedito Machado and Davi Moraes are among the authors.

PORGES, S. W. (2026). When a Critique Becomes Untenable: A Scholarly Response to Grossman et al.’s Evaluation of Polyvagal Theory. Clinical Neuropsychiatry.
Presents Porges’s response to the 2026 criticism, arguing that parts of the critique confuse levels of analysis and do not adequately evaluate Polyvagal Theory as a systemic and pathway-specific model.

The anchor sentence for this Blog 7 remains very strong in English: “Before interpreting a state of the brain, we need to know the state of the blood that reached it.”