One Breath Has Four Phases

Inhale, hold full, exhale, hold empty: what do the heart, brain, and blood do while we breathe?

Before dividing breathing into parts, notice one complete breath.

Do not try to improve it.

Inhale.

Perhaps there is a brief moment before you begin to exhale.

Exhale.

Perhaps another small interval appears before the next inhalation.

What we usually call simply “breathing” can be observed as four movements:

inhale
→ hold full
→ exhale
→ hold empty.

These four phases are not four independent systems.

They are different moments of a single cycle in which the lungs, heart, blood vessels, brain, muscles, and metabolism continue communicating.

In the previous blog, we followed air from the territory to the mitochondrion and back to the atmosphere.

Now we will reduce the scale even further.

We will follow a single breath.

First, we need to know where each phase begins

It sounds simple.

Experimentally, however, we need a reference.

A band around the chest can record thoracic expansion.

Another around the abdomen records a different component of respiratory movement.

A nasal or oral airflow sensor shows when air is actually entering and leaving.

Combining these signals allows us to identify:

the beginning of inhalation,
the end of inhalation,
the beginning of exhalation,
the end of exhalation.

Then we can ask where each heartbeat, each electrical change in the brain, or each hemodynamic change occurred in relation to that respiratory cycle.

This distinction is fundamental.

The sensors do not “know” that someone is inhaling.

Synchronization is what places all signals within the same time.

This will become one of the foundations of our future experiment using LSL.

The heart already knows this rhythm

An electrocardiogram records differences in electrical potential generated by cardiac activation.

Within the ECG, the R peak of the QRS complex provides a highly precise temporal marker for each heartbeat.

We measure:

R → next R = RR interval.

When a healthy person breathes spontaneously, there is usually an oscillation related to breathing:

during inhalation, heart rate tends to increase and the RR interval tends to shorten;

during exhalation, heart rate tends to decrease and the RR interval tends to lengthen.

An international expert recommendation published in 2025 proposed calling this phenomenon Respiratory Heart Rate Variability — RespHRV, rather than respiratory sinus arrhythmia. Among the authors are Brazilian researchers Benedito Machado and Davi Moraes from the University of São Paulo.

But there is an important precision for our study.

It does not make sense to calculate an “HRV of inhalation” from only one or two seconds of data.

Conventional HRV requires longer time windows.

What we can do is something different:

locate each RR interval within the respiratory phase.

We can then observe the trajectory of the heart across dozens or hundreds of cycles.

This gives us something closer to:

how RR changes within breathing

rather than simply asking “how much HRV exists during inhalation.”

1. Inhale

When we inhale spontaneously, the diaphragm descends and intrathoracic pressure becomes more negative.

This modifies venous return, cardiac filling, and pressures within the chest.

At the same time, respiratory circuits in the brainstem modulate autonomic circuits that control the heart. Modern physiology describes these interactions as a coupled system rather than two independent clocks.

In simple terms:

inhalation → HR tends to rise → RR tends to shorten.

Blood pressure also oscillates with breathing, but we need to be careful here. Changes in venous return, stroke volume, and arterial pressure do not all occur at exactly the same moment; delays may exist between the right heart, left heart, and arterial circulation.

So we will not adopt the simplistic rule:

“inhaling always lowers blood pressure.”

We will measure pressure continuously.

And CO₂?

During inhalation, the capnograph detects inspired gas containing very little CO₂.

But this does not mean that blood CO₂ falls instantly.

Capnography uses infrared absorption to measure CO₂ in the gas passing through the sensor. During exhalation, the concentration rises; the maximum value near the end of exhalation is called ETCO₂.

Therefore, we need to distinguish:

CO₂ at the mouth or nose

from

arterial and cerebral CO₂.

The latter change according to accumulated ventilation, not simply because an inhalation has begun.

2. Hold full

Now mentally pause the cycle at the end of inhalation.

The lungs are relatively full.

There is no airflow.

But metabolism has not stopped.

Cells continue producing CO₂ and consuming O₂.

If the pause is very short, changes in gases will be small.

If it lasts longer:

CO₂ tends to rise
and O₂ tends to fall.

This creates an interesting experimental problem.

Without exhalation, there is no new ETCO₂ measurement.

The capnograph needs expired gas.

So during a breath hold we can follow time, SpO₂, and other signals, but we only obtain a new ETCO₂ value when exhalation occurs. To follow CO₂ continuously during a hold, other approaches would be needed, such as transcutaneous CO₂ or more invasive measurements.

The way a person “holds” the breath also matters.

Holding the breath calmly is not the same as straining against a closed glottis.

A maneuver resembling Valsalva can dramatically alter intrathoracic pressure and circulation.

