First, let’s explore a factual curiosity that directs us towards the right question. Why is it that a sagging soft palate, overweight condition or drinking does not cause us to stop breathing for short periods as we go through the waking day?
Why is it that these physical and habitual problems don’t cause us to “snort” or “gasp” in a rapid inhalation that disturbs us during the day? Why can we lay down on our backs and breathe without interruption when we are awake?
Just sitting at a desk or performing the duties of a job driving or operating a vehicle, ship or plane, the position of the soft palate with respect to gravity is at its worst. Yet, we can go about our duties throughout the day and not stop breathing or suck the sagging tissues into the airway.
When we sleep, we have the same body with the same musculature as when we are awake. Clearly something changes when we are asleep. What is it and why? Let’s examine how the body controls breathing and what happens as we begin to drift into sleep.
First of all, it is important to understand the basics of sleep. Sleep Stage I (one, 1) is drowsiness. During Stage I sleep, the body relaxes the skeletal muscles that are used for gross motor movement and prepares the body for sleep. We mentally and physically relax. With some individuals this can last for 30 minutes to an hour. Others can pass through Stage I sleep in just a few minutes.
Once the body and mind have been sufficiently relaxed they prepare for entry into Stage II (2) sleep. Stage II sleep serves as an entry point to dreaming and an exit point from dreaming.
In order to prepare for dreaming (REM or Rapid Eye Movement sleep) certain muscles must be inhibited. This is because the brain will show activity during dreams that is identical to the activity shown during the waking performance of the observations and actions contained in the dreams. Specifically, your body will not know the difference between your walking down a flight of stairs in a dream and your walking down those same stairs when you are awake.
For this reason, the body inhibits these signals occurring in the brain from reaching the muscles. If you are dreaming of walking, the signals are stopped before they get to your legs. If they were not, you would find yourself walking while lying in bed. This would tend to disturb and affect your sleep. Thus, this signal “softening” between the brain and the musculature is an important pre-cursor to entering the dream state.
After you finish dreaming in REM sleep, you return to Stage II and the muscular inhibition is removed. Then you typically move into Stage III and Stage IV sleep. This is often called Delta Sleep and it is where you get the “deep rest” that you need each night.
During these stages of sleep, movement of skeletal muscles is re-enabled and you can roll over, tuck the pillow and move your legs under the commands from the brain. This allows gross positioning of the body during the longer stages of sleep. In most normal individuals, all of this is done without even waking. After a period of Stage III and IV sleep, you will return to Stage II sleep where the muscles will once again be inhibited and re-enter the dream state for another period of dreaming.
You may have noticed that some muscles can be controlled directly by the brain and some cannot. For instance, you can move your fingers and toes at will, but you cannot control the stomach muscle or your esophagus at will. There are some muscles that operate directly from subconscious control, but also can be overridden by conscious direction.
An example of this is breathing. If you don’t think about breathing, you still breathe. However, should you choose to, you can make yourself breathe as rapidly or as slowly as you wish. The same is true to a lesser extent with your heart.
When a person enters Stage II sleep and the inhibition of muscular tonus is imposed to prevent “acting out our dreams” in sleep, the signals that would go to large skeletal muscles are blocked. These signals travel in adjacent nerve pathways of the spinal cord to the signals that allow conscious control of the muscles used to breathe.
Some inhibition of the large skeletal muscles actually “bleeds over” to cause inhibition of the muscles that we use to breathe. This results in an unwanted reduction of the depth (amplitude) of breathing. In fact, this reduction in the depth of breathing during the inhibition that occurs during Stage II sleep can be significant enough that breathing stops altogether.
The cessation of breathing is the key factor of Sleep Apnea.
Our bodies have numerous types and styles of control systems. Some systems regulate and maintain physiological conditions. For example: your core body temperature is maintained within a degree F or so (when you are healthy) by way of a control system that is always operating.
Your body’s metabolism is regulated to smoothly and continuously provide just enough heat from the digestion of food and stored fat to maintain the desired body temperature. When the ambient temperature gets too high, you begin proportionately releasing sweat in order to cool your body down. When the temperature gets too low, you burn more stored fat to release heat energy.
This is an illustration of a proportional control system. That is, one which makes continuous corrective actions that are “in proportion” to the error that the system is sensing and experiencing. The error, of course, is the difference between the temperature that the body should be at for normal functioning and the body’s actual temperature.
Your respiration is also such a system. As the blood oxygen level starts to drop and the level of carbon dioxide begins to rise, your respirations become deeper and more regular while your heart pumps faster. This system operates all day, every day, and maintains a fairly consistent oxygen level in your blood. It is relatively able to accommodate variations in carrying capacity of your blood, performance levels of your lungs and circulation potential of your vasculature.
It is important also to discuss another type of system that controls your physiology and needs to be discussed. It is a “bi-valent” system. This is a system that has two states: either active or inactive. In other words the system’s response is either “full-on” or “full-off.”
A good example of this is the gag reflex. When a foreign object becomes lodged down your throat, your body will convulsively try to expel it by a rapid contraction of the esophagus and stomach.
