You’re stuck in traffic and are about to be delayed to an important meeting. The kitchen is a mess, the kids are hungry and unruly, the phone is ringing and the meatballs you intended to cook are gone. You receive a tiring text message or e-mail. Your partner is angry and is screaming at you. What happens to your breathing when you read these lines? Does it get stressed? When you experience stress, your breathing also becomes stressed. One of the most effective ways to take control of internal stress is by taking control of your breathing.
Impaired breathing increases fear and worry
What happens when we get scared or worried? “Oh, help! A tiger!” “Oh, a tiring text message.” We gasp for breath, right? This reaction is simply a way to wake up the body and make us alert and ready to face the emerging situation.
The feelings of fear we experience at the dentist, in the hospital when we are getting a shot or when we see a spider often make us gasp for breath, get tense and our breathing gets “stuck.” The phrase “Now the danger is over, we can breathe out” is an example of this.
Or if we are going make a speech at a wedding and are a little worried, then we’re likely to get anxious and breathe faster and higher up in the chest. Unpleasant feelings often have their center in the stomach, which reaffirms the expression “butterflies in your stomach.”
As we move our breathing up into the chest, it’s like we’re running away from our fears. This reduces the movement of the diaphragm, our main breathing muscle, which gives our feelings of discomfort the opportunity to grow bigger.
And it’s not just shallow breathing that results from unprocessed feelings. We also take the elevator up into our head and experience increased mental stress. A vicious circle is created and if it isn’t broken, the worsened breathing, mental stress, and unprocessed feelings will become worse, which can lead to anxiety, panic, and phobia.
Maintain good breathing – one of the biggest challenges of our time
One of the greatest challenges of our time is being able to handle the huge amount of stimuli we’re exposed to each day AND at the same time maintain a breathing pattern that is rhythmic and relaxed.
Experiencing war and accidents, in reality, or through news, newspapers, and movies gives rise to thoughts and feelings that change your breathing. You may sit still, but your breathing is ready for fight or flight.
Over time, it may be enough to hear the news intro or to see the front page of the newspaper to trigger stressed breathing, thus initiating a domino effect in which your thoughts, feelings and physical body are adversely affected. This, in turn, causes further deterioration in breathing and a vicious circle is established.
Low levels of carbon dioxide is the problem
Some good examples of how breathing greatly influence our feelings are panic attacks and fear of flying. At times like those it’s common for you to breathe into a bag in order to re-breathe some previously exhaled air. But why?
Exhaled air contains 100 times more carbon dioxide than inhaled air, and when we re-breathe the exhaled air, the carbon dioxide levels in our body are raised. The person with panic attacks or fear of flying begins to feel calmer. So during times of panic and fear, lowered carbon dioxide levels are the basic problem.
Ask a flight attendant the next time you fly, and they can confirm that breathing into a bag almost always works.
Carbon dioxide pressure – our main stress indicator
Carbon dioxide pressure may not be as well known as blood pressure, but is far more important. Carbon dioxide pressure varies with each breath and reveals how you feel – mentally, emotionally and physically, which compared to the blood pressure provides a much better snapshot of your health.
An optimal carbon dioxide pressure is between 40 and 45 mmHg (millimeters of mercury, the same unit as blood pressure is measured in), and it’s absolutely crucial for your well-being. Because there is such a close link between a deteriorated breathing (which lowers carbon dioxide pressure) and stress, it’s undoubtedly your most important stress indicator. The table below shows the relationship between carbon dioxide, breathing, and stress.
|Carbon dioxide pressure||Breathing||State of health|
|40-45 mmHg||Optimum breathing||Health, energy, and harmony|
|35-39 mmHg||Over breathing||Stressed|
|30-34 mmHg||Hyperventilation||Very stressed|
|25-29 mmHg||Foreceful hyperventilation||Extremely stressed|
Stress and deteriorated breathing affects the brain negatively
When we experience stress, our deeper instincts take over because it’s not convenient to try to make conscious choices like thinking about whether we should run left or right when a tiger attacks us.
A part of the stress response, therefore, means that activity decreases in both the cognitive parts of the brain, the center of our conscious choices, and in our limbic system, the brain’s emotional center. At the same time, the activity increases in the oldest part of our brain, the reptile brain, which manages instincts and survival.
The picture to the left shows brain activity at normal breathing and the image to the right after one minute of hyperventilation. The more colorful —red, yellow, green— the more activity. After one minute of hyperventilation, the activity in the brain has decreased drastically due to oxygen deficiency induced by hyperventilation.
