Attend a Buteyko course in Sydney
By international instructor and
author Patrick McKeown.
Cardiovascular health amongst young athletes
Every year, young and healthy athletes die from sudden adult death syndrome or cardiac arrest. Annually, there are approximately 300,000 sudden cardiac deaths in the USA, 100,000 in the UK and 6,000 deaths in Ireland. While statistics are one thing, a review of athletes who died in their prime is another. (Heart Rhythm Foundation 2002)
Cormac McAnallen aged 24, John McCall aged 18, Stephen Lyness aged 20, Catherine Hand aged 20, Rory McGee aged 26, Ciara Agnew aged 14, Nicholas Collins aged 16, Gerard Gallagher aged 25, Robert Finnerty aged 22, Shane Kennedy aged 20, Eoin Sheill aged 22, Robbie Simpson aged 19, Darius Vasseghi aged 18, Conor Martin aged 16, Cliona Murphy aged 30, Brian Bergin aged 34, Darragh Kelly aged 21, Richie Doyle aged 27, Kevin Quinn aged 18, Robert Manning aged 16. (The Cormac Trust 2004).
While there is no warnings, signs such as abnormal heart rate, chest pain, light-headiness and flu like symptoms often occur. Athletes collapse during training, stop breathing, loosing consciousness quickly due to a lack of blood and oxygen to the brain. Unless a normal heart rate is sustained within minutes, death ensues.
In my studies over the last decade of breathing volume and breath hold time, there is an urgency to spread awareness of correct breathing technique. Some of the heaviest breathers are athletes that I have worked with, performing a few hours daily, five days a week.
There is a connection between the breathing volume and the amount of blood flow reaching the heart. The most important function of the body is the heart, like all muscles it requires a sufficient blood flow and oxygen.
The next section deals with the physiological effects of overbreathing on heart circulation, drawing attention to evidence that links chronic overbreathing to cardiac arrest and myocardial infarction (heart attack).
Over-breathing and cardiovascular health
Breathing in excess of normal requirements causes a loss of carbon dioxide from the blood leading to hypocapnia. this alters oxygenation of the heart and cardiac rhythm. (Gravenstein). Reduced arterial carbon dioxide affects cardiac functioning in three ways; firstly it causes reduced blood flow to the heart (Kazmaier 1998 and Neill 1975 and Foex 1979), secondly, the bond between red blood cells and oxygen is strengthened leading to a reduced delivery of oxygen to the heart muscle (Bohr effect) (Neill 1975) and thirdly, there is increased oxygen demand on the heart due to myocardial contractibility (Boix 1994) and blood vessel constriction. (Richardson 1972 and Okazaki 1991).
Voluntary overbreathing reduces the arterial partial pressure of carbon dioxide from normal levels of 40mmHg to 20mmHg increased coronary blood vessel resistance by 17%, decreased coronary blood flow by 30% and increased the affinity of Hemoglobin for oxygen by 25%. (Rowe 1962 and Neill 1975).
Hashimoto et al presented the effects of CO2 on oxygenation of the heart during hemorrhagic shock under normocapnia (normal CO2), hypocapnia (low CO2) and hypercapnia (high CO2) carbon dioxide conditions. It was found that hypocapnia decreased blood flow and oxygenation of the heart, whereas hypercapnia (high CO2) increased it. (Hashimoto 1990).
Similar findings were found by Tateyama et al who investigated the effects of increased arterial carbon dioxide (PaCO2 not equal to 60 mmHg) on heart tissue oxygen tension and metabolism in anesthetized dogs. The authors found that hypercapnia increased blood flow and oxygenation of the heart. ( Tateyama 1995).
Hyperventilation and Cardiac arrest
The rhythm of the heart is controlled by an internal electrical system. When the heart beats abnormally; for example too fast, too slow or stops beating- it is termed arrhythmia. Sudden cardiac arrest is when the heart develops an arrhythmia that it stops beating causing cessation of normal blood circulation. (Jameson 2005). “The causes of cardiac arrest are numerous; by far the most common in adults is ischemic cardiovascular disease.” (Davies 1981 and Eisenberg 2001).
Ischemia is derived from Greek, meaning a restriction in blood supply to tissues, causing shortage of oxygen and glucose needed for cellular metabolism. (Merck 2010).
Hyperventilation causes ischemia, leading to cardiac arrest and heart attack in individuals. Rutherford et al notes that “during voluntary hyperventilation in unanesthetised humans, hypocapnia causes coronary vasoconstriction and decreased oxygen (O2) supply and availability to the heart. This can induce local epicardial coronary artery spasm in susceptible patients.”
Hypocapnia reduces the T wave of the electrocardiogram in normal human subjects (Rutherford 2005).
This is supported by King et al stating that “Hyperventilation causes hypocapnia and respiratory alkalosis and thereby predisposes to coronary vasoconstriction and cardiac arrhythmia.” (King 1990).
In a study of 329 patients investigating the significance of hyperventilation-induced ST segment depression, the test induced ST segment depression in 79 patients. In 36 of these 79 patients, the electrocardiographic changes occurred early during overbreathing whereas in 26 they occurred late during recovery. (Ardissino 1989). Other researchers have clearly linked hypocapnia to the development of arrhythmias. (Mazzara 1974 and Hanashiro 1990).
Hyperventilation and heart attack
Myocardial infraction also known as a heart attack, occurs when the blood flow bringing oxygen to the heart is severely restricted. When lack of blood leading to oxygen starvation results in damage to the heart muscle, its a heart attack.
Cardiac arrest is different to a heart attack as the principle cause is electrical signals controlling the timing and organisation of the heartbeat becoming completely chaotic. When the signals degenerate into total chaos, the heart suddenly stops, cutting off normal circulation to the rest of the body. Heart attacks take place often during or following physical exercise or emotional stress. Both activities increase breathing and when breathing volume is greater than metabolic needs, carbon dioxide is washed from the lungs resulting in a reduced blood flow and oxygen to the heart. Similar to development of cardiac arrest, evidence shows that hyperventilation reduces blood flow leading to myocardial infarction. (Chelmowski 1998 and Takaoka 1988 and Okazaki 1991 and Fragasso 1989).
In a paper entitled Hyperventilation and myocardial infarction, Chelmowski et al wrote; ” In addition to causing peripheral and cerebral vasoconstriction, hyperventilation has also been shown to cause diminished coronary blood flow. Oxygen delivery to the myocardium and other tissues is further decreased in alkalosis because of increased hemoglobin oxygen affinity according to the Bohr effect.” ( Chelmowski 1988).
The following sections will investigate whether patients with chronic heart disease breathe heavier than normal, whether hyperventilation during CPR adversely affects outcomes and whether breathing exercises aimed at correcting breathing volume can reduce cardiac problems.