800m: Caster Semenya & Robby Andrews

800 m musings - Caster Semenya, Robby Andrews and contrasting pacing strategies

Thanks all for the huge response to the previous post on barefoot running.  I can think of only one other topic that has produced the kind of discussion we've seen in the last few days, and those were our posts on Caster Semenya, who I discuss a little more below.

Some of the comments and discussion on the barefoot running issue were extremely enlightening and if you're eager to learn even more, then going through that discussion is as enlightening as any article, so thanks again and do take time to browse the discussion if you haven't already - we'll outsource it as a post all by itself!

800m - Caster Semenya's performances under the spotlight

Today though, I wanted to discuss the 800m event, specifically to highlight two really great talking points in the last week or so, beginning with Caster Semenya.

Semenya was always going to be one of the most scrutinized athletes in the world, her return to competition after a gender controversy bringing human interest, athletic interest, and scientific interest angles.

Ours is all three, but primarily the scientific and athletic, and so we've been watching closely to see how she performs now that she's had a full off-season to prepare and build to competitive shape.  Her comeback was actually in 2010, and she even won a few races in Europe, but that season was hampered by sporadic training caused by injury and the doubts over whether she would be able to compete.  The same can't be said now - she's known since this time last year that she would be eligible to run.

So her 2011 performances were always going to be the subject of discussion.  This situation became inevitable when Semenya, her lawyers and the IAAF decided that no public announcement of what happened in the aftermath of Berlin would be made.  The result was that the whole world knew there was a question mark, but it was followed by speculation and assumption, rather than an answer, even a basic one.

Speculation no matter what the result - the catch-22 for Semenya

As a result, every race for Semenya would be followed by one of two responses.  Either she would win convincingly, and the world's athletics followers would say "She has an unfair advantage, they obviously didn't change anything, and now thanks to her lawyers, no other women can even compete".  Or, if she didn't win her races, the world would say "This proves that she must have had surgery or treatment".   A catch-22 for Semenya.

But now a third response has appeared - she doesn't win, and everyone says she is losing on purpose.  And that's been the case after her first two races - the came second in Eugene a week ago, and third in Oslo on Thursday, and the talk on athletics websites is that she is deliberately losing races so as to avoid attention and further discrimination. 

No matter how you look at it, it's an impossible situation to be in.  And from the observer point of view, it's similarly difficult.  It would be great to just leave it alone and let her run, but the way things unfolded, that is basically impossible, because people want to know that they are watching a fair race, a competitive event.

So the current speculation was inevitable and this was exactly the reason we argued many times that she (through her lawyers) needed to make some kind of statement to at least assure people that something had changed.  Not the full medical details, those are hers and should be confidential.  But something along the lines of "I have worked with the IAAF and a team of medical professionals over the last six months, and all parties are satisfied with the resolution and progress, and that I can now compete fairly as a female.  I look forward to running and and competing again".

The IAAF could have made a similar statement, supporting that their experts were confident that she no longer had an unfair advantage, and perhaps some of the speculation would have been dealt with.  It would not have removed doubt or controversy, but at least there wouldn't be a shadow hanging over every performance, doubt that she's cheating by running too SLOWLY when she could dominate the event.  And if you think this is an isolated opinion, it's not, I suspect many people are wondering "why is that athlete wearing red trying NOT to win?"

I don't know the answer to this - I would find it difficult to believe that any athlete would deliberately finish second when they could win by a small margin (in a relatively slow time of 1:58.xx too - it's not as though she'd be running 1:54 to win every race).  And to finish third when they could finish second?  I find it difficult to believe, so I'd almost want to give her the benefit of the doubt.  Also, I'm not sure she or her team is that calculating, but perhaps I'm naive.  She is currently 4 seconds off her best, around 3.5%, which is a big distance off your best.  But that could mean one of three things - training hasn't gone well, she's running slowly on purpose, or she had treatment and the 1:54 from 2009 is now never going to be possible.

Also, I've seen her race BEFORE the controversy, and she looked pretty much the same as she does now, even when losing.  For example, in her World Junior Championships in Poland in 2008, she finished 7th in her heat, and looked much the same as she does now.  It may be that she just looks like that, that she never seems to be straining - short, chopped stride, no major upper body rotation - it would easily look like someone wasn't working hard enough.

But, then I see her race in Eugene and Oslo, and I can appreciate what people are saying - she led for 700m in Oslo and then in the final straight, just seemed to coast through to a third place finish.

But, you can see for yourselves if you haven't already.

First, here is the race in Oslo:




And here is the race in Poland, 2008.  As an aside, note the difference in her physical development from 2008 to when she won the World Title in 2009 in Berlin.  Truth is, if it hadn't been for controversies about gender, there'd have been a lot of people speculation about doping, such is the cynical age of elite sport we live in.



Your thoughts?  No matter what one believe, it's a difficult situation - the more I've written about this, and spoken about it, the more I've realized the problem of intersex conditions in sport is basically insoluble - there's no solution to satisfy everyone.  Of course, Semenya's case was handled so poorly and unfairly for her, and her response to it has been admirable.  But for the sport, the questions have to be asked.

Robby Andrews - great finish, interesting contrast in pacing

On a more racing-specific note, here is a fantastic men's 800m from the NCAA championships over the weekend.  It's fast, and competitive, one of the better finishes you'll see in an 800m race.  Watch the clip before reading on, spoilers to follow!



So the interesting thing for me is the pacing strategy - I'm biased, but I read quite a bit into it!  And the guy who ends up second, Charles Jock, runs a first 400m in 49.85s.  Super quick, and followed by a second lap in 54.90s.

Now that's a huge positive split - 5 seconds, which I don't believe is optimal.  Robby Andrews, who catches him, runs the first lap in a low 51s, which means his second lap is around 53.5 seconds.  That's a far more reasonable balance to the race, much more in line with how the best 800m performances have been recorded.

But the point I'd make is that Robby Andrews' super quick finish (which is amazing, don't get me wrong) only appears that fast because the rest of the field was far too fast early on.  To give you more numbers, Jock was recorded at 1:17.1 at 600m.  That means after a first lap of 49.85s, his next 200m took 27.3s. And his final 200m took 29.65s - he was getting progressively slower.

So was Andrews, to be honest, and it's a safe bet that Andrews was a little quicker than 27s to the 600m mark.  But then Andrews finishes with a final 200m of about 26.5 seconds (assuming he's ± 1 second down on Jock at 600m), compared to Jock's final 200m of around 27.65 seconds.

In other words, Andrews just slowed down the least, and that one second gap which looked so enormous at 200m to go, was overcome as a result of a better overall pacing strategy, combined with a huge slow down for the rest of the field.

Pacing strategy is not a precise science, at least with the knowledge we currently have.  But a + 5 second differential in an 800m suggests to me too fast a first lap, whereas the + 2 for Andrews is a much more controlled, and probably closer to optimal, performance.

But a great race, nevertheless.  Can Andrews go faster?  Probably.  Can Charles Jock?  Definitely, because he should have a big improvement there if he gets the pace right!

But more on pacing in the series coming up when I'll share the video of my presentation on the subject from the recent ACSM!

Enjoy the Diamond League!
Ross

le Tour de France 2008: Feed them well

Why eating is important

The 2008 edition of le grande boucle, as it is affectionately known, is now fully underway, and so far each stage has been quite exciting. The tour started without the traditional prologue, and instead was a full on stage. It's slightly uphill finish effectively neutralized the sprinters, and so it was not surprising to see all the main GC contenders at the front. In fact Alejandro Valverde won the stage and took yellow, although we spoke about how much of a challenge it would be to go "wire to wire" in yellow.

