Normal breathing:
the
key
to
vital health
by Artour Rakhimov, Ph.D.
Revised 2-nd edition:
February-May 2008
1-st
edition: April 2005
Copyright (C) 2005,
2008 Artour Rakhimov
Normal breathing:
the
key to vital health
Disclaimers and warnings
While the author has used
reasonable efforts to include accurate and up-to-date information in this book,
there are no warranties or representations as to the accuracy of such
information and no guarantee or promise about effects and treatment of any
health conditions is given.
The information provided in this book and its
pages is for guidance only and should be used under the supervision of a
qualified medical physician, or a family doctor, or a Buteyko practitioner. The
user of this book should not alter any medication without professional medical
advice. Before undertaking any breathing exercises one should seek medical
advice from one’s physician, family doctor or a qualified Buteyko practitioner.
The author assumes no liability for the
contents of this book, which may or may not be followed at one’s own risk.
Thus, any liability for any impact, problems, or damages is expressly
disclaimed.
Please be aware that breathing exercises,
including breath holding, have powerful effects on the human organism. These
effects may cause serious health problems in the event of incorrect application
of breathing exercises.
Special warnings for people
with serious health problems
Breathing exercises can cause large and rapid
changes in blood flow to the brain, heart, liver, kidneys, stomach, large and
small intestines and other organs, as well as changes in blood concentrations
of certain hormones. Such changes may result in different adverse effects.
There are many other consequences of manipulation in breathing that can lead to
stress and various problems. These effects can be particularly dangerous for
people with serious existing health problems or special conditions (diabetes,
severe renal disease, chronic acute gastritis, intestinal ulcers, Crohn’s
disease, inflammatory bowel disease, irritable bowel syndrome, acute brain
traumas, any bleeding or acute injury, pregnancy, etc.).
Copyright
This book is copyrighted. It is
prohibited to copy, lend, adapt, electronically transmit, or transmit by any
other means or methods without prior written approval from the author. However,
the book may be borrowed by family members.
Normal breathing:
the
key to vital health
Book content
Introduction
Chapter 1.
Scientific studies about breathing-health connection
Introduction
1.1 Minute ventilation in health and disease
1.2 Do people notice their over-breathing (hyperventilation)?
1.3 The main effect of hyperventilation
1.4 Do we need this “poisonous” CO2?
1.5 CO2 deficiency: the main physiological effect of
hyperventilation
1.6 Medical studies of hyperventilation
1.7 Studies about the hyperventilation provocation test
1.8 Hypoventilation as a health problem
1.9 End-tidal CO2 and different health problems
1.10 Hypoxia and blood shunting
1.11 Critical care patients and arterial CO2
1.12 Breath-holding time and its clinical significance
1.13 Role of nitric oxide
1.14 Changes in the ANS (autonomous nervous system)
1.15 Focus on
diseases
1.16 Why breathing?
1.17 Evolution of
air on Earth
Conclusions
Q&A section for chapter 1
References for chapter 1
Chapter 2. The
physiological mechanism of immediate regulation of breathing
Introduction
2.1 Biochemical control of respiration
2.2 The main
physiological parameter, which controls breathing of healthy people
2.3 Hypoxia and
its contribution to regulation of breathing
2.4 Control of
breathing during breath holding
2.5 Control of
breathing in people with chronic hyperventilation
2.6 Breath holding
control in diseased states
2.7 Connection
between BHT (breath holding time after normal expiration) and arterial CO2
Conclusions
Q&A section
for chapter 2
References for
chapter 2
Chapter 3. Lifestyle
factors that matter
Introduction
3.1 Stress, anxiety and strong emotions
3.2 Physical inactivity
3.3 Overeating
3.4 Deep breathing exercises
3.5 Overheating
3.6 Talking with deep inhalations, a loud voice, or a high pitch
3.7 Mouth breathing
3.8 Morning
hyperventilation
3.9 Embryonic and foetal development in a woman hyperventilating during
her pregnancy
3.10
Special factors for infants
3.12 Exposure to toxic chemicals
Conclusions
Q&A section for chapter 3
References for chapter 3
Chapter 4.
Western methods of breathing retraining
Introduction
4.1
4.2
4.3
4.4 St. Bartholomew's Hospital,
4.5
4.6 Department of Psychiatry,
4.7 Department of Psychiatry,
4.8
4.9
4.10 Lothian Area Respiratory Function Service,
4.11 Service de Psychosomatique, Hospital du Sacre-Caeur
4.12 Laboratory of Pneumology, U.Z.Gasthuisberg, Katholieke
4.13 New Zealand Guidelines Group,
4.14
4.15 Common features and some differences of Western methods of
breathing retraining
Q&A section for chapter 4
References for chapter 4
Chapter 5. History and advance of the Buteyko breathing method
Introduction
5.1 Some
historical facts about the origins of the method
5.2 Breathing and
modern diseases
5.3 Development of
specific health problems
5.4 Practical
discoveries and their application
5.5 Advance of the
method in the
5.6 Advance of the
method in western countries
5.7 Experimental trials of the Buteyko breathing method
Q&A section for chapter 5
References for chapter 5
Chapter 6. The
control pause
Introduction
6.1 The HVPT (hyperventilation provocation test)
6.2 The CP test
6.3 Life-style
factors that influence the personal CP
6.4 How CP
measurements relate to aCO2 values
6.5 Conditions for
correct CP measurements
6.6 CP and various
breathing patterns
6.7 The CP and
general health
6.8 CP and various
systems and parameters of the organism
6.9 The link
between the CP and symptoms
6.10 Maximum,
average and minimum daily CPs
6.11 Other pauses
and their definitions
6.12 Potential
dangers of long breath holds and strong air hunger
6.13 Short pauses
as safer alternatives
Q&A section for chapter 6
References for chapter 6
Chapter 7. Level
1: First steps for
better health
Introduction
7.1 Nasal
breathing only
7.2 Mouth taping
7.3 Prevention of
sleeping on the back
7.4 The Emergency
Procedure during acute or life threatening situations
7.5 Other possible
applications of the Emergency Procedure
7.6 Constant basic
control of breathing
Q&A section for chapter
7
References for chapter 7
Chapter 8. Level
2: Breathing exercises, sleep, focal infections, and cleansing reactions
Introduction
8.1 General goals
of the breathing exercises
8.2 Preliminary
requirements for learning breathing exercises
8.3 Learning the RB (reduced breathing)
8.4 More about
relaxation and posture
8.5 Gradualism –
an approach to learning air hunger
8.6 Which
breathing exercises to choose from?
8.7 What are the criteria of success?
8.8 How much to exercise?
8.9 Day-after-day progress in breathing retraining
8.10 Evening and morning CPs
8.11 General observations about sleep
8.12 Why
breathing gets deeper during sleep
8.13 Modern Western sleep
8.14 Methods to
prevent night hyperventilation
8.15 Supplements
8.16 Steroids
8.17 Order or priorities of actions
8.18 Focal infections
8.19 Practical
actions in relation to focal infections
8.20 Breathing and
focal infections: practical cases
8.21 Cleansing
reactions: their causes, basic mechanisms, and symptoms
8.22 Practical
steps during the cleansing reaction
Q&A section for chapter
8
References for chapter 8
Chapter 9. Level
2: Personal changes, physical exercise and other useful tools
9.1 Personal
changes due to the first breathing sessions
9.2 Exercise
9.3 Some practical
suggestions regarding your personal hygiene and oral health
9.4 Diet and
nutrition
9.5 Heat/cold
adaptation
9.6 Development of
correct speaking skills
9.7 Prevention of
hyperventilation conditioned to favourite activities
9.8 A typical long
session of the Buteyko breathing with light intensity
9.9 What to expect
and goal setting
9.10 Imagery and
visualization
9.11 Measurements
of pulse and its significance
9.12 Possible
intensities and durations of the breathing sessions
Q&A section for chapter 9
References for chapter 9
Chapter 10. Level
3: CP 60 or excellent health
Introduction
10.1 Constant
breathing control
10.2 Why it is
difficult to break through 40 s threshold
10.3 Physical
activity and breathing exercises
10.4 Strengthening
the weakest parts of the organism
10.5 Posture
10.6 Sleep
10.7 Avoidance of
allergies
10.8 Other special
activities
10.9 Other dietary
suggestions
10.10 Negative
emotions and their relation to muscular tension and physical activity
10.11 The check
list of questions for getting CP 60
Q&A section
for chapter 10
References
for chapter 10
Chapter 11. Breathing
and some GI problems
Introduction
11.1 Normal
digestion and abnormalities
11.2 Chronic
hyperventilation and its effects on the GI system
11.3 Interaction
of these destructive CHV factors with the organism
11.4 Factors that
define the time of digestion
11.5 Breathing
control during and after meals
11.6 Chewing and
particle size of the swallowed food
11.7 Effects of
various foods on breathing
11.8 Focal infections and their GI effects
11.9 Positive effects of high CPs on the GI tract
11.10 Triggers of
GI problems and the soft diet
11.11 Mechanical
shaking of the body
11.12 Use of
spices
11.13 Other
observations and suggestions
References
for chapter 11
Chapter 12.
Special topics related to the Buteyko method
12.1 Review of
some effects that take place at 10 and 20 s CP.
12.2 Emphysema and
breathing retraining
12.3 Sleep apnoea
and breathing retraining
12.4 Hypercapnic
vasoconstriction
12.5 Practical
suggestions for the youngest Buteyko students (0-1 years old)
12.6 Teaching
young children (from 2 up to 14-16 years old)
Q&A section
for chapter 12
References for
chapter 12
Chapter 13. Various other breathing-related subjects
Introduction
13.1 Hatha yoga teaching and
breathing
13.2 Hibernation
13.3 Breath holding abilities in
animals
13.4 Breathing in relation to
metabolic and health states
13.5 Breathing analogy in health
and disease
13.6 Homeostasis and various simple
parameters that reflect it
13.7 Socio-psychological aspects of
breathing
References for chapter 13
Chapter 14. Future
of the Buteyko movement and challenges of Buteyko breathing teachers
14.1 Current
trends
14.2 The hidden
challenge of the modern world: the Buteyko team vs. abnormal lifestyle factors
14.3 Teaching the
method: what is the core?
14.4 The method
and its impact on environmental and lifestyle factors
14.5 Ten
typical mistakes made by breathing practitioners
14.6 Teaching and
promoting the Buteyko method in new places
Appendix 1.
Summary and explanation of normal respiratory and some related values
Appendix 2.
Approximate relationship between breath holding time and alveolar CO2
concentration
Appendix 3.
Symptoms of hyperventilation syndrome treated in
Appendix 4.
Clinical effects of the Buteyko breathing method on common health problems
(based on work of Russian Buteyko doctors and own experience)
Appendix 5. Macro-minerals and their signs
of deficiency
Appendix 6. Typical changes due to the Buteyko
breathing exercises and subsequent normalization of breathing
Normal breathing:
the
key to vital health
Introduction
What do we need in order to be healthy? Most
people, including many medical doctors and health professionals, would probably
say that a good diet, exercise, healthy environment, and proper rest are all
important. Other people may add relaxation exercises, supplements, herbal
remedies and other factors. Meanwhile, there is one factor, which is usually
missing in typical answers. That is normal
breathing (or breathing in accordance with existing medical and
physiological norms).
Humans can live for days without water and
for weeks without food. However, we can survive without breathing for not more
than a few minutes. Can it be so, then, that breathing is as important as water
and food? In my view, breathing is the missing link in the modern philosophy of
health. We know too little about its importance and its effects on various
processes, systems, and organs of the human body.
This book is written for an inquisitive
reader who has keen interest in respiration, its basic theory, hyperventilation
and its effects, the regulation of respiration in health and disease and
breathing retraining therapies. The book will also separately describe the
discoveries and practical work of Doctor Buteyko, a detailed description of his
breathing method, and relevant known medical investigations and physiological
experiments. Such attention to the Buteyko method seems justified to me due to
its remarkable success in the treatment of various chronic health problems,
which are often considered incurable.
While this book does contain scientific terms
and methods, it is not required that the reader be medically trained in order
to understand the information presented here.
Each chapter of this book starts with an
introduction formulating the questions to be discussed. After the main text of
theoretical chapters, general conclusions are suggested. Each chapter has a
Q&A (Question & Answer) section and chapter-related references.
Finally, let me express my gratitude to all
people whose help made the existence of this book possible. In particular,
sincere thanks to Stuart B. Wiley (Canada), Paul Ryner, Carol Baglia,
Roger Young, Suzanne Nicole (USA), Patrick McKeown, Anne Burns (Ireland),
Carolina Gane (Holland), Elizabeth MacDomnic and Duncan Robertson (UK) for
proofreading and/or valuable remarks which improved the quality of the
manuscript.
Chapter 1. Scientific
studies
about breathing-health
connection
Introduction
In this chapter we will examine what medical
science has been studying during last hundred years. Our goal is to establish a
relationship between breathing and both health and disease.
How should we breathe? How do sick people
breathe? Is there any connection to the severity of the health problems? What
has been found out about breathing of severely sick and critically ill patients?
How do most people breathe when they die and before that? Are there any simple
practical tests, which indicate if personal breathing is normal or not?
1.1 Minute ventilation in health and disease
What is the norm of breathing? How many
litres of air per minute should we breathe while sitting at rest? The
physiological norm of minute ventilation can be found in many physiological and
medical textbooks. It is about 6 litres per minute (Guyton, 1984; Ganong,
1995). So, let us keep in mind this important number: 6 litres of air per minute.
Table 1.1 summarizes information about minute
ventilation at rest in different diseased states.
|
Disease |
Minute ventilation (± standard deviation) |
Number of patients |
Reference |
|
Chronic heart failure1 |
15 (±4) l/min |
22 |
Dimopoulou et al, 2001 |
|
Chronic heart failure1 |
16 (±2) l/min |
11 |
Johnson et al, 2000 |
|
Chronic heart failure1 |
14 (±4) l/min |
88 |
Clark et al, 1995 |
|
Diabetes |
10-20 l/min |
28 |
Tantucci et al, 1997 |
|
Asthma |
15 l/min |
8 |
Johnson et al, 1995 |
|
Asthma |
14.1 (±5.7) l/min |
39 |
Bowler et al, 1998 |
|
Asthma |
12 l/min |
101 |
McFadden & Lyons, 1968 |
|
COPD2 |
12.2 (±1.9) l/min |
10 |
Sinderby et al, 2001 |
|
Hyperthyroidism |
14.9 (±0.6) l/min |
42 |
Kahaly, 1998 |
|
Cystic fibrosis3 |
10.4 (±1.4) l/min3 |
10 |
Bell et al, 1996 |
|
Epilepsy4 |
7.88 l/min4 |
12 |
Esquivel et al, 1991 |
Table 1.1 Minute ventilation
of patients with different health problems.
Table 1.1
comments:
• 1. There are many dozens of other medical investigations into minute
ventilation of patients with chronic heart failure, which show similar results
to those listed above. (The reason for this is the commonness of this health
problem among people and the popularity of the stress-exercise test for heart
patients among respiration researchers). Here I have quoted only the results of
some typical recent studies.
• 2. “COPD” means chronic obstructive pulmonary disease.
• 3. Sometimes, measurement of ventilation produces results, which are
smaller than in real conditions. This can happen when the test interferes with
the normal breathing pattern, such as when the experiment involves the use of
facial masks. Since it is harder to breathe through them, these masks reduce
minute ventilation. Breathing through a mouth-piece also leads to breathing
less air than in reality. Another effect is connected with body weight: people
of a lighter weight need less air, as they normally have lower metabolic rates.
All these effects should be taken into account when analysing experimental
results. For example, in the quoted study (Bell et al, 1996) patients with
cystic fibrosis had minute ventilation of 10.4+-1.4 l/min. Not only were they
wearing masks during measurement, but also the average weight of these people
was 56.5 kg. Hence, the quoted minute ventilation would probably be equivalent
to about 15 l/min for typical adults.
• 4. Similarly, weight should be taken into account when analysing minute
ventilation of children. For example, it was reported that 12 children with
epilepsy had an average minute ventilation of almost 8 l/min (Esquivel et al,
1991). Their average weight was 43 kg, which corresponds to about 12-15 l/min
for adults with normal weights, therefore indicating hyperventilation. Numerous
other studies also found evidence of hyperventilation in patients with this
health condition.
Note, that virtually all tested patients with
chronic heart failure over-breathe.
The same was true for these limited studies
in relation to diabetes, asthma, and other disorders. However, more experiments
are required for these and other health problems in order to be certain about
the existing links between breathing and diseases.
It is normal, that such studies can find
prevalence of over-breathing in investigated subjects. A few health conditions
where patients breathe less than the norm will be considered below.
Now we can conclude that many sick people
breathe too much.
1.2 Do people notice their over-breathing (hyperventilation)?
They very rarely do. Usually, people agree that their
breathing is heavy when they breathe more than about 20 l/min at rest (or over
3 times the norm!).
Why
is this? Air is weightless, and breathing muscles are powerful. During rigorous
physical exercise or during maximum voluntary ventilation, an average person
can breathe about 160 l/min, with about 40 breaths per minute and 4 liters of
air for tidal volume for each breath (p.545, Straub, 1998). Some athletes can
breathe up to 200 l/min during strenuous exercise. So it is easy to breathe
only a small portion of our maximum abilities: for example, "only" 16
l/min (or “only” 10% of the maximum capacity) at rest, throughout the day and
night and overlook that it is, in fact, a high rate of breathing. It is
nevertheless normal during rigorous exercise to breathe 100 l/min or more since
CO2 and O2 concentrations in the arterial blood can remain nearly the same as
at rest.
