Hyperbaric Oxygen Therapy Diabetes / Obesity Hypothesis – Part Two…

Continued from part one…

Volume of oxygen and VO2 Rates


VO2 (or oxygen consumption) is a measure of the maximum volume of oxygen that is used by your body [13 – Bruno et al – 2013] to convert the energy from the food you eat into the energy molecules, called adenosine triphosphate (ATP), that your body uses at the cellular level. VO2max (or maximal oxygen consumption) is simply the maximum possible VO2 that a given person can achieve. VO2 and VO2max are important in the context of exercise, because they are a measure of your body’s ability to generate ATP, and ATP is the energy source that allows your muscles to continue working while you are exercising. [14 – Knowles – 1980 – quoted]

Divers from both commercial and recreational disciplines are taught extensively about what they know as the ‘Volume of Oxygen’ calculation (VO2). Such teaching is done to demonstrate that consumption of breathing oxygen under pressure, (whether pure or as a component gas in a mix), increases proportionately with an increase in ambient pressure. In other words, the deeper one goes, the more oxygen the body will burn proportionate to the depth. Oxygen is not consumed by metabolism at a constant fixed rate when we add increased ambient pressure to the equation, and we can indeed exceed “VO2 Max” in a hyperbaric environment. From a practical standpoint, this is taught to enable student’s skills for calculating the rate at which oxygen in a closed-circuit rebreather type system will be depleted, allowing for more accuracy in dive planning and profiles based on available oxygen. [2 – USN 2017]

Such Divers and supervisors are also taught this to effectively manage required volumes of oxygen for the treatment of divers, in a hyperbaric Chamber, (usually a DDC – Deck Decompression Chamber), for the treatment of decompression sickness by means of therapeutic treatments, (Rx tables), or the preventative and routine decompression method known as surface decompression or SurdO2. It is also, and more importantly, taught to enable supervisors and chamber technicians to calculate the rate of CO2 production, as a by-product of metabolism, which can potentially render a chamber atmosphere deadly to its occupants in minutes. [15 – Naval Sea Systems Command – 2004]

The spin off from this is, it becomes obvious that the very same oxygen depletion rate, (measurements of CO2 production), in terms of volume is also an indication of increased metabolism. In fact, it could be said that the prime metabolic indicator is the production of CO2. The depletion is not a measure of depletion as it would be calculated in an open circuit situation, where gas density is the primary reason for increased usage, but rather a calculation of how oxygen is used in metabolism, and then breathed out and scrubbed as carbon dioxide, and replaced with a measured amount of new oxygen from the breathing circuit. It must go somewhere, and that somewhere is the metabolic process, since it is not an inert gas and does not simply dissolve into solution to come back out later, as is the case with say, nitrogen for example. Divers are always taught that basal metabolic rate increases when diving. Anecdotes of ‘A dive is as good as a run without the exertion’ are common. Mostly dismissed as wishful thinking, these claims turn out to be true in fact. A dive is indeed as good as run to some measure, in metabolic terms at least, as will be visited later under the heading ‘Exercise’.

By measuring how much oxygen a divers body consumes in a closed-circuit/system environment in terms of flow, allows one to then also measure its volume or weight. The higher consumption rate indicates a higher oxidative function in the body which essentially is an increase in metabolic rate. This is evidenced by the functioning of carbon dioxide scrubbers, which remove the by-product of metabolism – CO2, and an observable increase in atmosphere CO2 content, expressed as a percentage on flow/content meters, and as calculated below by the University of Utah.

Metabolic Rate:

CALCULATIONS The volume (V) of oxygen consumed per unit time is calculated as V = flow rate × (FIO2 – FEO2) where FIO2 is the fractional volume of O2 in the ambient air (assumed to equal 0.2095) and FEO2 is the fractional volume of O2 in the effluent air coming out of the metabolic chamber.

 Note that the oxygen analyser records %O2 of the effluent air. Therefore, the specific equation for V in this case is

 V = flow rate × (20.95 – %O2) ÷ 100 Flow rate in these experiments is 500 ml/min.

Volumes need to be standardized to 0°C (i.e., 273°K) and 760 mmHg of pressure. The volume measurements used in these experiments are made across a range of different temperatures, but the pressure at which the measurements are made is always approximately 640 mmHg because of the altitude at U of U. Therefore, standardized volumes can be calculated as VSTPD = V × [229.9 ÷ (273 + °C)] where °C is the temperature at which the %O2 measurement is made

The above calculations are for all intents and purposes the same as diving calculations used in saturation diving, air diving, rebreather diving and consumption in chambers and closed systems, with the exception of accounting for increased pressure. The fact that pressure is accounted for though, indicates that VO2 is subject to ambient pressure.  It is simply a method of measuring how much CO2 is produced from oxygen metabolism.

Since the oxygen depletion is calculable, and can be measured, it is concluded that metabolic function increase is a direct result of breathing oxygen at higher than Normobaric conditions.


Basal metabolic rate is an estimate of how many calories one would burn, or rate of energy expenditure if doing nothing but rest per unit time. [17 – McNab – 1997] It represents the minimum amount of energy needed to keep the body functioning, including breathing and keeping the heart beating.