Sunday's Stage 2 had its fair share of bumps with four categorized climbs and also a slightly uphill finish. It seemed that again the sprinters would be neutralized, and it was Fabian Cancellara that attacked with one km to go. He could not hold it, though, and even Valverde had a go, but also faded. In the end a big man took victory---Thor Hushovd from Norway powered across the line for his fifth stage win in le Tour. Valverde remained in yellow, however.

During the first two stages there were crashes as the riders passed through the feedzones. These are designated areas where support crew hold out bags full of food and drink. The riders slow down a bit and grab them as they whiz by. Fortunately Stage 3 saw no crashes in the feed zones, but let's looks at why it is so important to eat on the bike.

Energy balance

We can all agree that the energy demands placed on tour riders are pretty astronomical, but it makes more sense to break it down into a specific context. Therefore let's take your "average" 75 kg cyclist and his daily energy demands. His resting metabolic rate, or RMR, is the amount of energy he requires to sit there do nothing all day long. In other words, it is the energy required by his body to maintain all of its life-sustaining functions. For him it is around 1500 calories.

But our cyclist is not just sitting there all day. . .in fact, he is covering upwards of 180 km per stage, often with significant uphill sections which require more energy. Cycling is a pretty efficient activity, however, and it costs our cyclist in the range of 0.3-0.4 calories per km cycled per kg of body mass---or about 25-30 calories per km. The bottom line here is that a 180 km stage will cost our athlete around 4000 calories, depending on the amount of drafting.

It's a lot of cheeseburgers!

Any way you calculate it, our cyclist's total energy expenditure for one day of the tour is very high. His RMR (1500 cal) plus his exercising energy expenditure (4000 cal) adds up to a whopping 5500 calories, which is probably the equivalent of 15+ cheeseburgers! So just to remain in energy balance our rider must consume 5000+ calories a day. Believe us when we say it: that is a lot of food. Add to this the fact that he is on the bike for four or more hours during the day, plus the "anorexic effect" of exercise, plus 8-10 hours of sleep. Suddenly he has only a relatively small window of time to consume large amounts or calories.

If we assume he is otherwise occupied for up to 16 hours a day with riding, sleeping, and other activities, he has only about 7-8 h to ingest 5500 calories, which works out to about 700+ calories an hour during the time he is available to eat and drink. So remaining in energy balance is actually a huge challenge for our tour rider.

Fortunately the race organizers allow the cyclists to grab the feed bags and eat while riding. This is crucial for two reasons. First, it provides more opportunity to choke down a portion of the 5500 calories he needs in a day. Second, the ingestion of carbohydrates during exercise prevents the dreaded "bonk," or hypoglycemia. Many of you probably have bonked before, and therefore you know that when it happens you are finished---no more racing for the day as you limp home and consume gross quantities of food along the way to fill the hole in your tummy!

How much to eat then?

Klaas Westerterp and his colleagues in Maastricht (Netherlands) actually measured the energy intake and estimated the energy expenditure in five cyclists in the 1988 Tour de France. Their average intake was almost 6000 calories per day, while their average expenditure was nearly 6100 calories per day---indicating that these cyclists did a remarkable job of (nearly) maintaining energy balance. They accomplished this by ingesting 49% of their energy while riding, which amounted to whopping 94 g of CHO per hour during each stage! Furthermore, a full 30% of their carbohydrate intake was in fluid form, which makes it substantially easier to meet energy requirements during the 7-8 h when they are not racing or otherwise occupied.

Given this information now, it should now make total sense when you watch the riders rolling through the French countryside, shoving energy bars and other products down their gullets. Hungry or not, they must get the calories into their bodies. Failure to do so will almost certainly result in fatigue and an early exit from the race, because when cycling four or more hours each day it does not take long to accrue a serious energy deficit. When your body does not get enough energy, cycling four hours or more a day becomes an unnecessary activity, and our bodies have an uncanny way of keeping us healthy---suddenly getting on the bike and pedaling requires substantial effort, more so than a few days ago, and eventually you will not be able to keep up with the bunch.

Stay tuned to le Tour---plenty of action ahead

Looking ahead to Tuesday's stage, we see the first individual time trial. It is a pancake flat 29 km ride and will do two things. First, it will create a pecking order for those who will contend for the GC. Second, it will limit any one rider's gains or losses as the distance is so short, and therefore the race should remain close and within reach for the contenders. It also will set the stage for Stage 6 on Thursday, which is the tour's first mountain top finish, and is sure to produce some fireworks!

Fatigue Series Part 5: Exercise in the heat

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:

1. 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.
2. 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?
3. 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!

Ross

Fatigue Series Part 4: Exercise in the Heat

Exercise in the heat: Predicting the physiological future - African runners outperform white runners in the heat

We're back with Part 4 (or is it 5 or 6? I've lost count!) of our Series on Fatigue during exercise. In our last post, we looked at exercise in the heat, and found that:

• Laboratory research shows that human beings will stop exercise when their body temperature rises to a certain level. That level is of course dependent on the athlete's motivational levels, though interestingly, not necessarily on their training status or performance.
• We also saw that the science has shown that when the body temperature rises to reach about 40 degrees, the brain actually activates less muscle than a "cooler" brain, and that there is evidence for reduced arousal and motivation.

So, the hypothesis, based on these constant workload studies, is that the heat affects performance because:

A high body temperature DIRECTLY inhibits the ability of the brain to activate muscle.
Therefore, exercise stops (because in these studies, remember, slowing down is not an option)

What happens when the athlete CAN slow down? Self-paced exercise

Today we turn our attention to the case where athletes can slow down - this is arguably more representative of what you will see in Beijing later this year, since any athlete can, at any stage, choose to drop off the pace. Of course, they lose their medal chance this way, but it's a much more applicable form of testing.


And to understand this, we look a few studies. We'll do it in a couple of posts, because otherwise the length would become enormous. So today, we consider one study, with more to come in the next few days.

In 2000, a study by Tatterson (J Sci Med Sport) found that cyclists slowed down soon after they started a 30-minute performance trial in hot, but not cold conditions. What was significant is that their body temperatures were not higher in the hot than in the cold when they slowed down. Obvious, yes, but quite contrary to the theory that your brain stops activating muscle AFTER your body temperature hits the "threshold". They didn't measure any index of muscle activation, however, but it was a crucial observation that something else (and not direct body temperature) was playing a role in the heat.

African runners in the heat - anticipatory regulation thanks to their smaller size?

Then, a study done by Frank Marino while he visited Cape Town a few years back, was one of the first to use the words "anticipatory", because his finding (discussed below) found differences in the pacing strategy of African runners compared to white runners in hot conditions. So the conclusion is that something is happening BEFORE the body temperature rises, slowing the runner down so that they don't overheat.


And this is obvious. Think for a moment about when you go and train on a very hot day. You do not simply go out and run or cycle at your normal pace until suddenly, overcome with a sensation of hyperthermia, you slow down! Rather, your entire approach to the session is changed and you slow down LONG BEFORE you ever get hot in the first place! Within the first few strides, you're probably already going slower. So this is one of those examples we spoke about a long time ago - intuitively, we know what happens.


The question is HOW? And also, we have to consider the prevailing expert opinion of the time. In this case, remember, the "textbook" knowledge says that exercise is impaired because the HOT BRAIN directly inhibits muscle activation after body temperatures are raised by exercise.

So, let's look at the study by Frank Marino. I'm sure he'll forgive my very rudimentary depiction of his methods below:





So he had 6 African and 6 white runners, quite well trained, doing a performance trial after a 30 minute steady run in either HOT (35 degree) or COOL (15 degree) conditions.


The starting hypotheses for this study, had you read the theories about exericse in the heat, would be:

• Performance would be impaired in the heat, so the runners would be slower during the 8km trial in the hot condition. This is fairly obvious.
• They'd slow down in the HOT trial because they'd be much hotter than in the cool trial - the high body temperature (and HOT brain) is failing to activate muscle, as we're told by other research.