Usually
it is possible to estimate the breathing rate (or minute ventilation) of a
person visually. If the chest is moving at rest, the person is breathing at
least twice more air than the physiological norm (over 12 l/min for a 70 kg
man). If his shoulders are moving, he is breathing four times the norm. Normal
breathing is invisible, inaudible, and regular. Moreover, when healthy people
are asked about their breathing, they usually say that they feel nothing, while
sick people have various sensations about movements of the air through the
nostrils, at the back of the throat, and in the area of the abdomen.
Unfortunately, modern medical doctors are not trained to pay attention to the breathing rate of their patients. A patient can come to the doctor's office while heavily panting, even through the mouth, and the GP or MD will not even mention or suggest to breathe through the nose or to reduce his or her breathing rate.
1.3 The main effect of hyperventilation
The previous section demonstrated that many
sick people chronically over-breathe. It is possible to assume that, maybe
these people got sick in the first place, and then started to breathe heavier.
Alternatively, it is also possible that they got sick because of over-breathing.
In order to find out what causes what let us look at the main physiological
effects of such over-breathing for healthy people. What would happen with a
healthy person, who starts to breathe too much?
Respiration is the process of regulated
exchange of two gases, CO2 (carbon dioxide) and O2
(oxygen). The human body, as a form of life, produces energy by oxidizing
different substances, mainly fats and carbohydrates. Both these substances are
mainly composed of carbon with some hydrogen and oxygen. Hence, the main end
products of this energy production are CO2 and water. Normally, one
of the functions of breathing, apart from bringing new O2 for cells
to use, is to remove excessive (but
not all) CO2.
When healthy people breathe near the norm,
their CO2 level in the organism is also near the physiological norm.
However, breathing too much delivers more O2 to the lungs and
removes more CO2 from the body.
Let us look at the basic course of events in
a case of acute over-breathing. When the person starts to breathe deeply and
frequently, the total concentration of CO2 in the lungs gets smaller
since the person intensively blows off carbon dioxide from the lungs. It takes
about one to two minutes to reduce the concentration of CO2 in
blood. About 1-10 minutes later, CO2 concentrations in the nervous
tissues, muscles, and most other organs and cells are also reduced due to CO2
diffusion from these parts to the blood.
Thus, the first effect of hyperventilation is
lowered CO2 concentrations in all body cells. If hyperventilation is
chronic, CO2 deficiency is also chronic.
1.4 Do we need this “poisonous” CO2?
Carbon dioxide gas is used for killing
animals. In small mammals (e.g., rats and mice) the loss of consciousness is
quick (seconds). In larger mammals (e.g., guinea pigs) the animals first become
very distressed and disturbed. They are restless, breathe deeply, and salivate
profusely. For discussion of animal euthanasia with the use of carbon dioxide
one may see (Coenen et al, 1995) and (Paton, 1983). Very large relative
concentrations or pure carbon dioxide gas are normally used.
Also, there are many books, newspaper
articles, and even some medical publications, which claim that one of the main
functions of human respiration is “to
remove the poisonous carbon dioxide from the human organism”. In addition,
there are many popular health articles, which state that carbon dioxide is a “waste” gas. It follows from this
approach that it is better to breathe deeper and faster in order to expel the
“poison” at higher rates.
However, there
are thousands of medical and physiological publications, studies, trials, and
experiments that state the opposite. Namely, they strongly discourage
over-breathing (hyperventilation), both in its acute and chronic forms.
Why? Over-breathing removes too much carbon
dioxide from the organism, while carbon dioxide is absolutely necessary to
sustain life. When its level becomes about 3-4 times less than the
physiological and medical norms, death is an immediate outcome.
Probably, these ideas about CO2 appeared after French scientist
Antoine-Laurent Lavoisier discovered in 1788 the role of CO2 and O2 in
breathing. He explained why mice and candle both died in CO2, but could live
longer in O2.
What about killing of animals with high
levels of carbon dioxide in air? Could we die in similar conditions? Let us
look at another related phenomenon, drowning. Thousands of people die every
year because of too much water being taken in through the mouth. About 4-5
litres of water in taken at once would be enough to fill the whole stomach and
parts of the lungs with water causing death in a few minutes. However, nobody
claims that water is a “poison”
because water is equally important and vital (in sensible quantities, not 4-5
litres at once) for human and any cellular life. The situation with carbon
dioxide is exactly the same.
Every living thing needs normal levels (not
too much and not too little) of carbon dioxide for healthy functioning.
Moreover, numerous medical studies cited in this chapter clearly show that
carbon dioxide is the substance that is most needed by patients with various
modern chronic degenerative disorders and ailments.
1.5 CO2 deficiency: the main physiological effect of hyperventilation
Let us look at some of the known carbon
dioxide effects, which are confirmed by professional Western studies. Note that
these effects can be found, in varying degrees, in any normal human organism.
Stabilizer of transmission of signals between nervous cells
The normal work of our senses, conscious
thinking, decision making, and all other mental activities require stable
transmission of electrical signals between nervous cells. Such transmission is
possible when CO2 content in nerve tissues is normal. Logic, sense, reason,
wisdom, focus, memory, concentration and many other qualities are based on this
stability of signal transmission.
The signal is passed from one nervous cell to
another only when the strength or voltage of the signal is higher than a
certain threshold value so that accidental signals will not be amplified
causing disruption in the work of the CNS. This threshold value is very
sensitive to the local CO2 content.
When we hyperventilate and CO2 content is
suboptimal, accidental weak signals can be amplified and transmitted further
interfering with the real signals based on senses, memory, logic and other
objective factors.
Hence, CO2 has a calming effect on
excessive excitability of brain areas responsible for conscious thinking (e.g.,
Krnjevic, 1965). Other researchers (Balestrino & Somjen, 1988; Huttunen et
al, 1999) also concluded that increased CO2 pressure generally
reduces cortical excitability, while hyperventilation "leads to spontaneous and asynchronous firing
of cortical neurons" (Huttunen et. al., 1999).
Hence, breathing too much makes the human
brain abnormally excited due to reduced CO2 concentrations. As a
result, the brain gets literally out of control due to appearance of
spontaneous and asynchronous (“self-generated”) thoughts. Balestrino and Somjen
(1988) in their summary directly claimed that, "The brain, by regulating breathing, controls its own excitability".
These effects of CO2 on brain
cells are of special importance in understanding anxiety, insomnia, panic
attacks, epilepsy and other psychological and neurological problems and
disorders to be discussed later. Besides, this effect is important in order to
understand the mechanism of the mind-body connection.
Bohr effect (or supply of oxygen
to all body cells)
CO2 is a catalyst for the chemical
release of O2 from haemoglobin cells. This phenomenon is called the
Bohr effect and it can be found in many medical textbooks (e.g., Ganong, 1995,
Starling & Evans, 1968). Bohr and his colleagues (1904) first described
this effect. How does it work?
In normal conditions (when we breathe about 6
l/min), arterial blood is 96-98% saturated with O2 due to a fresh
air supply to the lungs. When the arterial blood arrives at the tissues, some O2
is released by its carriers, the haemoglobin cells (red blood cells). What is
the reason for this chemical release? The cells of the organism also breathe,
and the more they breathe the more CO2 is produced. These elevated
values of CO2 in tissues increase the CO2 level in the
blood due to CO2 diffusion from the tissues. As a result, the
greater the amount of CO2 in the blood, the more O2 is
going to be released from the haemoglobin cells for the tissues to use, since
CO2 is a catalyst causing this chemical reaction.
This mechanism is especially effective during
physical exercise. Indeed, depending on the type of exercise, some of our
muscles work harder than others. Those muscles that produce more CO2,
are going to get more O2 in exchange (due to the Bohr effect), so
they can continue to work at high rates. Were this mechanism to be absent, a
human organism would quickly tire at the slightest physical exertion due to
lack of oxygen.
Therefore, carbon dioxide is a necessary
factor for oxygenation of tissues. No carbon dioxide means no oxygen in the
tissues, while no oxygen means no energy for various processes and no life.
Let us look at the events when people
over-breathe. On the one hand, breathing more can raise blood saturation from
normal 96-98% to 97-99% (by about 1%). However, it follows from the Bohr effect
that those who chronically breathe too much (in comparison with physiological
norms) suffer from hypoxia (low oxygen concentrations) in tissues due to the
low carbon dioxide level in the blood and tissues. (Low tissue oxygenation is
normally found in malignant cells, diseased nervous cells, and inflamed tissues
of various organs). Meanwhile, normal breathing (about 6 l/min) provides more O2
for the tissues of the organism.
Hence, the paradox of breathing is in the
fact that acute over-breathing, while bringing more oxygen during first
seconds, creates the opposite effect: in a few minutes (or even earlier). The
cells start to suffer from the lack of oxygen. Therefore, chronic deep
breathing causes chronic tissue hypoxia.
Prolonged forceful over-breathing can have
disastrous consequences, as Yale Professor Yandell Henderson and his colleagues
demonstrated in their work with dogs almost a century ago (Henderson et al,
1908). In these experiments, forceful respiration was created using a suction
and exhaust pump. The dogs after many minutes were disconnected from the
machine and died without attempting to draw a single breath due to failure of
the cardiovascular system. This result was completely unexpected by the
researchers. Later, it became clear that hypoxia was one of the factors
contributing to these deaths. However, there was also another factor:
constriction of small blood vessels due to low carbon dioxide level.
Local vasodilation
CO2 locally dilates arteries and
arterioles making the work of the heart easier, creating conditions for
delivering more oxygen to tissues, and removing more waste products.
Vice versa: low carbon dioxide stores have a
local vasoconstrictive effect leading to spasms, hypoxia (this time due to poor
blood supply) and accumulation of metabolic wastes in different vital organs
and tissues.
One may argue that there are many other blood
vessels which also contribute to total resistance to blood flow. Why should we
concentrate on CO2 effects on arteries and small blood vessels?
Basic physiology of the human organism explains, that the total relative
resistance to blood flow in arteries and arterioles is about 3-8 times greater
than in any other type of blood vessels (Ganong, 1995). The effect of
vasoconstriction due to hyperventilation is so powerful, that Soley and Shock (1938)
reported their difficulty in obtaining blood samples from fingers of their
patients following voluntary hyperventilation. It is more difficult for the
heart to pump the blood through the body when small blood vessels, due to low
carbon dioxide, are constricted. Moreover, the heart muscle itself receives
less blood if the person is over-breathing.
Therefore, low CO2 level in the
organism produces profound adverse impact on the cardiovascular system and
blood supply to the heart and other organs.
What about the
human brain? Does it suffer from heavy breathing? The following results were
obtained by measuring blood flow through the main artery (the carotid artery)
leading to the brain. Voluntary hyperventilation led to 35% reduction in the
blood flow to the brain in comparison with the conditions at rest. This result
is quoted in the medical textbook written by Starling & Evans (1968), while
the effect is well documented and has been confirmed by dozens of professional
experiments.
By the way, do you notice that when people
passionately argue with each other, or are angry, or violent, they usually
breathe heavily? Would it be reasonable, in the light of these physiological
studies, to conclude that it is useless to argue or try to reason with the
person whose brain is not normally oxygenated due to excessive breathing?
There are numerous studies which indeed do
reveal the negative effects of over-breathing on different skills (motor,
memory, logic) and general performance, which require combinations of various
human abilities.
Hence, a low carbon dioxide level not only
reduces oxygenation of tissues, but also impairs blood supply to vital organs
of physiological functioning.
Relaxation of smooth muscles
CO2, when applied locally, is a
relaxant of smooth muscles (e.g., Hudlicka, 1973). Dr. Brown in his article “Physiological effects of hyperventilation”
analysed almost 300 professional studies and stated, “Studies designed to determine the effects produced by hyperventilation
on nerve and muscle have been consistent in their finding on increased
irritability” (Brown, 1953).
This fact, together with the properties of CO2
mentioned previously, will help us to understand the mechanism by which normal
carbon dioxide concentrations can restore the harmonious work of different
muscular groups (such as the heart, respiratory muscles, muscles of the
digestive tract, etc.) in order to eliminate muscular spasms (e.g., heart
attacks, asthma attacks, constipation, etc.). Moreover, since muscles get
irritated it is normal to expect that when people breathe too much, they are
more likely to be tense, anxious, stressed, aggressive, and violent. Vice
versa, normal carbon dioxide concentrations would result in muscular
relaxation, composure, and sensible actions.
Bronchodilation
Normal level aCO2 eliminates possible
constriction of bronchi and bronchioles which can appear due to low aCO2. The
article "The mechanism of
bronchoconstriction due to hypocapnia [low CO2 concentrations] in man" (
Therefore, over-breathing can cause
bronchoconstriction (as it is observed in asthma) leading to the feeling of
suffocation.
Blood pH balance
CO2 is the most important factor
in controlling blood pH, balance of electrolytes and pH of other body fluids
(urine, saliva, stomach secretions, etc). Indeed, bicarbonate is the largest CO2
component of the blood, as well as intra-cellular and extra-cellular fluids,
while a typical medical or physiological textbook will indicate its leading
role in the control of pH of blood and other body fluids (e.g., medical
textbooks by Starling & Evans, 1968; Guyton, 1984; and Ganong, 1995).
Hence, changes in bicarbonate concentration must influence the ionic
composition of every human cell.
As one of the numerous effects in this area,
Carryer (1947) found that “While no
significant change in total calcium of the blood takes place, the readily
available, or ionized portion is affected markedly [due to
hyperventilation]… The decrease in
available calcium increases excitability of the neuromuscular mechanism,
inducing tetany”.
These medical conclusions point out the cause
of problems (low carbon dioxide due to hyperventilation) with calcium
metabolism, which is found in osteoporosis, arthritis, and other health
conditions.
Participation and catalisation of chemical reactions
CO2 is a participant of numerous
other biochemical reactions involving virtually all vitamins, minerals, amino
acids, hormones, carbohydrates and other vital substances. Some of the chemical
reactions, all requiring CO2 as a catalyst or as one of the
reagents, were described by Kazarinov (1990).
Apart from these known effects, there are
probably many other processes of the human organism that require normal CO2
levels and normal breathing for optimum physiological functioning.
The first respiratory physiologists were
called “cardio-respiratory physiologists” since the link between the
cardiovascular and respiratory systems, as they found it, was very intimate.
Professor Yandell Henderson was one of the most prominent scientists in this
area. His article “Carbon dioxide”
was published in 1940 in Cyclopedia of
Medicine. In the section with the title “Relations of Carbon Dioxide and Oxygen in the Body” he wrote,
“Carbon dioxide is, in fact, a more fundamental component of living
matter than is oxygen. Life probably existed on earth for millions of years
prior to the carboniferous era, in an atmosphere containing a much larger
amount of carbon dioxide than at present. There may even have been a time when
there was no free oxygen available in the air…
Another natural,
but very obstructive misconception is that oxygen and carbon dioxide are so far
antagonistic that in blood a gain of one necessarily involves a corresponding
loss of the other. On the contrary, although each tends to raise the pressure
and thus promote the diffusion of the other, the 2 gases are held and
transported in the blood by different means…
A sample of blood
may be high in both gases, or low in both gases. Moreover, under clinical
conditions low oxygen and low carbon dioxide—anoxemia and acapnia—generally
occur together. Each of these abnormal states tends to induce and intensify the
other. Therapeutic increase of carbon dioxide, by inhalation of this gas
diluted in air, is often the effective means of improving the oxygenation of
the blood and tissues.”
In the section “As a factor in the Acid-base Balance of the Blood”, he continued,
“Modern
physiology has shown that, in addition to the control and regulation exerted by
the nervous system, there are many chemical substances produced in the body
that influence function and form. To these active principles Starling gave the
name of “hormones.” Among the hormones are epinephrine (often called
adrenaline), pituitrin, thyroxin, insulin and many other products of the glands
of internal secretion and other organs. Carbon dioxide is the chief hormone of
the entire body; it is the only one that is produced by every tissue and that
probably acts on every organ. In the regulation of the functions of the body,
carbon dioxide exerts at least 3 well defined influences: (1) It is one of the
prime factors in the acid-base balance of the blood. (2) It is the principal
control of respiration. (3) It exerts an essential tonic influence upon the
heart and peripheral circulation.”
Finally, he stated in the section “In the Control of Respiration and the
Circulation”,
“Carbon dioxide is the chief
immediate respiratory hormone.”
1.6 Medical studies of hyperventilation
The previous section described some effects
(there are many more as we are going to see later) of hyperventilation on
healthy people. While these effects are normal for any human organism, the
degree of particular negative changes and the location of the most affected
organs are various in different individuals. Therefore, the individual problems
created by over-breathing are going to be different. In order to investigate
this issue, let us turn our attention to medical studies.
Medical doctors and professors have written
extensive reviews of professional literature and described their own case
histories of hyperventilation (Bass, 1990; Brasher, 1983; Lum, 1975; Magarian,
1982, 1983; Morgan, 1983; Tavel, 1990). These studies showed the symptoms of
over-breathing and the profound negative influence of both acute and chronic
hyperventilation on the whole biochemistry of the human organism.
The first medical article containing a
description of the symptoms of hyperventilation, but without understanding
their cause, was published by DaCosta (DaCosta, 1871). One group of researchers
described the biochemical mechanism by which hyperventilation can gradually
cause problems with high cholesterol (hypertension) and high blood sugar levels
(diabetes) (Lavrent'ev, 1993).
Acute and, especially, chronic
hyperventilation, according to these and many other references, affects every
system and organ of the human body causing a wide variety of symptoms. Many
medical doctors have mentioned that the physiological response to
hyperventilation is individual. Thus, individual genetic predisposition and
certain other factors define which system or organ is the most affected by
hyperventilation. It can be the heart, brain, kidneys, liver, intestines,
stomach, lungs or one of many others. Additional references on the negative
effects of hyperventilation can be found in the previously cited works.
