Challenging Conventional Paradigms of Maximal Exercise Performance
VO2max As The Maximum Integrated Capacity of The Pulmonary, Cardiovascular, & Muscular System
VO2max refers to the maximum rate of oxygen consumption measured during intense exercise, typically measured in ml of O2 per Kg per minute.
The concept that there exists a finite rate of oxygen transport from the environment to the mitochondria of exercising muscles began with Hill, Long, and Lupton. Since then, VO2max has become one of the most ubiquitous measurements in all of exercise science.
VO2max is calculated by Fick Equation, which states that VO2max = Q*[Ca-vO2] where Q stands for cardiac output (expressed as heart rate x stroke volume) and Ca-Vo2 represents the arteriovenous oxygen concentration difference.
From these calculations we can deduce that there are two primary ways that VO2max can be limited. Oxygen supply or utilization. Yet, the classical view of VO2max is that interindividual variability in VO2max is due almost entirely to differences in peak SV and CO between individuals.
“The dominant and deterministic physiological pathways that account for a vast majority of interindividual variability in VO2max are well known and center on total body hemoglobin content and peak cardiac stroke volume and as a result cardiac output” -Lundby, Montero, & Joyner, 2017
It makes sense that stroke volume would play a large role in VO2max given that the enlargement in cardiac dimension, improved contractility of the heart, and an increase in blood volume are all common cardiovascular adaptations to exercise training, all of which allow for a greater filling of the ventricles and consequently, increased stroke volume. We also need to factor in other things that will increase stroke volume as well, like the thoracic pump, as well as changes in blood HB concentration .
Per-Olof Åstrand also showed a close relationship between total Hb mass and VO2 max such that the differences between adults and children and between men and women were primarily due to differences in total hemoglobin. Additionally, it has been shown that an acute reduction in Hb concentration, even when blood volume is maintained, results in lower endurance performance due to a decreased oxygen-carrying capacity of the blood. Conversely, an increase in Hb concentration is associated with enhanced endurance capacity and is also proportional to the increase in the blood’s oxygen-carrying capacity. Because increases in blood volume will also thereby lead to an increase in end-diastolic volume, ejection fraction, and stroke volume, there is a clear association between increases in Hb concentration and blood volume and an increase in VO2max.
Effectively, this information is in support of a delivery limitation.
However, the presence of one limitation does not mean that VO2max cannot be limited by other factors like the pulmonary system or oxygen utilization within the working skeletal muscle or that there aren’t cases where improving maximal cardiac output does not improve VO2max. Simply put, the existence of one phenomenon does not disprove the presence of another. Similarly, the efficacy of one training method that has shown to be efficacious for improving VO2max, like high-intensity interval training, does not mean that different exercise prescriptions will not also show an improvement in the same variable.
For example, in elite athletes with very high maximal cardiac outputs, the decreased transit time of red blood cells in the pulmonary capillaries can lead to a pulmonary diffusion limitation. This was demonstrated in 1965 when the former mile world record holder Peter Snell performed a maximal treadmill step test, where he finished with a SpO2 level of 80%. Additionally, this finding was later confirmed by Dempsey et al. and Powers et al. when they showed that arterial oxygen desaturation occurs in some highly trained endurance athletes and they when these subjects breath hyperoxic gas mixtures, their hemoglobin saturation and VO2max increase. It has also been shown that arterial desaturation occurs in intermediate to advanced Crossfit competitors when performing maximal step tests and sport-specific competitions. This data suggests that pulmonary gas exchange may contribute significantly to the limitation of VO2max in highly trained athletes who exhibit exercise-induced reductions in SpO2 at sea level, as well as the fact that a healthy pulmonary system may become a so-called ‘limiting’ factor to oxygen transport and utilization as well as CO2 transport and elimination during maximum short-term exercise in the highly trained.
According to the Fick equation, every change in VO2max is matched by a concomitant change in maximal cardiac output or arteriovenous difference. One mechanism by which impaired pulmonary diffusion would limit VO2max would be by lessening the arteriovenous difference. If that reason holds, then a widening of the arteriovenous difference, in individuals with a pulmonary limitation, should be accompanied by an increased VO2max, which has been shown to occur. Additionally, an oxygen extraction limitation may be present, which would also truncate the arteriovenous oxygen difference. As a result, an improvement in oxygen extraction would be accompanied by an increase in VO2max in individuals with impaired oxygen extraction due to an increase in the arteriovenous difference.
As a result, I propse we make an afforance of david Poole’s definition of VO2max and redefine the term as the maximum integrated capacity of the pulmonary, cardiovascular, and muscular systems to uptake, transport, and utilize oxygen, respectively.
This is in opposition to the traditional definition of VO2max, which is the maximum rate of oxygen consumption measured during intense exercise. The later is a reductionist take on a complex variable, whereas the former is more holistic. In spite of the fact that there is mounting evidence that VO2max can be limited by multiple different physiological variables including pulmonary diffusion capacity for oxygen, maximal cardiac output, peripheral circulation, and metabolic capacity of skeletal muscle, most coaches and physiologists still do not hold this view. Instead, most coaches and physiologists believe that the central cardiovascular system’s capacity to transport oxygen to the working muscles is the principal determinant of VO2max.
This paradigm emerged as a result of Archibald Hill’s work in the early 1900’s. Archild Hill’s work undoubtedly contained many partial truths, but its partial validity should not mask its shortcomings. It is crucially important to remember that Archibald Hill formulated his hypothesis based on a small number of measurements, specifically of expired respiratory gases. He included no measurements of cardiovascular function or detailed respiratory function, nor did he take any measurements of skeletal muscle, metabolic, or contractile function. An unfortunate consequence of this is that generations of exercise scientists have been taught that you can simply use respiratory gas analysis to give you answers on the factors that limit human performance, but I believe this inherited wisdom is incorrect. For example, in Hill’s quantitative estimates, he calculated that arterial blood would be 90% saturated during all-out exercise, and mixed venous blood would be 10–30% saturated, and these values would be generalizable to all exercising athletes. This assumption leads one to assume that the arteriovenous difference would be nearly fixed, which would lead to the natural conclusion that cardiac output would be the primary determinant of VO2max, as Hill asserted.
