Anticipatory regulation of exercise in the heat: Discussion continues
About a week ago, in our last post of our Series on Fatigue, we looked in some detail at a study by Frank Marino which found that African runners paced themselves differently to White runners during 8km time-trials in hot, but not cool conditions. Part of this difference was likely the larger body size of the white runners, which meant that their rate of heat storage would be higher than the African runners’ at the SAME SPEED. Therefore, the theory put forward was that the RATE OF HEAT STORAGE mediates a reduction in running speed well before any potentially limiting level of hyperthermia is reached.
A couple of things arose out of this post. First, we got quite a few posts by people saying that they should have controlled for body size, and made sure that the two groups were equally large (or small, as they case may be). This is probably correct, technically speaking, but a little harsh and maybe missing the point of the study. The key here was not so much the mechanism for the different pacing strategies of Africans and White runners, but rather the fact that they did it at all. Perhaps it’s genetic, perhaps size-related, perhaps metabolic, perhaps related to running economy? That’s all for future work to establish, hopefully. But the point is that athletes pace themselves differently and the rate of heat storage is a very likely candidate that mediates this difference.
One reader said that they should have controlled for calf-size as well, which is also probably true, but if you go down that road, then you have to control EVERYTHING. And physiology is simply too complex to do this. That is why, as you may recall, we discussed how for many years, scientists used to limit themselves to these fixed work rate trials to exhaustion – they are simpler to manage. As soon as you allow pacing, the complexity becomes enormous, but it’s the only realistic way to assess how PHYSIOLOGY works in the field.
Today, we look at further studies that have attempted to assess this, but this time, with a possible mechanism. For that, I get to summarize my own study, which is a little self-indulgent. It was not intended in this way, but was rather the result of the fact that five or six years ago, nobody was doing this kind of work. Still today, there are some problems with it (again, the motto is “Nobody can PROVE anything”), but it’s worth looking at.
Anticipatory regulation of performance in the heat
Refresh your memory on the state of the knowledge prior to 2003. The thinking regarding exercise in the heat was that you fatigued because you were hot. That is:
- Exercise increased heat production
- In hot and humid environments, you are not abe to lose that heat
- Your rate of heat storage is positive, so your body temperature rises
- It rises until it reaches a critical limiting level of about 40 degrees Celsius
- At that point, your brain fails to activate the muscle, your level of effort hits maximum, and you stop exercise
Impaired performance in the heat is thus the result of GETTING TOO HOT, to put it simply. This theory was borne out by studies that showed how brain activity was altered and EMG activity was lower when the body temperature was 40 degrees celsius. The problem was, these studies all fixed the cycling power output (or running speed), and so there was no room to slow down – it’s either go or stop.
So, in 2002, I did a study in Cape Town that aimed to determine WHEN the decision is made to slow down or speed up, or, in the case of the existing theory, stop altogether?
This study, which was published in the European Journal of Physiology (Tucker et al. Eur J Physiol; 448: 422-430, 2004, for those interested), aimed to answer the following questions (in lay terms):
- During exercise in the heat, WHEN does the athlete slow down? The current thinking was that they slowed down BECAUSE they got too hot. But Marino and some others were suggesting it happened before this.
- What mechanism might exist to cause this slow down during exercise in the heat?
The study was relatively simple: 12 well-trained cyclists performed 20 km time-trials in the lab, either in the hot condition (35 degrees, 60% humidity), or cool (15 degrees, 60% humidity). During the trials, we measured something called EMG activity, which is basically the electrical signal sent from the brain, to the muscle to cause it to contract. This method, which is the same as was used previously to show how the brain activated less muscle when it reached 40 degrees, always ends up being the point of attack for people who don’t buy into the whole regulation of exercise argument, but more on that later.
