Recent breakthroughs in cystic fibrosis treatments and research
Several medical studies very recently (2009-2011) discovered that CFTR (cystic fibrosis transmembrane conductance regulator), the cystic fibrosis mutation protein gene, is controlled by oxygen pressure in body cells (see references below). While most people, including many medical professionals, believe that cystic fibrosis is a genetic disease, these new findings suggest that main symptoms of cystic fibrosis can appear only in conditions of tissue hypoxia.
This is not a big surprise since it has been well known for decades that ionic pumps or transporters of sodium, potassium, chloride and water are highly sensitive to oxygen deprivation (see references below). As a result, when oxygen availability is reduced, viscosity of mucus is increased and, this causes key abnormalities related to cystic fibrosis.
As a result, Russian medical doctors developed 2 therapies for people with low oxygenation: the Buteyko breathing technique and the Frolov respiratory device to increase body oxygen levels naturally. Both techniques lead to slower automatic breathing at rest and higher arterial CO2 levels. Higher CO2 causes improved oxygen transport, while breathing more than the norm (deep breathing) leads to opposite effects: less oxygen in the brain and body cells.
These Russian MDs found that symptoms of cystic fibrosis are reversible if the patients can increase their body oxygen levels up to 40-50 seconds. Some their patients are now in their 40's and 50's enjoying excellent health.
What this has to do with exercise?
There are 2 problems with mouth breathing during physical exercise: losses in nasal nitric oxide (produced in sinal passages) and reduced levels of carbon dioxide in the lungs and arterial blood.
Nasal nitric oxide is particularly crucial for people with cystic fibrosis. First of all, nasal nitric oxide is low in people with cystic fibrosis, and the reasons are poorly understood. People with asthma, bronchitis and many other inflammatory conditions have higher levels of nitric oxide and this helps them to fight respiratory infections since nitric oxide is a powerful agent to fight various pathogens. Second, nitric oxide is a powerful vasodilator that increases oxygen delivery to body cells.
Carbon dioxide is another potent vasodilator. It is also necessary for effective Bohr effect (release of oxygen in capillaries).
For these reasons, these Russian MDs insist that all physical exercise should be done with nose breathing, and, in case of cystic fibrosis, this makes absolute sense.
What are the benefits of nose breathing during physical exercise vs. mouth breathing for cystic fibrosis? Nasal breathing increases arterial CO2 levels during exercise. This causes adaptation of the respiratory center to higher CO2 values. Hence, such exercise improves oxygen content in body cells later after exercise. In addition, nasal respiration delivers nasal NO to other parts of airways.
Gradual transition to nose breathing exercise
However, for people with heavy breathing at rest, most CF people included, intensive exercise with nose breathing is impossible. Initially, they need to slow down their intensity to accommodate strictly nasal breathing. Later, day after day it is possible for them to increase intensity, but they need to do it very gradually. When the results of the body oxygen test are above 20 seconds, most people are able to exercise with nose breathing in and out.
Resources from NormalBreathing.com
What causes cystic fibrosis - Low oxygen levels in body cells
Treatment for Cystic Fibrosis - Increase body oxygen levels with correct breathing
Vasodilators - Medical research summary about vasodilating effects of CO2 and nitric oxide.
References: Ionic transporters and hypoxia
Ann Surg. 2011 May 10.
Hypoxia Inhibits Colonic Ion Transport via Activation of AMP Kinase.
Collins D, Kopic S, Bachlechner J, Ritter M, Winter DC, Geibel JP.
Int J Colorectal Dis. 2011 Apr 26.
Electrogenic transport, oxygen consumption, and sensitivity to acute hypoxia of human colonic epithelium.
Carra GE, Ibáñez JE, Saraví FD.
FASEB J. 2011 Feb;25(2):535-43. Epub 2010 Oct 13.
Hydroxylase inhibition attenuates colonic epithelial secretory function and ameliorates experimental diarrhea.
Ward JB, Lawler K, Amu S, Taylor CT, Fallon PG, Keely SJ.
Hydroxylases are oxygen-sensing enzymes that regulate cellular responses to hypoxia. Transepithelial Cl(-) secretion, the driving force for fluid secretion, is dependent on O(2) availability for generation of cellular energy.
Cell Physiol Biochem. 2010;25(1):123-34. Epub 2009 Dec 22.
Beta2-adrenergic stimulation blunts inhibition of epithelial ion transport by hypoxia of rat alveolar epithelial cells.
Loeh B, Baloglu E, Ke A, Bärtsch P, Mairbäurl H.
Hypoxia impairs alveolar fluid clearance by inhibition of Na(+) reabsorption, and also impairs beta(2) adrenergic signaling in alveolar epithelium.
Oxygen levels and CFTR gene
Bebök Z, Tousson A, Schwiebert LM, Venglarik CJ, Improved oxygenation promotes CFTR maturation and trafficking in MDCK monolayers, Am J Physiol Cell Physiol. 2001 Jan;280(1):C135-45.
Guimbellot JS, Fortenberry JA, Siegal GP, Moore B, Wen H, Venglarik C, Chen YF, Oparil S, Sorscher EJ, Hong JS, Role of oxygen availability in CFTR expression and function, Am J Respir Cell Mol Biol. 2008 Nov;39(5):514-21
Zheng W, Kuhlicke J, Jäckel K, Eltzschig HK, Singh A, Sjöblom M, Riederer B, Weinhold C, Seidler U, Colgan SP, Karhausen J, Hypoxia inducible factor-1 (HIF-1)-mediated repression of cystic fibrosis transmembrane conductance regulator (CFTR) in the intestinal epithelium, FASEB J. 2009 Jan;23(1):204-13.