This is what was found:

Graph of running speed (km/hr) against time for the 12 runners during 8km time-trial performances preceded by 30minutes run in hot and cold conditions

I've highlighted with a red circle one of the more significant findings - the white runners started the 8km trial much slower than the black runners did, from the first minute. Of course, both groups eventually slowed down in the heat compared to the cold (the black symbols on the graph), but it's this difference between black and white runners that should be of interest. So, why then, do the white runners start so much more slowly?

Option 1 is that they are already hot. They might be finishing the 30 minute steady run with higher body temperatures. That would agree with the theory that the hotter you are, the slower you go...

However, look at the graph below:

Graph of rectal temperatures during the course of the trials in hot and cold conditions

Again, I've highlighted the key point there - the black and white runners had THE SAME rectal temperature when they started the 8km run. And not only this, but the temperature was "only" 38.2 degrees, so they were way cooler than the supposed "limiting temperature".

Yet, for some reason, despite the fact that the black and white runners have the same temperature and are not in any danger, the white runners "chose" to START an 8km time-trial slower than the black runners. We can therefore dismiss Option 1 from above, and say that it's clearly not a case of a hot athlete slowing down! If it was this simple, with some "direct effect" on the athlete, then the slowing down would happen equally in the two groups. This is an amazing finding given the prevailing view that the heat impairs performance directly, I hope it strikes you that way too!

So what, then, is the reason? Well, that's of course difficult, if not impossible to PROVE (as we've seen recently courtesy the CAS, "proof" in science is not as easy to do as people think), but here's a theory from the Marino paper:

• The African runners were much smaller than the White runners - 59 kg compared to 77kg, to be exact. The white runners were taller, however, and had a larger body surface area.
• We know from previous research that a smaller runner produces less heat while running at the same speed as a larger one. That is, the total heat PRODUCTION is dependent on body mass, and smaller people produce less heat.
• Smaller runners also lose less heat, however, because they have a smaller body surface area to lose heat to environment.
• But the key is: These two factors don't exactly cancel one another out. The result is that even though they lose less heat, smaller runners are still able to lose more heat RELATIVE to heat production than larger runners. This has to do with the ratio their mass to body surface area - they may lose on surface area, but their lighter weight more than makes up for it.
• The net result of all this, is that smaller athletes have a reduced RATE OF HEAT STORAGE than bigger runners.
• Now, given this fact, if two runners are going along at the same speed, the smaller one will be storing less heat, and therefore his/her body temperature will be climbing slower than that of the big runner.
• Put differently, it means that if both athletes are concerned about how hot they are getting, then the bigger runner will have to slow down in order to prevent his heat storage from rising, which would ultimately increase his heat production.

Now, with all those facts on the table, the results start to offer an interesting theory:

The rate of heat storage is responsible for Anticipatory Regulation of exercise and pacing strategy in the heat

The theory is that the white runners, by virtue of their bigger size, have an increased rate of heat storage. (Note that this effect (the different pacing strategies, that is) is likely due to size - had the groups been matched for mass and height, the result might have been different - see the comments section to this post!)

The brain is "clever" enough to know that if the athletes starts their 8km time-trial at a fast pace, then their very high rate of heat storage is going to see their body temperature RISE very rapidly. They are in danger of reaching a core temperature of 40 degrees BEFORE the end of the time-trial (which they know is 8km long). Remember, at this temperature, the brain says "Enough" and exhaustion usually occurs (or soon after).

Therefore, the brain says "Whoa, back off a little!", long before the athlete overheats, and with the intention of making sure that they do not reach this limiting temperature before they are able to finish the trial - it would be a complete failure to do this, and reach the 6km mark by the time their brain says "enough". So instead, it REGULATES their performance IN ANTICIPATION of ever reaching that limit. That Anticipatory Regulation is achieved or mediated by the rate of heat storage, which is different from the very early stages of exercise.

On the other hand, the African runners, who are smaller, have no such problems. They thus maintain a higher speed, and a similar rate of heat storage, leading ultimately to an improved performance. Note, very importantly, that in the cold, this difference between black and white runners does not exist. Therefore, it's not a case that the white runners are just inferior to the black runners - it applies only in the heat, when the environmental temperatures bring this heat storage aspect into play.

Looking ahead

What this study does not do is measure anything related to brain function. Now, that's very difficult to do during dynamic exercise, and is often criticized, but we'll discuss a study tomorrow that looked at EMG activity (a measure of how much muscle is being activated by the brain) during trials in the hot and cold. This was the first study to find evidence for it. It was also a study I did for part of my PhD, though I'm not claiming anything here - it was be default, more than anything else!

So that's coming up in our next post - evidence of Anticipatory Regulation of Exercise Performance, along with a few more concepts to build on the ideas put forward here.

Join us then!

Ross

Fatigue Series: Part III - Exercise in the heat

Exercise in the heat: The "off-switch," the limiting temperature, and the Beijing Olympics

We're back with more on fatigue, and as promised, the strategy we'll adopt over the next few posts is to look at fatigue in very specific situations. These situations, often the intervention controlled by the scientists, offer a glimpse into how exercise performance is either limited or regulated, and help us understand how performance might be improved (by working backwards from the regulation or limit).

As we discussed in our last post, studies can look at exercise performance as being "limited" by some failure, or as a "regulated" process, where the body aims to maintain homeostasis by regulating what we've defined as the pacing strategy.

In today's post, we look at exercise in the heat. This is especially topical this year, because the Beijing Olympics promises to bring the influence of heat and humidity into the public eye in a big way. Elite athletes the world over are preparing for the heat by using special chambers to replicate the likely Beijing conditions, and it's also one of the reasons we discussed a few weeks ago that the Kenyan runners, the big favourites for the marathon, might have their work cut out, given the "levelling effect" that the heat can have.

Exercise in the heat: What ultimately limits performance?

We start our investigation of the heat by asking this question, which represents, of course, the "limitations" model for exercise. This is a crucial question, however, because if we want to know how exercise is regulated, it's important to recognize that it is ultimately limited by some variable.

The early theory - blood supply limitations

And until about 30 years ago, the early understanding of exercise in the heat is that it was limited because the body did not have enough blood to get to both the muscles and the skin, where it was needed for cooling. The result of this limited blood supply was that the muscles were deprived of oxygen, became anaerobic, and exercise stopped. Alternatively, the blood pressure was challenged to the point where exercise was completely impossible. This would, according to our discussion of constant workload vs. self-paced exercise, represent the point at which the "bridge breaks", or the light goes off!

However, in 1979, a scientist called Nadel published a study showing that blood flow was in fact not limiting during exercise in hot conditions. This was followed by studies in the 1990's from Denmark (where a lot of heat research comes from) which showed the same thing - there may be a challenge to blood supply during exercise in the heat, but the body is more than capable of meeting it in healthy individuals. And so that theory was disproven.

A clue to the limit - mental confusion

But around the same time, it was recognized that when these athletes were exercising in the laboratory, there came a point at which they actually developed mental symptoms - lack of co-ordination, dizziness, confusion and loss of ability to control their limbs! This led scientists to speculate that in fact, the limit to exercise in the heat was central, involving the brain. The speculation at the time, as far back as 1987 by a Canadian pair (Bruck and Olschiewski), was that a high body temperature affected brain function and the drive to exercise.

The famous video, shown at the end of this post, captures this situation - it is Gabrielle Andersen, staggering and swaying through the Olympic stadium in Los Angeles, typifying the human response observed in the research subjects at the point of exhaustion during exercise in the heat - paralysis on one side of the body, confusion, loss of co-ordination and balance.

Limiting body temperature - the "off-switch"

Subsequent work showed this "central fatigue hypothesis" to be a distinct possibility. It turned out that animals and humans all stopped exercise at a very distinct body temperature.