Magarian (1982), for example, quoted over 180 other scientific articles in
order to back up his conclusions about the physiological consequences of
hyperventilation.
Since
hyperventilation is an important part of our fight-or-flight response, the
blood is generally diverted from vital organs to large skeletal muscles.
Studies found decreased perfusion of the heart (Okazaki et al, 1991), brain
(discussed above), liver (Hughes et al, 1979; Okazaki, 1989), kidneys (
Typically,
the blood flow to vital organs is directly proportional to aCO2. Such a linear
relationship (between brain blood flow and carbon dioxide concentration) can be
found, for example, in Handbook of
Physiology (Santiago & Edelman, 1986).
Chronic hyperventilation interferes with normal digestion.
Decreased perfusion and oxygenation of GI organs can lead to lack of digestive
enzymes, accumulation of metabolic waste products, slow digestion, putrefaction
of certain nutrients and mal-absorption. That should cause problems with
protein metabolism (which usually appear before problems with fat and
carbohydrate metabolism), thus adversely affecting normal repair of the body
(especially the GI tract, the largest consumer of amino acids) and the immune
system.
In order to experience the effects of breathing
on digestion, one may voluntarily hyperventilate after a meal. While normal
digestion can take 2 hours, hyperventilation may extend this time up to 5-8
hours or more, depending on the degree of hyperventilation.
Warning. By mild voluntary hyperventilation, you may almost halt digestion. For many people that can cause GI distress and aggravation of existing gastrointestinal problems. Breathing less (or voluntary hypoventilation) can also make some digestive problems worse.
It would be normal to expect that the degree of
all these negative effects may vary from individual to individual.
Similarly, according to the article entitled
"The effects of hyperventilation;
individual variability and its relation to personality" (
Thus, when we over-breathe, there are certain
factors (both, genetic and environmental) which create our specific
physiological responses to hyperventilation. While the above-mentioned negative
consequences of deep breathing are typically found in a normal human organism,
genetic predisposition and some other factors (previous events which influenced
the organism) probably define the organs, their parts and the systems which are
going to suffer most from low carbon dioxide stores and other effects of
chronic hyperventilation. More research is required in order to find the
effects of hyperventilation and individual differences.
1.7 Studies about the hyperventilation provocation test
One may realize the dangers of over-breathing
by performing a HVPT (hyperventilation provocation test), during which the
person should breathe very quickly and deeply, usually for about 2-3 minutes.
(It would be impossible to do it much longer due to losing consciousness, while
forceful involuntary over-breathing, when a pump is used, would cause death in
dozens of minutes). This short over-breathing test has a well-recorded history
of clinical use and was employed by many medical doctors to provoke the
symptoms of the main health problem in order to diagnose it, as well as to
demonstrate to patients that hyperventilation was the main cause of their
symptoms. Thus, using deep and fast breathing, you can reproduce your specific
health symptoms.
Over-breathing
is an excellent tool used by medical doctors around the world to find out the
most sick organs and systems in any particulat patient.
For example, voluntary over-breathing in
asthmatics causes the asthma attack, in people with hypertension – the heart
attack, in epileptics – epilepsy attack, etc. Here is a short summary of
medical studies regarding different health conditions, number of patients
investigated, and the percentage of patients who reproduced their specific
health problem.
- coronary artery spasms (Nakao et al, 1997) 206 patients, 100%
specific;
- bronchial asthma (Mojsoski N & Pavicic F, 1990) 90 patients, 100%
specific;
- panic attacks (Bonn & Readhead, 1984; Holt PE, Andrews, 1989;
Nardi et al, 2000), 95% specific;
- epileptic absence seizures (Esquivel, 1991; Wirrel, 1996).
Important notice. The hyperventilation provocation test should not be
performed by people who have certain severe health problems, without professional
supervision, due to possible complications.
The symptoms experienced can be reversed by
reducing ventilation and raising carbon dioxide stores to previous values.
Another important finding of these and other authors is that most people,
including numerous above-mentioned patients, were unaware of their abnormal
breathing pattern and believed that they breathed normally.
1.8 Hypoventilation as a health problem
As shown above, many disease states are
characterized by hyperventilation. Are there any health problems in which sick
people breathe less than the norm?
Low minute volume can be found, for example,
in cases of hypothyroidism. Such people usually have abnormally low levels of
thyroid hormones. As a result, their cells cannot generate enough energy.
Typical symptoms of hypothyroidism are low energy, hypoxia, apathy, sleepiness,
and weight gain. Indeed, since little CO2 is produced by cells, less
O2 is released to them by haemoglobin cells, due to the suppressed
Bohr effect.
Chronic mountain sickness patients can have
lower than normal ventilation, but this rare health condition is observed only
in those who live about 3,000 m or more above sea level.
Abnormal breathing may be observed in sleep
apnoea, in which sleeping patients stop breathing for 10-20 or even up to 40-50
seconds. Such apnoeic spells interrupt the normal functioning of the nervous
system. As a result, these spells can awaken the patients many times during the
night, interfering with physiological and psychological recovery. These people
can breathe too little during spells. The inter-event ventilation (i.e. between
spells) has been observed to be usually more than 20 l/min.
Patients with hypothyroidism and sleep apnoea
can normalize their breathing patterns using the method described in later
Chapters. Moreover, practical work of breathing practitioners revealed that
normalization of breathing of these patients dramatically improves their health
state. Even more surprising is the fact that these patients can use virtually
the same methods and breathing exercises (to be discussed) in order to restore
their health.
1.9 End-tidal CO2 and different health problems
Minute ventilation, although a very important
respiratory parameter, needs special equipment and does not always indicate hyperventilation
and small aCO2. Inaccuracies occur in cases of small body weight
(found, for example, in children), irregular or very shallow breathing found in
some obese patients, and obstruction of airways leading to partial or total
closure of some lung areas. This last phenomenon will be discussed in the next
section.
As a result, many professional researchers,
when investigating respiration, often measure etCO2 (end-tidal CO2)
as a more accurate characteristic reflecting CO2 content of the
lungs. A device called a "capnometer" can continually measure CO2
level in the expired air. The level of CO2 gradually rises during
exhalation showing an approximate equalization with the CO2 value in
alveoli in the lungs (hence, the phrase "end-tidal"). The normal alveolar
CO2 pressure is about 40 mm Hg pressure (Guyton, 1984; Ganong, 1995)
or partial pressure of 5.3% of normal air at sea
level. According to "Handbook on physiology" (Severinghaus JW, 1965),
"A PCO2 below 35 mm Hg is indicative of alveolar hyperventilation"
(p.1476). 35 mm Hg corresponds to 4.6% CO2 at sea level (see Appendix 2 in
order to find the relationships between aCO2% and absolute aCO2 pressure at
different altitudes).
All
previously quoted studies (section 1.1) indicating hyperventilation should find
abnormally low etCO2 for tested patients. Indeed, people who breathe more
should generally show smaller CO2 concentrations in expired air.
What also follows from many studies is that
with the deterioration of health etCO2 tension gets even lower.
The investigation of over 100 patients
(Tanabe et al, 2001) with different degrees of chronic heart failure revealed
that class I patients (light degree) had about 34.5 mm Hg etCO2
pressure, class II patients: 32.5 mm Hg, and class III patients: 30.8 mm Hg. Thus,
the heart patients with the more serious heart problems had lower CO2
levels and, therefore, heavier breathing in terms of minute ventilation.
American scientists from the
Expired end-tidal CO2 values are
considered by many emergency professionals as an accurate predictor
(life/death) of cardiac arrest. For example, authors of the article "End-tidal carbon dioxide during
cardiopulmonary resuscitation in humans presenting mostly with asystole: a
predictor of outcome" investigated 120 French patients during
non-traumatic cardiac arrest. The researchers found that "end-tidal CO2 could provide a
highly sensitive predictor of return of spontaneous circulation during
cardiopulmonary resuscitation (MPR)" (p.791, Cantineau et al, 1996).
More recently a large group of medical doctors from several American hospitals
tested over 100 patients and wrote an article "End-tidal carbon dioxide measurements as a prognostic indicator of
outcome in cardiac arrest" with the same conclusion (Ahrens et al,
2001). There are several other studies written by emergency professionals, with
the same conclusions.
Therefore, emergency patients (with cardiac
arrest) with the most deep and frequent breathing have the least chances of
survival.
Rosen and his colleagues (1990) in the
abstract of the article “Is chronic
fatigue syndrome synonymous with effort syndrome?” wrote: "Chronic fatigue syndrome (CFS), including
myalgic encephalomyelitis (ME) and postviral syndrome (PVS), is a term used
today to describe a condition of incapacity for making and sustaining effort,
associated with a wide range of symptoms. None of the reviews of CFS has
provided a proper consideration of the effort syndrome caused by chronic
habitual hyperventilation. In 100 consecutive patients, whose CFS had been
attributed to ME or PVS, the time course of their illness and the respiratory
psychophysiological studies were characteristic of chronic habitual
hyperventilation in 93. It is suggested that the labels 'CFS', 'ME' or 'PVS'
should be withheld until chronic habitual hyperventilation - for which
conventional rehabilitation is available - has been definitively excluded."
Paulley started his article "Hyperventilation" (Paulley, 1990),
with "Physicians’ and specialists’
continued failure to recognize, diagnose and treat adequately the majority of
hyperventilators is a disgrace. Hyperventilation Syndrome (H.V.S.), incorrectly
labelled myalgic encephalomyelitis (M.E.), is the latest example of the
profession’s incompetence."
These doctors claim that chronic fatigue
syndrome, myalgic encephalomyelitis, and postviral syndrome can be directly
caused by over-breathing since normalization of breathing results in recovery
of the patients with these health concerns.
Capnometers (devices to measure carbon
dioxide levels in the expired air) have become especially popular among
psychologists. For example, Fried and colleagues (1990) studied several groups
of subjects with anxiety, panic phobia, depression, migraine, and idiopathic
seizures. The abstract claims that "virtually
all the noncontrol subjects were found to show moderate to severe
hyperventilation and the accompanying EEG dysrhythmia" (p.67).
Abnormally low carbon dioxide values (etCO2)
were found in all (over 60) patients with neurotic depression and non-retarded
endogenous depression (Damas Mora et al, 1976).
Asmundson and Stein (1994) measured carbon
dioxide concentrations in over 20 patients with panic disorder. Their average
CO2 was also below the medical norm.
Therefore, various psychological problems are
connected and can be the consequences of chronic over-breathing.
1.10 Hypoxia and blood shunting
McFadden & Lyons (1968) showed that in
mild and severe asthmatic patients, some parts of the lungs could not carry out
adequate air exchange due to airway obstruction. This causes an ineffective
exchange of CO2 for O2 in venous blood in the obstructed
alveoli of the lung. Therefore, this venous blood, after leaving the lungs
almost unchanged, is mixed with oxygenated arterial blood. This effect is
called “blood shunting”. As a result, hypoxia of such patients becomes worse
since less O2 is present in the blood. Meanwhile, aCO2
rises to or even exceeds, in severe cases, the physiological norm (40 mm Hg).
Thus, with further deterioration of health, large aCO2 (hypercapnia)
is observed. In spite of increased aCO2 pressure and greatly
improved Bohr effect, tissue hypoxia is greater than before due to very low
arterial oxygenation (it would not be correct to expect that higher aCO2
concentrations can compensate for lack of oxygenation in the damaged lung
areas. The balance between these two gases is indeed delicate.) This problem of
ventilation/perfusion mismatch (inadequate air supply to some lung parts) and
corresponding blood shunting is especially severe in patients with emphysema.
Normally, in healthy lungs each lung area
requires air ventilation, which is approximately proportional to its volume.
Meanwhile, in severe cases of ventilation/perfusion mismatch, the working lung
part can hyperventilate, but the total ventilation can be less than the norm.
Indeed, if, for example, only one-third of the lungs is functional, as in
emphysema, this third may use, say, about 3-4 l of air per minute, indicating
general hypoventilation (3-4 l/min is less than the physiological norm).
Meanwhile, under normal conditions, this working lung part would need only
about 2 l/min.
Ventilation/perfusion mismatch is common in
patients with mild or severe asthma, emphysema, and cystic fibrosis, and for
some patients with obesity, hypertension, and diabetes. However, for most
people very low aCO2 does not cause severe airway obstruction and
corresponding blood shunting. Taking into account individual variability of the
effects of CO2 depletion (discussed in section 1.3), it is possible
that asthmatics and other groups of people as above have air passages, which
are more sensitive to hyperventilation due to their genetically inherited
characteristics.
Hypoxic hypoxia can also be the result of the
ventilatory failure due to fatigue of respiratory muscles or depression of the
respiratory neurons in the brain by morphine and other drugs. (Hypoxic hypoxia
is hypoxia resulting from a defective mechanism of oxygenation in the lungs.)
1.11 Critical care patients and arterial CO2
It was shown above that, in cases of cardiac
arrest, carbon dioxide concentration is a reliable predictor of human survival.
Meanwhile, critical care professionals often use the most sophisticated and
advanced devices to measure different physiological parameters. Analysis of
arterial blood usually includes investigation of blood gases (blood
concentrations of bicarbonates, total CO2, oxygenation, etc.) of
critically ill patients.
All 29 patients with severe liver damage (in
most cases due to metastatic cancer or cirrhosis of liver) had low CO2,
while for 25 patients "it was also
clinically evident that respiratory exchange was increased markedly"
(p.762, Wanamee et al, 1956). Thus, hyperventilation was visually observed by
the authors of this publication, "Respiratory
alkalosis in hepatic coma". They also found that heavy over-breathing
led to severe electrolyte abnormalities. These abnormalities included decreased
sodium ions and increased chloride ions in the blood. Abnormally high lactic
and pyruvic acid concentrations were other frequent effects.
Blood gases and respiratory patterns provided
accurate information for survival prognosis in acute cerebrovascular accidents.
When these parameters were normal, patients survived. Out of 11
hyperventilating patients with less than 35 mm Hg aCO2, only one
survived (Rout et al, 1971).
The same conclusion (regarding aCO2
and survival prognosis) was made for head injuries (Huang et al, 1963;
Vapalanti & Trouph, 1971).
Summarizing the results of these works and
their connection with brain dysfunction, Dr. Plum wrote, "The combination of hyperpnoea [increased
breathing] with an elevated pH, and a
subnormal or moderately low oxygen tension occurs in many serious illnesses
that entirely spare the brain. These include the alveolar-capillary block of
diffuse pulmonary carcinomatosis; heart failure; advanced cirrhosis, with or
without hepatic coma; acute pulmonary infarction; and many others, including
the cryptic pulmonary congestion that accompanies most serious disease in the
obtunded and elderly" (Plum, 1972). Interestingly, all above-mentioned
effects (low carbon dioxide concentration, elevated pH, and hypoxia) quoted by
Dr. Plum are caused by heavy breathing.
Hence, one can conclude that over-breathing
is a normal feature of these severe diseases.
When suffering various serious health
problems (heart disease, diabetes, cancer, AIDS, etc.) the patient’s life is
usually threatened, not by the main health problem, but by complications and
infections, such as in the case of bacteremic shock. Analysing a group of
patients initially diagnosed with arteriosclerotic heart disease,
cerebrovascular insufficiency, diabetes, arthritis, several forms of cancer,
fatty liver, and alcoholism, one study showed that complications due
to pathogenic microorganisms in the blood caused 46 deaths in 50 patients
(Winslow et al., 1973). Pneumonia and urinary tract infections were the foci of
pathogenic microorganisms. Now we may ask the following: what was observed with
their breathing, when not only a part of the organism, but even the blood was polluted
with pathogens? All 50 patients, according to a table accompanying this
article, had very disturbed blood gases corresponding to severe over-breathing.
Dr. Simmons and his colleagues wrote an
article "Hyperventilation and
respiratory alkalosis as signs of gram-negative bacteremia"
(bacteremia being the presence of bacteria in the blood). This extract is from
the beginning of their abstract:
"Visible
hyperventilation was observed clinically in patients with Gram-negative
bacteremia. Eleven patients with Gram-negative infections and either proved or
probable bacteremias were therefore studied to see if hyperventilation might be
a common response to such bacteremia. In every case there was laboratory
evidence of hyperventilation, and in 8 cases the hyperventilation was visible
to the observer. Since only patients were studied who had no other cause for
increased ventilation, this appears to be a primary response to the bacteremia..."
(abstract, Simmons et al, 1960).
Another group of US medical professionals
found that the degree of over-breathing has a strong correlation with over-all
mortality (Mazarra et al, 1974). Heavier breathing indicated smaller chances of
survival. Here is what they wrote in their scientific abstract:
"Respiratory
alkalosis [blood alkalisation is the normal physiological result of
over-breathing] was the most common
acid-base disturbance observed in a computer analysis of 8,607 consecutive
arterial blood gas studies collected over an 18 month period in a large
intensive care unit.
Through a
retrospective review of the randomly selected hospital records of 114 patients,
we defined four groups based upon arterial carbon dioxide tension (PaCO2)
and mode of ventilation. Group I, with a PaCO2 of 15 mm Hg or less,
consisted of 25 patients with an over-all mortality of 88 per cent. Group II,
with a PaCO2 of 20 to 25 mm Hg, consisted of 35 patients with a
mortality of 77 per cent. Group III, with a PaCO2 of 25 to 30 mm Hg,
consisted of 33 patients with a mortality of 73 per cent, and Group IV, with a
PaCO2 of 35 to 45 mm Hg, consisted of 21 patients with a mortality
of 29 per cent (p<0.001). Shock and sepsis were most common in group I
patients.
These findings
suggest that extreme hypocapnia [low level of carbon dioxide] in the critically ill patient has serious
prognostic implications and is indicative of the severity of the underlying
disease" (Mazarra et al, 1974).
