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Carbon Dioxide: The missing piece in a metabolic jigsaw puzzle

Our body’s capacity to produce energy is dependent on oxygen. Our cells  are capable of producing much more energy in the presence of oxygen compared to a non-aerobic state *. Approximately 90% of the oxygen in our cells is used for energy production (1). So how can we ensure the delivery of adequate oxygen to our cells?

When most people are out of breath, they tend to breathe faster and take bigger breaths. Both of these actions will offer a temporary release for the air-hunger sensation but will not improve cell oxygenation – at least not in the long run.

 

In order to grasp how erroneous the idea of air hunger equating lack of oxygen is, think of the following: During an asthma attack patients are advised to breathe through a brown bag. If they need more oxygen, why should they restrict their oxygen intake?

 

 

The two breath parameters: Frequency & volume

Most people take between 10 and 16 breaths per minute. The volume of air that we inhale is approximately 500 millilitres per breath . This translates to approximately 6 litres per minute. When increasing the frequency of breaths, the volume of air per breath is reduced and vice versa, keeping the total volume of air inhaled the same.

 

Strange as it may sound, the increase of air in the lungs is not what is required for better oxygenation of our cells. Inhalations allow the body to take oxygen in. Most of the time though, the body retains high oxygen saturation levels. By using an oxygen meter we can prove that our blood contains 95-99% of its total oxygen capacity most of the time. If our blood constantly contains good levels of oxygen, why do we “run out of breath” at the end of a strenuous workout or when walking quickly up stairs?

 

 

The role of carbon dioxide in oxygen transport

Carbon Dioxide** is a by-product of fat and carbohydrate metabolism (aerobic and anaerobic). It exists in the fresh air at concentrations of 0.036-0.041% (36-41ppm). At 1% (10,000 ppm) concentration it can cause sleepiness and between 7 – 10%*** suffocation.

In 1904 **** physiologist Christian Bohr discovered the Bohr effect. Based on the Bohr effect, haemoglobin in the blood requires Carbon Dioxide (CO2) in order to release Oxygen (2). Low levels of CO2 in the blood, increase the affinity of oxygen to haemoglobin, preventing it from moving to the cells.

 

So, while at high levels CO2 can be toxic (3), at low levels it can deprive our cells of oxygen (based of the Bohr effect). Which raises the question, “what is the optimal level of CO2”? Before answering this question we need to review one more function of CO2: its role to signal our need to inhale!

Our brain is responsible for the control of our breathing cycle. Receptors in the brain continuously monitor a number of blood markers to signal the need for the next inhalation (4). Among these, the most critical, marker, is the levels of CO2 in the blood (5). When the levels of CO2 reach our tolerance point we get the urge for the next inhalation. Those familiar with the sport of underwater diving are aware of this concept.

 

 

So in order to deliver oxygen to our cells efficiently we need to prolong our urge for the next inhalation (i.e. increase our tolerance to CO2) and not increase our body’s levels of CO2. The beneficial metabolic effects of temporary exposure to an elevated CO2 state has been demonstrated in scientific studies. In one study the application of CO2 to transcutaneous tissue led to the proliferation of  mitochondria, similar to the one observed during aerobic exercise (6).

 

 

It is worth pointing out that in most medical centres the saturation of oxygen (SpO2) in the blood is monitored regularly. Nonetheless, good levels of SpO2 in the blood do not equate good levels of SpO2 in the organs. Our ability to deliver oxygen to our cells is dependent on our tolerance to CO2.

A good reference book on this topic is: “Oxygen Advantage” by Patrick Mckeown. On the Youtube Oxygen Advantage channel you can find several exercises to improve your tolerance to CO2.

 

 

Fun fact

The concept of better delivery of oxygen to cells is also the reason for which some athletes train at high altitude. High-altitude training became popular after the 1968 Mexico Olympics. Mexico is located at 2,300 metres above sea level. During this Olympiad, many athletes surpassed their previous performances, which prompted coaches to question if the location, was conducive to athletic performance. At high altitude the oxygen is reduced. At a hypoxic (low in oxygen) environment, the body is forced to produce more red blood cells. More blood cells means more available vehicles to carry oxygen to the cells. However, soon after an athlete, returns to sea level, the number of red blood cells returns to normal levels.

 

 

Footnotes

* One molecule of glucose will produce two molecules of Adenosine Triphosphate (ATP – our body’s energy currency) in an anaerobic state, as opposed to thirty six molecules of ATP in an aerobic state.

** Carbon Dioxide, a natural-occurring product of metabolism, that should not to be confused with Carbon Monoxide, a flammable gas that does not occur naturally in the atmosphere.

*** In one study subjects were exposed to air containing 7-14% of CO2 for 10-20 mins. All subjects had a complete recovery of their physiology 10 mins after the end of the experiment (7).

**** That was 33 years before Han’s Krebs’ discovered the eponymous Krebs cycle.

 

References

  1. Bland, J., Costarella, L., Levin, B., Liska, D., Lukaczer, D., Schiltz, B. and Schmidt, M.A., 1999. Clinical nutrition: A functional approach. The Institute for Functional Medicine, Gig Harbor, Wash, USA.
  2. Bohr, C., Hasselbalch, K. and Krogh, A., 1904. Über einen in biologischer Beziehung wichtigen Einfluss, den die Kohlensäurespannung des Blutes auf dessen Sauerstoffbindung übt. Acta Physiologica16(2), pp.402-412.
  3. Satish, U., Mendell, M.J., Shekhar, K., Hotchi, T., Sullivan, D., Streufert, S. and Fisk, W.J., 2012. Is CO2 an indoor pollutant? Direct effects of low-to-moderate CO2 concentrations on human decision-making performance. Environmental health perspectives120(12), p.1671.
  4. Huckstepp, R.T. and Dale, N., 2011. Redefining the components of central CO2 chemosensitivity–towards a better understanding of mechanism. The Journal of physiology589(23), pp.5561-5579.
  5. Cheung, S., 2010. Advanced environmental exercise physiology. Human Kinetics.
  6. Oe, K., Ueha, T., Sakai, Y., Niikura, T., Lee, S.Y., Koh, A., Hasegawa, T., Tanaka, M., Miwa, M. and Kurosaka, M., 2011. The effect of transcutaneous application of carbon dioxide (CO 2) on skeletal muscle. Biochemical and biophysical research communications407(1), pp.148-152.
  7. Sechzer, P.H., Egbert, L.D., Linde, H.W., Cooper, D.Y., Dripps, R.D. and Price, H.L., 1960. Effect of CO 2 inhalation on arterial pressure, ECG and plasma catecholamines and 17-OH corticosteroids in normal man. Journal of Applied Physiology15(3), pp.454-458.