This is not a response that is proportional to the amount of penetration of the foreign object, nor is it proportional to the size of the object. It is an “all or nothing” response to expel the foreign object. It is bivalent; either you “gag” and vomit or you don’t.
There are many control systems active in your body, as well as many protective systems. The two that we need to discuss are directly relevant to the respiration system; one is proportional and the other is bivalent.
As mentioned previously, there is a control system that is responsible for maintaining the blood oxygenation level. This is a proportional control system and it relies on several devices. Most importantly, it must be able to control the diaphragm muscles in order to regulate the depth of respiration. With respect to sleep apnea, this is where the trouble begins.
As mentioned above, when one starts to fall asleep, one moves from Stage I (drowsiness) into Stage II sleep. Stage II sleep is the transition stage before entering REM (rapid eye movement) sleep.
REM sleep is where we dream. Dreaming is critical to a good night’s sleep. When we have begun to fulfill our need for REM sleep, the body will spend periods of time in Delta sleep. REM sleep is usually encountered every 30 to 90 minutes. It occurs in more frequent intervals at the end of a good night’s sleep.
When we enter Stage II sleep in preparation for dreaming, muscular activity is inhibited. This is called “reduction of muscle tonus.” This function occurs primarily to keep the dreamer from physically acting out the movements of their dreams since the part of the brain that controls muscular movement cannot tell the difference between activity in a dream or in the waking state.
These signals, if uninhibited, would go out to your muscles and you would perform what you were dreaming. This muscular inhibition is absolutely necessary. It is accomplished by suppressing the movement of signals from the brain along the spinal cord. Unfortunately, as we age, a couple of problems develop.
The first problem is that the muscles of the soft-palate in your mouth become weaker with age. This allows the soft-palate to sag. This is not particularly unusual since most people are not professional vocalists and don’t regularly exercise their soft palates. As we age and our levels of human growth hormone (HGH) drop, many muscles in our body atrophy to lower levels of capability and performance.
The second problem is that the communication between the diaphragm and the brain becomes somewhat obstructed. The nerves that reach the diaphragm emanate from the spinal column at vertebrae C3, C4 and C5. These are cervical (i.e, in the neck) vertebrae that are located at the insertion of the upper trapezius muscles.
The upper trapezius muscles are the most common site for the expression of stress and tension in humans. This tension reduces the size of the intervertebral foramen space from which the nerves emanate and restricts the electrical flow along the root of the nerve through direct restriction.
Unfortunately, a large amount of this tension is residual and does not dissipate when the subject enters Stage II sleep.
Another issue is one that can aggravate the proper inhibition of muscular movement due to the degradation of the myelin sheath surrounding different portions of the nerves within the spinal cord. This “blurring” of the boundaries allows some interference of the inhibition of skeletal muscles with the signals for the diaphragm.
The result of these issues is that upon entering Stage II sleep, the muscle tonus holding the soft-palate out of the airway is reduced. This allows the soft-palate to sag into the airway. While this is happening, the same inhibition of muscle tonus is attenuating (reducing) the signals to the diaphragm on an already obstructed communication channel.
The result is that our breathing becomes shallower and shallower due to insufficient signal strength to the diaphragmatic muscles. This occurs as we drift into Stage II sleep in preparation for entrance to REM sleep.
As our breathing becomes shallower, the blood oxygen level drops and the carbon dioxide level rises. In a young and healthy individual, this would elicit stronger and deeper breathing from the control system that regulates these activities.
In an older individual, especially one who may also be a smoker, drinker, and/or overweight and exhibit with restricted nervous flow to the diaphragmatic muscles, there is no residual ability to increase the respiration rate or intensity for the purpose of offsetting the slowdown caused by Stage II sleep entry and restricted nervous flow related to muscular tension in the neck region. Consequently, respiration reduces in intensity and the blood oxygenation drops.
When the blood oxygen level drops and the level of carbon dioxide rises, the normal proportional control loop is unable to maintain the desired levels.
This is where the safety backup system comes in. When the blood oxygen level gets low enough and the carbon dioxide level high enough to cause the individual to suffer physiological damage, a bivalent system intervenes and forces the body to make a large and immediate inhalation or “gasping” motion.
This large and rapid inhalation causes a large pressure differential in the pharynx and literally sucks the sagging-soft- palate into the airway. This then obstructs the flow and causes a loud “SNORT” or “GASP” that arouses the sleeping subject.
Often, the arousal does not bring the subject to full consciousness. More often than not, it is simply enough to get the subject to return to a Stage I sleep state where there is no muscular inhibition.
Upon awakening or returning to Stage I sleep, the inhibition causing the reduction of muscle tonus for entry into Stage II sleep is released and respiration begins again in a somewhat normal manner. As the subject starts to drift off to sleep again, he ultimately moves into stage II sleep, the muscle tonus drops, the soft-palate sags, the signal to the diaphragm diminishes and the cycle repeats itself.
The result of this cycle is diminished breathing to the point of stoppage, followed by “snorting or gasping arousals” that typically occur every minute or so as the subject repeatedly attempts to enter Stage II sleep so that they can spend the required amount of time in REM sleep, which is necessary for proper rest and body recuperation on a daily basis.