This article indicated that the names of the
most common diseases to occur in all 4 groups of people were cerebrovascular
disease, hepatic coma, bronchopneumonia, and arteriosclerotic heart disease.
Finally, let us look at the conclusion drawn
by a group of US researchers who recently wrote an article with the title
"Can cardiac sonography and
capnography be used independently and in combination to predict resuscitation
outcomes?" (Salen et al, 2001).
"CONCLUSIONS:
Both the sonographic detection of cardiac activity and ETCO(2) levels higher
than 16 torr were significantly associated with survival from ED resuscitation;
however, logistic regression analysis demonstrated that prediction of survival
using capnography was not enhanced by the addition of cardiac sonography" (Salen et al,
2001).
In other words, they found, probably to their
surprise, that monitoring of the heart, as an addition to the monitoring of
breathing, does not provide any further information about chances of survival.
A review of these professional studies
indicates that critically ill patients usually have very low carbon dioxide
level due to visible hyperventilation. Laboured breathing of such patients
probably corresponds to minute ventilation of 20-25 l/min or more.
The analysis of Westren medical literature
suggests that many critically ill patients die in conditions of heavy and deep
breathing.
Deep breathing, as we showed above, reduces
oxygenation of the body. Are there any simple tests that reflect our
ventilation and oxygenation? “Oxygen content in the organism can be
found using a simple method: after exhalation, observe, how long time the
person can have no breathing without stress” (Buteyko, 1977).
1.12 Breath-holding time and its clinical significance
All breathing parameters described above need
to be measured using special equipment. Meanwhile, there is a simple test,
which can be done at almost any moment by everyone, since only a watch or a
clock is required. This is BHT (breath-holding time), or how long one can be
without breathing. What are the results of medical studies regarding this test?
According to textbook “Essentials of exercise physiology” (McArdle et al, 2000), “If a person breath-holds after a normal
exhalation, it takes about 40 seconds before breathing commences” (p.252).
Breath holding can be started at different
phases of breathing (e.g., after normal inhalation, or exhalation, or taking a
very deep inhalation, or a complete exhalation). These different conditions can
produce large variations in results (by more than 200%). Moreover, sometimes
patients are asked to take 2 or 3 deep breaths before the test. Since
researchers use different methods for BHT measurements, the standardization of
results is necessary in order for them to be compared.
“Handbook
of physiology”, after analysing numerous relevant publications, suggested
the following proportions for BHT measurements (Mithoefer, 1965). If BHT after
full inhalation is 100%; then BHT after normal inhalation is 55%; BHT after
normal exhalation is 40%; BHT after full exhalation is 24%. Taking an
additional full exhalation or inhalation before starting the test increases BHT
by about 5 or 15% respectively for each full manoeuvre. This information allows
us to compare different BHT tests done during almost a century of clinical
investigations, if we use some standard conditions for the test. In order to do
that, let me introduce the BHT: BHT
is BHT after quiet or usual expiration. The under-line can remind the
reader about BHT measured at the base level, as when we are totally relaxed (as
after usual exhalation).
Different studies and their results can be
now compared by changing their BHTs to the standard of measurements, the BHT.
These results are given in Table 1.2.
Warning. Usually
BHT in physiological or medical studies is measured for as long as possible.
This procedure is dangerous if you have certain serious health conditions with
inflammation, irritation, ulcers or any other damage to internal organs (this
will be fully explained later). The conditions requiring caution include:
certain heart conditions, diabetes, hypoglycaemia, severe kidney disease,
gastric or intestinal ulcers, acute gastritis, IBS, etc.
|
Types of people
investigated |
Number of subjects |
BHT, S |
BHT, s |
Test conditions (order of
actions just before BHT test) |
% of BHT for BHT1 |
Reference |
|
Fit instructors |
22 |
46 s |
67 s |
Full exhalation, normal inspiration |
70% |
Flack, 1919 |
|
Home defence pilots |
24 |
49 s |
72 s |
|||
|
British candidates |
23 |
47 s |
69 s |
|||
|
US candidates |
7 |
45 s |
66 s |
|||
|
Delivery and test pilots |
27 |
39 s |
57 s |
|||
|
Pilots training for scouts |
15 |
42 s |
62 s |
|||
|
Pilots taken off flying
through stress |
|
34 s |
49 s |
|||
|
Normal subjects |
30 |
23 s |
58 s |
Full inspiration |
40% |
Friedman, 1945 |
|
Neurocirculatory asthenia |
54 |
16 s |
40 s |
|||
|
Normal subjects |
22 |
33 s |
45 s |
Normal inspiration |
73% |
Mirsky et al, 1946 norm.
inspir., alap, |
|
Anxiety states |
62 |
20 s |
28 s |
|||
|
Normal subjects and class
1 heart patients |
16 |
16 s |
48 s |
Full inspiration, full
exhalation, full inspiration |
33.3% |
Kohn & Cutcher, 1970 |
|
Class 2 and 3 heart patients |
53 |
13 s |
39 s |
|||
|
Pulmonary emphysema |
3 |
8 s |
23 s |
|||
|
Functional heart disease |
13 |
5 s |
15 s |
|||
|
Normal subjects |
6 |
28 s |
76 s |
Full exhalation, full inspiration |
38 % |
Davidson et al, 1974 |
|
Asymptomatic asthmatics |
7 |
20 s |
55 s |
|||
|
Asthmatics with symptoms |
13 |
11 s |
27 s |
Full inspiration |
40 % |
Perez-Padilla et al, 1989 |
|
Normal subjects |
14 |
25 s |
74 s |
Deep breath of 50% O2, 50% N22 |
33.3% |
Zandbergen et al, 1992 |
|
Panic attack |
14 |
11 s |
34 s |
|||
|
Anxiety disorders |
14 |
16 s |
49 s |
|||
|
Outpatients |
25 |
17 s |
43 s |
Full inspiration |
40 % |
Gay et al, 1994 |
|
Inpatients |
25 |
10 s |
25 s |
|||
|
COPD or CHF (congenital
heart failure) |
7 |
8 s |
21 s |
|||
|
12 heavy smokers |
12 |
8 s |
21 s |
|||
|
Normal subjects |
26 |
21 s |
21 s |
Normal exhalation |
100% |
Asmudson & Stein, 1994 |
|
Panic disorder |
23 |
16 s |
16 s |
|||
|
Normal subjects |
30 |
36 s |
36 s |
Normal exhalation |
100% |
Taskar et al, 1995 |
|
Obstructive sleep apnoea
syndrome |
30 |
20 s |
20 s |
|||
|
Normal subjects |
76 |
25 s |
67 s |
Full exhalation, full inspiration |
38% |
McNally & Eke, 1996 |
|
Normal subjects |
10 |
38 s |
38 s |
Normal exhalation |
100% |
Flume et al, 1996 |
|
Successful lung
transplantation |
9 |
23 s |
23 s |
|||
|
Successful heart
transplantation |
8 |
28 s |
28 s |
|||
|
Normal subjects |
31 |
29 s |
32 s |
Normal exhalation in supine position |
90% |
Marks et al, 1997 |
|
Outpatients with COPD |
87 |
8 s |
9.2 s |
Table 1.2 Breath holding
time according to various medical references
Table 1.2
comments.
• 1. “% of BHT for BHT” means the percentage of BHT used to
calculate BHT.
• 2. Zandbergen et al, 1992 conducted their experiments with the mixture
of 50% O2 and 50% N2. According to Ferris with his
colleagues (1945), such mixture increases normal BHT by about 50%.
Analysing the results of Table 1.2, the
following conclusions can be made.
• Normal subjects have
the longer BHT (maximum pause) in comparison with sick people who suffer
from various health problems.
• The stronger the
severity of the health problem, the shorter the BHT.
• Recovering and
asymptomatic people have intermediate BHT values.
Let us now turn our attention to the comments
expressed by medical professionals about the breath holding time of healthy and
sick people.
In 1919 The Lancet published one of the first
articles describing the medical application of BHT investigated by military
medical doctor and Lieutenant-Colonel Martin Flack (Flack, 1919). As Dr. Flack
indicated, less than 35 s BHT was considered to be sufficient to take pilots
"off flying through stress"
(Flack, 1919). The possible reason for such a drastic measure was described by
him on the next page. On one occasion a medical doctor wanted to suspend from
flying one experienced pilot due to his unusually low BHT (23 s BHT).
The pilot was allowed to fly, lost control, crashed the plane and was killed.
The commanding officers decided that this test was, indeed, an indicator of the
personal health state, especially stress. At the end of his publication Flack
suggested, "...that these tests
would also be of value for measuring trench fatigue, industrial fatigue, and
fatigue in women workers..." (Flack, 1919).
According to Dr. Wood, who investigated
patients with a variety of symptoms diagnosed as DaCosta’s syndrome (one of the
previous names for the chronic fatigue syndrome), low BHT was the most common
symptom found in his 200 patients (Wood, 1941).
A few years later Dr. Friedman, Director of
the Harold Brum Institute for Cardiovascular Research, San Francisco, after
analysing his patients with neurocirculatory problems wrote, "... the breathholding time was found to be
directly related [inversely proportional] to the severity of the dyspnea suffered" (Friedman, 1945).
Dr. Mirsky and his colleagues (1946)
concluded that "the difference [in
breath holding time] between the normal
and abnormal patients [with variety of anxiety states] is of clinical significance".
Two American medical doctors, Robert Kohn and
Bertha Cutcher, in their article "Breath
holding time in the screening for rehabilitation potential of cardiac patients"
(Kohn & Cutcher, 1970) described the testing of more than 100 cardiac
patients. It was found that "...an
individual unable to hold his breath for at least 20 sec [7 s BHT] is a poor candidate for vocational
rehabilitation". Furthermore, "It is now suggested that the determination of the breath-holding time
is an effective screening test for rehabilitation potential" (Kohn
& Cutcher, 1970).
Apparently, healthy obese patients were
"unable to hold their breath much
beyond 15 s", whilst all normal non-obese subjects could breath hold
for more than 30 s (Hurewitz et al, 1987).
Similarly, African researchers
noticed that, “Significant differences
were observed in the mean of the Quetelet index, percent predicted vital
capacity and the breath holding time between the normal female and the obese
female subjects. A high but inverse relationship was found between estimated
body fat and each percent predicted vital capacity and breath holding time in
subjects whose Quetelet index was above 30 kg/m2” (Sanya &Adesina,
1998)
A review of publications on leprosy (Katoch,
1996) revealed that "respiratory
function test studies have shown impaired breath holding time"
(abstract).
Authors of the article "Rating of breathlessness at rest during
acute asthma: correlation with spirometry and usefulness of breath-holding time"
(Perez-Padilla et al, 1989) wrote,
"These
results suggest that: 1) magnitude of dyspnea and breath-holding time correlate
with severity of airflow obstruction in acute asthma attacks associated with dyspnea
at rest; and 2) breath-holding time varies inversely with dyspnea magnitude
when it is present at rest" (abstract). Thus, BHT has correlation with
the most important parameters officially accepted for the diagnosis of asthma.
Later Mexican scientists published the same
result in their article, Estimating forced expiratory volume in one
second based on breath holding in healthy subjects. Their conclusion was “FEV1 [forced expiratory volume] can be reliably
estimated using BHT” (Nevarez-Najera
et al, 2000).
Japanese doctors compared breath holding times for normal subjects and
patients with COPD (chronic obstructive pulmonary disease). “The period of no respiratory sensation [a certain period of no particular
respiratory sensation which is terminated by the onset of an unpleasant
sensation and followed by progressive discomfort during breath-holding] was
also measured in eight patients with chronic obstructive pulmonary disease. The
values of the period of no respiratory sensation in patients with chronic
obstructive pulmonary disease were apparently lower than those obtained in
normal subjects. These findings suggest that measurement of the period of no
respiratory sensation can be a useful clinical test for the study of genesis of
dyspnoea” (Nishino et al, 1996).
Kendrick and colleagues used breath holding
for more accurate measurements of pulmonary blood flow (Kendrick et al, 1989).
It was important for testing that the subjects hold their breath as long as
possible for better measurements. The researchers had 33 patients with cardiac
problems (but without overt cardiac failure) and noticed that, "for very dyspnoeic patients a breath-hold
time of less than 10 s would be desirable...e.g., 6 s is acceptable. However,
in very ill patients, even a 6 s breath hold time may be too long"
(Kendrick et al, 1989). The authors were clearly disappointed by the short BHTs
of their patients.
Magnetic resonance imaging (MRI) is a test in
which X-ray films are taken of patients, who must remain motionless during the
procedure. Patients must therefore be able to hold their breath for the
duration of the test. Sick patients with numerous health problems have been a
challenge for MRI professionals since these patients could not hold their
breath a sufficiently long enough time in comparison with normal subjects.
For example, one abstract claimed that
patients with coronary artery disease "found
it significantly more difficult to perform a steady breath-hold … or attain the
same diaphragm position over multiple breath-holds than normal subjects"
(Taylor et al, 1999).
In order to solve this problem, new magnetic
imaging techniques requiring shorter BHTs (even as short as a few seconds only)
were developed. However, some, most seriously ill patients could not achieve
even multiple 1 s breath holds, as reported by Posniak and colleagues (1994):
"OBJECTIVE.
Chest and abdominal CT scans using 1.0-sec scan times are often limited by
motion in patients who are unable to hold their breath. With our scanner we can
obtain images in 0.6 sec (partial scan)" (abstract). The breathing
pattern of some patients was so strong that they could not stop for even a
single second.
Russian medical Doctor K.P. Buteyko and his
colleagues tested thousands of patients with a variety of cardiac and bronchial
problems and found that sick people usually have about 10-20 s BHT, and the
very sick as low as 3-5 s. With approaching death, the breath holding time
gradually, day after day, goes down: 5 s, 4, 3, 2, 1 (last frantic gasps for more
air), death… (Buteyko, 1977).
Are there any health conditions in which BHT
is long in spite of poor, but stable health? It is possible, according to my
research, in such rare cases as obesity hypoventilation syndrome, chronic
mountain sickness, after carotid body resection (these nervous cells monitor
carbon dioxide concentration in the blood and brain and, as a result, control
respiration), and curarisation of respiratory muscles (a procedure during which
respiratory muscles are cut and cannot obey the central nervous system).
Obviously, more research is required before final conclusions can be made.
We can see that the BHT (breath
holding time after normal expiration) is an excellent indicator of our health.
The sicker the person, the lower the BHT.
Finally it can be noted that these low BHTs
were found for sick and severely sick patients. Apparently, there are certain
people who have low BHTs (due to chronically heavy breathing), but are
not diagnosed (yet?) with any serious organic disease.
1.13 Role of nitric oxide
There are
numerous studies published over the past 80 years regarding the negative
effects of hypocapnia (low level of CO2). Hence, CO2 is the most known and
investigated factor that relates to overbreathing. Which other parameters of
the body become abnormal during and because of hyperventilation?
Normal
nasal breathing helps the body to use its own nitric oxide. This substance is
produced, among other places, in nasal passages. During normal breathing, we
have quiet prolonged exhalations (that do not prevent accumulation of nitric
oxide in some areas of nsal passages) and relatively quick inhalations (that
allow inhalation of the accumulated nitric oxide). Duirng hyperventilation
exhalations are forceful and quick (as one can observe in many sick people) and
inhalations are slow. This reversal of the main stages of breathing decreases
the utilization of nitric oxide.
The roles
and some important effects of this hormone on the body have been discovered
very recently and there are still many questions in relation to this substance.
Nitric oxide is found and synthesized in endothelial cells that line
the lumen of blood vessels, neurons, and
macrophages. As a gas, it is routinely found in nasal passages and measured in
exhaled air. The known functions of the NO include:
1. Vasodilation of arteries and arterioles
(and hence regulation of blood flow to tissues). In this respect, NO is similar
to CO2 acting on the smooth muscles of blood vessels.
2. Regulation of binding and release of O2
to haemoglobin. This NO function is again similar to the CO2 function known
as the Bohr effect.
3. Destruction of parasitic organisms,
viruses, and malignant cells by inactivating their respiratory chain
enzymes in mitochondria.
4. Inhibition of inflammation in blood
vessels.
5. Neurotransmission. Learning, memory,
sleeping, feeling pain, and some other processes require NO for transmission of
neuronal signals. On the other hand, brain cells can probably be killed during
a stroke due to excessive production of nitric oxide.
6. Hormonal effects. NO influences secretion from
several endocrine glands. It stimulates the release of adrenaline from the
adrenal medulla, pancreatic enzymes from the exocrine portion of pancreas, and
Gonadotropin-releasing hormone from the hypothalamus.
Abnormal NO production and its availability
are now associated with hypertension, heart failure, stroke, obesity, diabetes
(both type I and II), atherosclerosis, rheumatism, aging, and dyslipidemias
(particularly hypercholesterolemia and hypertriglyceridemia).
Currently there are numerous studies
world-wide related to the role of NO in human health and diseased states. It is
beyond the scope of this book to provide these studies.
Practice
shows that possibly for some people some health improvements can be achieved
mainly through the correction of one’s breathing pattern, which can normalize
production and utilization of nitric oxide, while CO2 changes could be small.
Hence, in these people nitric oxide can play, during some stages of breathing
normalization, the leading role in health restoration.
1.14 Changes in the ANS (autonomous
nervous system)
Most of
the time, breathing is regulated by the ANS (autonomous nervous system). In
healthy people movement of the diaphragm provides at least 75% of the changes
in air volume in the lungs during inhalation at rest, as one may see in many
medical textbooks (e.g., p. 312, Castro, 2000; p. 595, Ganong, 1995).
