Central Governor Model

[Robh]

A review of Professor Noake’s Revolutionary Model of Performance

Part 1

Introduction

The most enduring model of endurance physiology is the Cardiovascular/Anaerobic model. Initially suggested by British physiologists A.V. Hill and associates in the mid-1920s, this model has been promoted by scientists, coaches, and athletes world-wide for nearly 80 years. This model basically posits that a lack of oxygen to working muscles is what ultimately limits exercise performance. Most adherents to this model use the terms VO2max, lactate threshold, and running economy when discussing training or physiology; terms which are used to describe particular aspects of this model. Though this model continues to be accepted today by most runners and coaches since the 1970s an increasingly large body of research has challenged the validity of the cardiovascular/anaerobic model. However, despite the increasing volume of evidence against it, the model has persisted as the primary model of endurance physiology.

I believe the main reason the cardiovascular/anaerobic model has persisted in the face of the large body of evidence to the contrary is that no other comprehensive model of endurance physiology has been proposed. So, while the deficiencies of the cardiovascular/anaerobic model are well known, the absence of another model to replace it has allowed continued support for the cardiovascular/anaerobic model.

Recently one of the primary opponents to the cardiovascular/anaerobic model, noted researcher and author Dr. Tim Noakes, proposed a new, revolutionary, comprehensive model of endurance performance that he has termed the Hill/Noakes Central Governor Model. The existence of a physiological governor was first suggested by A.V. Hill, the same physiologist credited with the cardiovascular/anaerobic model. However, Hill’s idea of a physiological governor have been overlooked or ignored by those supporting the cardiovascular/anaerobic model attributed to him and hence, remained in obscurity for many years. During a review of Hill’s original work Dr. Noakes re-discovered Hill’s governor theory. Intrigued by the idea, Dr. Noakes reviewed existing research and conducted new research designed to test the validity of Hill’s theory. The compelling results of his research combined with the previous unexplained results of prior research convinced Dr. Noakes of the accuracy of this model. He substantially updated the model and introduced it to the physiology world as the Hill/Noakes Central Governor Model.

I believe that his new model may well be the missing ingredient that will finally cause the abandonment of the cardiovascular/anaerobic model. As Dr. Noakes said to me, it will become increasingly difficult to continue to support the cardiovascular/anaerobic model and that at a minimum his new model clearly delineates the battle lines such that people will have to decide which side of the line they care to take. If this is correct, then in the next few years we will see a large migration of scientists, coaches, and athletes to the Central Governor Model. Undoubtedly accompanying a change in belief in the underlying physiology will be changes in accepted training methods. How significant those changes may be remains to be seen. If Dr. Noakes’ model is truly the heir apparent to the cardiovascular/anaerobic model I thought it would be appropriate to review his model, its training implications, and to compare and contrast it with my power running model of performance. We begin with fatigue.

Fatigue Defined

What causes muscular fatigue? Why during the final miles of a long run or race does it become increasingly difficult to maintain a set pace? Why can’t runners maintain maximum speed for an entire 100 meter sprint? Why do high ambient temperatures affect performance so dramatically, especially in the later stages of a race? These and other examples are all evidence of fatigue, but they don’t tell us what is causing the fatigue. Scientists have long sought the causes of fatigue. However, before we can fully discover what causes fatigue, we have to properly define fatigue.

The traditional definition of fatigue used by physiologists is an inability to either continue a pre-defined amount of work or equal a previous level of work, despite a strong desire and effort by the subject to do so. It is common for researchers to have subjects exercise at some set work load, say a pace that initially equals 80% of VO2max, and when the subject can no longer maintain that pace they are said to have fatigued.

While that definition is a good as far as it goes, it doesn’t go far enough. Even though a subject may not be able to maintain a set work load they can continue at a lesser work load, i.e. the pace slows but the subject continues. The point being that outside of death fatigue is not absolute. A subject is not either fatigued or not fatigued. Fatigue falls on a scale, with greater or lesser amounts. The subject can always continue, albeit at a slower pace. Saying a subject is fatigued because they can’t maintain a pre-determined level of output is not incorrect, but it doesn’t account for the fact that the subject could continue at a new, slower pace.

Where does fatigue occur?

Now that we have established that fatigue is not an absolute event and is instead a relative event -you could even call it a pacing strategy - we have to determine where fatigue occurs. Do the muscle fibers themselves become fatigued and not contract as quickly and/or powerfully or is fatigue occurring elsewhere and then interfering with the muscle contraction? Perhaps it is occurring in multiple locations at the same time? These are very important questions to answer accurately in order to determine the cause or causes of fatigue.