A lot of the stress we experience in our daily lives is mental and emotional and isn’t accompanied by any physical activity. Therefore, it’s very common for many of us to walk around with a low-grade form of hyperventilation, i.e., we breathe in a way that doesn’t reflect our body’s needs.
The difference won’t be as dramatic as shown in the picture above, but when over breathing is repeated hour after hour, day after day, it will eventually have a significant negative impact on your brain’s ability to work.
Lower levels of carbon dioxide decreases the blood flow to the brain
Already in the 1940s the researchers Seymour Kety and Carl Schmidt made a groundbreaking discovery, namely that there is a direct connection between the carbon dioxide pressure and the blood flow to the brain. The reason for the study was to find out how pilots during the second world war could make better decisions while under stress.
When the carbon dioxide pressure was increased, the blood flow to the brain increased, while a decrease led to a reduction in the blood flow. The researchers found that when the carbon dioxide pressure dropped below 30 mmHg, there was a markedly increased risk of mental fatigue and also unconsciousness.
In a study from 1964, M. Reivich demonstrated how blood flow to the brain decreases by 2% for each 1 mmHg reduction in carbon dioxide pressure.
The mechanism is used to facilitate brain surgery. By adjusting the respirator to cause the patient to hyperventilate, the blood flow to the brain is reduced. It decreases the brain volume, constricts blood vessels and reduces hemorrhaging in the brain. These factors facilitate the operation.
Another technique is to allow the patient to hyperventilate at the end of an operation. Therefore, you don’t have to give as much anesthetic and the patient can wake up sooner after surgery.
Adrenaline increased by 360% at carbon dioxide deficiency
In one study, twelve healthy medical students hyperventilated for 20 minutes. On one occasion during hyperventilation, they breathed normal air, which reduced the carbon dioxide pressure to an average of 25 mmHg. On the other occasion, the subjects breathed air containing five percent carbon dioxide, i.e., 100 times more than normal, which generally kept the carbon dioxide pressure unchanged.
The stress hormones adrenaline and norepinephrine increased by 360 and 151 percent respectively, as they breathed normal air. In hyperventilation with carbon dioxide-enriched air, the levels of both adrenaline and norepinephrine were largely unchanged. Thus, low carbon dioxide levels lead to a strong hormonal stress response.
All participants also had enlarged pupils that didn’t respond to light, called mydriasis, and convulsive muscle contraction. The latter is something I can confirm as I have hyperventilated on several occasions, and the muscles in my legs and hands shook uncontrollably for several minutes after I quit hyperventilating, as if I had Parkinson’s.
Carbon dioxide is our body’s most important stress relieving hormone
In your body’s cells, carbon dioxide is constantly produced, at a rate of about one liter for every four minutes when you’re at rest. As you breathe, you breathe out the carbon dioxide that has been built up in the body. The more active you are, the more carbon dioxide is produced. That’s why you breathe more if you’re running, compared to sitting on the couch and relaxing.
The two major causes of lower levels of carbon dioxide are a) over breathing / hyperventilation, when you exhale too much carbon dioxide and b) inactivity as it reduces carbon dioxide production. The main reason to why we feel good when breathing more slowly or doing different types of physical activity, is that the body’s carbon dioxide levels increase.
When you experience mental or emotional stress, but the stress is not accompanied by physical activity or low, slow and rhythmic breathing, the stress might build up in your body and sooner or later cause serious damage.
This article is based on the book Conscious Breathing.
Stress hormones increases during low levels of carbon dioxide
|Title||Hyperventilation-induced changes of blood cell counts depend on hypocapnia|
|Journal||Eur J Appl Physiol Occup Physiol. 1994;69(5):402-7|
|Author||Stäubli M1, Vogel F, Bärtsch P, Flückiger G, Ziegler WH.|
Voluntary hyperventilation for 20 min causes haemoconcentration and an increase of white blood cell and thrombocyte numbers. In this study, we investigated whether these changes depend on the changes of blood gases or on the muscle work of breathing. A group of 12 healthy medical students breathed 36 l.min-1 of air, or air with 5% CO2 for a period of 20 min.
The partial pressure of CO2 decreased by 21.4 mmHg (2.85 kPa; P < 0.001) with air and by 4.1 mmHg (0.55 kPa; P < 0.005) with CO2 enriched air. This was accompanied by haemoconcentration of 8.9% with air (P < 0.01) and of 1.6% with CO2 enriched air (P < 0.05), an increase in the lymphocyte count of 42% with air (P < 0.001) and no change with CO2 enriched air, and an increase of the platelet number of 8.4% with air (P < 0.01) and no change with CO2 enriched air.
