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- Alex Hutchinson (@sweatscience)

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Last spring, I had the opportunity to visit the sports science research group at the University of Cape Town. While I was there, I heard about some very surprising new research raising questions about the definition of VO2max. Since the research hadn’t yet been published, I agreed not to write about it; that paper has now been published in the January issue of the British Journal of Sports Medicine, so here goes.

A little background to start. The concept of VO2max — the absolute limit on how much oxygen you can deliver to your exercising muscles — is controversial these days, because it implies a physical limit on endurance performance. That idea, entrenched for the last century, has been challenged recently by researchers led by Cape Town’s Tim Noakes, whose “Central Governor Theory” argues that we never actually reach our ultimate physical limits — instead, our brains hold us back to protect us.

The new issue of BJSM actually contains eight different papers that could be interpreted as supporting Noakes’s basic thesis. And Noakes himself has an introductory article that offers a good overview of the debate and why it matters, for those who aren’t familiar with it. The full text of that intro is freely available here. Here’s Noakes’s somewhat oversimplified summary of the current status quo thinking:

In 1923, Nobel Laureate Archibald V Hill developed the currently popular model of exercise fatigue. According to his understanding, fatigue develops in the exercising skeletal muscles when the heart is no longer able to produce a cardiac output which is sufficient to cover the exercising muscles’ increased demands for oxygen. This causes skeletal muscle anaerobiosis (lack of oxygen) leading to lactic acidosis. The lactic acid so produced then ‘poisons’ the muscles, impairing their function and causing all the symptoms we recognise as ‘fatigue’.

We already know for sure that lactic acid doesn’t “poison” the muscles. But what about the idea of VO2max?

According to Hill, during the period between progressive exercise and exhaustion, whole body oxygen consumption reached a maximum value – the maximum oxygen consumption (VO 2max ) – ‘beyond which no effort can drive it’.

Two studies in the new issue of BJSM appear to show that VO2max isn’t actually “maximal” — you can get a higher value. As Noakes argues:

Had Hill shown this in 1923, he could not have concluded that maximal exercise performance is controlled by a limiting cardiac output. Instead a more complex explanation is required to explain why athletes always terminate exercise before they reach an ultimate oxygen limitation.

Okay, so much for intro. The study, by Fernando Beltrami and his colleagues in Cape Town, introduces a new VO2max protocol. VO2max is usually tested with an incremental design: you get on a treadmill (or an exercise bike), and the speed/workload gets higher/harder every minute or so until you reach failure. At some point before you reach failure, the amount of oxygen you’re using will have reached a plateau. Beltrami’s test is a decremental protocol. You start at a speed/workload slightly higher than what you were able to reach in a conventional incremental test, and then the speed is progressively reduced.

The subjects in the study all did a series of tests, as shown below. The key test was on visit number 4, when the experimental group did their decremental test:

Now, why would you expect a different result from a decremental test instead of an incremental test?

We reasoned that if subjects knew beforehand that the test would become progressively easier the longer it continued, the possibility was that any biological controls directing the termination of exercise might be relaxed, thus allowing the achievement of a VO 2max higher than that achieved with conventional INC.

In other words, if the plateau observed in conventional VO2max tests is mediated by the brain in some way, rather than being purely physical, then it might be possible to change the plateau. And here are the VO2max produced in those multiple tests by the two groups:

Sure enough, the VO2 produced in the decremental test is higher by 4.4% (with p=0.004) than in the incremental test. Strangely, it stays at this new higher value in the subsequent incremental test — even though there were no related physiological changes. Heart rate, breathing rate, and ventilation at VO2max were the same in the different protocols. So what’s going on?

Emotional stress can affect blood flow during exercise and stimulation of sympathetic cholinergic fibres are thought to promote arteriolar vasodilatation and to induce changes in metabolism, producing a switch from aerobic metabolism to increased oxygen-independent glycolytic pathways… We propose the interesting possibility that an anticipatory difference in perception of the future workload might impact the sympathetic or parasympathetic drives and lead to differences in the metabolic response during exercise.

That’s just speculation. But what’s not speculation is that the subjects in this study did conventional VO2max tests and produced reproducible plateaus; then they did another test that just involved changing the order of the speed, and produced higher Vo2max values. Whatever is happening here, it’s not tenable to argue that the VO2max values measured in conventional incremental tests represent some absolute physical limit on the body’s ability to deliver oxygen to working muscles.