Overtraining, Overeaching and all the Rest Part 6

Having finished my tedious definition of overtraining in previous parts of the series, I moved onto more practical issues and looked at two different ‘types’ of overtraining in Overtraining, Overeaching and all the Rest Part 5 on Tuesday.  In that part, I examined the idea of a parasympathetic (aka A-type or Addisonic) and sympathetic (aka B-type of Basedowic) overtraining.

I finished by listing a handful of common symptoms of overtraining with the list deliberately meant to demonstrate that some of the symptoms appear to be relegated to muscle and the others to the brain or more central parts of the body.  I’ll pick up there today by looking at another common distinction of overtraining ‘types’ and then look a bit more at what ’causes’ overtraining to try to tie all of this together.
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Type of Overtraining Part 2: Central vs. Peripheral

For reasons primarily of practicality and convenience, the body is often divided rather roughly into central (meaning the brain and central nervous system) and peripheral (muscle and peripheral nervous system) systems.  While this helps simplify discussions, it’s critical to realize that the systems aren’t separate in the least.

As I discussed in a very different context in the article Dieting Psychology vs. Dieting Physiology, the central and peripheral systems are interacting and communicating with one another constantly. In the case of eating behaviors and body weight regulation, the gut, fat cells and everything peripheral is sending signals to the brain (about such things as how much you’re eating, energy balance, fuel utilization) and the brain is sending signals back out or adapting to them (e.g. making you hungry if you’re dieting, slowing metabolic rate, etc.).

In the case of the body and training, while the brain is sending signals to the muscles about how to contract or what to do, the muscles are sending signals back to the brain (about energy store, damage and other factors).  Separating the two systems may be convenient for discussion or study but it’s ultimately wrong; I’ll come back to this at the end of today.

In any case, in the early days of overtraining, there was an idea that central overtraining and peripheral overtraining were distinct entities and that different types of training would impact on/cause each.  And certainly there is an element of truth to the idea.  We all know, having read the Internets, that certain types of training tend to ‘stress’ the central nervous system more than others; and certain types of training tend to stress the muscles more.

But it’s not as if it’s one or the other; it’s simply an issue of proportion (e.g. 20 rep squats are stressful all over and studies actually show a great deal of neural stress from what usually thought of as muscular training).  All training has effects on both muscles and nervous system factors just to different degrees.  That’s on top of the communication going on between the two.  Put differently, it’s critical to realize that the muscles ‘talk’ to the brain in the same way that the brain ‘talks’ to the muscles.

But ideas that you couldn’t overtrain so long as you rotated what muscles you trained every day or that you could only overtrain with certain types of training did become entrenched in the lore of training because of this artificial separation.  And it caused people to make some big mistakes.

As a singular example, Fred Hatfield not only wrote that central overtraining didn’t exist, but that you could train as much and as hard as you wanted so long as you alternated muscle groups.  That is, so long as you avoided local overstress of a given set of muscles, you were fine because there was no such thing as central overtraining.  Sadly he was completely and utterly wrong as many who tried to follow his ABC system found out the hard way.

Going back to my time in SLC, I saw a fantastic example of this, again with the Russian coach who had buried our team in volume; he believed that it was impossible to overtrain if you weren’t doing training that stressed the cardiovascular system.  So long as it was just local muscular work, he felt you were fine.  Which is an idea that got discredited by probably the 1980’s or so; sadly he hadn’t learned anything new since the 70’s.

Because of this belief, he then proceeded to destroy Eva as, despite her constantly telling him that she was becoming overtrained (she had all the symptoms), he ‘knew’ that it was impossible.  They weren’t doing central work and, in his mind, that made overtraining impossible.  All because of a 30 year old discredited idea and the fact that he was a moron.

Again, there is certainly some merit to the idea that peripheral and central fatigue/overtraining do have distinct causes or at least manifestations, which I’ll come back to in a second, but at the end of the day you can’t separate the two out in the simplistic fashion that many have done.  Everything is literally communicating with everything else.  Central versus peripheral systems or overtraining (or fatigue) can be a separation of convenience, just keep in mind that it’s not a separation that exists in reality (or ‘for reals’ as the kids say these days).  You’ll see why I’m beating this particular dead horse so hard in a moment.

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What Causes Overtraining Redux

In Overtraining, Overeaching and all the Rest Part 3, I presented the idea that the global ’cause’ of overtraining was a long-term imbalance between training (and other) stressors and recovery processes.  While that’s useful in a practical sense, it doesn’t get to the real root of the matter; that is, what at the biological/physiological level is causing the problem.  As I noted, those processes may be useful to delve into if they help on a practical level.  Perhaps they let us modulate diet, or supplementation (or drugs), or training structure or what have you.

So what, at the end of the day ’causes’ overtraining?

For decades researchers have looked for an answer and many ideas have been tossed around.  An early one was simply glycogen depletion, it was felt that insufficient carbohydrate was leading to progressive glycogen depletion and that caused the problem.  And some studies seemed to bear this out, glycogen would get depleted over the course of a hard training week and the athletes would start to show early signs of problems.

The idea certainly looked good on paper but studies where glycogen levels were maintained with high-carbohydrate intakes in the face of a heavy training still couldn’t prevent underperformance.  Glycogen depletion wasn’t helping but simply maintaining glycogen levels wasn’t sufficient either.  It might have been part of the issue but it wasn’t the whole issue.

A myriad other things have been looked at and many of the biological things that researchers look at (such as the free testosterone/cortisol ratio) are probably more markers of overtraining than causes per se; that is they indicate that recovery isn’t keeping up with stress but aren’t actually causing the problem.