Inhalation involves activation of the diaphragm (the initially dome-shaped
diaphragm is stretched sideways and becomes more flat), and, hence, inhalation,
as a process of muscular activation, is normally controlled by the sympathetic
part of the ANS. Exhalation, in health, involves relaxation or passive recoil
of the diaphragm (p. 314, Castro, 2000) indicating parasympathetic control of
this part of the process. In normal conditions (12 breaths per minute) one
breathing cycle (inhalation-exhalation) takes 5 seconds. Inhalation lasts about
2 s and exhalation about 3 s (p. 313, Castro, 2000; p.541, Straub, 1998).
Since an
average person takes many thousands breaths every day, the parameters of his or
her breathing can be considered as a window, through which certain disturbances
in the ANS can be detected. Let us consider the typical breathing parameters of
sick people.
The above
studies in minute ventilation show that people with asthma and heart disease
breathe about 2.5 times more air every minute (about 15 l/min instead of 6).
How is it possible that they breathe so much? Such breathing rates are possible
by breathing faster (not 12 times per minute, but 15-20 or even more times per
minute) and deeper (up to 700-1,000 ml of air per breath instead of 500 ml as
it should be in health). If a healthy person needs about 3 s to exhale 500 ml
through the relaxation of the diaphragm, there is no way for a sick person to
exhale more air (700-1,000 ml) in less time using only relaxation. Hence, sick
people unconsciously apply muscular efforts to exhale air from the lungs at
resting conditions. These muscular efforts need sympathetic control indicating
that hyperventilation means abnormal control of this vital function (breathing)
by the ANS. Moreover, this fast and deep breathing is usually, but not always,
accompanied by chest breathing, when the rib cage, not the diaphragm, does the
main job of air movement. Hence, hyperventilation also means abnormal
innervations or dis-regulation of control of the breathing muscles by the ANS.
Furthermore, practice shows that hyperventilation is usually accompanied by the
reversal of the two phases of breathing: inhalations often become longer than
exhalations. One may notice how sick people take a prolonged inhale and then
the rib cage collapses to expel air with force and an audible noise. Finally,
the breathing of sick people is often uneven and irregular with sighing,
coughing, snorting, sneezing, etc.
All these
abnormal processes take place 24/7 and they indicate pathologies in the
functions of the ANS. The ANS, in its turn, regulates contractions of the
heart, digestion, production of hormones and many other vital processes. It is
logical to expect then that chronic overbreathing can lead to various health
abnormalities through negative effects on the ANS, but too little research
about these negative effects is currently available.
1.15 Focus on diseases
The modern Western approach to respiration is often based on
the following understandings about breathing. “Respiration
is the total process of delivering oxygen to the cells and carrying away the
by-product of metabolism, carbon dioxide”, or “Respiration is the process of
taking in oxygen from inhaled air and releasing carbon dioxide by exhalation”, or “Respiration is the process by
which animals take in oxygen necessary for cellular metabolism and release the
carbon dioxide that accumulates in their bodies as a result of the expenditure
of energy”.
About a century ago leading world’s physiologists had a
different understanding about the role of breathing and CO2 in human health
(see Professor Yandell Henderson’s quote above). First of all, it is the
primary role of breathing to regulate CO2 (not just to release this
by-product). Secondly, while regulation of CO2 is an important factor, there
are many other functions of normal breathing. These other functions can be
disturbed or disrupted. Possible abnormalities of breathing are: dominance of
chest breathing at rest; fast shallow breathing and diaphragmatic flutter; slow
inhalations and quick exhalations; periodic breathing; coughing; sighing; and
sneezing. All these and many other irregularities and infringements are
connected with pathological processes or abnormalities in the respiratory
system, autonomous nervous system, endocrine system, musculoskeletal system,
cardiovascular system, gastrointestinal and other systems of the human organism.
Let us now review some diseases and their relations to breathing.
Asthma
In 1968 The New England Journal of Medicine published the
results of a large study (McFadden, 1968) in which breathing and blood gases of
a group of asthmatics were investigated. The researchers found that all 101
tested patients had chronic alveolar hyperventilation. Those asthmatics who had
a light or moderate degree of the disease breathed about 15 l of air per min or
2.5 times more than the official medical norm (6 l/min).
More recently, in 1995, American researchers from the Mayo
Clinic and Foundation (
Finally, medical professionals from
Clinical
Science published in 1968 an article, The
mechanism of bronchoconstriction due to hypocapnia in man (hypocapnia means abnormally low CO2 concentrations). In
this paper,
What
about modern textbooks on physiology? One states, “Agents
that tend to dilate airways include increased PaCO2 (hypoventilation or
inspired CO2)...” (p.545, Straub, 1998). This
textbook directly claims that slowing down breathing (hypoventilation) or
increased CO2 level dilates airways. Moreover, CO2 is suggested as the chief
chemical substance that promotes this effect.
Did anybody ever suggest before recent years the connection
between asthma and ventilation? Doctor Buteyko proposed this link in the 1950s
(his first official publications appeared in the 1960s), when he discovered the
central role of overbreathing in the development and degree of asthma. (He and
his colleagues also found that asthma patients got immediate relief from their
asthma attack symptoms, if they practiced reduced breathing). Dr. Herxheimer
independently suggested that low CO2 was the cause of bronchial asthma
in 1946 and 1952 (Herxheimer, 1946; 1952).
Let us consider the possible mechanism suggested by Doctor
Buteyko. Low CO2 values in the bronchi cause chronic constriction of airways
(that happens in all people). In addition to this direct effect, chronic hyperventilation
makes immune reactions abnormal. The immune system becomes too sensitive in
relation to intruders from outside (coming with air or food), but weakens the
responses to various pathogens, like viruses and bacteria. (Why?
Hyperventilation is a defensive reaction and a part of the fight-or-flight
response. Hence, hyperventilation indicates a state of stress, increased
alertness and emergency for the whole organism, the immune system included.
Hence, various intruders are to be attacked.)
The immune system becomes hypersensitive and seemingly
innocent events (like breathing cold air or inhaling dust particles, dust mite
proteins, cat proteins, tree pollen, etc.) can trigger an inflammatory response
in the airways of asthmatics, enlargement of mast cells, excessive production
of mucus, a sense of anxiety or panic, more hyperventilation, and further
constriction of airways.
As a result, mucus makes air passages narrower (or even
blocks some of them) creating a feeling of suffocation and causing asthma
attacks. During an attack, an asthmatic may try to clear the mucus by coughing
it out, but that further reduces CO2 concentrations in the lungs and makes air
passages narrower.
Heart disease
In 1995 the British Heart Journal published a study (Clark et al, 1995) done by researchers
from the National Heart and Lung Institute in
In 2000, in a study from the Chest magazine, a group of American cardiac professionals
revealed that patients with chronic heart failure had breathing rates in the
range of 14 to 18 l/min (Johnson et al, 2000).
More recently, Greek doctors from the
These and many other similar results raise many questions.
Are there any heart patients (with primary hypertension, angina pectoris, and
other problems) who have normal breathing parameters? Does the normalization of
breathing mean no symptoms and no disease for all heart patients? What are the
details of interactions between breathing and heart disease? These questions
will be discussed later.
Above-mentioned physiological effects, resulting from a CO2
deficiency, influence the cardiovascular system.
· Low blood CO2 values lead to the narrowing of small blood
vessels (vasoconstriction of arteries and arterioles) in the whole body. That
causes two problems. First, as a group of Japanese medical professionals found,
in conditions of CO2 deficiency, blood flow to the heart muscle decreases
(Okazaki et al, 1991). Hence, heart tissue gets less oxygen, glucose and other
nutrients. Second, since small blood vessels are the main contributors to the
total resistance in relation to blood flow, CO2 deficiency increases resistance
to blood flow and makes the work of the heart harder.
· The suppressed Bohr effect, due to low CO2 values in the
blood, also reduces oxygenation of the heart muscle. That increases anaerobic
metabolism and produces excessive amounts of lactic acid. Note that lactic acid
is often implicated as a source of pain in any tissue. In the case of the
heart, a person can suffer from angina or chest pain.
· The excited nerve cells in the heart (the cells that are
called pacemakers) interfere with the normal synchronization and harmony in the
working of the heart muscle. (The valves should open and close in proper time,
much like a well-tuned engine.) Desynchronization can make the whole process of
blood pumping less efficient or more energy- and oxygen-demanding possibly
causing pathological adaptive changes in the heart tissue.
· Abnormal metabolism of fats leads, as Russian medical
studies revealed, to increased blood cholesterol level in
genetically-predisposed people. That condition gradually, over periods of weeks
or months, produces cholesterol deposits on the walls of blood vessels. Such
deposits can induce primary hypertension. As their published work suggests, the
BHT has a linear correlation with the blood cholesterol level. These
results are discussed later in more details.
· Chronic hyperventilation affects the normal utilization and
conversion of essential fatty acids into prostaglandins causing changes in
inflammatory responses and the malfunctioning of the immune system.
· Mouth breathing (at rest, during sleep, exercise, etc.) is
an additional adverse stimulus. It further reduces aCO2 and prevents normal
absorption of nitric oxide (a hormone and powerful dilator of blood vessels)
synthesized in the nasal passages while the main effect of taking
nitroglycerine medication, in case of heart problems, is to provide the organism
with additional nitric oxide.
· Since heart patients breathe 2-3 times more than the
official norm, they usually have a more frequent and deeper breathing pattern.
That must result in other breathing abnormalities, for example, chest
breathing, as well as slow inhalations and quick exhalations. These
irregularities indicate abnormal states of the autonomous nervous and
musculoskeletal systems.
The father of cardiorespiratory physiology, Yale University
Professor Yandell Henderson (1873-1944), investigated some of these effects
about a century ago. Among his numerous physiological studies, he performed
experiments with anaesthetized dogs on mechanical ventilation. The results were
described in his publication Acapnia and shock. -
Which parts of the
cardiovascular system are going to be most affected? That depends on genetic
predisposition, life style and environmental factors. There are so many
parameters that can adversely affect the normal work of the cardiovascular
system. People are different. Some may get chronic heart failure, others high
blood pressure, or stroke, or various abnormalities in the heart muscle.
Western experimental studies suggest that the
following cardio-vascular problems can appear as a result of hyperventilation
(courtesy of Peter Kolb, Biochemical Engineer,
- palpitations (Bass C, 1990; Cluff, 1984; Demeter & Cordasco,
1986; Lum, 1975; Magarian et al., 1983; Nixon, 1989; Sher, 1991)
- cardiac neurosis (Bass C, 1990; Cluff, 1984; Nixon, 1989)
- angina pain (Nixon, 1989)
- myocardial infarction (Nixon, 1989)
- Wolfe-Parkinson-White syndrome (Nixon, 1989)
- arrhythmias (Cluff, 1984; Demeter & Cordasco, 1986; Nixon, 1989)
- stenosis of coronary artery (Demeter & Cordasco, 1986; Nixon,
1989; Sher, 1991; Waites, 1978)
- tachycardia (Cluff, 1984; Lum, 1975; Nixon, 1989; Tavel, 1990)
- failure of coronary bypass grafts (Nixon, 1989)
- right ventricular ectopy (Nixon, 1989)
- silent ischemia (Nixon, 1989)
- elevated blood pressure (Nixon, 1989)
- flat or inverted ECG T-wave (Demeter & Cordasco, 1986; Nixon,
1989; Sher, 1991; Tavel, 1990)
- vasoconstriction (Cluff, 1984; Demeter & Cordasco, 1986; Lum,
1975; Nixon, 1989; Sher, 1991)
- reduced cerebral blood flow (Cluff, 1984; Lum, 1975; Magarian et al.,
1983; Sher, 1991; Waites, 1978)
- mitral prolapse (Bass C, 1990; Cluff, 1984; Nixon, 1989; Tavel, 1990)
- low cardiac output/stroke volume (Waites, 1978).
Do you know that it is possible to get abnormal ECG tracing
from a healthy heart just by voluntary heavy breathing? Later, many cardiac
professionals, while analyzing such ECGs, can claim pathological changes in the
heart. These changes are different in different people. Vice versa, normal
breathing naturally eliminates, either immediately or in due course of time,
various, already detected, ECG abnormalities.
Modern medicine and physiology have a very limited
understanding of what is going on with the cardiovascular system when breathing
gradually change in one or the opposite direction. There are many questions
related to individual variability, mechanisms of developing pathologies, and
the interaction of hereditary and environmental factors.
Cancer
Let us consider some facts about the appearance, growth and
development of malignant tumours; their spread to distant tissues and resistance
to standard methods of treatment. What is the abnormal background, which is
rarely discussed in popular books and articles about cancer, but which is known
to professional oncologists?
It has
been known for decades that malignant cells normally and constantly appear and
exist in any human organism due to billions of cell divisions and mutations.
These abnormal cells, in normal conditions, are quickly detected by the immune
system and destroyed. However, the work of macrophages, enzymes and other
agents of the immune system is severely hampered under the conditions of
hypoxia. That was the conclusion of various studies. For example, Dr. Rockwell
from Yale University School of Medicine studied malignant changes at the
cellular level and wrote, "The
physiologic effects of hypoxia and the associated micro environmental
inadequacies increase mutation rates, select for cells deficient in normal
pathways of programmed cell death, and contribute to the development of an
increasingly invasive, metastatic phenotype" (Rockwell, 1997). The
title of this publication is "Oxygen
delivery: implications for the biology and therapy of solid tumors".
Summarizing
the results of numerous studies, Ryan with colleagues chose the following title
of their article, "The hypoxia inducible
factor-1 gene is required for embryogenesis and solid tumor formation"
(Ryan et al, 1998).
In normal
conditions, even a group of hypoxic cells dies (or is easily destroyed by the
immune cells). What about cells in malignant tumours? Researchers from Gray
Laboratory Cancer Research Trust (
"Cells undergo a variety of biological responses when placed
in hypoxic conditions, including activation of signalling pathways that
regulate proliferation, angiogenesis and death. Cancer cells have adapted these
pathways, allowing tumours to survive and even grow under hypoxic
conditions..." (Chaplin et al,
1986).
Moreover, American scientists from
There is
so much professional evidence about fast growth of tumours in the condition of
severe hypoxia, that a large group of Californian researchers recently wrote a
paper "Hypoxia - inducible factor-1
is a positive factor in solid tumor growth" (Ryan, 2000). As an echo,
a British oncologist from the Weatherhill Institute of Molecular Medicine (
When the
solid tumour is large enough and the disease progresses, cancer starts to
invade other tissues. This process is called metastasis. Does poor oxygenation
influence it? "...Therefore, tissue
hypoxia has been regarded as a central factor for tumor aggressiveness and
metastasis" (Kunz & Ibrahim, 2003) was the conclusion of German
researchers from
Since
dozens of medical and physiological studies yielded the same result, what about
just a title again? "Tumor
oxygenation predicts for the likelihood of distant metastases in human soft
tissue sarcoma" (Brizel et al, 1996). The harder one breathes, the
faster cancer invades.
Probably,
the reader now can guess about the effect of cancer treatment and the chances
of survival for those who suffer from severe chronic hyperventilation. Indeed, "... tumour hypoxia is associated with
poor prognosis and resistance to radiation therapy" (Chaplin et al,
1986).
"Low tissue
oxygen concentration has been shown to be important in the response of human
tumors to radiation therapy, chemotherapy and other treatment modalities.
Hypoxia is also known to be a prognostic indicator, as hypoxic human tumors are
more biologically aggressive and are more likely to recur locally and
metastasize" (Evans & Koch, 2003).
"Clinical
evidence shows that tumor hypoxia is an independent prognostic indicator of
poor patient outcome. Hypoxic tumors have altered physiologic processes,
including increased regions of angiogenesis, increased local invasion,
increased distant metastasis and altered apoptotic programs” (Denko et al,
2003).
Could breathing influence the tumors and if so, how? The
authors of one of the studies cited above mused about the origins of all these
problems, “Surprisingly little is known, however, about the
natural history of such hypoxic cells”
(Chaplin et al, 1986). Why could they appear? What is the source of tissue
hypoxia? We can again suggest that our breathing does influence the breathing
process of all body tissues, tumours included.
Is there any experimental evidence indicating
the usefulness of CO2 for malignant tumours?
During the last decade, there has been a
steady progress in the investigation and application of CO2-O2
gas mixtures called "carbogen" in clinical practice. Carbogen
breathing is usually applied for several hours during administration of certain
anti-cancer medications. Let us review
some results in this area and the reasons for carbogen application.
Several studies from
A large group of British scientists from the
Paul Strickland Scanner Centre revealed that when 14 cancer patients breathed
various carbogen mixtures (with 2%, 3.5% and 5% CO2 content, the
rest was O2) "arterial
oxygen tension increased at least three-fold from basal values"
(Baddeley et al, 2000). They also found that "There were no significant changes in the respiratory rate, heart
rate and blood pH. The results suggest that 2% CO2 in O2
enhances arterial oxygen levels to a similar extent as 3.5% and 5% CO2
and that it is well tolerated" (Baddeley et al, 2000).
Another group of British researchers directly
measured oxygen pressure in cancer cells and concluded, "This study confirms that breathing 2% CO2 and 98% O2
is well tolerated and effective in increasing tumour oxygenation"
(Powell et al, 1999).
These results generate the following
question. Which gas, CO2 or O2 is the main contributor to
increased oxygenation and by how much? The amounts of both gases in mixtures
were much higher than the amounts of O2 and CO2 in normal
air.
Let us, first, consider the influence of O2.
