Exercise physiology
VO₂max sums up what the oxygen chain (lungs, heart, blood, vessels, capillaries, muscles and mitochondria) produces when it runs at full capacity. Understanding the workings of this integrated system makes it easier to identify what training should stimulate to make VO₂max “climb”.
Most of us roughly know the definition: VO₂max is the maximal rate at which the body can use oxygen during maximal exercise. In other words, it is the maximal amount of oxygen we are able to use per minute. It is a “ceiling”, a limit on oxygen uptake that the body cannot exceed, however intense the exercise. This limit varies greatly from one person to another: it is individual and depends on many factors. The good news: your VO₂max is dynamic, in the sense that it can change over time. It can be partly shaped by appropriate training that stimulates the various components underlying VO₂max.
But what really lies behind VO₂max? VO₂max is in fact a marker that integrates a complex reality… and the journey begins in the air around us. The oxygen it contains enters the lungs and crosses the wall of the alveoli into the blood, where haemoglobin binds it. The heart pumps this blood, the vessels distribute it to the active muscles, and it is in the capillaries, the finest of them, that oxygen leaves the blood to enter the muscle fibre. There, the mitochondria, small specialised structures inside cells, use it to regenerate ATP (adenosine triphosphate), the well-known molecule whose breakdown supplies the energy our muscle cells need to contract.
VO₂max: the maximal output of an integrated system
VO₂max is usually expressed in two ways. The absolute value is expressed in litres of oxygen per minute, whereas the relative value is expressed in millilitres per kilogram per minute. The latter relates the rate to body mass: it can therefore change with body weight, without any change in the absolute rate. It is often this relative figure that athletes like to compare.
The gold standard for determining VO₂max is an exercise test with analysis of respiratory gases. A mask channels inspired and expired air; the device measures the volume of air passing through and the concentrations of oxygen and carbon dioxide in that air. The difference between what goes in and what comes out gives the oxygen actually consumed and the carbon dioxide actually produced. What we observe is therefore the overall output of the chain (lungs, heart, blood, vessels, capillaries, muscles and mitochondria together), not the work of any one of these links taken separately [2].
During an incremental exercise test, oxygen uptake rises with intensity, supplying the mitochondria with more and more O₂ so that they can meet part of the rising energy demand. When the effort is maximal (and in fact slightly before), a saturation phenomenon may be observed: a plateau in oxygen uptake. This is the limit of what the body can consume per minute: VO₂max.
That said, a truly maximal effort is not always guaranteed during an exercise test: we therefore need to be able to judge whether the effort really was maximal. Strictly speaking, we should in principle speak of VO₂peak in an exercise test, because there is never any certainty that the body has actually reached its absolute maximum oxygen uptake: VO₂max. In practice, if several criteria are met (which must be analysed in detail), we can reasonably assume that VO₂peak does reflect VO₂max. Out of caution and intellectual honesty, we should always report VO₂peak or, at the very least, qualify what we call VO₂max [2,19].
Several things feed the uncertainty about whether VO₂max has really been reached.
The Fick equation, term by term
The Fick equation helps us understand what makes up oxygen uptake per unit of time (usually per minute) and what it depends on:
VO₂ = Q × (CaO₂ − CO₂)
This equation tells us that oxygen uptake per minute, VO₂, depends directly on cardiac output, Q, and on the oxygen extracted by our cells from each litre of blood, (CaO₂ − CO₂).
Their difference, (CaO₂ − CO₂), known as the arteriovenous difference, therefore represents the oxygen taken up by our cells from each litre of blood, at whole-body level, taking all tissues into account (not only the active muscles).
Let us take a concrete example and calculate VO₂ using the Fick equation. Consider a 70 kg person at rest: their heart beats 70 times per minute and ejects 70 mL of blood with each beat (stroke volume), and their tissues take up 5 mL of oxygen from every 100 mL of blood, which is their arteriovenous difference.
One level down: the ingredients of each term
The Fick equation has only two terms: cardiac output and the arteriovenous difference. Each in turn depends on several ingredients. Let us take them in order.
Its two factors (heart rate and the volume of blood ejected with each beat) do not follow the same rules. Maximal heart rate depends mainly on age and cannot be trained: endurance training does not increase it and, if anything, it tends to decrease [16]. What can be trained is stroke volume: the amount of blood the left ventricle sends to the tissues with each beat. It increases with appropriate training [6] and it is what primarily distinguishes athletes from non-athletes [4].
How much blood can the ventricle send out with each beat? This depends first on how much blood it holds just before contracting, i.e. on its filling. Filling depends on the return of blood to the heart, on how quickly the ventricle relaxes between beats and on its compliance, as well as that of the pericardium surrounding it. A larger blood volume could also facilitate this filling [11]. The volume ejected also depends on the force of contraction (contractility, which nervous stimulation increases during exercise [10]) and on the pressure in the arteries, against which the heart must push the blood. Yet what distinguishes athletes is not contractility but a more compliant ventricle, which relaxes faster and fills more: it can therefore send out more with each beat [4].