So our protocol will need to distinguish:

breath retention

from

pressure-generating effort.

3. Exhale

During quiet exhalation, the cardiac phenomenon usually reverses.

Cardiac vagal activity related to the respiratory cycle tends to increase.

Heart rate decreases.

RR lengthens.

This is why breathing with a longer exhalation can significantly alter RespHRV.

But once again, we should not conclude:

“exhaling produces more HRV.”

The variable is the entire cycle and the temporal relationship between breathing and the heart.

Recent studies also show that respiratory frequency, breathing depth, and posture can modify the amplitude of RespHRV without representing equivalent changes in “vagal tone.”

During exhalation, the capnogram begins close to zero with gas from anatomical dead space, rises as alveolar gas reaches the sensor, and reaches its highest value near the end of exhalation.

This is where we obtain:

ETCO₂.

Values around 35–45 mmHg are often used clinically as a reference range for normal ETCO₂, although ETCO₂ is not exactly the same as arterial PaCO₂.

For our experiment, it may be even more important to observe:

ΔCO₂ relative to the individual baseline.

A person moving from 39 to 44 mmHg has undergone a physiologically relevant change even though both values remain within a broadly normal range.

4. Hold empty

Now we reach the interval after exhalation.

Lung volume is relatively low compared with the end of inhalation.

No new air enters.

Cells continue producing CO₂.

So, as the pause becomes longer:

CO₂ progressively rises
and O₂ progressively falls.

This begins to activate chemoreceptors and increases the urge to breathe.

The cardiovascular response can vary considerably with duration, training, emotional state, and the way the breath hold is performed.

This is also where cerebral hemodynamics become especially interesting.

CO₂ is a powerful modulator of cerebral blood vessels.

Relative increases in CO₂ favor vasodilation and increased cerebral blood flow; reductions in CO₂ during hyperventilation favor vasoconstriction.

Recent studies of cerebrovascular reactivity use breath-hold tasks precisely to provoke CO₂ changes and observe the cerebral vascular response. A 2023 study showed that ETCO₂ can be used to model both the amplitude and the delay of cerebrovascular responses during breath-hold protocols.

This will be central to interpreting our NIRS data.

How will we observe the brain with EEG?

EEG measures electricity.

Electrodes placed on the scalp record differences in electrical potential, typically in the microvolt range, generated by the coordinated activity of large populations of neurons, especially cortical postsynaptic currents.

A 2023 review highlights one of EEG’s major advantages: neural changes can be followed on the scale of milliseconds.

This is ideal for respiratory research.

We can mark:

0° = beginning of inhalation
→ inhalation–exhalation transition
→ exhalation
→ 360° = new cycle

and ask whether power, phase, or other EEG properties change systematically around that circle.

Recent research already shows that both oscillatory and non-oscillatory components of brain activity can be coupled to respiratory phase.

But there is a challenge.

Breathing also moves:

the neck,

the face,

the scalp,

the jaw,

the electrodes.

So part of what appears in the EEG may be muscular or mechanical artifact.

Our study will need to distinguish:

the brain changing with breathing

from

the electrode moving because the person breathed.

And how does NIRS see the brain?

NIRS does not measure electricity.

It sends near-infrared light through the scalp and detects the light that returns after being absorbed and scattered by tissue.

Oxygenated and deoxygenated hemoglobin absorb different wavelengths of light differently.

Using at least two wavelengths and a modified form of the Beer–Lambert law, we can estimate relative changes in:

HbO — oxygenated hemoglobin

and

HbR — deoxygenated hemoglobin.

It is a hemodynamic window.

Not “EEG with light.”

And this changes everything in our experiment.

If HbO rises during a breath hold, we might be tempted to say:

“the brain became more active.”

But perhaps what happened was:

CO₂ ↑
→ cerebral vasodilation
→ cerebral blood flow ↑
→ HbO changes.

Breathing, blood pressure, and scalp circulation can also alter the optical signal.

This is why modern systems use short-separation channels, which mainly capture superficial tissue signals and help distinguish scalp-related changes from changes more likely to come from the cortex.

Our question will not be:

“Did HbO increase or decrease?”

It will be:

“What was happening simultaneously with CO₂, SpO₂, pressure, heart activity, and EEG when HbO/HbR changed?”

SpO₂ is another window, not the same thing as CO₂

A pulse oximeter uses red and infrared light.

The absorption of these wavelengths changes according to the proportion of oxygenated and deoxygenated hemoglobin in pulsatile arterial blood, allowing an estimate of SpO₂.

During quiet breathing, SpO₂ usually changes very little from one respiratory phase to another.

During short breath holds it may also remain apparently stable for some time.