There are two O2 states namely O2 that is combined with
haemoglobin and dissolved O2, which can increase oxygenation of the
arterial blood. As we considered in Chapter 1, the saturation of haemoglobin
with O2 under normal conditions (or when breathing normal air) is
about 98%. Increased O2 pressure can raise this value to almost
100%. This would cause about a 2% increase in arterial blood in comparison with
the initial value. In addition, when patients breathe carbogen mixtures more O2
can be dissolved in the arterial blood (this O2 is not bound to red
blood cells). In normal conditions the contribution of dissolved O2
is about 1.5% of the total blood O2 as the remaining 98.5% O2
is combined with haemoglobin. Increasing O2 almost five times
increases total arterial O2 content by about 6% in relation to the
initial normal value.
Hence, increasing the O2 component
in breathing air (up to almost 100%) causes about 8% increase in total O2
content in arterial blood.
Similarly, British researchers, as mentioned
above reported "arterial oxygen
tension increased at least three-fold from basal values" (Baddeley et
al, 2000). How was it possible to get such a large increase in tissue
oxygenation (about 200%) if arterial blood could carry only about 8% more O2
during carbogen breathing in comparison with initial conditions?
The remaining increase in tissue oxygenation
could be due to larger CO2 values, which shift the Bohr curves down
and enhance O2 release from haemoglobin cells, and due to the
dilation of blood vessels. Therefore, the increase in oxygenation of tissues is
mainly due to the larger CO2 content.
Indeed, the British professionals decided “to assess the
relative contributions of carbon dioxide and oxygen to this response and the
tumour oxygenation state, the response of GH3 prolactinomas to 5% CO2/95% air,
carbogen and 100% O2” (Baddeley et al,
2000). That was done using magnetic resonance
imaging and PO2 histography. They found that,
“A 10-30% image intensity increase was observed during 5% CO2/95%
air breathing, consistent with an increase in tumour blood flow, as a result of
CO2-induced vasodilation, reducing the concentration of deoxyhaemoglobin in the
blood. Carbogen caused a further 40-50% signal enhancement, suggesting an
additional improvement due to increase blood oxygenation. A small 5-10%
increase was observed in response to 100% O2, highlighting the dominance of
CO2-induced vasodilation in the carbogen response” (Baddeley et al, 2000).
It is not oxygen, but carbon dioxide that is
the substance responsible for the main improvement in oxygenation of tissues.
Diseases of the brain and the central nervous system
Physiology and medicine teach us that a CO2 deficiency
produces the following abnormalities in the nerve cells:
· Increased excitability of all nerve cells. We are
too excited when we hyperventilate since overbreathing “leads to spontaneous and asynchronous firing of cortical neurons"
(Huttunen et. al., 1999).
· Reduced blood flow to the brain. Our brains get less blood
supply. This physiological fact can be found in many textbooks. As Professor
Newton from the
· The suppressed Bohr effect. Not only is the inflow of
oxygen less, but also oxygen release from red blood cells is hampered by low
CO2 concentrations in tissues. That further reduces brain oxygenation.
In addition, there are similar negative effects due to
likely abnormalities with production and delivery of nitric oxide causing
hypoxia, lowered blood perfusion, faulty transmission of signals, and
inflammation. Imbalances in the ANS and hormonal system are other destabilizing
factors. It is likely that there are other effects of abnormal breathing on the
nervous system. Hyperventilation is virtually always manifested in abnormal
breathing patterns, including a higher frequency of breathing, shorter
exhalations and inhalations, absence of periods of no-breathing, abnormalities
in the work of respiratory muscles (e.g., chest breathing), etc.
Do clinical studies show that patients with mental or psychological
problems have heavy breathing?
In 1976 the British Journal of Psychiatry published a study of CO2 measurements in 60 patients with
neurotic depression and non-retarded endogenous depression (Mora et al, 1976).
All patients had abnormally low carbon dioxide values.
Later, in 1990, American psychiatrists from
Canadian scientists from the Department of Psychiatry (
It has been known in neurology for over 50 years that poor
oxygenation and reduced blood supply of the brain are the foundations of
virtually all “mysterious” and known neurological and psychological
pathologies, ranging from insomnia, depression, addictions and phobias to
Parkinson, Alzheimer, and senile dementia. Indeed, if one considers the places
and people who tried breathing retraining (Chapter 4), almost all of them
relate to psychology and neurology.
GI (gastrointestinal) problems
How hyperventilation affects the GI system?
· Small blood vessels in the digestive organs get
constricted. That reduces their blood supply. Physiological measurements
confirm this effect on the stomach, liver, spleen, and the colon. Hence, GI
organs get less oxygen, glucose, and other nutrients for their normal work and
repair.
· The suppressed Bohr effect, due to low CO2 values in the
blood, reduces the oxygenation of the digestive organs.
· The excited state of the nerve cells in the GI system (the
enteric nervous system that orchestrates the normal work of the whole digestive
conveyor) interferes with the normal work of the GI organs. That can influence
the contraction of the muscular layers, the production and secretion of
digestive enzymes and other functions. Indeed, a group of American gastroenterologists
from the Mayo Clinic in
· Chronic hyperventilation can cause autoimmune GI reactions
since it is not normal to breathe two-three times the norm 24/7. The immune
system, as in case of asthma, can start searching for enemies coming from
outside (i.e., with food). This can contribute to the pathology of inflammatory
bowel disease, irritable bowel syndrome, Crohn’s disease and other problems and
complaints.
Hyperventilation can create numerous abnormalities in the GI
system. There are no studies that compare these effects or define the
individual differences. Similarly, the impact of permanent changes in breathing
is also not investigated.
Hormonal problems
How do people with hormonal (endocrine) problems breathe? A
group of Italian medical researchers from the
How can deep breathing cause hormonal or endocrine
problems? Since hyperventilation is a state of emergency for the whole body, it
can interfere with the normal production and secretion of various hormones. For
example, the immediate effects of stress include surges of adrenalin and
cortisol. Chronic hyperventilation often leads to gradual development of
deficiencies in these hormones. In addition, all tissues, hormonal glands
included, suffer from reduced oxygenation and blood supply. Above-mentioned
abnormalities with nitric oxide production and its bioavailability directly
cause problems with several hormones (see above). The function of the ANS is
compromised in conditions of overbreathing creating another cascade of
imbalances in the circardian cycles regulated by these hormones. However, there
were no systematic studies that identified the long-range hormonal changes due
to heavy breathing. Individual differences, together with life style and
environmental parameters, should play their role when it comes to expected
effects.
Other health concerns and summary
What about Western research concerning the breathing of
people with various other problems? There were few studies relating the quality
of breathing to other health problems. However, medical science knows little or
nothing about the breathing/disease interaction for many common health problems
like cancer, arthritis, diabetes, etc. That especially relates to the
situations when breathing parameters gradually change.
What other diseases are related to abnormal breathing?
Breathing regulates blood supply and oxygenation of all cells, tissues and
organs. Breathing also reflects the state of the autonomous nervous system that
regulates the work of all body organs. In conditions of chronic
hyperventilation vital organs suffer from reduced blood supply and hypoxia. In
addition, chronic hyperventilation interferes with the normal work of the nervous
and immune systems. Hence, a wide variety of negative effects is present when
we breathe too much.
Furthermore, if reduced blood and oxygen supply, together
with abnormalities of the immune and nervous systems, are part of the main
problem, then breathing can play a role in the further development of this
health problem. There is some limited but encouraging practical evidence about
the healing influence of normalization of breathing on a variety of health
conditions.
What diseases are not related to chronic hyperventilation?
People with, for example, color-blindness lack certain structures in the retina
of their eyes. Whatever their breathing patterns, there are no known cases of
the appearance or disappearance of this medical condition. Likely, breathing
has nothing to do with this problem. Hemophilia is usually manifested in the
absence of one blood clotting substance. Again, this problem is purely genetic
and unrelated to breathing.
There are over 30,000 various health problems and
abnormalities known to modern medicine. Doctor Buteyko and his Soviet (Russian)
medical colleagues, based on their clinical experience with over 200,000
patients, hypothesized that about 150-200 health conditions are connected with
abnormal breathing. Hence, less than 1% of all health problems might be
affected by our breathing. However, many of these health problems are fairly
common for modern people. This, for example, relates to our main killers, like
heart disease, cancer, and many others.
1.16 Why breathing?
Patients with modern degenerative diseases
usually have many dozens of physiological and biochemical parameters which seen
to be abnormal. For critically ill patients this number is much larger and is
often estimated to be many hundreds. That means that the concentrations of
numerous minerals, vitamins, hormones and many other substances are out of
their norms. Why, then, are breathing in general and CO2 related parameters in
particular chosen for our consideration?
Based on still limited studies, when
breathing is normal, many diseases are absent. When people are sick, they
over-breathe. Even partial normalization of their breathing results in better
health, as we saw above and are going to consider later. What exact role
breathing plays in the pathology of various diseases is a very big and hard
question that needs further studies and trials.
The unique position of
breathing among many other health parameters is due to its semi-automatic
nature. Professor Ronald Ley, State University of New York, recently wrote a
large review “The modification of
breathing behavior” starting with the statement, “Breathing is the only vital function under direct voluntary control as
well as involuntary control” (Ley, 1999).
Most of the time the "breathing
centre" governs human respiration by keeping minute ventilation, carbon
dioxide and oxygen concentrations, and breath holding time or the BHT
(breath holding time after normal expiration) within relatively narrow ranges
at rest. Meanwhile, people can voluntarily change many breathing parameters.
For example: minute ventilation, breathing frequency, and tidal volume (the
amount of air taken in per breath) can be decreased or increased by at least a
factor of two. The duration of such wilful breathing can be sustained for many
minutes or even hours every day. Thus, breathing, to some degree, can be
controlled in the short run by human willpower and, over long periods of time,
can be normalised through self-discipline and persistence. Moreover, there are
numerous life style and environmental factors (to be discussed) that directly
influence breathing and that can be adjusted to meet the needs of the human
organism.
A person cannot directly order the heart to
slow down, the air passages to open, the kidneys and liver to intensify their
work and cleanse the blood of pathogens, or any spasm to disappear. However,
these and many other problems can be solved by breathing exercises, as will be
discussed later.
1.17 Evolution of air on Earth
How is it possible that a human being, one of the smartest species on
Earth, can kill itself, and over 90% people die this way, by over-breathing? Is
it nature so silly to create this way? In order to answer these questions we
need to consider changes in air composition on Earth.
When there were no life on Earth, air has no oxygen (since oxygen is a
very reactive substance), while CO2 was a part of the volcanic gases that
formed air during those times. Geological studies suggest that CO2
concentration was up to 10-12% or even more. Thus, when the first organic
substances and life forms appeared on Earth (from about 5 billion to 1 billion
years ago), our atmosphere did not have any measurable amounts of O2,
according to Professor Maina (Maina, 1998), who wrote the book The gas exchangers: structure, function, and
evolution of the respiratory processes about development
of respiration and breathing in various creatures living on Earth in the past
and now. He is one of the leading modern authorities on respiration of
different life forms.
Appearance of the first vertebrates
(about 550 millions years ago) and the development of prototypes of human lungs
took place when air was made up of only about 1% O2, while having
many % CO2 (Maina, 1998), likely over 7%. Normal air today has many
times more O2 (about 20%) and
only a fraction of the CO2 (0.03%). However, our cells now still
live in the air that existed hundred millions years ago: “But the cells of animals and humans need about 7 %
CO2 and only 2% O2 in the surrounding environment. This is the way how our cells
live: cells of the heart, brain, and kidneys” (Buteyko, 1977).
Hence, most of the time our lungs were
developing and evolving in conditions when the CO2 content was high (up to
7-12% during the first stages of development), with gradual decline, and low O2
values (about 1% or less during the first stages). During these stages the
process of control of breathing by the nervous system was also developed. Since
this primitive air had very little O2, our evolutionary predecessors could get
more oxygen in tissues by breathing more. Since any stressful situation,
digestion, search for food, mating, playing, and any other activity required
more oxygen, hyperventilation became the fundamental reflex or instinct. Only
totally peaceful stress-free rest had low metabolic rate where heavy breathing
would not give any advantage for survival.
On the other hand, however heavy was
breathing of these primitive creatures in the past, they would still get the
main nutrient, CO2, from air. The CO2 content in tissues had to be even higher
than in air and these creatures would never develop spasms of coronary vessels,
bronchi, other smooth muscles, or abnormal excitability of the nerve cells, or
muscular tension or any other above-mentioned negative effects. Hence, nature
did provided primitive creatures with ability to function without all
above-discussed physiological flaws.
However, the main parameter of our
environment, our air, had dramatic change during later stages of our evolution
due to advance of green life that transforms CO2 into O2 during photosynthesis.
These events could be reflected on the following picture.
Fig 1.1 CO2 and O2 values in air
during early stages of development of our lungs, in our cells now and in modern
air.
We can see that air had dramatic
change during evolution. It now has too much oxygen and almost no CO2. Hence,
the chief parameter of our environment (we can survive for days or weeks with
no water or food, but only for minutes with no air) became abnormal in its
composition. It is only existence of our lungs that protected us from
extinction. Nature could not anticipate this cardinal change in air, but it did
provide us with the means for survival.
Conclusions
• Many sick people with
modern degenerative health conditions chronically breathe 10-25 l/min, or 2-5
times more than the physiological and medical norms (about 5-6 l/min).
• Such chronic
over-breathing usually reduces CO2 stores in the organism causing,
according to physiological laws and studies, the following consequences:
- hypoxia of all cells and organs (especially of the brain and heart);
- local constriction of arteries, arterioles, and capillaries, leading
to poor blood perfusion in the heart, brain and other vital organs;
- tension and irritability in smooth muscles;
- excessive excitability of many brain areas and other parts of the
nervous system;
- constriction of air passages;
- abnormal changes in blood pH and electrolytic composition of each
human cell;
- abnormal biochemical reactions involving vitamins, minerals, amino
acids, lipids, hormones, carbohydrates and other vital substances.
• Medical studies have
revealed personal variability of physiological and psychological symptoms due
to chronic hyperventilation.
• Acute over-breathing,
which is produced by the hyperventilation provocation test, often reproduces
the symptoms of the main health problem.
• There are only a few,
rare health conditions, which are characterised by breathing less than the
norm.
• Since over-breathing
causes low CO2 concentrations in the exhaled air, results of such
measurements revealed that the carbon dioxide level is low for different groups
of sick people, and dangerously low in the severely sick.
• Breathing of
critically ill patients is usually visible, audible, and corresponds to very
low carbon dioxide stores and heavy hyperventilation.
• BHT (breath holding
time) or the BHT (breath holding time after normal expiration) is a
simple and clinically significant indicator reflecting the individual health
state of people with asthma and heart disease.
• Breathing has a unique
position among other vital physiological functions due to the human ability to
control it.
• During early millennia
of evolution of the lungs, hyperventilation, as a reaction to psychological,
physiological, chemical, bacteriological, viral and any other stress, became
the most fundamental reflex of the human organism.
• Despite of dramatic
change in air composition during evolution of life on Earth and despite of our
ability to kill ourselves just by heavy breathing, Nature provided us with the
means of survival: our lungs.
Q&A section for Chapter
1
Q: What were the historical
origins of concerns about the dangers of CO2?
A: In the 1780s, French scientist Antoine-Laurent Lavoisier determined
the composition of air. He also discovered the mechanism of gas exchange during
respiration and burning. Oxygen is consumed for the production of energy and
carbon dioxide is expelled as an end product. In his classical experiments, mice
died in a closed glass jar in an atmosphere containing large quantities of
carbon dioxide and almost no oxygen. A candle also quickly expired in such air.
That was probably the time when a superficial
understanding of respiration produced the idea that carbon dioxide was a “toxic, waste and poisonous” gas while
oxygen brought life and vigor. “Take a
deep breath”, “Breathe more air, it
is good for your health”, “Breathe
deeper, get more air into your lungs, we need oxygen”, etc. became popular
phrases for which there is no scientific basis. Even now, some scientific
publications contain such misleading sentences, as “Respiration is the process of oxygen delivery.”
Professor Yandell Henderson gave the
following explanation of this ignorance, “Likeness
of Life to Fire. - Lavoisier's supreme contribution to science, and
particularly to physiology was the demonstration that, in their broad outlines,
combustion in a fire and respiratory metabolism in an animal are identical.
Both consist in the union of oxygen from the air with carbonaceous material:
and both result in the liberation of heat and the production of carbon dioxide…
The human mind is
inherently inclined to take moralistic view of nature. Prior to the modern
scientific era, which only goes back a generation or two, if indeed it can be
said as yet even to have begun in popular thought, nearly every problem was
viewed as an alternative between good and evil, righteousness and sin, God and
the Devil. This superstitious slant still distorts the conceptions of health
and disease; indeed, it is mainly derived from the experience of physical
suffering. Lavoisier contributed unintentionally to this conception when he
defined the life supporting character of oxygen and the suffocating power of
carbon dioxide. Accordingly, for more than a century after his death, and even
now in the field of respiration and related functions, oxygen typifies the Good
and carbon dioxide is still regarded as a spirit of Evil. There could scarcely
be a greater misconception of the true biological relations of these gases…” (
Q: How did the parameter “40 mm Hg CO2” appear in
textbooks?
A: This number is important because it is present in all main
physiological textbooks used nowadays by western students. This is the current
medical norm for CO2 content in alveoli and the arterial blood. The number was
established about a century ago by the famous British physiologists Charles G.
Douglas and John S. Haldane from
Q: How many people have
normal breathing?
A: If we accept medical standards (6 l/min for ventilation, as in most
medical and physiological textbooks, and 40 s for the BHT), only a small
percentage (less than 10%) of the population satisfies this criterion.
Experience shows that on average, only a few, if any, per 1,000 people have
breathing with Doctor Buteyko norm (60 s BHT or more).
Q: How much oxygen is retained in the
human organism? In other words, are we efficient in oxygen extraction from air?