Basal metabolic rate is dependent on oxidative metabolism which in turn is driven by inward gradients of oxygen. The more oxygen being driven into cells the higher the metabolic rate of that cell as established above. Conversely the less pressure driving oxygen into cells reduces metabolic function as is observed in altitude sickness and hypoxia. [17 – Coote – 1995]

Consciousness is maintained above partial pressures of about 0,16 ATA partial pressure of oxygen (ppO2). An individual remains conscious due to the pressure of the gas not the percentage. The pressure determines the amount of oxygen transported in blood. Evident when flying and in other altitude related activities. Above a certain height, an individual will fall into unconsciousness because the pressure of oxygen (ppO2) drops below a point required to maintain blood saturation (SaO2) of around 90% or more limiting brain function.

HBOT works on the premise that an increase in pressure increases the inward gradient of oxygen and in turn increases the tension of oxygen in blood plasma and in a knock effect, also the tissues that blood feeds. This creates a differential between oxygen tension in blood plasma and cellular fluid, or an ‘inward gradient’, resulting in a desire for equilibrium and inward gassing and solvency of oxygen into cellular fluid and tissue, (Henry’s Law).

As the tissues saturate with oxygen to higher tension levels, metabolic process increases facilitating improved cellular function allowing for what is known as accelerated healing, optimal mitosis, improved vasculogenesis and improved angiogenesis, etc. [6 – Boykin et al – 2007] [7 – Van Neck et al – 2017]

Metabolism doesn’t only provide the body with a means to heal however. It is also part of the glucose cycle which is where type 2 diabetes comes into it. By stimulating the metabolism, one also stimulates the glucose cycle which is compromised in metabolic disorders such as type 2 diabetes and obesity.

The glucose cycle including glycogenesis and gluconeogenesis is included in this.

As discussed above an increase in Vo2 rate is indicative of an increase in metabolic rate. Even if it is only basal rate that increases the body still functions at higher than normal rates. Much as it does during exercise.


Sports medicine determines that aerobic exercise increases metabolism by increasing muscle function and strength as well as mitochondrial use of oxygen. The mitochondrial need for more oxygen during periods of exertion stimulates a higher than normal oxygen intake by means of increased heart rate and respiration. The higher the oxygen consumption the higher the metabolic rate.

Exercise does not however allow for further saturation of plasma. This much is governed by pressure gradients as discussed. In the absence of any pressure or tension differential plasma will only become as saturated as ambient pressure allows. Henry’s law dictates that gas solubility in a liquid is determined by the ambient pressure applied to that gas’s partial pressure as it compares to the tension of that gas in the liquid. Haemoglobin will saturate to the full extent however, which is not far of its normal SAo2 condition in healthy people. (more on this later) Haemoglobin can only carry a finite number of oxygen molecules however. Increased breathing rate and blood flow facilitate a higher VO2 consumption and in turn a higher metabolism during and shortly after exercise. Sound familiar?

Hyperbaric oxygen has been established as a metabolic stimulator during and shortly after treatment session. It’s the reason it works. [18 – Fujita et al – 2012] While most treatments are seeking optimised vascularisation or improved mitosis for accelerated healing of damaged capillary structures and tissue, it also stimulates metabolism, which is overlooked when considering the glucose cycle and obesity as well as metabolic disorders such as type 2 diabetes. It is in fact treated as a side effect to be cautious of. Granted the number of patients suffering from type 2 diabetes in the UK alone is far too high to treat exclusively by means of HBOT but it should not be overlooked for people who are unable to take glucose regulators such as metformin and those unable to exercise adequately for other medical reasons.

In both HBOT and exercise, the body returns to normal function relatively quickly after treatment or exertion. The effect is not permanent. Consequently, it can be said that a single workout is not going to change much but rather a regular regime will maintain overall higher average metabolic function allowing the body’s own glucose management to operate more optimally.

The same can be suggested for HBOT treatments. A regular regime of treatments should indeed have a similar result as regular exercise and potentially even more so given that plasma saturates in HBOT treatments whereas it does not during exercise. Exercise relies on increased respiration and heart rate to deliver more oxygen to cells.

It is suggested that HBOT treatments could be a suitable and even superior replacement for physical exertion. This is not to suggest that the population in general should have chamber sessions rather than exercising, but rather to suggest that those individuals unable to exercise can benefit immensely, and in the same manner other people benefit from exercise, from a similar metabolic result with regular HBOT treatments. Restoration of normal glucose metabolism usually normalizes glycogen metabolism, as well.

This provides a potential pathway to breaking the obesity / type 2 diabetes recurring circle of mutual support of each other. Less adipose tissue will result in less insulin absorption and consequently better insulin response, and effectively better fat management by the body. At that point the body should begin to manage its own glucose cycle and effective use of glycogen.

When diagnosed, many diabetics are informed that a diabetic body is great at making fat. We are excellent fat makes, but very bad at eradicating it. As suggested above, and explained further below, breaking the seemingly one-way fat making cycle for many diabetics is key to improving the reversal of glycogenesis (creation of glycogen and ultimate consequential increase in fat mass) and how it relates to the Cori cycle.

It is suggested, and supported by Fujita et al 2012, in their paper “Effects of Hyperbaric Oxygen on Metabolic Capacity of the Skeletal Muscle in Type 2 Diabetic Rats with Obesity “, [18] that HBOT can do this at the root of the cause. Imagine even then exercising under pressure or shortly afterward as many athletes do.

To be continued in part three…

© Copyright 2017

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