For example, in cheetahs (running on treadmills, believe it or not!), it was noticed as far back as 1973, that at a particular point, the animals displayed very strange behaviour - they simply "gave up" running and lay down! In the words of the authors (Taylor and Rowntree):

“…the cheetahs refused to run… They would simply turn over with their feet in the air and slide on the tread(mill) surface".

Later, it became possible to actually measure the body temperature of animals and humans during exercise (I can't imagine it's very easy to measure the body temperature of a Cheetah during running! Rats and goats, perhaps, are easier propositions!). It was found that all animals seemed to have a very narrow range of body temperatures at which they would stop exercise. For example, beagles stopped at body temperatures of about 42 degrees, antelope 42 degrees, and goats 43 degrees. Rats, the most tested of all, were found to stop at about 41 degrees celsius.

Human beings - a thermal limit to exercise and a proposed mechanism

Then came humans. And perhaps not surprisingly, research found that humans tended to stop at a body temperature of about 40 degrees celsius. What was most interesting is that this temperature was consistent regardless of pre-cooling, the rate of heat storage, and the degree of heat adaptation. In other words, it seemed that humans have this "off-switch" at 40 degrees celsius, irrespective of the external intervention. The only thing that changed was the time it took to get there - for example, a person who is well adapted to the heat is able to sweat more, lose more heat and therefore takes much longer to reach this limit than someone who goes straight into a hot environment. But they still stop at around the same temperature, according to this lab research.

Remember that this is found when humans exercise in a laboratory at a constant workload until they themselves decided "enough is enough" and choose to stop. When given a little more motivation (like when an Olympic gold medal is on the line, or that 10km PB you've been training for), it's likely that you'll get this body temperature up to 41 degrees, but beyond that, it seems that exercise is very nearly impossible, at least in the absence of some pathology or abnormal response.

Remember also that heat stroke, which is a very serious medical condition, happens at a temperature of 42 degrees, so the limit to voluntary exercise happens well before this level is attained. That of course raises the interesting question of why heatstroke happens - a malfunction of the "off-switch", perhaps? Or a failure of the signal to actually reach the brain to stop exercise? It's a difficult one, for which there are theories, and we'll cover them at some stage.

The mechanism - reduced muscle activation and arousal levels

So once this was discovered, science began looking for the mechanism, the HOW of the "off-switch". Because the thinking was that the central drive (from the brain) was the culprit, it made sense to look at brain function for clues, and that's exactly what the Danish researchers did. So, in a series of studies, cyclists were made to ride in the heat at a fixed workload until exhaustion, and then various measurements were made of brain function and muscle function. There were two key findings:

1. At very high (40 degrees) body temperatures, immediately after the athletes had become exhausted, they found that the activation of muscle by the brain was actually LOWER than when the body temperature was only 38 degrees. The graph below shows the EMG activity in the quadriceps muscles after exercise in the hot and cool conditions. It's quite clear that the EMG, which is a measure of activation of muscle, is lower when the body is hot. So that gives an indication of why the cyclists were no longer able to push out the required force - their brain simply prevented them from activating the required amount of muscle.
2. There was evidence of reduced arousal/motivation levels once the body temperature rose. In fact, what was found is that there was a very good correlation between a rise in body temperature and a reduction in arousal. Motivation or arousal, incidentally, was measured using EEG and the ratio of certain brain waves which are known to indicate this parameter. The key point here is that as the body temperature gets higher, the motivation declines, and this in turn is responsible for a rise in the perception of effort. They therefore found a good correlation between RPE and a rise in body temperature, though of course, correlations are often a slightly misleading. The key is: Increased body temperature = decreased motivation/arousal = increased effort perception.
   

The problem with this research: What happens before the "off-switch" is reached?

Again, the key question one should be asking is whether this solid science is actually relevant to what you are going to witness in Beijing later this year? Because in Beijing, the world's best atheltes will line up, highly motivated, take part in a race, where they can speed up or slow down, depending on the innumerable factors that go into racing strategy.

The studies have shown that when athletes go at a fixed pace until they are exhausted, they'll stop when their body temperature hits about 40 degrees. Perhaps, given the incentive of Olympic Gold, that temperature will be higher. And perhaps, when they push themselves hard enough for the rewards that are on offer in Beijing, they'll be able to raise their body temperatures so high that they end up looking like the famous Gabrielle Andersen from the 1984 Olympic Games marathon (see video below).

But, realistically, you know that this doesn't happen, because Olympic competition is not a fixed workload trial to exhaustion in a lab, and the athlete is able to slow down if they wish. And so what you will see in Beijing is athletes dropping off the lead pace after only 7 km of a 10km race, and then you have to wonder: Are they hot, or is something else in play? And you should be asking: What happens when the body temperature is 39 degrees, and there are still 20 km of the marathon left to run? Does the brain allow the athlete to just run and run until it the body temperature hits 40 degrees, and the athlete stops? Of course, you suspect the answer is no.

So the "limitations" theory for exercise in the heat, while proven in the lab, fails to explain what you'll see in Beijing later this year, and will have experienced in your own training, many times.

And that's what we'll cover in our next post. Join us then!

Ross

Fatigue Series: Part II - Models and implications

Fatigue in "real life": How exercise type influences conclusions and our understanding of fatigue

Back in the saddle for Part 3 of our series on Fatigue today. In previous posts, we've introduced the concept of Anticipatory Regulation, and contrasted it with the theory of "limitations" of exercise performance. We introduced the pacing strategy concept, which is often dismissed as "obvious" (because it is!), but is in fact one of the most complex, and meaningful characteristics of exercise performance for physiologists.

What we'll do next is go through a number of different situations, scenarios and "challenges" faced by the body during exercise in order to delve into the concept of anticipatory regulation vs. peripheral fatigue a little more. That series of posts will look at:

• The physiological basis for why pacing strategies exist during exercise
• The special cases of:
• Exercise in the heat
• Exercise at altitude and with MORE oxygen
• Exercise with different availability of energy - the fuel limitations theory
• Studies of exercise where subjects are deceived as to how long they will exercise for

But before we tackle that, it's important to discuss briefly how these studies are done, because it has major implications for what conclusion is eventually drawn from them. So today's post looks at "real-life" vs laboratory science, and its implications.

Scientific testing modes

There are, of course, an infinite number of possible study designs and combinations of different exercise types. But it's worth discussing the two predominantly used exercise modes, which are:

1. Constant workload trials to exhaustion
2. Time-trial studies

1. Constant workload trials to exhaustion

In constant workload trials to exhaustion, the exercising athlete is "forced" to cycle, run, row (or do any other exercise) at a predetermined intensity until they themselves choose to terminate the exercise bout because they are unable to maintain that required intensity. This includes the well known VO2max test, where a runner or cyclist starts off at a comfortable pace, and the intensity is increased every minute or two until the athlete cannot continue any longer (or falls off the treadmill, something most physiologists have experienced!).

In this test, performance is measured as either time taken to reach the point of voluntary exhaustion (the athlete says "that's it, I feel close to death and can't carry on!") or the total work done (distance covered, kilojoules used etc.) before that point is reached. What is crucial to recognize is that the athlete has no idea of how long they will exercise for - the instruction is to "go until you have to stop", which means exercise is completely open-ended with the athlete determining the duration. This removes any aspect of pacing, and since there's no known "endpoint," adjusting the pace appropriately would be meaningless and impossible anyway.

In this kind of exercise mode, the researcher is:

1. Defining fatigue as an "event". That is, fatigue is a distinct moment in time when the athlete decides to stop. It is therefore an "all-or-nothing" event, black or white, yes or no, on or off. One could compare it to an "off-switch," where the athlete exercises until such time as "the lights go off!". This definition is clearly not appropriate for cycling or running races (though it's entirely appropriate in this kind of study), for when you are taking part in a race, you recognize that fatigue is more complex than simply a point at which your lights go off!
   
