Hi Everyone,
I've been charging through a bunch of data recently on a group of cyclists. We tested for CP + W' at various alttiudes, and they also did an interval workout which contains some max effort 5 sec sprints (see attached). This workout is done at 2250m btw. Anyway, this is the integral model shown, and what we can see is that the sprint efforts make a huge impact on Wbal, such that W'bal goes negative. I didn't find this previously in another study in which we only did 60 s intervals, although in that study we estimated CP using the 3min AOT, which definitely leads to high values for CP.
What I think is going on here has something to do with central regulation of descending motor drive (see study below). The central effect probably recovers much more rapidly than peripheral mechanisms of fatigue. I don't think the integral formula deals with this very effectively because it is monoexponential. Therefore, after very short periods of recovery you are able to produce almost near peak power. If your W'bal was reduced to say 2 or 3 kJ from a previous longer duration interval, then it just doesn't recovery quick enough. So then you do a sprint effort and it can be dropped negative. In Phil Skiba's original article which introduced the W'bal integral formula, he discusses a biexponential approach. So what I think is that a biexponential approach might potentially work better, since the fast tau could represent rapid recovery of muscle activation, whereas the slow tau would represent recovery of peripheral fatigue mechanisms.
Task Failure during Exercise to Exhaustion in Normoxia and Hypoxia Is Due to Reduced Muscle Activation Caused by Central Mechanisms While Muscle Metaboreflex Does Not Limit Performance.
On the flipside (ie: power production as opposed to recovery), it looks as though a similar concept may apply ie: explosive all out sprint activity induces a rapid central mode of 'fatigue' (which is probably better described as regulation) that rapidly reduces muscle activation, hence leading to decreased force output. This central component probably occurs well before there is even enough time for peripheral fatigue to develop.
Central fatigue contributes to the greater reductions in explosive than maximal strength with high-intensity fatigue.
The biggest challenge in understanding W' is that there is no doubt it is a combination of both central and peripheral mechanisms, but knowing the relative contribution of each at any moment in time is highly complex. The way we currently test for CP + W' though dictates that the peripheral mechanisms dominate. Similarly, the current versions of the W'bal formula probably model the peripheral component reasonably well, but if central fatigue rises or falls rapidly, then the model doesn't account for this effectively. I think this is part of the reason why the basic 2p CP model tends to overestimate power at short duration ie: it predicts that you have not generated enough peripheral fatigue to cause "task failure" at a given power since it doesn't account for the effect of central fatigue which is overlayed on top, and contributes an additonal mechanism that reduces the power (or duration) compared to predicted. The 3p model tries but falls short because the parameter of Pmax is not dynamic. The same limitation exists in the WKO4 model btw ie: there is no term which describes the dynamic influence of central regulation of muscle activation. It is becoming very clear (to me at least) that any model of power v duration, which is essentially a model of fatigue versus time, is conceptually incomplete unless a parameter which describes central regulation is included, and we get the behaviour of that parameter right.
Lastly, lets assume you do a work which does not contain sprint efforts.... if you're fatigued from previous training, well then you expect W'bal to stay positive when you have a crack at a max effort. But if you've improved fitness without updating the CP + W' values (which can easily occur), then you'll be able to push it negative.