Muscles contract because they receive a signal from the brain that causes them to contract. If they do not receive the signal they don’t contract. The brain controls physical activity by the signals it sends to the muscles. If a higher workload is required, the brain alters its signal and activates more fibers. If a lesser workload is desired, the brain alters the signal and reduces the number of fibers activated. This is the basic process of muscle contraction.

If the muscle fibers are the singular point of fatigue during exercise then as the muscle fibers fatigue the brain, in order to maintain work rate, would need to activate an increasing number of muscle fibers, eventually activating 100% of the fibers in order to maintain the desired workload. At the point that 100% of fibers were fatigued, then the workload would necessarily decrease despite attempts by the brain to the contrary. The fatigued fibers simply would not contract as quickly or powerfully as before, resulting in a drop in power output and a slowing of the pace. So, if fatigue is a muscular phenomenon we should see an increasing mass of muscle fiber being activated as exercise continues, cumulating in 100% fiber activation at the end of exhausting exercise.

What would cause muscle fibers to fatigue? It could be many things including a weakening of the contractile proteins within the muscle fiber, lack of oxygen within working fibers, increased muscle fiber acidity, hypoglycemia, heat buildup within a fiber causing a decrease in contractility – all of which have been pointed to as a source of fatigue - or it could be any number of other things not yet identified.

A competing theory would be that fatigue occurs elsewhere in the body and interferes with the contractile function of the muscles. For example, if the central nervous system were fatiguing during exercise the signals it produces and sends to the muscles, commanding them to contract, could be weakened or delayed resulting in a de-recruitment of muscle fibers.

To test if the muscle fibers themselves are the root location of fatigue we would only need to measure muscle activity during exhausting exercise and determine if an increasing mass of muscle fibers are being activated. This is exactly what scientists have done. Scientists can measure muscle fiber activation and studies that have done so have established that an increasing volume of muscle mass is not being activated during exercise and that 100% of available muscle fibers are not activated at the end of exhaustive endurance exercise. Instead, the number of muscle fibers activated falls during exhaustive exercise. For example, a team of researchers examined power output and muscle fiber activation during a one hour cycling time trial (1). During the course of the test the researchers intersperse 6 maximal one minute sprints. Power output and muscle activation decreased steadily from sprints 2 – 5, despite the effort of the cyclists to perform to their maximum ability. The drop in muscle activation and power of the subjects demonstrate that central drive to the muscles was decreasing, not increasing.

Interestingly, in contrast to an increasing drop in power and muscle activation in sprints 2-5 during the 6th sprint, which was conducted in the last minute of the time trial, power output and muscle activation increased significantly. (A last minute surge by competitors at the end of a race is a commonly observed occurrence in endurance competitions, especially cycling, hence the researchers placement of the 6th sprint.) If the muscles themselves had been fatigued the cyclists would have been unable to suddenly increase power output. So the evidence points away from muscle fatigue as the source of fatigue during exercise. This is not to say that muscles don’t fatigue, only that decreases in work output that define fatigue is not driven directly by muscle fiber fatigue.

If fatigue is not found primarily with the muscle fiber itself, then what causes fatigue? While the data points away from muscle fiber fatigue as the singular source of fatigue it does point to the brain as the source of fatigue. The drop in muscle activation suggests that the central drive to the muscles has decreased. The sudden return of both power output and muscle activation during the 6th and final sprint is evidence that there is at least some conscious influence of central drive. With the knowledge that the end of the sprint coincided with the end of the time trial the cyclists could consciously influence the subconscious brain to provide a final all-out effort resulting in a suddenly increased power output.

These observations from this and other studies led Dr. Noakes and his associate, Alan St. Clair Gibson, to devise a new definition of fatigue that stated

“…fatigue is actually a central (brain) perception, in fact a sensation or emotion and not a direct physical event. This stems directly from our interpretation that exhaustion results from changes in central (brain) commands to the muscles, rather than as a result of changes in the muscles themselves.”(2)

Essentially they are saying that the central nervous system (brain) reduces force output by reducing neural drive to the muscles. The reduced drive results in a reduction in the number of motor units activated during exercise. In other words, the brain itself is the source of fatigue. Additionally, the feelings of fatigue that a runner consciously senses during exercise is an emotion or sensation sent by the sub-conscious mind to the conscious mind. Though you may feel like your legs are fatigued the origination of that feeling of fatigue is your brain, not your legs.

