Mechanisms of Breathing

Breathing isn't a muscle "pushing" or "pulling" air directly — it's a pressure-driven process built on the pleural cavity and diaphragm covered in the previous section. This page breaks that process into three parts: the pressure changes that move air in and out, the lung volumes used to measure breathing, and the neural and chemical signals that set breathing rate.

Key Takeaways

• Inhalation: diaphragm and external intercostal muscles contract, increasing intrathoracic volume and decreasing intrapleural pressure, which pulls air in (negative pressure breathing).

• Passive exhalation relies on elastic recoil and alveolar surface tension; active exhalation adds internal intercostal and abdominal muscle contraction.

• Surfactant reduces alveolar surface tension, preventing alveolar collapse.

• Six lung volumes/capacities describe breathing: TLC, RV, VC (= TLC − RV), TV, ERV, and IRV (TV + IRV + ERV = VC). RV cannot be measured directly by spirometry.

• The medulla oblongata's ventilation center sets breathing rhythm, driven mainly by chemoreceptor detection of CO₂ (central chemoreceptors) rather than O₂ (mainly sensed by peripheral chemoreceptors).

• Hyperventilation drops CO₂ and can cause alkalosis or fainting; hypoventilation raises CO₂.

Pressure-Driven Ventilation

Breathing relies on pressure differences between the lungs and the intrapleural space — the narrow, fluid-filled space between the visceral and parietal pleura. These pressure differences are what allow air to move in and out of the lungs.

Inhalation and Negative Pressure Breathing

During inhalation, the diaphragm contracts and flattens downward while the external intercostal muscles — the muscles between the ribs — pull the rib cage upward and outward. Together, these actions increase intrathoracic volume, expanding the space inside the chest cavity.

As that volume increases, intrapleural pressure decreases. Because the pressure inside the lungs is now higher than the pressure in the intrapleural space, the lungs expand to fill that space, and air flows in to equalize the pressure. This is called negative pressure breathing, because it's the drop in pressure that pulls air into the lungs.

Passive and Active Exhalation

In passive exhalation — like at rest — the diaphragm and external intercostal muscles relax, causing the chest cavity to shrink. As thoracic volume decreases, intrapleural pressure rises, and the lungs recoil. This recoil comes from two sources: the elastic nature of lung tissue and surface tension inside the alveoli.

In active exhalation — like when speaking, singing, or exercising — additional muscles get involved. The internal intercostal muscles and abdominal muscles contract, further compressing the chest cavity and forcing air out more quickly.

MCAT Callout — Inhalation vs. Exhalation: intrapleural pressure decreases during inhalation (pulling the lungs open) and increases during exhalation (letting the lungs recoil).

Surfactant and Alveolar Stability

To keep the alveoli from collapsing completely as the lungs deflate, the body produces surfactant. Surfactant reduces surface tension in the alveoli, stabilizing them during recoil and keeping them open for the next breath.

Measuring Breathing: Lung Volumes and Capacities

To assess how well the lungs are functioning, clinicians use a spirometer — a device that tracks how much air is inhaled and exhaled, and how quickly. It's commonly used to evaluate lung health and diagnose respiratory conditions.

Six lung volumes and capacities describe the full range of air movement in and out of the lungs:

Tidal volume, inspiratory reserve volume, and expiratory reserve volume together make up vital capacity (TV + IRV + ERV = VC). Adding residual volume to vital capacity gives total lung capacity (VC + RV = TLC).

Neural and Chemical Control of Breathing

The Ventilation Center and Chemoreceptors

Breathing is primarily regulated by the ventilation center, a region of the brainstem located in the medulla oblongata. This center automatically sends rhythmic signals to the diaphragm and other respiratory muscles, controlling the pace of breathing even during sleep or without conscious thought.

The medulla receives information from chemoreceptors, which monitor the chemical composition of the blood — especially carbon dioxide levels. If CO₂ starts to accumulate (a condition called hypercarbia or hypercapnia), chemoreceptors detect the change and signal the medulla to increase respiratory rate, clearing the excess CO₂ by breathing it out faster.