The number of neutrophil granulocytes did not change during the experiments, but 75 min after deep breathing of air, band-formed neutrophils had increased by 82% (P < 0.025), whereas they were unchanged 75 min after the experiment with CO2 enriched air.
Adrenaline and noradrenaline increased by 360% and 151% during the experiment with air, but remained unchanged with CO2 enriched air.
It was concluded that the changes in the white blood cell and platelet counts and of the plasma catecholamine concentrations during and after voluntary hyperventilation for 20 min were consequences of marked hypocapnic alkalosis.
Increased nerve cell activity during hyperventilation
|Title||Corticospinal excitability is associated with hypocapnia but not changes in cerebral blood flow|
|Journal||J Physiol. 2016 Jun 15;594(12):3423-37. doi: 10.1113/JP271914. Epub 2016 Feb 24|
|Author||Hartley GL, Watson CL, Ainslie PN, Tokuno CD, Greenway MJ, Gabriel DA, O’Leary DD, Cheung SS|
|Links||Abstract, Full text|
KEY POINTS: Reductions in cerebral blood flow (CBF) may be implicated in the development of neuromuscular fatigue; however, the contribution from hypocapnic-induced reductions (i.e. PETCO2) in CBF versus reductions in CBF per se has yet to be isolated. We assessed neuromuscular function while using indomethacin to selectively reduce CBF without changes in PETCO2 and controlled hyperventilation-induced hypocapnia to reduce both CBF and PETCO2.
Increased corticospinal excitability appears to be exclusive to reductions in PETCO2 but not reductions in CBF, whereas sub-optimal voluntary output from the motor cortex is moderately associated with decreased CBF independent of changes in PETCO2. These findings suggest that changes in CBF and PETCO2 have distinct roles in modulating neuromuscular function.
ABSTRACT: Although reductions in cerebral blood flow (CBF) may be involved in central fatigue, the contribution from hypocapnia-induced reductions in CBF versus reductions in CBF per se has not been isolated. This study examined whether reduced arterial PCO2 (PaCO2), independent of concomitant reductions in CBF, impairs neuromuscular function.
Neuromuscular function, as indicated by motor-evoked potentials (MEPs), maximal M-wave (Mmax ) and cortical voluntary activation (cVA) of the flexor carpi radialis muscle during isometric wrist flexion, was assessed in ten males (29 ± 10 years) during three separate conditions: (1) cyclooxygenase inhibition using indomethacin (Indomethacin, 1.2 mg kg(-1) ) to selectively reduce CBF by 28.8 ± 10.3% (estimated using transcranial Doppler ultrasound) without changes in end-tidal PCO2 (PETCO2); (2) controlled iso-oxic hyperventilation-induced reductions in P aC O2 (Hypocapnia), P ETC O2 = 30.1 ± 4.5 mmHg with related reductions in CBF (21.7 ± 6.3%); and (3) isocapnic hyperventilation (Isocapnia) to examine the potential direct influence of hyperventilation-mediated activation of respiratory control centres on CBF and changes in neuromuscular function.
Change in MEP amplitude (%Mmax ) from baseline was greater in Hypocapnia tha in Isocapnia (11.7 ± 9.8%, 95% confidence interval (CI) , P = 0.01) and Indomethacin (13.3 ± 11.3%, 95% CI , P = 0.01) with a large Cohen’s effect size (d ≥ 1.17). Although not statistically significant, cVA was reduced with a moderate effect size in Indomethacin (d = 0.7) and Hypocapnia (d = 0.9) compared to Isocapnia.
In summary, increased corticospinal excitability – as reflected by larger MEP amplitude – appears to be exclusive to reduced PaCO2, but not reductions in CBF per se. Sub-optimal voluntary output from the motor cortex is moderately associated with decreased CBF, independent of reduced PaCO2.
The threshold for nerve cell activity lowered during hyperventilation
|Title||Paraesthesiae and tetany induced by voluntary hyperventilation. Increased excitability of human cutaneous and motor axons|
|Journal||Brain. 1991 Feb;114 ( Pt 1B):527-40|
|Author||Macefield G1, Burke D|
Anxiety can induce hyperventilation, and the resultant hypocapnia and hypocalcaemia can lead to paraesthesiae and tetany. To define the nature of the disturbance created in peripheral nerve, the excitability of cutaneous and motor axons was monitored in 6 normal subjects requested to hyperventilate until paraesthesiae developed in the hands, face and trunk. This occurred when alveolar PCO2 (PACO2) had declined on average by 20 mmHg.