2. Establishing at what physiological point the "off" switch is reached. The researcher is able to narrow physiology down to one or two variables and control for others. It reduces the complexity of performance quite dramatically (though it's certainly still very complex), and enables the scientist to adopt what one might call a "black box" approach. They can measure as much as possible, and then infer backwards from the "fatigue point" in order to appreciate what caused fatigue in the first place. When we talk about exercise in the heat, you'll see a great example of how this has been done.
   

The "collapsing bridges" theory for fatigue

Before moving onto the next type of exercise mode, we'll let Calvin and Hobbes give you a little illustration of the principle of constant workload trials and fatigue:


Basically, this cartoon illustrates what physiology is doing when we fix the workload and let the athletes exercise to fatigue. Effectively, it is stressing the human body to the point where it "breaks", and fatigue occurs. Then, once that has happened, the researcher goes back, analyses the physiological situation when that fatigue "occurred" and deduces that the cause of fatigue was X, Y or Z.

For example, one might make athletes exercise in hot conditions, and find that fatigue always happens at a body temperatures of about 40 degrees Celsius (104 F) (this is true, as we shall see in the series moving forward). In that case, one could conclude that the high body temperature has caused fatigue, as we have controlled for everything else. Similarly, you might find studies where athletes exercise to exhaustion in a VO2max test. And because they reach the "VO2max", the conclusion is made that a limitation of oxygen delivery caused the athlete to eventually stop exercise (or fall off the treadmill again!). The fatigue, then, is analogous to the "load limit" in the cartoon, with factors like temperature, metabolites, and oxygen availability all representing "trucks" that cause the bridge to break!

This kind of constant workload test, as I'm sure you can appreciate as you read this, is not exactly representative of what happens when you go out and exercise. Because regardless of what you do, either in training or racing, there is hardly ever a situation where you do not have a choice to slow down before you stop. In a laboratory, doing exercise at a fixed work rate, this choice does not exist for you! You either exercise or you don't, whereas any other exercise affords you the chance to slow down. And, as we've discussed in Part IB of this series, it's this ability to slow down (and the regulation that controls HOW and WHEN you slow down) that is crucially important for understanding physiology.

So what then, is the point of this kind of constant workload study? I certainly don't wish to dismiss it as meaningless, because it is in fact responsible for some of the best research done. It is science at its best, in many ways, as we must control for all the other variables except the one which we are investigating, and this includes the workload. However, what it does is establish the limits of performance in a simplified, manageable model. By defining fatigue so specifically as a single "event" or point, one is able to study the upper or lower limits of exercise quite elegantly. It's extremely useful for scientists to know that fatigue coincides with a body temperature of 40 C, for example, as it allows us to know what is happening at the extremes of performance, and therefore reveals the physiology of "homeostatic failure."

But this technique does NOT explain how performance is regulated, and problems develop when scientists begin to apply these findings to all situations. For example, when a physiologist proclaims that "Impaired exercise performance in the heat of Beijing will be the result of high body temperatures causing fatigue", then they are stretching the truth, and lying to you by taking their finding out of context! This happens very often, and is a big reason for the sometimes aggressive debate between the two models we introduced in our last post.

Then finally, in terms of application, when you are watching the Olympic Games this year, you're not watching this kind of exercise, you are watching the second kind of study, the self-paced trial (with a few differences!)

2. Self-paced exercise time-trials

This is a rather obvious concept - the athlete in the lab is made to do a "simulated" time-trial, over a known duration, and the power output or running speed is free to vary, at the athlete's discretion. Performance in this kind of model is defined by the time taken to complete a known distance, or a known amount of work, or distance covered in a known time. The key to this kind of study is that there IS a known end-point, so the athlete has an idea of what lies ahead when they start exercise. This enables the "pacing strategy" to come into play, as discussed previously.

If the Constant Workload Trial we discussed above represents the "ON-OFF" switch, then this kind of self-paced trial is the "DIMMER" control on your lights. Because instead of a situation where the light is on until it goes off, here we have a situation where the athlete is able to constantly modulate the workrate, up and down depending on the set of INPUTS they are receiving. The key question for physiologists everywhere, then, is how is this achieved? Returning again to the heat example, the challenge is to figure out how the athlete is able to adjust work rate to prevent the limit from ever being attained.

This kind of exercise is also more "realistic" if you want to compare it to most exercise types and actually apply the findings from your study. That is, when you go out for an 8km training run, you are effectively doing a sub-maximal exercise bout which is self-paced, with known duration, just as you would do in the lab. That means that application and inference from this kind of model is possibly more realistic than a model where workrate is fixed and duration is unknown.

Some key differences - "real" exercise is not purely self-paced

There are, of course, some big differences. For one thing, when you go out to run a 10km race, you're not really doing a "self-paced" trial, because there are other athletes in the race who have an equally large impact on your selected pace. So perhaps, for a race situation, one might say "freely paced", and then acknowledge that other runners, motivation, and numerous other factors affect the "self-paced" intensity! The point is that ultimately the athlete is still able to increase or decrease the exercise intensity, and this is a "self-selected" pace, regardless of which INPUTS are responsible for the pace. This sets the scene for the previously discussed "Anticipatory Regulation" (see the model at the end of Post IB for more on this concept).

Another difference is that exercise outdoors throws up a number of variables that are difficult to replicate in a lab. For example, changing wind and temperature conditions, gradients, road surfaces, and surroundings all exert an effect on performance during training or racing, but are limited in labs. We can, and do, try to control for this, but it does of course limit the contextual application of research to outdoor competition, and is one reason why to this day, with so much knowledge, we still actually know relatively little about performance physiology! As we've said, if anyone tells you that they know the TRUTH, they're lying...ignorant...or both...!

Looking ahead - why this is important

As I mentioned at the top of this post, the next few posts will look at pacing strategies during exercise in different conditions. But we'll also look at the constant workload model, and compare the conclusions made from these studies with those made in the self-paced, time-trial studies.

Once again, exercise in the heat provides the best example of this, because in this area, there have been some excellent research studies using constant workrate trials, which have concluded that fatigue is the result of high body temperatures acting on the brain. As described above, the problem is that these types of trials create a situation where that is really the only conclusion possible, because the trial is set up to evaluate a "forced" physiology leading to a distinct failure of exercise. In self-paced trials, one can look at what happens to performance and perceptions of effort long before the "fatigue point" is reached, to help understand how performance is regulated. That reveals that in fact, athletes slow down long before they are hot, and suggests that performance in the heat is regulated in advance of the "failure" so easily observed when athletes are forced into maintaining one intensity.

But this is all for the next batch of posts, where we'll tackle those four scenarios in turn, and we'll constantly be coming back to this concept of fatigue as a distinct event vs. fatigue as a regulated process!

Join us then!
Ross

Fatigue and Exercise Part I B

The pacing strategy continued: Setting the scene with two examples and a summary of models

In yesterday's post, we looked at the admittedly rather obvious question of why a pacing strategy exists. It's a question that is often dismissed as non-sensical and irrelevant with an obvious answer, but hopefully, it's possible to recognize that in fact, this question has profound implications for exercise physiology. First of all, it has no explanation according to the prevailing theory for fatigue. Secondly, it stimulates one to think a little more deeply about why such an obvious thing exists. In otherwords, is it conscious or sub-conscious, or perhaps even "pre-conscious"? Is it simply a function of training and experience? But then, how does training help you understand how to pace yourself? What is the mechanism?

In any event, the next step to take is to delve a little more into the issue, and I thought that two examples of fatigue-models might help to explain some lingering questions. Once again, I must stress that I have no definitive answer here - no one does. But it's a stimulating discussion, and we're working towards a model for fatigue which will be evidence-based (promise!)