A:
Typical patients with asthma and heart disease breathe about 15 l/min at rest
and have about 15 s BHT. They utilize or absorb only about 10% of
inhaled oxygen, the remaining 90% is exhaled back in air. People, who are
considered normal by medical standards (6 l/min and 40 s BHT) retain
only about a quarter (25%) of the oxygen that they inhale. Their lungs are more
efficient at extracting oxygen. Those healthy people, who breathe in accodance
with Buteyko norm (4 l/min; 60 s BHT), can extract up to 30-35% of the
oxygen they inhale. People with over 3 min BHT (hatha yoga masters. Dr.
Buteyko and many of his colleagues, etc.) would have about 2 l/min for minute
ventilation and retain up to 60% of inhaled oxygen.
Q: Which body parts or tissues are
particularly sensitive to tissue hypoxia? In other words, how long can various
organs and tissues survive without oxygen?
A: The time of survival will relate to initial oxygenation
(reflected in the breath holding time) and existing pollution of tissues. This
table from the British Medical Journal (Leach & Treacher, 1998) reflects tolerance to hypoxia of various tissues for an
ordinary person.
|
Tissue |
Survival time |
|
Brain |
< 3 min |
|
Kidney and liver |
15-20 min |
|
Skeletal muscle |
60-90 min |
|
Vascular smooth
muscle |
24-72 hour |
|
Hair and nails |
Several days |
Q: Some people claim that
over-breathing can help the organism to "expel toxins". Is this
opinion correct?
A: Although some medical and physiological textbooks on respiration
state that unwanted substances can be removed from the organism through the air
passages, their quantities are small. In addition, over-breathing or
hyperventilation is unlikely to be useful due to greatly decreased blood supply
to other organs of elimination, which will then function less efficiently.
Moreover, poor blood supply to the tissues is going to diminish the rate at
which these substances are collected by body fluids and eliminated.
Meanwhile, normal breathing (about 6 l/min),
in addition to the described normalisation of body physiology, means that
smaller amounts of polluted air, smoke, dust, etc. are taken in to the organism
through the lungs.
Q: Does deep breathing help
to deliver more fresh air to poorly ventilated parts of the lungs filled with
old stale air?
A: Often people also ask, “Is it true that, if I breathe little, I do
not exercise my lungs and can develop some lungs problems?” Vice versa. All
people with asthma, emphysema, bronchitis, and many other problems are heavy
breathers. They need CO2 to heal their lungs. In addition, people with heavy or
deep breathing are often chest-breathers since the smooth muscle of the
diaphragm is in the state of spasm. Hence, their lower layers of the lungs get
much less, if any, fresh air. Normal breathing is diaphragmatic allowing
homogeneous inflation of the whole lungs with fresh air, similar to what
happens in the cylinder of a car due to the movement of the piston.
Q: Can a few deep breaths or
sighing relieve tension in the chest?
A: During the first of several deep breaths, not only are all alveoli in
the lungs greatly expanded providing more oxygen for all tissues, but also any
tightness in the chest muscles can be temporarily relieved, due to their
stretching and subsequent relaxation. Periodic sighing (a typical symptom of
diabetics, CFS sufferers, cardiac patients, asthmatics, etc.) is an example of
chest tension relief, but such deep breaths also remove more CO2,
first, from the lungs, and finally, from all cells.
As a result, any beneficial effects of deep
breathing are very short-lived. Moreover, lowered CO2 levels lead to
worsening of the problems which deep breathing was intended to solve causing:
1) further bronchoconstriction, up to partial or total closure of some lung
areas and less effective gas exchange; 2) more muscular tightness due to increased
hypoxia, excessive excitability and tension in the chest and other muscles,
constriction of arteries and capillaries, and certain other physiological
disorders discussed above.
Thus, the temporary relief provided by
periodic deep breaths or sighing can become a part of the vicious circle. It is
no surprise that various medical professionals, authors of the already cited
publications, viewed sighing as a clear symptom of the chronic hyperventilation
syndrome.
Q:
How does breathing affect the quality of sleep?
A: A normal person needs about 5-6
hours of sleep. He falls asleep within a few minutes, sleeps the whole night in
the same position without awakening, does not remember his dreams and wakes up
fully refreshed. That corresponds to normal breathing and normal breath holding
time (about 40 s).
A typical
asthmatic with 15 l/min ventilation and about 15 s BHT tends to have 8-10 hours
of sleep. He is likely to need some 5-20 minutes to fall asleep. During the
night he can awaken, get anxious, change positions, have dreams, etc. In spite
of the long period of sleep, he may still feel tired in the morning. How and
why are these abnormalities possible?
As
mentioned above, hyperventilation "leads
to spontaneous and asynchronous firing of cortical neurons" (Huttunen
et. al., 1999). This phrase, from the professional magazine Experimental Brain Research, has very
serious personal and even social ramifications (as we are going to see in
Chapter 9).
For example, when this asthmatic
goes to sleep he has thoughts, which are self-generated by his brain in spite
of his conscious attempts to calm down, relax, put everything aside, etc. These
“spontaneous and asynchronous” thoughts
often cause problems with falling asleep.
Let us consider the duration of
sleep. Two main known physiological purposes of sleep are to give rest to the
brain (especially to cortical areas) and the muscles. The normal person, due to
normal aCO2 concentrations, has
had a relaxed, easy attitude, with normal perception during the whole day. He
has experienced less stress (since stress in modern people is mainly due to
distorted attitudes to outer events and stimuli, not due to life-threatening
situations). His muscles have been relaxed (again due to carbon dioxide).
Hence, he needs only 5-6 hours of sleep.
The asthmatic, due to chronic
hyperventilation, has had tense muscles and over-excited brain during the whole
day. Normally, he needs more time for sleep in order to relax and rest his
muscles and brain.
Moreover, severely sick and
hospitalised people with 5-8 s BHT may need up to 12-14 hours of sleep,
usually of miserable quality: with frequent awakenings, changed body positions,
dreams, nightmares, etc. The causes are the same: tense muscles and “spontaneous and asynchronous firing of cortical
[and other] neurons”.
Certain practical evidence and
hatha yoga studies also have found that, when breath holding time is about 1
minute, people need on average only about 4 hours of sleep, while for 2-3
minutes BHT, 2 hours of sleep is sufficient. In my view, that
corresponds to the way Nature designed the human organism.
The relationships between sleep
and breathing will be considered in more detail later.
Q: Are concentration and other mental skills (like logic, analytical
abilities, memory, etc.) similarly affected and why?
A: We know from above, that brain
blood flow is proportional to aCO2. In addition, brain
oxygenation is impaired in such conditions due to the Bohr effect. Both factors
produce predictable effects on all our senses and communication within the
nervous system. At some moments of time, these “spontaneous and asynchronous
firings of cortical” and other neurons may coincide with the normal image of
the world. However, considering long periods of time, it is unreasonable to
expect that a chronically hyperventilating brain can function normally.
Q: I have heard that in some
places pure O2 can be bought for breathing. Is it good for health?
A: While breathing pure O2, “Free radicals (and other toxic metabolites of oxygen) are generated in
most cells as a consequence of normal metabolic processes, but cells are
protected from injury by antioxidant mechanisms. Several forms of lung injury
appear to result from generation of toxic metabolites of oxygen in quantities
which exceed the antioxidant capacity of lung cells…”, as stated at the
very beginning of the abstract by Brigham (1986).
Moreover, detailed investigation of lung
tissues revealed that, “Exposure of
animals to oxidant gases produces a mild emphysema, and O2-derived
free radicals are capable of degrading connective tissues in vitro. It is
postulated that degradation of connective tissue by O2-derived free
radicals leads to emphysema in these models” (abstract, Kerr et al, 1987).
A review, “Data on oxidants and antioxidants”, conducted by Junod (1986), also
found that “Since O2
intermediates can affect the general cellular metabolism and inhibit cell
replication or reduce protein synthesis, all the biological effects of O2
and its metabolites should therefore be considered in the pathogenesis of
emphysematous lesions in the lung” (Junod, 1986).
Another related question is why anti-oxidants
are important supplements. They are used in order to diminish the possible
damage done by oxidants generated by, among other sources, excessive freely-dissolved
O2 concentrations.
Finally, a textbook on medical physiology
(Ganong, 1995) contains a section entitled "Oxygen toxicity". It starts with: "It is interesting that while O2 is necessary for life in
aerobic organisms, it is also toxic. Indeed, 100% O2 has been
demonstrated to exert toxic effects not only in animals, but also in bacteria,
fungi, cultured animal cells, and plants. The toxicity seems to be due to the
production of the superoxide anion (O2-), which is a free radical,
and H2O2. When 80-100% O2 is administered to
humans for periods of 8 hours or more, the respiratory passages become
irritated, causing substernal distress, nasal congestion, sore throat, and
coughing. Exposure for 24-48 hours causes lung damage as well. In animals, more
prolonged administration without irritation is possible if treatment is briefly
interrupted from time to time, but it is not certain that periodic
interruptions are of benefit to humans" (Ganong, 1995).
In subsequent paragraphs, Professor Ganong
describes development of lung cysts and serious visual defects due to retinal
damage in infants treated with O2 for respiratory distress syndrome.
Increased O2 pressure (in some places pure O2 is
administered at increased pressure) accelerates the harmful effects of O2.
Meanwhile, breathing O2 for a few
minutes would probably not be very harmful. Generally, breathing pure oxygen
can be useful as a short-term emergency measure in cases of life-threatening
hypoxia.
Q: What is the long-term
influence of different air compositions on human health? Has anybody
investigated the optimum composition of air?
A: The first experiments in this area were done about a century ago by
Yale researchers. Professor John Haldane was, probably, the most prominent
scientist of those times. He wrote a classic textbook “Respiration” (Yale University Press, New Haven, UK, 1922) which is
mostly devoted to the interaction between breathing and arterial blood CO2
concentrations. During the later years of his career he served in the British
Navy, working on air supply for submarines (where people can spend several
months). The results of his research are still classified by British government
agencies.
Available information about air composition
on spaceships indicates that during the first three
In 1960s Doctor Buteyko was the manager of
the laboratory of functional diagnostic and studied various breathing –related
effects on cardiovascular and other systems of the human organism. His research
was supported and funded by the Soviet Ministry of Aviation and Space
Exploration for first Soviet space missions. According to Doctor Buteyko, the
optimum air for long-term health benefits should be about 10-12% O2
(as found on high mountains) and 2% CO2 (Buteyko, 1977). Probably,
this extra 2% CO2 increases aCO2, improving tissue
oxygenation and producing other positive changes, while 10-12% O2
(twice less than normal air) is small enough to minimize oxidative lung damage.
Surprisingly little information is published
about research on optimum air for submarines. Also, very little is published
about the growth processes of plants and animals in CO2 rich air,
while known results are very encouraging.
Q: Plant respiration is the
opposite process: consumption of CO2 and production of O2.
Thus, plants fix CO2 for synthesis of other chemical substances. Can
animals do the same?
A: A review of numerous publications devoted to this subject was given
by Waelsch and colleagues (1964) in an article entitled “Quantitative aspects of CO2 fixation in mammalian brain in
vivo”. They found that aspartic and glutamic amino acids and glutamine were
the substances chemically synthesised in mammalian brains.
Glutamine is the most abundant amino acid in
the human organism (hence, its popularity among some bodybuilders). It is also
the amino acid most required for tissue repair, but “since the supply of glutamic acid from the circulating blood is
insufficient for the formation of additional amount of glutamine, the
dicarboxylic acid has to be synthesized in the brain.” (Berl et al, 1962)
This last substance is a CO2 derivative.
Thus, CO2 can be fixed by the
human organism in order to rebuild nervous tissues in the brain. The rate of CO2-derived
glutamine production is proportional to CO2 concentration in the
brain. It follows that low CO2 in the brain not only makes the brain
unreasonably excited (possibly causing anxiety, fears, panic attacks,
aggression, hostility, violence, or other strong emotions), but also has
adverse effects on its cellular repair.
There are several other reactions, in which
CO2 is one of the necessary components. These reactions relate to biosynthesis
of amino acids, carbohydrates, lipids and several other vital substances. The
formulas of these reactions are provided in the article “The Role of Carbon Dioxide in the Vital Processes of the organism”
(Kazarinov, 1991)
[Available at:
http://members.westnet.com.au/pkolb/biochem.htm].
“Q: Could you [doctor KP
Buteyko] please explain us shortly your principle of breathing?
A: Here it is: we know that deep breathing decreases
the concentration of carbon dioxide in the blood, lungs and cells. A Russian
scientist from
References for chapter 1
Ahrens T, Schallom L, Bettorf K, Ellner S, Hurt G, O'Mara V, Ludwig J,
George W, Marino T, Shannon W., End-tidal
carbon dioxide measurements as a prognostic indicator of outcome in cardiac
arrest. Am J Crit Care 2001 Nov; 10(6): 391-398.
Asmundson GJ & Stein MB, Triggering
the false suffocation alarm in panic disorder patients by using a voluntary
breath-holding procedure, Am J Psychiatry 1994 Feb; 151(2): 264-266.
Baddeley H, Brodrick PM, Taylor NJ, Abdelatti MO, Jordan LC, Vasudevan
AS, Phillips H, Saunders MI, Hoskin PJ, Gas
exchange parameters in radiotherapy patients during breathing of 2%, 3.5% and
5% carbogen gas mixtures, Br J Radiol 2000 Oct; 73(874): 1100-1104.
Balestrino M, Somjen GG, Concentration
of carbon dioxide, interstitial pH and synaptic transmission in hippocampal
formation of the rat, J Physiol 1988, 396: 247-266.
Bass C, The hyperventilation
syndrome, Respiratory Diseases in Practice 1990 Oct/Nov: 13-16.
Bazelmans E, Bleijenberg G, Van Der Meer JW, Folgering H, Is physical deconditioning a perpetuating
factor in chronic fatigue syndrome? A controlled study on maximal exercise
performance and relations with fatigue, impairment and physical activity,
Psychol Med 2001 Jan; 31(1): 107-114.
Bohr C, Hasselbach KA, Krogh A, Scand Arch Physiol 1904; 16: 402.
Bowler SD, Green A, Mitchell CA, Buteyko
breathing techniques in asthma: a blinded randomised controlled trial, Med
J of Australia 1998; 169: 575-578.
Brasher RE, Hyperventilation
syndrome, Lung 1983; 161: 257-273.
Brigham KL, Role of free radicals
in lung injury, Chest 1986 Jun; 89(6): 859-863.
Brizel DM, Scully SP, Harrelson JM, Layfield LJ, Bean JM, Prosnitz LR,
Dewhirst MW, Tumor oxygenation predicts
for the likelihood of distant metastases in human soft tissue sarcoma,
Cancer Reserach 1996, 56: 41-943.
Brown EB, Physiological effects
of hyperventilation, Physiol Reviews 1953 Oct, 33 (4): 445-471.
Buteyko KP, Carbon dioxide theory
and a new method of treatment and prevention of diseases of the respiratory
system, cardiovascular system, nervous system, and some other diseases [in
Russian], Public lecture for Soviet scientists at the Moscow State University,
9 December 1969, published in
the Soviet national journal Science and
life, Moscow, issue 11, October 1977.
Buteyko KP,
Russian national newspaper “Komsomol’skaya pravda” [“Komsomol’s Truth”]
Cantineau JP, Lambert Y, Merckx P, Reynaud P, Porte F, Bertrand C,
Duvaldestin P, End-tidal carbon dioxide
during cardiopulmonary resuscitation in humans presenting mostly with asystole:
a predictor of outcome, Crit Care Med 1996 May; 24(5): 791-796.
Carryer HM, Hyperventilation
syndrome, Med Clin North Amer 1947, 31: 845.
Chaplin DJ, Durand RE, Olive PL, Acute
hypoxia in tumors: implications for modifiers of radiation effects,
International Journal of Radiation, Oncology, Biology, Physics 1986 August;
12(8): p. 1279-1282.
Clark AL, Chua TP, Coats AJ, Anatomical
dead space, ventilatory pattern, and exercise capacity in chronic heart failure,
Br Heart J 1995 Oct; 74(4): 377-380.
Clark DM, Hemsley DR, The effects
of hyperventilation; individual variability and its relation to personality,
J Behav Ther Exp Psychiatry 1982 Mar; 13(1): 41-47.
Cluff RA, Chronic
Hyperventilation and its treatment by physiotherapy: discussion paper, J of
the Royal Soc of Med 1984 Sep; 77: 855-861.
Coenen AM, Drinkenburg WH, Hoenderken R, van Luijtelaar EL, Carbon dioxide euthanasia in rats: oxygen
supplementation minimizes signs of agitation and asphyxia, Lab Anim 1995
Jul; 29(3): 262-268.
DaCosta JM, On irritable heart: a
clinical study of a form of functional cardiac disorder and its consequences
, Am J Med Sci 1871; 61: 17-53.
Davidson JT, Whipp BJ, Wasserman K, Koyal SN, Lugliani R, Role of the carotid bodies in breath-holding,
New England Journal of Medicine 1974 April 11; 290(15): p. 819-822.
Demeter SL, Cordasco EM, Hyperventilation
syndrome and asthma , Am J of Med 1986 Dec; 81: 989-994.
Denko NC, Fontana LA, Hudson KM, Sutphin PD, Raychaudhuri S, Altman R,
Giaccia AJ, Investigating hypoxic tumor
physiology through gene expression patterns, Oncogene 2003 September 1;
22(37): p. 5907-5914.
Dimopoulou I, Tsintzas OK, Alivizatos PA, Tzelepis GE, Pattern of breathing during progressive
exercise in chronic heart failure, Int J Cardiol. 2001 Dec; 81(2-3):
117-121.
