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Hyperventilation explained

m0ses

Well-Known Member
Hyperventilation should be explained on every entry level freediving course and every freediver should have the knowledge about it. However not many actually know and understand the physiological effects on human body which hyperventilation produces.

Review article about hyperventilation and its influence on human body you can find here.
 
OP
OP
m0ses

m0ses

Well-Known Member
Full Text

Hyperventilation - a review, by Lily Crespy

Introduction

Hyperventilation in freediving is a very controversial issue. To start with, the very definition of hyperventilation is often debated, and freedivers can sometimes not agree whether a certain breathing pattern constitutes hyperventilating or not. Moreover, the debate on the advantages versus the drawbacks of hyperventilating before a dive on breath-hold, and to what extent, is still going strong in the freediving community.
For years, hyperventilation was widely practiced by freedivers as it was known to help divers hold their breath for longer and increase their performance in static, dynamic and deep disciplines. This theory has since largely been demonstrated to be wrong and to be actually dangerous for people practising apnea, as it could cause blackouts.
Here, we will explain what constitutes hyperventilation, its physiological effects on the human body, and why it should be avoided before breath-hold diving.

1) Definitions

There are two types of hyperventilation:
- Spontaneous hyperventilation is the normal reaction of an organism breathing air low in O2 or enriched in CO2, or increasing its metabolism (muscular effort, stress, cold environment) so as to conserve normal O2 and CO2 values ;
- Voluntary hyperventilation is a hyperventilation not ruled by O2 and CO2 values; often practiced in the past by apnea divers, it is now widely reproved, as it was at the origin of numerous syncopes (1).
For the rest of this study we will only focus on voluntary hyperventilation, and refer to it simply as “hyperventilation”.

Several criteria have been proposed to define what constitutes hyperventilation. Here are two of the most accurate ones:
- “An increase in ventilation out of proportion to any increase in metabolic VO2, therefore resulting in a low arterial pCO2. Reduced arterial pCO2 is therefore a criterion by which to determine whether a subject is hyperventilating or not.” (2) ;
- “Pulmonary ventilation rate greater than that metabolically necessary for gas exchange, resulting from an increased respiration rate, or increased tidal volume, or both. It causes excessive O2 intake and CO2 elimination. Hypocapnia and respiratory alkalosis then occur, leading to dizziness, faintness, numbness in fingers and toes, possibly syncope, and psychomotor impairment.” (3)

To summarize, hyperventilation is the action of breathing larger amounts of air than normal, either by taking bigger breaths or by breathing more rapidly, or both. One of the main measurable effects of hyperventilation, and also a criterion for defining it, is the arterial pCO2, which drops following hyperventilation.


2) Physiological effects

a) Effects on gas levels

- Oxygen: hyperventilation increases the content in O2 of the gases in the pulmonary alveoli. Indeed, after hyperventilating, the pO2 goes from 100 to 120 mm Hg, which can increase the O2 available in alveoli by around 150 mL. Regarding arterial blood, because the haemoglobin saturation on O2 is already close to 97%, hyperventilation can only increase this saturation weakly, reaching 98% without really going beyond this value. This results in an increase in the volume of O2 transported by the arterial blood that is insignificant (1). Norfleet and Bradley have shown that eucapnic hyperventilation (i.e. where CO2 levels remain unchanged) does not prolong the duration of voluntary apnea, suggesting the effect of hyperventilation on O2 levels alone is not enough to significantly improve breath-hold capacities (1).

- CO2: hyperventilation leads to a decrease of CO2 stocks. This hypocapnia suppresses the stimulus of CO2 on central chemoreceptors (under 40 mm Hg) and on peripheral chemoreceptors (under 30 mm Hg). As the CO2 stimulus on these chemoreceptors is the signal inducing the need to take a breath, this disappearance of the urge to breathe explains the comfortable sensation felt by freedivers after hyperventilation, but also the risk of syncope. Indeed, as the apnea progresses, the CO2 and pH stimuli remain weak for a long time, whereas the O2 stimulus increases slowly, but not enough to constitute by itself an alarm bell. Therefore the hypoxia progressively occurs until loss of consciousness (1). This will be explained with the mechanism of the shallow-water blackout in part three.
Moreover, the low pCO2 value during breath-hold delays the apparition of diaphragmatic contractions (appearing for pCO2 values above 47 mm Hg), which are another alarm bell indicating the start of the struggle phase. (1)