These same chemoreceptors can also sense oxygen levels, but the response to low oxygen (hypoxemia) is usually weaker and only becomes strong when oxygen levels drop significantly. This asymmetry reflects a division of labor in the body's chemoreceptors: central chemoreceptors in the medulla are primarily sensitive to CO₂ (via its effect on cerebrospinal fluid pH) and drive most day-to-day breathing regulation, while peripheral chemoreceptors in the carotid and aortic bodies are the body's main oxygen sensors, with weaker secondary sensitivity to CO₂. So while oxygen matters, carbon dioxide is the main driver of everyday breathing rate.

Hyperventilation and Hypoventilation

Breathing rate can be voluntarily overridden for short periods — you can hold your breath or breathe faster on purpose — but that control is limited. Hold your breath too long, and CO₂ builds up until the medulla forces you to breathe, overriding conscious control.

Hyperventilation (breathing too rapidly) removes too much CO₂ from the body. This drop in CO₂ can lead to alkalosis, and if CO₂ levels get low enough, it can cause fainting or a pause in breathing — because the medulla no longer senses a strong enough CO₂ signal to continue ventilation. Hypoventilation (not breathing enough) has the opposite effect: CO₂ accumulates because it isn't being cleared as fast as the body produces it.

MCAT Callout — CO₂ Drives Breathing Rate: under normal conditions, the body regulates breathing primarily to control CO₂, not oxygen. Hypoventilation raises CO₂; hyperventilation lowers it — both push the medulla to correct course.

Common MCAT Mistakes

• Thinking muscles "pull" air into the lungs directly. Breathing is pressure-driven: diaphragm and intercostal contraction change thoracic volume, which changes intrapleural and intra-alveolar pressure, and air follows the pressure gradient.

• Mixing up which pressure change happens on inhalation vs. exhalation. Intrapleural pressure decreases on inhalation (volume increases, lungs expand to fill the space) and increases on exhalation (volume decreases, lungs recoil).

• Assuming residual volume can be measured by spirometry. RV is the one lung volume a spirometer can't measure directly, because that air is never exhaled — it has to be calculated using other methods (e.g., helium dilution).

• Assuming oxygen is the primary driver of breathing rate. Under normal conditions, CO₂ — sensed mainly by central chemoreceptors in the medulla — drives breathing rate. Oxygen sensing (via peripheral chemoreceptors) is a secondary, weaker signal that only dominates when oxygen drops significantly.

MCAT-Style Concept Check

Question: A patient hyperventilates for an extended period. Which of the following correctly predicts the effect on blood CO₂ and pH, and the reason prolonged hyperventilation can cause fainting?

• A) CO₂ rises and pH falls (respiratory acidosis); fainting occurs because chemoreceptors overdrive breathing

• B) CO₂ falls and pH rises (respiratory alkalosis); fainting can occur because CO₂ drops too low for the medulla's chemoreceptors to sustain the drive to breathe

• C) CO₂ and pH stay unchanged; fainting results from decreased oxygen delivery alone

• D) CO₂ falls and pH also falls (metabolic acidosis); fainting occurs due to excess bicarbonate excretion

Answer: B

Explanation: Hyperventilation means breathing faster/deeper than the body's CO₂ production requires, so CO₂ is cleared from the blood faster than metabolism generates it — this is the same relationship described above, where hyperventilation lowers CO₂. Since CO₂ is the main input the medulla's central chemoreceptors use to set breathing rate, a large enough drop removes the chemical signal that normally keeps ventilation going, which can cause a pause in breathing or a fainting episode until CO₂ levels build back up and restore the drive to breathe.

FAQ

Why is breathing described as "negative pressure" ventilation?

Because inhalation is driven by a drop in intrapleural pressure, not by muscles physically pulling air in. Diaphragm and external intercostal contraction increase thoracic volume, intrapleural pressure decreases, and the resulting pressure gradient pulls air into the lungs.

What's the difference between passive and active exhalation?

Passive exhalation (at rest) relies only on elastic recoil of the lung tissue and alveolar surface tension as the diaphragm and external intercostals relax. Active exhalation adds contraction of the internal intercostal and abdominal muscles to force air out faster.

Why can't a spirometer measure residual volume directly?

Residual volume is the air that remains in the lungs after a full exhalation — it's never exhaled, so a spirometer, which only measures air that moves in and out, can't capture it directly.

Does the body regulate breathing based on oxygen or carbon dioxide?

Primarily carbon dioxide. Central chemoreceptors in the medulla are highly sensitive to CO₂ and drive most everyday breathing regulation; peripheral chemoreceptors sense oxygen but only respond strongly once oxygen levels drop significantly.