Douglas
CG, Haldane JS, The regulation of normal
breathing, Journal of Physiology 1909; 38: p. 420–440.
Esquivel E, Chaussain M, Plouin P, Ponsot G, Arthuis M, Physical exercise and voluntary
hyperventilation in childhood absence epilepsy, Electroencephalogr Clin
Neurophysiol 1991 Aug; 79(2): 127-132.
Evans SM & Koch CJ, Prognostic
significance of tumor oxygenation in humans, Cancer Letters 2003 May 30;
195(1): p. 1-16.
Ferris EB, Engel GL, Stevens CD, Webb J, Voluntary breathholding, III. The relation of the maximum time of
breathholding to the oxygen and carbon dioxide tensions of arterial blood, with
a note on its clinical and physiological significance, J Clin Invest 1946,
25: 734-743.
Flack M, Some simple tests of
physical efficiency, Lancet 1920; 196: 210-212.
Flume PA, Eldridge FL, Edwards LJ, Mattison LE, Relief of the 'air hunger' of breathholding. A role for pulmonary
stretch receptors, Respir Physiol 1996 Mar; 103(3): 221-232.
Ford MJ, Camilleri MJ, Hanson RB, Wiste JA, Joyner MJ, Hyperventilation, central autonomic control,
and colonic tone in humans, Gut 1995 Oct; 37(4): p. 499-504.
Fried R, Fox MC, Carlton RM, Effect
of diaphragmatic respiration with end-tidal CO2 biofeedback on respiration, EEG,
and seizure frequency in idiopathic epilepsy, Annals of New York Academy of
Sciences 1990; 602: p. 67-96.
Friedman M, Studies concerning the aetiology and pathogenesis of neurocirculatory
asthenia III. The cardiovascular manifestations of neurocirculatory asthenia,
Am Heart J 1945; 30, 378-391.
Ganong WF, Review of medical
physiology, 15-th ed., 1995, Prentice Hall Int.,
Gay SB, Sistrom C1L, Holder CA, Suratt PM, Breath-holding capability of adults. Implications for spiral computed
tomography, fast-acquisition magnetic resonance imaging, and angiography,
Invest Radiol 1994 Sep; 29(9): 848-51.
Gilmour DG, Douglas IH, Aitkenhead
AR, Hothersall AP, Horton PW, Ledingham IM, Colon
blood flow in the dog: effects of changes in arterial carbon dioxide tension,
Cardiovasc Res 1980 Jan; 14(1): 11-20.
Guyton AC, Physiology of the
human body, 6-th ed., 1984, Suanders College Publ.,
Harris AL, Hypoxia: a key
regulatory factor in tumour growth, National Review in Cancer 2002 January;
2(1): p. 38-47.
Hashimoto K, Okazaki K, Okutsu Y, The effects of hypocapnia and hypercapnia on
tissue surface PO2 in hemorrhaged dogs [Article in Japanese], Masui 1989
Oct; 38(10): 1271-1274.
Hasselbalch, Biochem Zeitschr, 1912, XLVI, p. 416.
Henderson Y, Acapnia and shock. -
Henderson Y, Carbon dioxide,
in Cyclopedia of Medicine, ed. by HH
Young, Philadelphia, FA Davis, 1940.
Herxheimer H, Hyperventilation
asthma, Lancet 1946, 6385: 83-87.
Herxheimer H, The late bronchial
reaction in induced asthma, Int Arch Allergy Appl Immunol 1952; 3: 323-328.
Huang CT, Cook AW, Lyons HA, Severe
cranio cerebral trauma and respiratory abnormalities, Arch Neurol 1963, 9:
545-554.
Hudlicka O, Muscle blood flow,
1973, Swets&Zeitlinger,
Hughes RL, Mathie RT, Fitch W,
Campbell D, Liver blood flow and oxygen
consumption during hypocapnia and IPPV in the greyhound, J Appl Physiol.
1979 Aug; 47(2): 290-295.
Hurewitz AN, Sampson MG, Voluntary
breath holding in the obese, J Appl Physiol 1987 Jun; 62(6): 2371-2376.
Huttunen J, Tolvanen H, Heinonen E, Voipio J, Wikstrom H, Ilmoniemi RJ,
Hari R, Kaila K, Effects of voluntary
hyperventilation on cortical sensory responses. Electroencephalographic and
magnetoencephalographic studies, Exp Brain Res 1999, 125(3): 248-254.
Johnson BD, Scanlon PD, Beck KC, Regulation
of ventilatory capacity during exercise in asthmatics, J Appl Physiol. 1995
Sep; 79(3): 892-901.
Johnson BD, Beck KC, Olson LJ, O'Malley KA, Allison TG, Squires RW, Gau
GT, Ventilatory constraints during
exercise in patients with chronic heart failure, Chest 2000 Feb; 117(2):
321-332.
Kahaly GJ, Nieswandt J, Wagner S, Schlegel J, Mohr-Kahaly S, Hommel G, Ineffective cardiorespiratory function in
hyperthyroidism, J Clin Endocrinol Metab 1998 Nov; 83(11): 4075-4078.
Katoch K, Autonomic nerve
affection in leprosy, Indian J Lepr 1996 Jan-Mar; 68(1): 49-54.
Kendrick AH, Rozkovec A, Papouchado M, West J, Laszlo G, Single-breath breath-holding estimate of
pulmonary blood flow in man: comparison with direct Fick cardiac output,
Clin Sci (London) 1989 Jun; 76(6): 673-676.
Kerr JS, Chae CU, Nagase H, Berg RA, Riley DJ, Degradation of collagen in lung tissue slices exposed to hyperoxia,
Am Rev Respir Dis 1987 Jun; 135(6): 1334-1339.
Kohn RM & Cutcher B, Breath-holding
time in the screening for rehabilitation potential of cardiac patients,
Scand J Rehabil Med 1970; 2(2): 105-107.
Krnjevic K, Randic M and Siesjo B, Cortical
CO2 tension and neuronal excitability, J of Physiol 1965, 176: 105-122.
Kunz M & Ibrahim SM, Molecular
responses to hypoxia in tumor cells, Molecular Cancer 2003; 2: p. 23-31.
Junod AF, Data on oxidants and
antioxidants, Bull Eur Physiopathol Respir 1986 Jan-Feb; 22(1): 253s-255s.
Lavrent'ev MM, Averko NN,
Leach RM, Treacher DF, ABC of oxygen, Oxygen transport, 2. Tissue hypoxia (Clinical review), BMJ 1998; 317: 1370-1373 (14 November).
Ley
R, The modification of breathing
behavior. Pavlovian and operant control in emotion and cognition, Behav
Modif 1999, Jul; 23(3): 441-79.
Lum LC, Hyperventilation: The tip
and the iceberg, J Psychosom Res 1975; 19: 375-383.
Magarian GJ, Hyperventilation
syndrome: infrequently recognized common expressions of anxiety and stress,
Medicine 1982; 61: 219-236.
Magarian GJ, Middaugh DA, Linz DH, Hyperventilation
syndrome: a diagnosis begging for recognition, West J Med 1983; 38:
733-736.
Maina JN, The gas exchangers:
structure, function, and evolution of the respiratory processes, 1998,
Springer,
Marks B, Mitchell DG, Simelaro JP, Breath-holding
in healthy and pulmonary-compromised populations: effects of hyperventilation
and oxygen inspiration, J Magn Reson Imaging 1997 May-Jun; 7(3): 595-597.
Mazarra JT, Ayres SM, Grace WJ, Extreme
hypocapnia in the critically ill patient, Amer J Med Apr 1974, 56: 450-456.
McFadden ER & Lyons HA, Arterial-blood
gases in asthma, The New Engl J of Med 1968
McNally
RJ & Eke M, Anxiety sensitivity,
suffocation fear, and breath-holding duration as predictors of response to
carbon dioxide challenge, J Abnorm Psychol 1996 Feb; 105(1): 146-149.
Mirsky I A, Lipman E, Grinker R R, Breath-holding
time in anxiety state, Federation proceedings 1946; 5: 74.
Mithoefer JC, Breath holding.
In: Handbook of physiology, Respiration,
Mojsoski N, Pavicic F, Study of
bronchial reactivity using dry, cold air and eucapnic hyperventilation [in
Serbo-Croatian], Plucne Bolesti 1990 Jan-Jun; 42(1-2): 38-42.
Mora
JD, Grant L, Kenyon P, Patel MK, Jenner FA, Respiratory
ventilation and carbon dioxide levels in syndromes of depression, Br J Psychiatry
1976 Nov, 129: 457-464.
Morgan WP, Hyperventilation
syndrome: a review, Am Ind Hyg Assoc J 1983; 44(9): 685-689.
Nakao K, Ohgushi M, Yoshimura M, Morooka K, Okumura K, Ogawa H,
Kugiyama K, Oike Y, Fujimoto K, Yasue H, Hyperventilation
as a specific test for diagnosis of coronary artery spasm. Am J Cardiol
1997 Sep 1; 80(5): 545-9.
Nardi AE, Valenca AM, Nascimento I, Mezzasalma MA, Lopes FL, Zin WA, Hyperventilation in panic disorder patients
and healthy first-degree relatives, Braz J Med Biol Res 2000 Nov; 33(11):
1317-1323.
Nevarez-Najera A,
Hernández-Campos S, Rodríguez-Morán M, Guerrero-Romero F, Estimating forced expiratory volume in one second based on breath
holding in healthy subjects [Article in Spanish], Arch Bronconeumol. 2000
Apr; 36(4): 197-200.
Newton E, Hyperventilation Syndrome 2004 June 17, Topic 270, p. 1-7
(www.emedicine.com).
Nishino T,
Sugimori K, Ishikawa T, Changes in the
period of no respiratory sensation and total breath-holding time in successive
breath-holding trials, Clin Sci (Lond). 1996 Dec; 91(6): 755-761.
Nixon PGF, Hyperventilation and
cardiac symptoms, Internal Medicine 1989 Dec; 10(12): 67-84.
Okazaki K, Okutsu Y, Fukunaga A, Effect
of carbon dioxide (hypocapnia and hypercapnia) on tissue blood flow and oxygenation
of liver, kidneys and skeletal muscle in the dog, Masui 1989 Apr, 38 (4):
457-464.
Okazaki K, Hashimoto K, Okutsu Y,
Okumura F, Effect of arterial carbon
dioxide tension on regional myocardial tissue oxygen tension in the dog [Article
in Japanese], Masui 1991 Nov; 40(11): 1620-1624.
Paulley JW, Hyperventilation,
Recenti Prog Med 1990 Sep; 81(9): 594-600.
Paton WDN, Is CO2 euthanasia
humane? Nature 1983, 305: 268.
Perez-Padilla R, Cervantes D, Chapela R, Selman M, Rating of breathlessness at rest during acute asthma: correlation with
spirometry and usefulness of breath-holding time, Rev Invest Clin 1989
Jul-Sep; 41(3): 209-213.
Plum F, Hyperpnea,
hyperventilation and brain dysfunction, Annals of Intern Med 1972, 76: 328.
Posniak HV, Olson MC, Demos TC, Pierce KL, Kalbhen CL, CT of the chest and abdomen in patients on
mechanical pulmonary ventilators: quality of images made at 0.6 vs 1.0 sec,
Am J Roentgenol 1994 Nov; 163(5): 1073-1077.
Powell ME, Hill SA, Saunders MI, Hoskin PJ, Chaplin DJ, Human tumour blood flow is enhanced by
nicotinamide and carbogen breathing, Cancer Res 1997 Dec 1; 57(23):
5261-5264.
Powell ME, Collingridge DR, Saunders MI, Hoskin PJ, Hill SA, Chaplin
DJ, Improvement in human tumour
oxygenation with carbogen of varying carbon dioxide concentrations,
Radiother Oncol 1999 Feb; 50(2): 167-171.
Respiration and Circulation, ed. by P.L.
Altman & D.S. Dittmer, 1971,
Rockwell S, Oxygen delivery: implications
for the biology and therapy of solid tumors, Oncology Research 1997;
9(6-7): p. 383-390.
Rout MW, Lane DJ, Wolliner L, Prognosis
in acute cerebrovascular accidents in relation to respiratory pattern and blood
gas tension, Br Med J 1971, 3: 7-9.
Ryan H, Lo J, Johnson RS, The
hypoxia inducible factor-1 gene is required for embryogenesis and solid tumor formation,
EMBO Journal 1998, 17: p. 3005-3015.
Ryan HE, Poloni M, McNulty W, Elson D, Gassmann M, Arbeit JM, Johnson
RS, Hypoxia-inducible factor-1 is a
positive factor in solid tumor growth, Cancer Res, August 1, 2000; 60(15):
p. 4010 - 4015.
Salen P, O'Connor R, Sierzenski P, Passarello B, Pancu D, Melanson S,
Arcona S, Reed J, Heller M, Can cardiac
sonography and capnography be used independently and in combination to predict
resuscitation outcomes? Acad Emerg Med 2001 Jun; 8(6): 610-615.
Santiago TV & Edelman NH, Brain blood flow and control of breathing,
in Handbook of Physiology, Section 3:
The respiratory system, vol. II, ed. by AP Fishman. American Physiological
Society,
Sanya AO, Adesina
AT, Relationship between estimated body
fat and some respiratory function indices, Cent Afr J Med. 1998 Oct; 44(10):
254-258.
Schmaltz C, Hardenbergh PH, Wells A, Fisher DE, Regulation of proliferation-survival decisions during tumor cell
hypoxia, Molecular and Cellular Biology 1998 May, 18(5): p. 2845-2854.
Severinghaus JW, Blood gas
concentations. In: Handbook of
physiology, Respiration,
Sher TH, Recurrent chest
tightness in a 28-year-old woman, Annals of allergy 1991 Sep; 67: 310-314.
Simmons DH, Nicoloff J, Guze LB, Hyperventilation
and respiratory alkalosis as signs of gram-negative bacteremia, J Amer Med
Assoc 1960, 174: 2196-2199.
Sinderby C, Spahija J, Beck J, Kaminski D, Yan S, Comtois N, Sliwinski
P, Diaphragm activation during exercise
in chronic obstructive pulmonary disease, Am J Respir Crit Care Med 2001
Jun; 163(7): 1637-1641.
Soley MH & Shock NW, Etiology
of effort syndrome, Amer J Med Science 1938, 196: 840.
Speckmann E-J & Caspers H, The
effect of O2- and CO2-tensions in the nervous tissue on neuronal activity and
DC potentials, Handbook of Electroencephalography and Clinical Neurophysiology
1974; 2C: 71-89.
Starling E & Lovatt EC, Principles
of human physiology, 14-th ed., 1968, Lea & Febiger,
Stanley NN, Cunningham EL, Altose MD, Kelsen SG, Levinson RS, Cherniack
NS, Evaluation of breath holding in
hypercapnia as a simple clinical test of respiratory chemosensitivity,
Thorax 1975 Jun; 30(3): 337-343.
Sterling GM, The mechanism of
bronchoconstriction due to hypocapnia in man, Clin Sci 1968 Apr; 34(2):
277-285.
Straub NC, Section
V, The Respiratory System, in Physiology, eds. RM Berne & MN Levy,
4-th edition, Mosby, St. Louis, 1998.
Tanabe Y, Hosaka Y, Ito M, Ito E, Suzuki K, Significance of end-tidal P(CO(2)) response to exercise and its
relation to functional capacity in patients with chronic heart failure,
Chest 2001 Mar; 119(3): 811-817.
Tantucci C, Scionti L, Bottini P, Dottorini ML, Puxeddu E, Casucci G,
Sorbini CA, Influence of autonomic
neuropathy of different severities on the hypercapnic drive to breathing in
diabetic patients, Chest. 1997 Jul; 112(1): 145-153.
Taskar V, Clayton N, Atkins M, Shaheen Z, Stone P, Woodcock A, Breath-holding time in normal subjects,
snorers, and sleep apnea patients, Chest 1995 Apr; 107(4): 959-962.
Tavel ME, Hyperventilation
syndrome - Hiding behind pseudonyms? Chest 1990; 97: 1285-1288.
Taylor AM, Keegan J, Jhooti P, Gatehouse PD, Firmin DN, Pennell DJ, Differences between normal subjects and
patients with coronary artery disease for three different MR coronary
angiography respiratory suppression techniques, J Magn Reson Imaging 1999
Jun; 9(6): 786-793.
Thorborg P, Jorfeldt L, Lofstrom
JB, Lund N, Striated muscle tissue
oxygenation and lactate levels during normo-, hyper- and hypocapnia. A study in
the rabbit, Microcirc Endothelium Lymphatics 1988 Jun; 4(3): 205-229.
Vapalanti M & Troup H, Prognosis
for patients with severe brain injuries, Br Med J 1971, 3: 404-407.
Waites TF, Hyperventilation -
chronic and acute, Arch Intern Med 1978; 138: 1700-1701.
Wanamee P, Poppel JW, Glicksman AS, Randall HT, Roberts KE, Respiratory alkalosis in hepatic coma,
Arch Intern Med 1956, 97: 762-767.
Winslow EJ, Loeb HS, Rahimtoola SH, Kamath S, Gunnar RM, Hemodynamic studies and results of therapy
in 50 patients with bacteremic shock, Am J Med 1973, 54: 421-426.
Wirrel CW, Camfield PR, Gordon KE, Camfield CS, Dooley JM, and Hanna
BD, Will a critical level of hypocapnia
always induce an absence seizure? Epilepsia 1996; 37(5): 459-462.
Wood P, Da Costa's syndrome,
The Brit Med J 1941, 1: 767.
Zandbergen
J, Strahm M, Pols H, Griez EJ, Breath-holding
in panic disorder, Compar Psychiatry 1992 Jan-Feb; 33(1): 47-51.