So the two examples for today are the "leaky calcium channel" theory and the model of exercise in the heat.

The leaky calcium channel theory

Yesterday's post also introduced a theory that hit the news earlier this year, when scientists discovered that a possible cause for fatigue might be what they called "leaky calcium channels". The one sentence summary of this theory is that exercised muscle becomes fatigued due to calcium channels which become progressively more and more "leaky", causing the force of contraction to go down. It was a landmark study, and caused much excitement in the field, thanks to a somewhat sensationalized article in the New York Times. (This is, incidentally, a great example of how people will find "silver bullet" explanations for complex issues. Fatigue is not a problem waiting to be "solved", but it's reported this way, for admittedly understandable reasons. We certainly would not claim to have any answer so exciting and definitive!)

Consider for a moment the implications of this theory for endurance exercise - the best example is if you are doing interval training on the track. Let's say you're doing 5 x 800m repeats. If you ran without a watch, and your goal was to run the TOTAL SESSION as hard as possible, and you were running alone (very important - we'll look at how "social factors" influence pacing later in the series!), then I can almost guarantee that your pace will go FAST-SLOWER-SLOWER-SAME-FASTEST for the five repeats. It's the same pattern as we saw yesterday from Haile Gebrselassie and just about any other athlete doing self-paced exercise.

But the leaky calcium theory is saying that the reason you slow down and develop fatigue is that your muscles becomes less and less able to exert their normal force. Now, the key requirement for this to be true, which I hope is obvious to people, is that all the muscle has to be active. Because if there is any muscle that is INACTIVE, then that muscle would surely not be affected by "leaky calcium channels"? The inactive muscle could simply be activated and the pace would be maintained.

"Ah", you say, "but that's not an intelligent pacing strategy!". To which my response is "Yes, but please tell me how the body knows this, when the problem is a leaky calcium channel in the muscle? How is it even remotely possible in this explanation that you can be aware of the fact that your slow down is being caused by a tiny channel in the muscle?" The point is, in this system, there is no allowance for your perception or "intelligence", and surely intelligent pacing requires that you somehow KNOW what is going on with your body?

Therefore, pacing during endurance exercise is also incompatible with the calcium channel theory. Note that this DOES NOT mean calcium channels are not somehow involved, for a I believe they are. I said in the first post of this series, the trick is to balance the extremes, and we'll hopefully manage to integrate all the information moving forward.

So here's the thing - we know that muscle is not 100% active during your 10km race. In fact, even when you do your best to exert maximal force for FIVE SECONDS, there is evidence that you still keep some "reserve" capacity. We know that because if someone is doing a maximal 5 second contraction, and you stimulate the muscle using an electric current, the force can go up, so clearly what the person thought was "everything" was actually still sub-maximal! So a reserve is a universal feature of any voluntary effort, regardless of how hard you try. Now, given that fact, one can appreciate that it is impossible to explain how any biochemical change - lactate, hydrogen, leaky calcium - can force you to slow down, either consciously (intelligent pacing) or unconsciously (acting on the muscle).

Exercise and pacing in the heat: The best comparison between "limitations" and "regulation"

To illustrate this point before we move onto Part II, perhaps the best example of how the pacing strategy comes into play is during exercise in the heat. This is a topic we'll devote an entire week to later on, because the heat is the best example of a "homeostatic failure" model compared to a model for "anticipatory regulation", because it changes the INPUTS, as we spoke about yesterday. Perhaps this example should have been used instead of the "endspurt" question, because it's a lot more logical to work through.

Basically, there are two lines of thought for why exercise performance in the heat is compromised:

The "Peripheral" model for fatigue in the heat - failure causes fatigue

This theory says that fatigue in the heat is the result of a failure to keep the body temperature down. When the body temperature rises, it causes fatigue because the overheated brain is less capable of activating muscle to keep exercise going. This theory was first developed through a series of very novel research studies by scientists in Denmark - Savard, Nybo & Nielsen are the common names, for those who are interested.

Basically, what they have done is find that once the body temperature hits 40 degrees, the athlete:

1. Stops exercise - fatigue co-incides with this "limiting" temperature, hence the name "critical core temperature hypothesis for fatigue in the heat"
2. Activates less muscle - muscle must be stimulated to contract, and what Nybo and Nielsen showed is that the activation of muscle by the "hot" brain is lower than that by the "cool" brain after exercise
3. Has altered brain function - they measured brain waves during exercise and found that certain waves are altered, which suggests "reduced arousal" levels.

Their conclusion? Exercise is impaired in the heat because the body temperature rises until it reaches limiting values. At this point, the brain fails to activate the required muscle, and the athlete can no longer continue exercise.

A couple of key points: Firstly, there are a few details in the explanation of why the brain fails to activate muscle that we'll get into later. However, what is key to realise is that these studies, while excellent and crucial to our understanding of the heat, have failed to recognize that during any form of exercise, it is possible to slow down long before you stop! In other words, because these studies force people to exercise at a fixed power output until exhaustion, the conclusion they make is that fatigue is caused by some "failure". They then extend this finding to say that "impaired performance" is caused by the same thing, when in fact, they don't measure what happens BEFORE the limiting temperature is reached!

An anticipatory regulation model for exercise in the heat

The alternative model is that performance is regulated well before the limiting temperature is reached. For this to be true, it would require that the athlete slow down at sub-maximal body temperatures. And there is evidence for this - Frank Marino from Australia found it in runners, Stephen Cheung of Canada found it for small muscle groups, and I found it a couple of times in the heat in studies that have all been published (If you'd like these references, please let me know - I'm not going to include them in the text because it breaks the flow - there are some below, however)

Thus, the athlete should start slowing down even though the body temperature is not different from that in the cool condition. As a result of slowing down, the athlete would be producing less heat, and so the fall in work rate will ultimately produce body temperatures that are not different to those measured in the cool conditions! In otherwords, you don't slow down BECAUSE you are hot, you slow down in order to prevent yourself from getting hot!

Perhaps most interestingly, we've actually measured that LESS MUSCLE is activated during cycling in the heat than in the cool conditions. This was a study I did in 2004, and it will be discussed in detail later, but the key point was that cyclists in the heat slowed down very early on, when nothing measurable was different, and they did so by activating less muscle. That's completely incompatible with the "peripheral fatigue" model.

This will, I'm sure, be dismissed as obvious by many, but again, the crucial question is HOW is this achieved? To refer to yesterday's post, what are the inputs, how are they interpreted, and what is the output in response? These, and many more questions, are on the way.

Summarizing the models: A platform to move forward

The two diagrams below are concise summaries of the last two posts. The first diagram, directly below, shows what I have called "The homeostatic limitation model".

This model shows the following:

1. Muscle contraction during exercise is responsible for producing changes, including biochemical ones (leaky channels, fall in pH, lactate, phosphates etc), as well as changes to the cardiovascular system, energy system (glycogen is depleted and blood glucose falls), and thermoregulatory (body temperature rises, as discussed). The figure shows, from top to bottom: A mitochondria, the liver for energy supply, the heart, and body temperature.
   
2. These changes DIRECTLY inhibit exercise, either by:

• Causing the muscle to lose its force generating ability. This is the theory for lactate, phosphates, oxygen supply (the "anaerobic" limit to exercise) and calcium ions; or
• By acting on the brain to force the muscle activation levels down. This is the case with high body temperatures, as discussed briefly above.

The key to this model is that failure is responsible for fatigue. Something has gone "wrong", either with oxygen delivery, biochemistry, blood supply, or body temperature, and this has impaired the athlete's ability to exercise at the same pace, so they slow down. One very important point I must make is that this model makes absolutely no allowance for pacing - I've said this many times before, but there is no feedback from these systems that would allow the suggested "intelligent" pacing to take place!

