Mind The [Arteriovenous Oxygen Concentration] Gap

An individual’s VO2max represents the maximum integrated capacity of the pulmonary, cardiovascular, and muscular system to uptake, transport, and utilize oxygen respectively. Additionally, VO2max is calculated from the product of cardiac output and the arteriovenous oxygen concentration difference, which is expressed by the Fick equation which states the following:

VO2max = Q * [Ca-vO2], where Q is cardiac output which is calculated from the product of heart rate and stroke volume (Q = HR x SV) and Ca-vO2 is the arteriovenous oxygen concentration difference, which represents the difference in oxygen saturation between arterial and venous blood.

Given the aforementioned parameters, it becomes clear that their are two ways that one can increase their VO2max:

1. They can increase their cardiac output; or

2. They can widen the arteriovenous oxygen concentration difference.

This article will be focused on the second of these two factors. Specifically, how to increase arterial oxygen saturation (SpO2), and how to increase muscle oxygen extraction (thus, lowering SmO2).

Increasing Arterial Oxygen Saturation:

It’s important to remember that the circulatory system is a closed loop where oxygen travels from the heart to the working muscle and back along the following route: heart → artery → arteriole → capillary → venule → vein → heart. When we record arterial oxygen saturation, often referred to as SpO2 or SaO2, we are measuring at the location of the artery. Arterial oxygen saturation depends on both on hemoglobin concentration as well as it’s oxygen binding capacity (alveolar PO2), pulmonary diffusion capacity, and alveolar ventilation. It’s commonly assumed that both arterial oxygen content and hemoglobin saturation are well maintained during exercise. However, during maximal effort exercise arterial hemoglobin concentration and oxygen carrying capacity can both rise by ~10%. This occurs when plasma water is lost into the active muscle cells and interstitial fluid as the concentration of osmotically active particles in the muscles rise.

Insofar as an individual’s arterial oxygen capacity rises, while their oxygen content remains constant, their arterial oxygen saturation will fall. This is why you’ll often see a decrease in SpO2 from ~98-99% down to ~94-95% during very high intensity exercise. Additionally, some of this fall is attributable to reductions in arterial pH (increased acidity) and a rise in temperature, both of which lower arterial oxygen saturation (SpO2) at a given oxygen binding capacity (PO2). In very extreme cases you may see SpO2 fall below ~90%, though this is much more common in elite endurance athletes. In these cases the extreme drops in SpO2 are caused by a pulmonary diffusion limitation, which is a form of respiratory limitation. To learn more about identifying and training respiratory limitations you can check out the following articles:

1. Extended Desaturation Training for Respiratory Limited Athletes;

2. Monitoring Respiratory Muscle Oxygenation; and

3. Training The Respiratory Limited Athlete.

Increasing Skeletal Muscle Oxygen Extraction:

When we are referring to the venous oxygen concentration component of the Fick equation we are referring to a measurement of oxygen saturation in the vein. Muscle oxygen saturation, or SmO2, as recorded with a NIRS device is measured in the microvasculature and capillaries, which approximates mixed venous oxygen content. The two populations where we see the lowest venous oxygen saturations are in cardiac patients, who have very low cardiac outputs (due to an insufficiency of the heart as a pump), and highly trained athletes who have augmented oxygen extraction capabilities (up to 85% in highly trained individuals).

Highly trained athletes increased oxygen extraction capabilities are explained by a number of factors. Unlike cardiac muscle where most capillaries are open at all times. only a small fraction of the total number of capillaries are perfused in resting muscle. As a result, the diffusion distances between the capillaries of muscle fibers are great. Additionally, the mean transit time of the red blood cells through so few capillaries is short, which means there is limited time for oxygen extraction and uptake by the skeletal muscle. During exercise though there is huge increase in the number of capillaries that are open which reduces diffusion distances and increases capillary blood volume so that transit time is extended allowing for more oxygen to be unloaded from the blood into the working muscle. 

As a consequence of the greater number of capillaries being 'recruited', each muscle fiber is now supplied by more capillaries than when it was at rest. Therefore, in order to maintain a high extraction of oxygen across the muscle there must be a delicate balance between the optimal rates of blood flow, capillary blood volume, and minimum mean transit tine available for the exchange of oxygen across skeletal muscle capillaries. This balance is preserved at high rates of muscle blood flow - in fact, extraction of oxygen increases as VO2max goes up (which warrants increases in flow as well). In these cases capillary blood volume needs to be large enough and capillary mean transit time needs to be long enough, to allow oxygen to be released from Hb and diffuse all the way from the capillaries to the mitochondrial of muscle cells.

Oftentimes, athletes with lower training ages (or advanced athletes with very high maximal cardiac outputs) will present with oxygen extraction limitations. I’ve written quit a bit about this topic in the past. If you're interested in learning how to address these athletes limiters you can check out the following article titled, Training The Utilization Limited Athlete.

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