It didn’t help that some of the factors being looked at were central, changes in neurochemistry and such that occurred.  That was on top of the observations that many of the manifestations of overtraining seemed to be emotionally or brain based as much as they were muscle based.

It was hard to figure out how all of these disparate pieces of data fit together to explain what caused overtraining.  That is, how could all of those different symptoms of overtraining, some of which look emotional/behavioral and some of which look muscular, be linked.  And then someone finally figured it out.

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The Cytokine Hypothesis of Overtraining

The most comprehensive model of the cause of overtraining that I’ve seen was presented in a paper titled Cytokine hypothesis of overtraining: a physiological adaptation to excessive stress? by LL Smith (he’s written several others in a similar vein).  In it he examined all of the different data points that had been developed over the years and built up a model of overtraining that I think is on the right track.  It may or may not be the entire picture but, at this point in the game, I think it’s the best model we have to explain all of these different data points.

Now, for background, cytokines are small, fairly short-lived chemical messengers that do a lot of different things in the body.  As a singular example is something called IL-6 or Interleukin-6.  Released from skeletal muscle and fat cells, IL-6 does a number of different things.  Acutely, it can increase fat oxidation (and IL-6 is released in response to glycogen depletion); chronically it causes inflammation.

IL-6 can also cause fatigue during exercise and it does so by altering neurochemistry in the brain.  So under experimental conditions, even if someone is well rested and such, if you inject IL-6 into them, their exercise performance goes down and they will report fatigue and lethargy.  And IL-6 does so by altering brain function and neurochemistry.  In other words, IL-6 is a chemical released from skeletal muscle that goes to the brain and makes you fatigue sooner than you otherwise would.  Now we’re onto something.

There are dozens of cytokines doing all kinds of things in the body and they are probably all interacting in horribly complex ways that it will take researchers forever to figure out (this keeps them off the streets and out of scientist gangs).  But cytokines and how they work provide one mechanism by which one area of the body (for example, skeletal muscle) can communicate with others such as the brain.

An easy to understand example that most are familiar with is what happens when you get the flu: you get achy muscles and joints, you lose your appetite, you want to sleep all the time.  Basically, the immune system response in one part of the body causes this cytokine response that goes to the brain and makes you feel crappy so that you’ll rest and get over being sick.  The peripheral response has an additional central manifestation, you don’t just get achy muscles and joints but your behavior changes in a way that hopefully gets you to rest up and get over being sick.

Your body is smart sometimes.  Unfortunately, people are sometimes not so smart.  But whereas people will rest when they have the flu, as I noted in Overtraining, Overreaching and all the Rest Part 4,  athletes often continue hammering themselves even in the face of this mounting fatigue and lethargy.  If they were sick, they’d take time off; faced with underperformance, they often train harder.  And they dig the hole deeper.

And this turns out to probably explain a lot about the disparate symptoms of overtraining.  Essentially, the paper I cited above took all the data and developed a model whereby chronic overwork of muscles and joints (in the face of insufficient recovery) causes a systematic inflammatory response in the body; studies have found an increase in a variety of inflammatory cytokines.

In addition to giving you that feeling of achiness, the cytokines released go to the brain and make you lethargic, sap motivation, depress you (or make you hostile depending on your overall personality type), blunt appetite, etc.  They do this by screwing with your neurochemistry.  Those changes then impact on your exercise performance because the signals sent to your muscles to do work is now impaired.  It’s just one big loop.

The chronic peripheral stress/damage/inflammation is the cause of the behavioral issues, mediated by shifts in the chronic levels of inflammatory cytokines.  Basically, it’s your body trying to tell you to knock it off, rest and recover by making you feel like crap.   But as noted above, whereas most people will rest when they are sick, certain athletic personalities interpret underperformance as a need to train harder; they ignore the feedback signals that their body is giving them and do more damage.  Which becomes a different kind of loop: excessive training leads to underperformance which drives more training which further harms underperformance which…..

Beyond that, the idea that central and peripheral overtraining are separate entities is simply wrong.  Rather, the chronically heavy training leading to underecovered/chronically damaged muscles leads to this inflammatory response that causes the central effects (fatigue, lethargy, depression).  It seems to explain most of what’s going on although newer data may develop a more complete model.  I doubt it will fundamentally change this one, it may simply add to it somewhat.

But that rather simple concept, that the muscles and brain are in constant communication with one another seems to wrap the overall set of data points on overtraining into a rather neat little package.  As I noted, many of the observed changes (e.g. biochemical) are probably secondary to the other changes but, at the end of the day, it’s constant heavy loading on muscles and joints that causes a systematic inflammatory response that, in addition to making your muscles feel bad, sends signals to your brain that inhibits you globally.

Hormones go whacky, sleep is disrupted, you get depressed or hostile (researchers have used the Profile of Mood States or POMS to try to measure overtraining for years, and certain characteristic changes occur with overtraining), lose your motivation, reaction time goes down (some have likened overtraining to chronic fatigue syndrome), etc.   It’s a shockingly simple and neat model but seems to explain most of what’s been observed over the past 30 years and all of the differently observed levels (muscular, neural, neurochemical, behavioral).

And that’s where I’ll wrap up today.  In the next one or two parts, I’ll wrap up and look at how to use some of this information to both avoid/prevent overtraining, deal with it when/if it happens and all the rest.

Read Overtraining, Overreaching and all the Rest Part 7.

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