The figure below shows the model for "Anticipatory regulation": Just a note to say that this is by no means the "definitive" model for anticipatory regulation (or the central governor, or anything else you may have heard it called!). This is just a summary of the last 3 posts, and as this series moves forward, I'll try to develop this in much, much more detail, until we have something hopefully more comprehensive

In this model, which was introduced yesterday, there are INPUTS and OUTPUTS.

The INPUTS are provided by the heart, liver (or energy supply), body temperature or rate of heat storage, biochemistry, and then, very importantly, the brain itself!

These INPUTS provide what is called afferent feedback to the brain, informing it of the situation. This feedback provides information on things like "How hot is it?", "How much energy is available today?", "What is the pH of the tissues?", "What is the heart doing?", and basically "Is it safe to keep going at this pace?".

In response, the brain integrates all this information, then evaluates it in the context of the exercise bout before enforcing some output on the system. Key to this evaluation is to know how far the athlete has gone, how far they still have to go, and a host of other inputs or "moderators". We'll discuss all these in turn. Regardless, the end result of this process is the OUTPUT - the activation or the inhibition of muscle. This is responsible for controlling the force output of the muscles, and hence the pacing strategy.

It's important to recognize the presence of the brain as an INPUT in this model. That is, the brain informs the brain (pardon the creative licence!) of certain key inputs before and during exercise. These include memory (the hippocampus, presumably, is the part of the brain involved), experience/training, and then crucially, social factors, or social facilitation. One cannot ignore these "conscious" cues that must also impact heavily on performance.

Also bear in mind that what you all know as true is that when you're in a race, you race with tactics and the presence of other athletes. There is no explanation for this, no mechanism, according to a "limitations" model...how would leaky calcium channels be integrated into racing? It can't be, because tactics and "intelligence" requires that the brain be involved...so you might actually be closer to this model than you realise!

Conclusion

So that is the model, which at this stage is just a theory, I admit! In the coming posts, we have to back-track a little, and look at pacing strategies, and then we'll move on to systematically evaluating and discussing each of the various INPUTS I've put forward. Importantly, we must gather the evidence, otherwise, this is all just conjecture! That evidence most definitely exists, and the next phase of this series will be to examine that evidence, logically and thoroughly. I'll be breaking it up into much smaller pieces, however, so don't worry, this is the last "mega-epic post" for a while!

Speaking of theory, we can now attempt to answer that most basic of questions that started this whole series: The "endspurt" is the result of an increase in muscle activation, controlled by the brain in response to numerous INPUTS during exercise. It occurs because the finish line is approaching, and the physiological changes are no longer deemed harmful or potentially limiting to continuing exercise. The reserve can thus be activated!

Stick with this, and hopefull that will evolve from being mere theory to fact!

Have a good weekend!

Ross

Some relevant references, for those interested:

• Savard et al (1988), J Appl Physiol 64: 649 - 657
• Nybo and Nielsen (2001), J Appl Physiol 91: 1055-1060
• Nybo and Nielsen (2001), J Apply Physiol 91: 2017-2023
• Nybo et al. (2002), J Physiol, 545: 697-704
• Marino et al. (2004), J Appl Physiol, 96: 124-130
• Marino (2004), Comp Biochem Physiol B Biochem Mol Biol 139, 561-569
• Tatterson (2000), . J Sci Med Sport 3, 186-193
• Tucker et al. (2006), J Physiol 574, 905-915
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Fatigue and Exercise Part I A

The pacing strategy - why the "obvious" is crucially important

On Tuesday, we introduced a new series on Fatigue and Performance, which, based on the comments and responses so far, promises to provide much food for thought, interesting discussion and a few strong opinions!

And thinking about the subject (see my thoughts at the bottom of this post), it's clear that the most difficult part of this whole series is going to be controlling the logical flow of the discussion. It's such a vast, enormous topic that it's going to be impossible to put across a vast amount of information without skipping over studies that some might consider relevant. That's the nature of science - if not, then every review article would have thousands of references! So literally, ten years of academic debate and research studies have to be translated into a (hopefully) understandable and readable summary! The only way to combat this is to stick to the plan we laid out two days ago, and so that means that many of your questions and comments might be quite relevant, and there will be "gaps" in the logic of each individual post, but hopefully, they'll all be answered eventually.

So with that on the table, knowing where to start is perhaps the most crucial thing of all - the first step on the journey (warning - it's quite a long post, so I have split it into two parts - the first is published today, the second will be published tomorrow! But you might want to read it in "shifts"!).

And I thought that perhaps I'd return to yesterday's post and the question I posed about pacing strategies and the mechanism for their existence. Today's post, then, is all about the pacing strategies, which are simultaneously the most obvious, the most complex, and the most important thing about fatigue and exercise performance.

What do we mean by pacing strategy? And why is it obvious? And important?

Yesterday's question involved pacing strategies, which anyone who has ever done exercise knows all about. In particular, we spoke about the "endspurt", which is the characteristically observed "kick" for the finish line in a race. I posed the question that if the athlete has the "reserve" to be able to speed up at the end, then what was keeping them from using that reserve earlier, and potentially running faster? (In hindsight, I probably could have chosen a better illustration of pacing strategy because people tend to dismiss this profound question rather frivolously, but there's plenty of time for all those questions to be asked!)

Take a look, for example, at the following two graphs. They show the power output during cycling (on the left), and the running speed during a 10km race (on the right):

This pacing strategy is, incidentally, typical of even the elite athlete. To let the cat out of the bag, the graph on the right belongs to a world-record performance - it is the 10km performance is that of Haile Gebrselassie when he ran his 10,000m world record of 26:22.75 in 1998. His final kilometer was run in 2:31.3, compared to high 2:37's and 2:38's before that. So even the greatest of the elite follow a similar strategy as a club-level cyclist - faster start, slowing in the middle, with an endspurt to finish. Obviously, the size of the difference is important, and the elite performance shows less variation than the club-level performance. Later in this series, when we discuss pacing strategies, we'll get to that in greater detail.

A "ridiculous" question with an obvious answer?

But let's get back to that question - Why the slow down in the middle, with the endspurt at the finish line? And what keeps the athlete from accessing the "reserve" sooner than the final kilomter?

Many say it's an irrelevant, absurd question, with an obvious answer. They dismiss it out of hand. Some of the typical responses are:

"It's obvious, because they know that if they ran faster early, they would not finish. It's training and experience, what a stupid question!"...or;

"It confuses me. To me what they are describing as "anticipatory regulation" is simply wise pacing." or;

"How can this question even be asked? Any person that has run seriously would not even ask it surely." The second and third responses are actual responses to this question, incidentally.

These answers reveal two things:

1. Academic exercise science is often quite far removed from "common sense",

Yes, it is actually obvious that people would speed up at the end. I'll never forget that having freshly graduated with Honours in Exercise Physiology, I was trying to explain to a very successful coach (Olympic champions in his group) the physiology behind performance. Having done my best rendition of the "truth", he nodded and said "Yes, well, we've known that since the 1970's, haven't we?". And he took me home, showed me a coaching book with worn pages saying pretty much the same thing...a humbling experience, to be sure!

However, as I thought about it, I realised that firstly, there was very little new under the sun (to quote Ecclesiastes) and so some humility was never a bad idea! But secondly, it was obvious that while people in coaching have always appreciated this endspurt and its meaning, those in the sciences have pursued quite a different course, developing a model that is incomplete and ultimately unable to explain this "obvious" endspurt!

We'll work towards explaining all that, but what people don't realise is that in exercise physiology, the usual explanation for fatigue is completely irreconcilable with this endspurt observation! So the answer, which might be obvious to athletes and coaches actually has no feasible explanation in academia!

So what is that irreconcilable theory?

