1.
In contrast to the heart, the lungs do not have their own pacemaker center.

2.
The lungs are inflated and deflated by the action of the rib muscles and the diaphragm. These, in turn, are activated by nerve cells located in the brain. (The muscles are striated skeletal muscles).

6.
When these cells “fire” (make action potentials), then these action potentials will propagate to the intercostal muscles and to the diaphragm and these will then contract; this is the inspiration phase.

7.
When they stop firing, then the ribs and the diaphragm will relax and this is the (passive) expiration phase. Remember; normal expiration is passive; it does not require any action potentials and muscle contractions.

1.
Notice the shape of the burst of action potentials in the diagram. They start very small (= very few action potentials) but the number of action potentials gradually grows until maximum is reached at the end of the inspiration. (see smooth tetanus)

2.
This behavior looks like a ‘ramp’; a slow and soft start followed by a progressive increase in activity until maximum is reached. This pattern has a purpose: it is good to start the inspiration slowly.

3.
Suppose that there was no ramp and that all nerve cells started to fire simultaneously, like in the right diagram.

4.
If all the neurons had started all together, then inspiration would suddenly start with a loud and strong ‘gasp’; not very nice.

5.
So the slope of the ‘ramp’ is very important as this determines how quickly and how strongly we inspire.

1.
Sometimes, you need to have stronger, deeper and/or a faster respiration. Then other centers will join the Dorsal Respiratory Center to control the respiration.

2.
The most important additional center is the Ventral Respiratory Center. This center will join the nerve cells from the Dorsal Center in sending more action potentials.

6.
Also, the expiration is now also activated because the ventral group also sends nerve fibers to muscles that will help in the expiration (green ramp).

7.
As shown in the diagram, nerves now also excite the external intercostals which help the expiration.

1.
Unfortunately (for the student), there are two more centers, located above the Dorsal and the Ventral group.

2.
These two regulate the behavior of the two lower groups.

5.
In experiments, it was even possible to keep the lungs in the inflated state, effectively stopping all respiration (hence its name; apneu!). (apneu = no pneu(matism)=no respiration).

6.
In general, both the pneumotaxic and the apneustic center fine-tune the work of the dorsal and the ventral Respiratory Centers.

1.
The Respiratory centers don’t work on their own but are influenced by excitatory and inhibitory signals from the body.

2.
There are about five (!) different type of signals that regulate the frequency and the depth of our respiration:

3.
These signals are:
   1. irritant signals from the lungs
   2. stretch reflex from the lungs
   3. pain and emotional signals from the hypothalamus
   4. voluntary signals from the higher brain (cortex)
   5. central and peripheral chemoreceptors

1.
Noxious substances in lung tissue (= alveoli) stimulate afferent fibers to the respiratory centers.

2.
Such irritating signals are induced by accumulating mucus, inhaled debris such as dust, smoking, etc.

3.
These same irritants, in the trachea or in the bronchi, would initiate coughing.

4.
These same irritants, in the nasal cavity, would initiate sneezing.

1.
There are numerous stretch receptors in the visceral pleurae and along the bronchi.

2.
As the lungs gets more and more inflated, during very deep inspiration, they will send inhibitory signals to the Dorsal group to stop the inspiration.

3.
It is therefore a safety system to avoid damage to the lungs by over inflation.

4.
In some countries, this inspiration reflex is called the Hering-Breuer reflex.

1.
Our emotions (through the hypothalamus) also affect our breathing.

2.
Emotional hyperventilation (when you are nervous) or a sudden stop in breathing, such as when you experience an emotional shock, are good examples of these signals.

1.
We can consciously influence our breathing (this you can not do that with your heart!)

2.
These impulses therefore come from the cortex of our brain; one of the higher brain centers.

3.
But there is a (safety) limit. We can for example hold our breath (=stop breathing) for quite a long time but at a certain moment we have to gasp for fresh air! So, the lack of oxygen overrules our wish to stop breathing!

4.
Unfortunately, you can also see this in people who have drowned. They have always water in the lungs!

1.
The chemoreceptors are sensitive to the O₂, CO₂ and pH concentrations in arterial blood (peripheral) and in the cerebrospinal fluid.

2.
In fact, the most important factor in regulating our respiration is NOT the O₂ concentration but the CO₂ concentration!!

3.
This is because a too high CO₂, produced by our body, if not swiftly expired, will influence our blood pH and thereby affect all our metabolic reactions!

4.
Therefore, an increase in CO₂ must quickly be acted upon. This occurs predominantly by the central chemoreceptors (70%) but also a bit by the peripheral receptors.

5.
A too high CO₂ quickly and easily crosses from the arterial blood into the cerebrospinal fluid. There it is converted to hydrogen ions by the bicarbonate pathway.

6.
It is the hydrogen ions (pH!) that actually activate the chemoreceptor on the surface of the medulla, close to the respiratory centers.

7.
An increase in pCO₂ in the blood will therefore, through this pathway, induce a strong increase in ventilation (depth and frequency). This will continue until the arterial pCO₂ is back to normal (approx. 40 mmHg).

8.
As said, a less important pathway is for CO₂ to activate the peripheral chemoreceptors. These are located in the wall of the aortic arch (= aortic bodies) and in the bifurcation of the carotids (=carotid bodies).

9.
From these peripheral chemoreceptors (or bodies), nerves go directly to the respiratory centers.

10.
Another important point about the CO₂ story is the situation when the pCO₂ is less than normal (less than 40 mmHg). This is important and sometimes crucial and is discussed a bit later, in “Hyperventilation”. >