Spontaneous EMG activity developed when PACO2 had declined by a further 4 mmHg. Changes in the excitability of cutaneous and motor axons were measured from changes in the compound action potentials evoked by stimulation of the median nerve at the wrist and recorded over the digital nerves of the index finger and over the thenar muscles, respectively. As PACO2 declined, the size of the compound sensory and muscle potentials evoked by a constant stimulus progressively increased, indicating an increase in axonal excitability.
These changes occurred before paraesthesiae or tetany developed. In each subject there was a statistically significant inverse correlation between PACO2 and axonal excitability. Independent of this increase in axonal excitability, there was no significant change in the supernormal phase of the recovery cycle of cutaneous axons. Microneurographic recordings from the median nerve in 2 subjects revealed spontaneous bursting activity of cutaneous axons, perceived as paraesthesiae.
It is concluded that the paraesthesiae and tetany induced by hyperventilation result solely from changes in the excitability of cutaneous and motor axons in the peripheral nerve, presumably due to an alteration in the electrical properties of the axonal membrane resulting from a reduced plasma . The supernormal phase may entrain the ectopic discharge and thereby determine the maximal discharge frequency of impulses in ectopically generated trains, but does not otherwise contribute to the physiological disturbance.
How the carbon dioxide pressure affects the blood flow to the brain
|Title||The effects of altered arterial tensions of carbon dioxide and oxygen on cerebral blood flow and cerebral oxygen consumption of normal young men|
|Journal||J Clin Invest. 1948 Jul;27(4):484-92|
|Author||Kety SS, Schmidt CF|
1. The effects of the inhalation of 5-7% CO, 85-100%o 02, and 10g% 02, were studied on the composition of arterial and internal jugular blood; on blood flow, oxygen consumption, and vascular resistance of the brain; on cardiac output and blood pressure.
2. CO2 inhaled in concentrations of 5-7%o produces an increase in cerebral blood flow averaging 75%. 02 inhaled in concentrations of 85-100% is associated with a reduction in cerebral blood flow of 13%o, while 10% 02 produced an increase of 35% in this function. These changes are statistically significant.
3. Calculation of cerebrovascular resistance indicates that in every case the change in blood flow is due to a change in the vascular resistance of the brain.
4. Cerebral oxygen consumption is not significantly altered by changes in the composition of inspired air over the ranges studied.
5. Mean arterial blood pressure rose significantly during the CO2 and high 02 inhalations and fell slightly with 10% 02.
6. The only significant change in cardiac minute volume was an increase which occurred during 10% 02 inhalation and resulted from an increase in rate rather than stroke volume.
What is a suitable carbon dioxide pressure during surgery?
|Title||Intraoperative end-tidal carbon dioxide concentrations: what is the target?|
|Journal||Anesthesiol Res Pract. 2011;2011:271539. doi: 10.1155/2011/271539. Epub 2011 Oct 25|
|Author||Way M, Hill GE|
|Links||Abstract, Full text|
|Abstract||Recent publications suggest that target end-tidal carbon dioxide concentrations should be higher than values currently considered as acceptable. This paper presents evidence that end-tidal carbon dioxide values higher than concentrations that are currently targeted result in improved patient outcomes and are associated with a reduced incidence of postoperative complications.|
The blood flow to the brain decreases by 2% for every decrease of the carbon dioxide pressure by 1 mmHg
|Title||Arterial PCO2 and cerebral hemodynamics|
|Journal||Am J Physiol. 1964 Jan;206:25-35|
The effect of arterial Pco2 in the control of cerebral hemodynamics over the full range of responsiveness of the cerebral vasculature was studied in the rhesus monkey. Cerebral perfusion pressure and arterial O2 saturation were controlled so that they produced no significant effect on the cerebral circulation.
Other possible sources of error, e.g., blood temperature, effect of anesthesia, development of metabolic acidosis, and validity of internal jugular measurements of cerebral blood flow were evaluated. Arterial Pco2 was varied from 5 to 418 mm Hg in eight animals. The minimum and maximum cerebral blood flows obtained were 18 and 140 ml/min 100 g, respectively. These values were approached when the arterial Pco2 was in the range of 10–15 mm Hg and 150 mm Hg, respectively.
At these levels of arterial Pco2 the maximum and minimum cerebrovascular resistance occurred. These values were 4.78 and 0.63 mm Hg/ml/min per 100 g, respectively. A mathematical analysis of the data enabled equations relating arterial Pco2 to cerebrovascular resistance and to cerebral blood flow to be derived. Values predicted by these equations compare favorably with the actual measured data and with similar data in the literature.