b) Effects on the blood

Hyperventilation leads to lower pCO2 and higher pH in arterial blood, and to a drop in arterial blood pressure. The decrease in blood pressure is due to vasodilation of the arteries, not to a change in cardiac output (4, 6).
The hypocapnia caused by hyperventilation also induces a muscular vasodilation, but induces a vasoconstriction in the skin and, more importantly, in the brain (1, 6). This cerebral vasoconstriction provokes a lower tolerance to hypoxia (1). For a pCO2 dropping from 37 mm Hg down to 19 mm Hg we observe a drop from 45 to 25 mL/100g/min in the cerebral blood flow (5). The effects of hyperventilation on pH and intracranial pressure are transient (5).
Since CO2 reacts with water to form carbonic acid, an increase in CO2 levels leads to a more acidic blood. Hyperventilation leads to a decrease of CO2 levels in the blood, and therefore this in turn, leads to an alkalinisation of the blood, i.e. and elevation of its pH, known as respiratory alkalosis.

c) Nerves and muscles

Studies have shown that over-breathing induces a decrease in phosphates, glucose and calcium ions in the blood (6). Differences in calcium content in particular can induce significant changes in the excitability of nerves and muscles. Indeed, over-breathing has been shown to induce increased irritability of the nerve and muscle, and to produce tetany (6).
The alkalinisation caused by hypocapnia has a debilitating action on the nerves and the muscles. Therefore, we can observe successively: dizziness, paraesthesia in the extremities, muscle spasms, facial myoclonies especially of the lips. The intensity of such effects varies greatly between individuals and from one day to the next for each person. It is practically impossible to establish any proportionality between pCO2 values and clinical effects (1).

d) Molecular level: the Bohr effect

Haemoglobin is carried in the red blood cells and is the protein responsible for the transport of oxygen in the body. Haemoglobin is a heterotetrameric protein comprising two alpha-subunits and two beta-subunits. Each subunit contains a heme core with one iron ion (Fe2+). It is this iron atom that binds a molecule of O2, making each molecule of haemoglobin able to carry up to 4 molecules of O2 in the blood.
The affinity of haemoglobin for oxygen and the strength of the bond between them is dependent on various factors, namely pH, levels of CO2 and of 2,3-biphosphoglyceric acid, and the pO2. There is also a cooperative effect by which, when one subunit binds to one molecule of O2, the affinity for oxygen of the other subunits increases, thereby favouring the binding of more O2 by that molecule of haemoglobin.
It should be noted that carbon monoxide (CO) binds to haemoglobin on the exact same binding site as O2. The affinity of haemoglobin for CO is 250 times greater than for O2. It goes without saying that freedivers should avoid smoking. Not only will the nicotine and tar accumulate inside the lungs and make the gas exchanges more difficult between the blood and alveoli, but also the carbon monoxide inhaled in cigarette smoke will bind to haemoglobin and therefore prevent good transport of oxygen through the blood.

The influence of hyperventilation, however, lies in its effect on blood pH. As described above, hyperventilation will induce a decrease of CO2 levels in arterial blood. CO2 naturally reacts with water to give the following reaction:
CO2 + H2O  H2CO3  HCO3- + H+
When CO2 levels drop following hyperventilation, the reaction producing CO2 is favoured, to counteract this. This provokes a decrease of H+ ions, and therefore an increase in blood pH. A higher blood pH favours the “relaxed” conformation of haemoglobin, which has a higher O2 affinity. Therefore, with low pH, oxygen tends to remain strongly bound to haemoglobin. So freedivers hyperventilate hoping to prolong their breath-hold but in the end, hyperventilation is preventing the release of oxygen to the tissues, which therefore actually shortens the breath-holding ability.

3) Shallow water blackout
[...]

more you can find here.


Disclaimer: This work has been compiled and created by Lily Crespy, Master Student of Apnea Bali Freediving Education school. It is free to copy and reproduce as long as it will be credited to: Lily Crespy and Apnea Bali Freediving Education
 

esom

Well-Known Member
Aug 17, 2010
196
10
58
seaside
Quote:
definition of hyperventilation is often debated, and freedivers can sometimes not agree whether a certain breathing pattern constitutes hyperventilating or not
...
Anyway, whether you are a beginner freediver or one of the top world’s champions, whichever way you choose to prepare for a dive on breath-hold, whatever your preferred breathe-up routine may be, whether you hyperventilate mildly or not at all, in the end just remember: the safest way to freedive is to NEVER FREEDIVE ALONE.