Central Governor Model

With the definition of fatigue now centered on central control rather than something occurring within the muscles, the next topic to be addressed is why does the brain reduce its neural drive? Is the brain itself becoming fatigued or are other things influencing the brain to decrease drive to the working muscles? How does the brain know when to de-recruit fibers? How does it determine what lower level of fiber recruitment is appropriate? How does the brain go about selecting the appropriate pace for any particular event?

There is good evidence that the brain reduces its neural drive in order to protect the body from irreversible damage. Basically the brain subconsciously monitors the status of all systems of the body, continuously computes the metabolic costs to continue at the current pace and compares that to the existing physical state. Based on this information the brain adjusts the optimum pace so that the event is completed in the most efficient manner while maintaining overall body homeostasis and a reserve of physical and mental capacity. The brain protects the body by regulating power output during any form of exercise with the ultimate goal of maintaining homeostasis and protecting life.

An example of this process would be a slower pace during events with high ambient temperatures. Runners have long known that if the outside temperature is high that the running pace will be slowed due to the heat. Previously this phenomenon has been unexplained by the cardiovascular/anaerobic model except to say that the runner has to slow down to prevent over-heating. Conversely, the Central Governor model is able to successful explain this well-known fact. The brain calculates the build up of heat due to the high ambient temperature and then selects a slower pace requiring a lesser power output, resulting in less internal body heat being generated. In this manner the brain protects the body from the dangers of over-heating.

Research studies provide evidence of this process. In one study scientists continuously measured the heart rate of cyclists during a 104 km cycling race (3). The researchers discovered that the cyclist’s heart rate, which is commonly used as a measure of exercise intensity, increased and decreased in an apparently random manner in all the subjects continuously throughout the event. These changes were not solely related to geographical changes along the race course either. During times when the course was flat the random changes in heart rate continued to occur. These findings are consistent with the brain’s on-going calculations of the known remaining distance to be covered and the physical state of the cyclists and then adjusting power output (and hence pace) accordingly. The findings of this study have been confirmed in another study of professional cyclists during the three-week Tour of Spain (4).

Summary

Based on the evidence the Central Governor Model suggests fatigue is a relative condition, not an absolute one – i.e. the athlete can always continue but at a slower pace. Muscle fiber power output is not regulated by factors in the muscle itself but is continuously reset by the brain based on continuous computations of the sensory feedback it receives from all of the body’s systems. Fatigue is a relative process as exercise intensity is constantly changed during exercise as the brain either recruits additional fibers to increase power output or decreases fiber activation to decrease power output based on its calculations.

In part 2 we will compare the Central Governor Model to the Power Running Model.

Reference:

1. Kay D, Marino FE, Cannon J, St Clair Gibson A, Lambert MI, Noakes TD. Evidence for neuromuscular fatigue during high-intensity cycling in warm, humid conditions. Eur J Appl Physiol. 2001 Jan-Feb;84(1-2):115-21
2. Noakes, T. Lore of Running, 2004, pg 147
3. Palmer G, Hawley J, Dennis S, et al. Heart rate responses during a 4-day cycle race. Med Sci Sports Exerc 1994; 26:1278-83.
4. Rodriguez-Marroyo J, Lopez J, Avila C. et al Intensity of exercise according to topography in professional cyclists. Med Sci Sports Exerc. 2003; 35:1209-15


part II
Exercise Physiology

The Science of Performance

Central Governor Model

A review of Professor Noakes' Revolutionary Model of Performance

Part 2 – Integrating Power Running into the Central Governor



Introduction

In part 1 of this review we established the basis for the Central Governor Model – namely that exercise performance is controlled centrally, by the brain. At its essence the central governor model holds that the brain continually monitors all of the body’s systems and uses the data to calculate the maximum rate at which exercise can be performed while preserving and protecting the body from irreparable harm or death.

In the article “Muscles Limit Performance” I built the case that muscles exert the greatest influence on performance. In that article I cited two research studies that found that distance running performance could be accurately predicted by both sprinting and jumping events. Specifically these studies found that 20m sprint times were a better predictor of 5k performance than VO2max and that the 50m sprint, 300m sprint, and plyometric leaping performance were excellent predictors of 10k run performance. In fact, plyometric leaping performance was a single better predictor of 10k performance than VO2max and was as good or better at predicting performance than lactate threshold (plyometric leaping is similar to the triple jump except that it is performed from a standing rather than running start).