Things like heart rate, Rating of Perceived Exertion, skin temperature, body temperature were all measured during the trials as well. I’ll sum up the two key findings below:
1. The pacing strategy differs, almost from the start of the trial
The graph below shows the power output measured through the trials. You’ll not that in the heat, for the first 5 km, the power was the same as in the cold, and then it started dropping, whereas it was maintained in the cool trial. The result was that the overall power output was lower in the heat. Nothing unexpected there…
The mechanism – muscle activation and anticipatory regulation
But, what you should be asking is the following:
Why did the cyclists slow down after only 30% of the trial was completed?
There are two possible answers to that question:
You could say, based on the theory of heat LIMITING performance, that they slow down because their body temperature has risen quite high in those first 5km, and they slow down, because as was shown recently, a high body temperature directly prevents the brain from activating muscle;
OR, you might say
They slow down at this point so that they don’t get hot later on during exercise. That agrees with the Marino theory for anticipatory pacing, and something other than high body temperature is responsible for reducing their power output.
The graph below shows the answer to this question:
What this graph shows is the EMG activity (as a % of maxium – we express it relative to some maximal value of muscle activity, measured before the trial when the cyclist pushes as hard as possible for 5 seconds) over the course of the trial.
You’ll notice two key things:
1) First, the EMG activity is lower in the heat than in the cold, almost from the outset
2) The EMG activity increases significantly at the end of the trial – the “endspurt”
These changes in EMG activity EXPLAIN the changes in power output in our previous graph. That is, the power output in the heat is lower BECAUSE the activation of muscle is lower from very early on. Then, at the end of the trial, the power output increases substantially because the brain is activating more muscle. More muscle activation means more force, and that means more power.
But perhaps the key to all this comes from the tables I’ve inserted over the graph, which show that:
- The athlete slows down (the power output graph on top) and activates less muscle (the EMG graph below) even though their body temperatures, heart rates and even their Perception of Effort (the RPE) are THE SAME as in the cool condition. If you compare the HOT to the COOL conditions, you see that the body temperatures are “only” 38.4 degrees celsius, which is not different from the COOL condition, and nor is it anywhere close to the supposed “limit” to exercise of 40 degrees.
- Think for a moment about that for a moment – they “choose” to activate less muscle, to cycle at a lower power output, despite the fact that they are NOT HOT, and nowhere near the supposed “critical limiting temperature”. This may strike you as obvious, but again, you need to ask HOW they could possibly know this, and based on what information is such a ‘decision’ made?
- Then, at the end of the trial, the athlete is able to SPEED UP in the cold trial, activate MORE MUSCLE, even though their body temperature is higher than it was before
Quite clearly, the decision to speed up or slow down has nothing to do with body temperature, which is what the textbooks say. These findings show that the activation of muscle, the power output and hence performance are regulated by something much more complex that simply the direct effect of body temperature.
The most amazing of all – you slow down, even though you feel the same!
What is perhaps most remarkable of all is that the cyclists slowed down in the heat even though their perception of effort was the same as in the cool condition. This perception of effort basically measures an overall Rating of Exertion, which is to say it’s a mix of fatigue, effort and general perception. It’s a highly complex measurement, and we’ll come back to it later in this series.
Point is, it’s not as though they felt worse, and therefore slowed down! That’s what you might think, but the finding above suggests this is not the case. In other words:
- you feel the same in terms of your effort and fatigue levels
- you’re equally as hot as you were in the cold condition
- your heart is working at about the same level
yet you slow down through the activation of less muscle.
Now, there are many issues here that I won’t get into for this post, but will gladly discuss in question and answer things (so do read the comments at the bottom of this post because your question may well come up there!). So yes, there are some grey areas, there are mechanisms still missing (what causes them to slow down, for example?) and there’s much to be discovered still. But the take-home message here is that:
A model that says that you fatigue in the heat because you get too hot is clearly incorrect. Rather, fatigue in the heat is complex, and impaired performances happen long before athletes ever get hot. The regulation of exercise happens in anticipation of overheating, and it’s mediated by factors that are still too complex to pin down exactly. However, there are theories, and that’s what we will address next.
Join us then!