"Never freedive alone" is good sometimes. This text is an example for this i think. Being able to balance the text, by stating "NFA!" in the end, apparently made it possible for the athor, to have a more sound look at a subject, which is also not as simple as the correspondent slogan suggests.
 

Dan Black

Member
Aug 25, 2017
6
1
13
20
Birmingham
youtu.be
Full Text

Hyperventilation - a review, by Lily Crespy

Introduction

Hyperventilation in freediving is a very controversial issue. To start with, the very definition of hyperventilation is often debated, and freedivers can sometimes not agree whether a certain breathing pattern constitutes hyperventilating or not. Moreover, the debate on the advantages versus the drawbacks of hyperventilating before a dive on breath-hold, and to what extent, is still going strong in the freediving community.
For years, hyperventilation was widely practiced by freedivers as it was known to help divers hold their breath for longer and increase their performance in static, dynamic and deep disciplines. This theory has since largely been demonstrated to be wrong and to be actually dangerous for people practising apnea, as it could cause blackouts.
Here, we will explain what constitutes hyperventilation, its physiological effects on the human body, and why it should be avoided before breath-hold diving.

1) Definitions

There are two types of hyperventilation:
- Spontaneous hyperventilation is the normal reaction of an organism breathing air low in O2 or enriched in CO2, or increasing its metabolism (muscular effort, stress, cold environment) so as to conserve normal O2 and CO2 values ;
- Voluntary hyperventilation is a hyperventilation not ruled by O2 and CO2 values; often practiced in the past by apnea divers, it is now widely reproved, as it was at the origin of numerous syncopes (1).
For the rest of this study we will only focus on voluntary hyperventilation, and refer to it simply as “hyperventilation”.

Several criteria have been proposed to define what constitutes hyperventilation. Here are two of the most accurate ones:
- “An increase in ventilation out of proportion to any increase in metabolic VO2, therefore resulting in a low arterial pCO2. Reduced arterial pCO2 is therefore a criterion by which to determine whether a subject is hyperventilating or not.” (2) ;
- “Pulmonary ventilation rate greater than that metabolically necessary for gas exchange, resulting from an increased respiration rate, or increased tidal volume, or both. It causes excessive O2 intake and CO2 elimination. Hypocapnia and respiratory alkalosis then occur, leading to dizziness, faintness, numbness in fingers and toes, possibly syncope, and psychomotor impairment.” (3)

To summarize, hyperventilation is the action of breathing larger amounts of air than normal, either by taking bigger breaths or by breathing more rapidly, or both. One of the main measurable effects of hyperventilation, and also a criterion for defining it, is the arterial pCO2, which drops following hyperventilation.


2) Physiological effects

a) Effects on gas levels

- Oxygen: hyperventilation increases the content in O2 of the gases in the pulmonary alveoli. Indeed, after hyperventilating, the pO2 goes from 100 to 120 mm Hg, which can increase the O2 available in alveoli by around 150 mL. Regarding arterial blood, because the haemoglobin saturation on O2 is already close to 97%, hyperventilation can only increase this saturation weakly, reaching 98% without really going beyond this value. This results in an increase in the volume of O2 transported by the arterial blood that is insignificant (1). Norfleet and Bradley have shown that eucapnic hyperventilation (i.e. where CO2 levels remain unchanged) does not prolong the duration of voluntary apnea, suggesting the effect of hyperventilation on O2 levels alone is not enough to significantly improve breath-hold capacities (1).

- CO2: hyperventilation leads to a decrease of CO2 stocks. This hypocapnia suppresses the stimulus of CO2 on central chemoreceptors (under 40 mm Hg) and on peripheral chemoreceptors (under 30 mm Hg). As the CO2 stimulus on these chemoreceptors is the signal inducing the need to take a breath, this disappearance of the urge to breathe explains the comfortable sensation felt by freedivers after hyperventilation, but also the risk of syncope. Indeed, as the apnea progresses, the CO2 and pH stimuli remain weak for a long time, whereas the O2 stimulus increases slowly, but not enough to constitute by itself an alarm bell. Therefore the hypoxia progressively occurs until loss of consciousness (1). This will be explained with the mechanism of the shallow-water blackout in part three.
Moreover, the low pCO2 value during breath-hold delays the apparition of diaphragmatic contractions (appearing for pCO2 values above 47 mm Hg), which are another alarm bell indicating the start of the struggle phase. (1)

