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Why Does Your Breathing Speed Up When You Run?

Category: The Body

Think of the last time you sprinted across a field. Afterward your chest heaved, and it felt as if you had used up all your air. Many people explain this by saying the body ran short of oxygen. An OpenStax physiology textbook tells a different story: it describes rising carbon dioxide as the main driver of breathing, with oxygen playing a weaker role. [1]

That creates a puzzle. If carbon dioxide is the signal, breathing should speed up only after carbon dioxide has built up. Yet during steady, moderate exercise, breathing rises in close step with the carbon dioxide being exchanged in the lungs. This page follows that puzzle: what the signal is, how the body seems to get ahead of it, and which parts scientists have not settled. [2]

1. Is Fast Breathing After Running Really About Running Out of Oxygen?

The idea sounds sensible: your muscles burn oxygen, so you breathe faster to bring in more. But an anatomy and physiology textbook from OpenStax describes the main driver of breathing differently. Cells in the body produce carbon dioxide, and when it rises in the blood, the brain detects the change and breathing becomes faster and deeper. [1]

Oxygen has a job as a signal too, but it is more of an emergency alarm. The textbook says breathing responds strongly to oxygen only when the level in the blood falls well below normal. So for ordinary exercise, “you are out of oxygen” does not match how the textbook describes the control of breathing. [1]

That leaves a new question: where in the body is carbon dioxide being watched?

2. Two Sets of Sensors Keep Watch on Your Blood

The body has sensors called chemoreceptors. Some sit in the lower part of the brain, in a region called the medulla, and react to changes in carbon dioxide and acidity in the fluid around the brain. Others sit in large blood vessels, in the neck and near the heart, and sample the blood passing by. When they detect more carbon dioxide or more acid, they send word to the breathing centers in the brain. [1]

A simple way to picture it is a thermostat for your blood: the more the reading drifts, the harder the system pushes back. That is only a comparison, and the real system has many more inputs than one dial.

3. Why Does Breathing Speed Up Before Carbon Dioxide Has a Chance to Rise?

Here is the puzzle. A review of exercise breathing by Dempsey and colleagues describes it as a very efficient control system: during rhythmic exercise, the air moved through the lungs rises in close step with the carbon dioxide exchanged in the lungs. [2] If breathing only reacted after carbon dioxide went up, you would expect carbon dioxide to wobble upward each time you started to run. A system that keeps it in step suggests that some signals arrive early.

The review lists three candidate inputs that might push breathing up. One comes from carbon dioxide exchange in the lungs. One is “central command,” a feed-forward message from the parts of the brain that order your muscles to move, which can also nudge the breathing centers. The third is feedback from the working muscles themselves, carried by nerve fibers called type III and IV muscle afferents. [2]

Think of a gym that is about to fill with people. Waiting until the air is stuffy is too late, so someone opens the windows when the doors open. Your body’s head start is a little like that. Again, this is only a picture: the real system does not have a single window.

4. What Changes When You Run Harder?

Hard exercise adds another signal. The textbook explains that blood can become more acidic, and the same chemoreceptors read a rise in acidity as a reason to breathe more. [1]

You may have heard that lactic acid builds up and “makes” you breathe hard. Scientists are careful about that claim. A rise in acidity and a rise in lactate can happen at the same time, but this does not prove that lactate causes the gasping, so it is better to treat it as a partial picture. [1]

5. Who Gives the Order to Breathe Faster? Scientists Still Disagree

The disagreement is about the muscles. In a series of human studies, researchers used a drug injected near the spinal cord to quiet type III and IV muscle afferents during steady exercise. In some of these blockade studies breathing dropped below its usual level, and the research group proposed that these muscle signals are required for the normal breathing of mild to moderate exercise. [2]

Other researchers read the same kind of evidence differently. Poon and Song, in a paper titled “Type III-IV muscle afferents are not required for steady-state exercise hyperpnea in healthy subjects and patients with COPD or heart failure,” argue that the muscle signals are not needed for steady exercise in healthy people. [3] As far as the sources I could read show, researchers hold different views on whether these muscle signals are needed during steady exercise.

That is a good place to stop and notice what we do know. Carbon dioxide and acidity are the main chemical signals. In steady, moderate exercise, breathing tracks carbon dioxide exchange in the lungs closely. What is less certain is how much each early signal contributes. [2]

6. Count Your Own Breaths and Look for the Head Start

Sit on a chair and count your breaths for one minute. Count one breath each time your belly rises and falls. Then march in place for one minute in a clear space and count again for another minute right after you stop. Stop at once if you feel dizzy or unwell.

Next, try a gentler march and a faster one and compare. Does harder exercise give a bigger count? You can also time how long it takes for your breathing to settle back to the first number. One try does not prove anything, so repeat it a few times.

If you would like to read more, the OpenStax chapter on the process of breathing is free online and has diagrams of the chemoreceptors. The two research articles in the source list show where the disagreement about muscle signals comes from. [1] [2] [3]

Sources

  1. OpenStax, Anatomy and Physiology 2e, 22.3 The Process of Breathing. https://openstax.org/books/anatomy-and-physiology-2e/pages/22-3-the-process-of-breathing (Carbon dioxide and acidity as the main signals, chemoreceptor locations, and the weaker role of oxygen. Only the opening of the chapter could be read with the tools available when this page was written; the statements in this article follow the summary of the chapter recorded for the Japanese edition of this site. Numbers such as oxygen thresholds are left out.)
  2. Dempsey JA, Blain GM, Amann M. “Are type III-IV muscle afferents required for a normal steady-state exercise hyperpnoea?” The Journal of Physiology, 2014. https://pmc.ncbi.nlm.nih.gov/articles/PMC3930433/ (Abstract and introduction read through Europe PMC. Used for the three candidate inputs, the close match between ventilation and carbon dioxide exchange, and the muscle-afferent blockade studies. Figures from the later sections, such as how large the increase is in hard exercise, were not read and are not used.)
  3. Poon C-S, Song G. “Type III-IV muscle afferents are not required for steady-state exercise hyperpnea in healthy subjects and patients with COPD or heart failure.” Respiratory Physiology & Neurobiology, 2015. https://pmc.ncbi.nlm.nih.gov/articles/PMC4575501 (Only the title, authors, and the start of the abstract could be read, through Europe PMC. The article is cited for the existence and direction of the disagreement, not for its data.)