Part 2. Tissue pollution and hypoxia: how they affect our breathing

There are two processes of respiration: respiration of living cells and our outer respiration or breathing. During their life, our cells consume oxygen for energy generation and produce carbon dioxide. This process is called inner or cellular respiration. Our cells breathe. They live in a certain gaseous environment. “But the cells of animals and humans need about 7 % CO2 and only 2% O2 in the surrounding environment. This is the way our cells live: cells of the heart, brain, and kidneys” noted a famous Soviet respiratory physiologist Dr. Buteyko KP (Buteyko, 1977.) The process of outer respiration, that is taking oxygen from the air and expelling some CO2 with each exhalation, constitutes our breathing.

How does our cellular respiration relate to our breathing? Imagine a healthy person with normal breathing parameters. Oxygenation of their body can be easily measured using the stress-free breath holding time test done after usual exhalation. (Exhale normally, pinch the nose, and see how long you can hold your breath but only until first signs of stress or discomfort. As soon as stress appears and starts to grow, release the nose and resume breathing. Your breathing rhythm should be the same both before and after the test.) The stress-free breath holding time (or index of oxygenation) of a healthy person is about 40-60 s indicating normal body oxygenation (Flack, 1920; Buteyko, 1977; McArdle et al, 2000). Hence, in health, our breathing defines breathing of our cells (or cellular respiration) providing them with sufficient oxygen for maintenance of normal homeostasis.

Now let us assume now that some tissues or cells of the body accumulate toxic or carcinogenic substances (e.g., tobacco smoke in the lungs, indigested toxins in the gastrointestinal tract, free radicals in the skin due to excessive sun radiation, etc.). This micro-pollution generates free radicals, alters the normal micro-environment, behaviour, and functions of normal cells, hampers blood supply, and creates local hypoxia. The degree of these effects depends on the dosage and toxicity of the carcinogens.

Apart from local effects, the toxins gradually diffusing into neighbouring tissues, can reach the blood and travel to other tissues and organs. It is a known physiological and toxicological fact that the presence of toxic substances intensify respiration (our outer breathing) due to stress on the immune system and organs of elimination (the kidneys, liver, skin, etc.). Hence, a person’s breathing will be deeper (increased tidal volume) and heavier (greater minute ventilation).

Similar effects are produced by most medical drugs. “Antibiotics (penicillin, streptomycin etc.) intensify breathing… Camfora, codein, cordiamin, adrenalin, theoephedrine, and ephedrine – also intensify breathing” (Buteyko, ibid.). The degree of intensification depends on toxicity, dosage, possible allergies, and individual abilities to eliminate them from the system.

Western research also demonstrated increased ventilation in humans due to endotoxin (Preas et al, 2001), flumazenil and midazolam (Kawauchi et al, 2000), testosterone (Ahuja et al, 2007), theophylline (Pesek et al, 1999), adenosine (Smits et al, 1987; Reid et al, 1987), and bronchodilators: pirbuterol and ipratropium (Ashutosh et al, 1995) and aminophylline (Montserrat et al, 1995). Generally, any drug with known toxicity for the liver or kidneys produces increased ventilation.

Even those drugs or substances which are classified as respiratory depressants (diacetylmorphine or heroin, morphine, alcohol, etc.) first suppress respiration for several hours, but later produce significant increase in minute volume above the initial values due to stress on organs of elimination.

Conclusion: Local pollution causes systemic stress and increased ventilation (outer respiration).

The next question is: what is the effect of deeper breathing (increased minute ventilation) on cellular oxygenation?

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References for part 2

Ahuja D, Mateika JH, Diamond MP, Badr MS, Ventilatory sensitivity to carbon dioxide before and after episodic hypoxia in women treated with testosterone, J Appl Physiol. 2007 May;102(5): 1832-1838.

Ashutosh K, Dev G, Steele D, Nonbronchodilator effects of pirbuterol and ipratropium in chronic obstructive pulmonary disease, Chest. 1995 Jan; 107(1): 173-178.

Buteyko KP, Soviet national journal Nauka i zshizn’ [Science and life], Moscow, issue 10, October 1977.)

Flack M, Some simple tests of physical efficiency, Lancet 1920; 196: 210-212.

Kawauchi Y, Oshima T, Saitoh Y, Toyooka H, Flumazenil abolishes midazolam-induced increase in the work of nasal breathing, Can J Anaesth. 2000 Dec; 47(12): 1216-1219.

McArdle WD, Katch FI, Katch VL, Essentials of exercise physiology (2-nd edition); Lippincott, Williams and Wilkins, London 2000, p.252.

Montserrat JM, Barberà JA, Viegas C, Roca J, Rodriguez-Roisin R, Gas exchange response to intravenous aminophylline in patients with a severe exacerbation of asthma, Eur Respir J. 1995 Jan; 8(1): 28-33.

Pesek CA, Cooley R, Narkiewicz K, Dyken M, Weintraub NL, Somers VK, Theophylline therapy for near-fatal Cheyne-Stokes respiration. A case report, Ann Intern Med. 1999 Mar 2; 130(5): 427-430.

Preas HL 2nd, Jubran A, Vandivier RW, Reda D, Godin PJ, Banks SM, Tobin MJ, Suffredini AF, Effect of endotoxin on ventilation and breath variability: role of cyclooxygenase pathway, Am J Respir Crit Care Med. 2001 Aug 15; 164(4): 620-626.

Reid PG, Watt AH, Routledge PA, Smith AP, Intravenous infusion of adenosine but not inosine stimulates respiration in man, Br J Clin Pharmacol. 1987 Mar; 23(3): 331-338.

Smits P, Schouten J, Thien T, Respiratory stimulant effects of adenosine in man after caffeine and enprofylline, Br J Clin Pharmacol. 1987 Dec; 24(6): 816-819.

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