As effort increases, stroke volume does not follow the same curve in everyone. It was long accepted that it stops increasing at around 40 to 50% of VO₂max [10,11], on the strength of old studies conducted on few subjects and at only two or three intensities: too few data points to draw a solid general conclusion. In reality, the response varies greatly between individuals: in some, stroke volume levels off, or even falls, well before maximal effort; in others, it keeps rising up to VO₂max, as shown by the studies compiled by Vella and Robergs [11]. Fitness level, age, sex, genetics: the explanation is multifactorial.
It can be read in two stages: what the arterial blood coming from the left ventricle delivers to the tissues (CaO₂), then what the tissues remove from it, which determines what is left on its return (CO₂).
What the blood delivers: arterial oxygen content, CaO₂. Oxygen in the blood is carried almost entirely by haemoglobin (Hb), a protein contained in red blood cells that binds oxygen:
CaO₂ ≈ 1.34 × [Hb] × SaO₂, plus a small fraction dissolved in plasma
In the expression above, [Hb] is the haemoglobin concentration, in grams per litre, and 1.34 is the number of millilitres of oxygen carried by one gram of haemoglobin [10]. As for SaO₂, this is arterial saturation, i.e. the proportion of that haemoglobin actually loaded with oxygen; it depends on ventilation and on the diffusion of oxygen from the alveoli into the blood [3]. Plasma, for its part, dissolves only about 3 mL of oxygen per litre, whereas 100 mL of whole blood carries about 20 mL, slightly less in women [10]. What matters is therefore not only haemoglobin concentration but the total amount in circulation, which also depends on blood volume, i.e. the total amount of blood circulating in the body: total haemoglobin = [Hb] × blood volume.
What the tissues remove: extraction. For oxygen to be taken up, the blood must first reach the working fibres, the elongated cells that make up muscle. During exercise, blood is redistributed: the arterioles, the small arteries supplying the active muscles, dilate, while those of other organs constrict. At rest, the muscles receive 15 to 20% of cardiac output; during intense exercise, this can rise to 90% [10]. What matters is not only how much blood reaches the muscle, but that this blood goes to the fibres that are consuming oxygen. An experiment reported by Heinonen [16] illustrates this: at maximal exercise, researchers injected the most powerful known vasodilator into the leg artery to force the vessels open. VO₂max did not increase. The fraction of oxygen extracted even decreased: the vessels had also opened towards fibres that were not working. Blood supply no longer matched the needs of the active fibres as precisely [16].
Oxygen must then pass from the blood to the fibre. At the end of the arterioles, blood flows through the capillaries, the finest vessels, which surround each fibre. There, oxygen leaves the red blood cells, crosses the capillary wall and reaches the fibre: this is diffusion, which is easier when the capillary network is dense, the exchange surface is large and the distance to the centre of the fibre is short, which depends on its size [17]. Inside the fibre, two elements take over [17]: myoglobin, a protein similar to haemoglobin that binds oxygen and helps it travel to the mitochondria, and the oxidative capacity of these mitochondria, i.e. the amount of oxygen they are able to use. And the transfer does not stop, because the mitochondria consume oxygen as it arrives: oxygen pressure stays lower in the fibre than in the capillary. It is this gradient that drives it in [5].
The arteriovenous difference therefore depends on arterial content, on the distribution of blood flow (to the active muscles, then to the working fibres), on diffusion and on the mitochondria: it is not an isolated measure of muscle quality.
Identifying them to make progress
Limits are the links that cap VO₂max at a given moment. This ceiling is not fixed: which limit weighs most changes with the type of exercise, training status, health and environmental conditions such as altitude, where barometric pressure falls and, with it, the partial pressure of inspired oxygen (hypobaric hypoxia). Oxygen delivery often plays a major role when many muscles are working, without the lungs or the muscles being secondary [3,4,5,16]. A gas exchange measurement (the PEAK option from Twin Peak Lab) sheds light on this overall functioning, but VO₂max alone does not tell where the limit lies in the chain: locating it requires other measurements [2,3].
Levers are what training can act on: loosening a limit when it is trainable (maximal heart rate, for example, is not), or strengthening a point that is already strong. When one limit is loosened, another takes over. And training never works on a single link: stroke volume, the capillary network and mitochondrial content progress together, at different rates; their weight varies with age, starting level and the duration of the effort [6,7,8,16]. Strengthening a single link is not enough anyway: in the mathematical model developed by Wagner [3], we see that degrading a single link makes VO₂max drop markedly, whereas improving it by a comparable amount barely raises it. The idea is therefore to pull these levers in a coordinated way, to get closer to the VO₂max each person can reach given their potential.
Now you understand why your watch can get it wrong
Estimating VO₂max, this integrated system involving so many components, seems very difficult from heart rate and external load profiles alone, i.e. power or speed. The watch does not measure gas exchange: it sees neither stroke volume nor what the muscles extract. The error can therefore be large from one person to another [9], which is why it is crucial to measure VO₂max through gas exchange (the PEAK option from Twin Peak Lab) if it is an important parameter for you to know.
In the next article, we will unpack how to stimulate the different components of this integrated system in practice. So you don’t miss it, subscribe to the newsletter.
Arnaud Collet, PhD, CPSS®
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