That does not mean nothing is happening.

CO₂ may be rising well before SpO₂ shows an important decline.

Therefore:

SpO₂ does not replace CO₂.

And CO₂ does not replace SpO₂.

They tell different parts of the story.

One breath is no longer four separate pieces

We can now bring the windows together:

But even this table is only a reduction.

In the real Body-Territory, everything happens together.

That is precisely what we want to measure.

One breath.

Many signals.

One shared time.

Perhaps the next step is not to ask which sensor contains “the truth.”

Perhaps we should place all of them in Jiwasa:

breathing + ECG + blood pressure + CO₂ + SpO₂ + EEG + NIRS

and ask what each one can perceive about the same event.

Because when inhalation begins, there is no separate heart waiting for its turn.

There is no isolated brain observing the lungs.

There is an entire organism passing through another cycle of relationship with the territory.

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 the RespHRV concept and clarifies that heart rate tends to increase during inhalation and decrease during exhalation without reducing the amplitude of this oscillation to a simple measure of “vagal tone.” The authors include Brazilian researchers Benedito H. Machado and Davi J. A. Moraes.

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 decades of evidence showing how respiratory networks, sympathetic activity, and cardiovagal control operate as coupled systems. The participation of Brazilian researchers helps connect the series to a strong Latin American tradition in cardiorespiratory neurophysiology.

FISHER, J. P.; ZERA, T.; PATON, J. F. R. (2022). Respiratory–cardiovascular interactions. Handbook of Clinical Neurology, 188, 279–308.
Supports the interpretation of breathing and circulation as interdependent physiological oscillators and explains how ventilation, autonomic control, venous return, and circulation continuously modulate one another.

GOHEEN, J. et al. (2024). Dynamic mechanisms that couple the brain and breathing to the external environment. Communications Biology, 7, 938.
Shows that breathing, brain activity, and external stimuli can display coordinated temporal relationships, supporting our interpretation of breathing as a bridge between brain and territory.

KLUGER, D. S. et al. (2023). Modulatory dynamics of periodic and aperiodic activity in respiration-brain coupling. Nature Communications, 14.
Demonstrates that respiratory phase is related not only to classical EEG/MEG oscillations but also to aperiodic components of brain activity.

ZHANG, H. et al. (2023). The applied principles of EEG analysis methods in neuroscience and clinical neurology. Military Medical Research, 10, 67.
Provides the methodological basis for understanding EEG as a noninvasive recording of cerebral electrical activity with high temporal resolution and multiple possible analyses in time, frequency, and connectivity domains.

SCHOLKMANN, F.; TACHTSIDIS, I.; WOLF, M. et al. (2022). Systemic physiology augmented functional near-infrared spectroscopy: a powerful approach to study the embodied human brain. Neurophotonics, 9(3), 030801.
Is central to our experimental design because it shows that fNIRS should be interpreted together with systemic physiology and explains why heart rate, blood pressure, CO₂, and superficial circulation are not merely “noise,” but necessary information for understanding the hemodynamic signal.

ZVOLANEK, K. M. et al. (2023). Comparing end-tidal CO₂, respiration volume per time, and average gray matter signal for mapping cerebrovascular reactivity amplitude and delay with breath-hold task BOLD fMRI. NeuroImage, 272, 120038.
Shows experimentally how breath holds and ETCO₂ can be used to map both the magnitude and delay of cerebrovascular responses, which will be important for interpreting NIRS during respiratory pauses.

WOLLNER, E. A. et al. (2023). Capnography—An Essential Monitor, Everywhere: A Narrative Review. Anesthesia & Analgesia, 137(5), 934–942.
Supports the use of capnography as a continuous measure of ventilation and expired CO₂ and helps distinguish ETCO₂ from arterial or cerebral CO₂.

LEPPÄNEN, T. et al. (2022). Pulse Oximetry: The Working Principle, Signal Formation, and Applications. Advances in Experimental Medicine and Biology, 1384, 205–218.
Explains the optical basis of SpO₂ using differential absorption of red and infrared light and supports the conceptual separation between measuring oxygenation and measuring ventilation/CO₂.

BrainLatam (2026). Respiración Entera: Puente entre APUS y Tekoha.
Provides the previous conceptual basis for understanding breathing not as an isolated function, but as a process crossing posture, viscera, circulation, metabolism, and Body-Territory.

BrainLatam (2026). From the R of the QRS to the Brain: The Heartbeat as Information.
Prepares the experimental interpretation of the R peak as a temporal marker capable of connecting heartbeat, RespHRV, EEG, and bodily perception within a synchronized multimodal architecture.

A strong anchor phrase for this blog is: “one breath, many signals, one shared time.”