b) Effects on the blood

Hyperventilation leads to lower pCO2 and higher pH in arterial blood, and to a drop in arterial blood pressure. The decrease in blood pressure is due to vasodilation of the arteries, not to a change in cardiac output (4, 6).
The hypocapnia caused by hyperventilation also induces a muscular vasodilation, but induces a vasoconstriction in the skin and, more importantly, in the brain (1, 6). This cerebral vasoconstriction provokes a lower tolerance to hypoxia (1). For a pCO2 dropping from 37 mm Hg down to 19 mm Hg we observe a drop from 45 to 25 mL/100g/min in the cerebral blood flow (5). The effects of hyperventilation on pH and intracranial pressure are transient (5).
Since CO2 reacts with water to form carbonic acid, an increase in CO2 levels leads to a more acidic blood. Hyperventilation leads to a decrease of CO2 levels in the blood, and therefore this in turn, leads to an alkalinisation of the blood, i.e. and elevation of its pH, known as respiratory alkalosis.

c) Nerves and muscles

Studies have shown that over-breathing induces a decrease in phosphates, glucose and calcium ions in the blood (6). Differences in calcium content in particular can induce significant changes in the excitability of nerves and muscles. Indeed, over-breathing has been shown to induce increased irritability of the nerve and muscle, and to produce tetany (6).
The alkalinisation caused by hypocapnia has a debilitating action on the nerves and the muscles. Therefore, we can observe successively: dizziness, paraesthesia in the extremities, muscle spasms, facial myoclonies especially of the lips. The intensity of such effects varies greatly between individuals and from one day to the next for each person. It is practically impossible to establish any proportionality between pCO2 values and clinical effects (1).

d) Molecular level: the Bohr effect

Haemoglobin is carried in the red blood cells and is the protein responsible for the transport of oxygen in the body. Haemoglobin is a heterotetrameric protein comprising two alpha-subunits and two beta-subunits. Each subunit contains a heme core with one iron ion (Fe2+). It is this iron atom that binds a molecule of O2, making each molecule of haemoglobin able to carry up to 4 molecules of O2 in the blood.
The affinity of haemoglobin for oxygen and the strength of the bond between them is dependent on various factors, namely pH, levels of CO2 and of 2,3-biphosphoglyceric acid, and the pO2. There is also a cooperative effect by which, when one subunit binds to one molecule of O2, the affinity for oxygen of the other subunits increases, thereby favouring the binding of more O2 by that molecule of haemoglobin.
It should be noted that carbon monoxide (CO) binds to haemoglobin on the exact same binding site as O2. The affinity of haemoglobin for CO is 250 times greater than for O2. It goes without saying that freedivers should avoid smoking. Not only will the nicotine and tar accumulate inside the lungs and make the gas exchanges more difficult between the blood and alveoli, but also the carbon monoxide inhaled in cigarette smoke will bind to haemoglobin and therefore prevent good transport of oxygen through the blood.

The influence of hyperventilation, however, lies in its effect on blood pH. As described above, hyperventilation will induce a decrease of CO2 levels in arterial blood. CO2 naturally reacts with water to give the following reaction:
CO2 + H2O  H2CO3  HCO3- + H+
When CO2 levels drop following hyperventilation, the reaction producing CO2 is favoured, to counteract this. This provokes a decrease of H+ ions, and therefore an increase in blood pH. A higher blood pH favours the “relaxed” conformation of haemoglobin, which has a higher O2 affinity. Therefore, with low pH, oxygen tends to remain strongly bound to haemoglobin. So freedivers hyperventilate hoping to prolong their breath-hold but in the end, hyperventilation is preventing the release of oxygen to the tissues, which therefore actually shortens the breath-holding ability.

3) Shallow water blackout
[...]

more you can find here.


Disclaimer: This work has been compiled and created by Lily Crespy, Master Student of Apnea Bali Freediving Education school. It is free to copy and reproduce as long as it will be credited to: Lily Crespy and Apnea Bali Freediving Education

Hi, just read through this article as a part of my subject I have chosen to study and I need to be able to refernce it but the link that you have provided is unfortunately out of date or invalid.

Is there any chance that you can update the link because I don't want to be convicted for plagarism and get sent to jail for 500 years.

Thanks, Dan
 
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