If you spent time studying exercise physiology, you would be taught that fatigue is caused by metabolite accumulation/depletion, high body temperatures, or some other peripheral change, as we introduced yesterday. This suggests that fatigue (or slowing down - even the definition is contentious) is a result of some change in the muscle. You may have heard, for example, of the theory of leaky calcium channels. In this theory, fatigue happens when muscle becomes "leaky" to calcium, which lowers the contractile capacity of the muscle.

I'll go into this theory much more in tomorrow's post, but consider that this theory suggests that you'll be slowing down progressively during exercise as your calcium channels become more and more leaky. Why then, would you not simply use muscle fibres that were previously inactive in order to maintain the speed? The "endspurt" which is often dismissed as "wise pacing" shows clearly that those muscle fibres were available. Yet the athlete "chose" not to use the reserve until the very end, rather getting slower or holding the pace. Conscious? Yes, probably part of it is, but what is the physiology behind this? The athlete knows that if they don't slow down, they'll become even more fatigued? But the "fatigue" is in the muscle, how do they know this? There has to be a signal, and how do leaky calcium channels fit with the conscious decision?

The point is, from the perspective of some biochemical cause of fatigue, the "obvious" pacing strategy becomes very difficult, even impossible, to reconcile and explain. In that sense, you have to be "priviledged" enough to become "educated" before the obvious question becomes relevant! That's a problem with academia sometimes - can't see the wood for the trees, but hopefully understanding this question and its answers reveals some useful information for performance.

But, more importantly, those dismissive answers mentioned above reveal that:

2. We're still failing to acknowledge the mechanism for this observation.

It may well be a conscious decision to speed up and slow down - "wise pacing" as people say. But apart from the fact that I'm not convinced it's simply a "decision", this is also not a mechanism, it's a description. When people dismiss the question as irrelevant or obvious, and say they know the answer, they never really give it, because the mechanism requires that we explain HOW the athlete knows to slow down?

And it's not enough to simply palm it off on "training" and "experience"! HOW does training alter pacing? How does experience influence the decision to slow down and speed up? Based on what INFORMATION is the "decision" made - time, distance, memory, pain? If you can honestly say that when you ran your last 10km race, you were consiously comparing it to the one you did in March, I'll take my hat off to you! So yes, I acknowledge it's pacing, but have you ever wondered how pacing is achieved? That's the question here, and I hope that this post so far has demonstrated that a biochemical cause of fatigue is not compatible with pacing.

Speaking of the "decision", is it conscious, or sub-conscious, and does it matter? In other words, does the athlete literally DECIDE to slow down through a process of rationalization and discussing it with himself: "Mike, time you slowed down now, because if you don't, you'll be in trouble at the 8km mark". But again, HOW does Mike know this? Or does something else cause that slowing down via an independent mechanism the athlete is not aware of?

The key concept - a co-ordinated system with INPUTS and OUTPUTS

All relevant questions, but the one with most merit is this:

What cues, what signals, what experiences, what training, and what physiology are responsible for enabling the athlete to consciously slow down in the middle, and then speeding up at the end of a race and still optimize performance?

Remember, the athlete is still running as "fast as they can" for the distance - Gebrselassie finished his 10km race having gone as fast as he could, just as you probably did in your last 10km race. So you finished, having balanced the requirements to avoid any limit to exercise with the requirement of running as fast as possible. Here, we have to also make mention that some people don't get it right - they start too fast, or too slow, fail to finish, and we'll discuss why that happens at some stage. But in general, most people, if left to their own devices and time-targets, will come very close to running an "optimal" race while still avoiding the physiological failures we introduced yesterday!

And here's the crux - the pacing strategy is the OUTPUT, the work done by the muscles, which are instructed to contract by the brain. But in order to produce this conscious decision to modify the OUTPUT, something (in the brain, you'd think?) must be taking into account a wide range of INPUTS in order to generate that conscious decision.

So, far from being dismissed as an obvious conscious decision, understanding the pacing strategy is going to give us insights into two key physiological features:

1. Inputs which will consist of changes in the periphery that ultimately have to be defended or regulated. One can quite easily appreciate how changing these inputs might alter performance. Therefore, if training and preparation can alter performance through these inputs, then understanding them is incredibly useful. In this series, the most interesting input to look at is HEAT, but we'll also spend some time on ALTITUDE, DIET/ENERGY, and also DECEPTION, when athletes are "tricked" into running or cycling further or shorter than they expect.

2. Outputs, which are going to comprise the muscles, which must of course be stimulated by the brain - remember the sequence is that muscle contracts only when stimulated to do so. So when the athlete slows down, there are only two possible causes: Either the muscle is fatigued and cannot do its job any longer (the peripherial model), or less muscle is being activated. The analogy here is that if you and five men are carrying a Grand Piano, it gets heavier either because each of your six-man team gets weaker, or one or more of your team leaves, leaving the rest of you to do the work. You'd slow down in response.

3. The set of inputs and outputs must be interpreted, co-ordinated and responded to. I'm sure it's not difficult to appreciate that this job must be done by the brain, and not some "little green Martian" as some have sarcastically joked in previous discussions!

Now, if this sounds suspiciously like a homeostatic loop for all of you with some biology training, you'd be 100% correct! For those who don't know, "homeostasis" is just a fancy term for the system which maintains the internal "balance" of the body - signals in, outputs out, all designed to regulate the system.

Also, if you want to call this the Central Governor, that's fine. As I wrote on Tuesday, I'm going to steer clear of this term, because it is too easily misconstrued as a centre or a "black-box" with a specific location in the brain. It's not that at all - if you look at the ten paragraphs above, we've already introduced at least four aspects of it, which would involve perhaps four areas of the brain that could contribute, and so to pin-point one location is a futile task. So I'll go with "Anticipatory Regulation" for this series, and hopefully, this post has portrayed this anticipatory regulation as more than a simple conscious pacing strategy. That pacing strategy is in fact merely the output component of a very complex, very interesting physiological system.

Wrap-up of Part I A - more to follow tomorrow...

That's it for the first part of Part I. As I said, I'm mindful that these are "epic" articles, which might be testing your own "fatigue" just to read them! I do apologize, but hopefully you are able to break the article up and squeeze some time out to get through it. I'd rather be "longer" and more detailed than make the mistake of cutting out valuable information, so do bear with me! The one consolation for you is that because they take so long, I'll only post once every two or three days, so there's time to grind through it!

Join us tomorrow for the conclusion and an example of what we've discussed today, taken from exercise in the heat!

Ross

P.S. The paragraph below is just some musings after reading some rather heated responses to this kind of discussion - thought I'd issue a call for "open debate"! It's not crucial to read!


Last word: Debating the issues moving forward

Last night, I read through a discussion forum on LetsRun.com, where the topic of the "Central Governor" was being discussed. It was quite clear from this forum that the fatigue issue will attract its fair share of opinion, argument and debate. And that's fantastic - it is, after all, the reason for our existence! However, what I would like to request is that any debate be done with an open mind, regardless of which side you're coming from.

The discussion on LetsRun reveals a characteristic trait of people - they approach debates with their minds already made up, and little can convince them to even listen to any other possibilities - we're all that way, to some extent. Our goal with this (or any other) series is not to change minds or win people over, but rather to encourage the recognition that if your perception is ever shown to be incomplete or incorrect, then by listening to others, you may improve your own understanding enough to move nearer to the "right" answer (whatever that may be!). The problem for many people is that the debate tends to rapidly degenerate into a situation where the facts are no longer discussed, and instead, abuse is hurled back and forth - let's hope that this series doesn't provide the platform to create this situation, as it did on the forum mentioned above!

So with the hope that it doesn't, and as I said in a response to a comment in the previous post, bear with us having to attempt to summarize literally thousands of articles and ten years worth of debate into a month-long series! Also, we're not here to indoctrinate, but to gradually work through a very complex topic, which, as I said, could literally be written as a dozen PhD theses (and has been!)