Using these two studies I argued that even though sprinting and jumping are anaerobic events their surprisingly potent ability to predict long distance performance indicates that whatever limits performance at sprinting and jumping must limit performance at endurance events too. I asserted that since muscle contractility is the only factor common to sprinting, jumping, and distance running that these studies support my contention that muscle contractility limits both sprinting and endurance performance.

The question arises then – does the central governor invalidate my power running model of performance? If the brain centrally controls muscle fiber activation rate then doesn’t that suggest that the central governor overrides any influence that muscle contractility has on performance? Or at a minimum that muscle contractility is secondary to central control at least in terms of the primary influencer of exercise performance? Let’s explore these questions in more detail.

Integration of Muscle Power and the Central Governor

To answer these questions let me use the following analogy. It’s not a perfect analogy but it is close enough to make my point.

Imagine that we have two motorcycles – one with a 125 cubic centimeter (cc) engine and the other with a 250 cubic centimeter (cc) engine. Both engines have governors which prevent the engines from running at excessive rpms and destroying themselves. Without a governor the 125cc engine makes a peak of 30 horsepower (hp). Due to its 125cc larger displacement the 250cc engine makes a peak of 40 horsepower (hp) without a governor. However, since both engines do have governors they are prevented from making peak horsepower. The governor on the 125cc engine is set so that horsepower peaks at 25 and on the 250cc engine the governor kicks in at 35 horsepower.

The motorcycle manufacturers set the governor at very conservative levels before they deliver the motorcycles to the consumer – hence the reason the 125cc makes only 25 horsepower as delivered and the 250cc makes just 35 hp as delivered even though they are capable of 30 hp and 40 hp respectively. With a little knowledge and a few tools you can modify the governor on either bike so that either one comes much closer to reaching its peak horsepower. With some modifications of their governors, the bikes would reach about 28 hp and 38 hp respectively. Of course, if you removed the governor the 125cc bike would achieve its max of 30 hp and the 250cc bike would achieve its max of 40 hp.

Despite being able to modify the governor you can not make the 125cc engine produce the same 40 hp that the 250cc engine makes. No matter what changes you make to the governor of the 125cc engine that engine will not produce 40 hp. In fact, due to its inherent design characteristics even if you removed the governor the 125cc engine is not going to produce 40 hp. With extensive engine modifications the 125cc engine will produce at most about 35 hp and then the lifespan of the engine will be severely shortened due to the immense strain it endures to produce that much horsepower. Due to its greater displacement advantage the 250cc engine will always be able to produce more horsepower than the 125cc engine.

Though you can modify the governor so as to allow the engine to work closer to its current maximum, ultimately, to go significantly faster will require engine modifications. Increase the displacement of the 125cc engine, to 150cc or 200cc for example, and you instantly have more hp and a faster motorcycle.

How does this relate to our bodies? The motorcycle is analogous to our bodies – our muscles are the human version of a motorcycle engine and our body’s central governor serves the same purpose as the motorcycle governor. Our muscles produce the power while the central governor ensures our muscles don’t work so hard so as to become permanently damaged. And like the governor on the motorcycle, the human central governor is set by the factory at a conservative level. And just like the motorcycle governor, with the proper knowledge and the right tools the human central governor can be re-set to a higher level.

This then is the integration of the muscle power model and the central governor model. Your muscles are the engine of your body and there is a maximum amount of power they can produce. The central governor regulates power output, preventing the muscles from working at their maximum level for extended periods so as to protect the body from permanent damage or death. The central governor regulates power output so that the task at hand is completed in the quickest, most efficient manner while maintaining a reserve of physical and mental capacity. The central governor can not cause muscles to produce more power than the muscles are capable of – it can only regulate the available power output.

These two physiological models – muscle power and central governor – are not in conflict and the central governor model does not invalidate the muscle power model. Instead they are complimentary, working together to maximize efficiency while maintaining homeostasis. Indeed, even Prof. Noakes addresses the issue of the integration of the muscle power model and the central governor model.

Before proposing his central governor model, Prof. Noakes believed that muscle power played a primary role in performance. In the 1991 edition of his book, Lore of Running, Prof. Noakes writes, "My personal bias is that the rate of oxygen transport is not the critical factor determining exercise performance. Rather, I suggest that the best athletes have muscles with superior contractility..."(1) Even more definitively, he writes, "A muscle factor determines running performance at any distance."(2)

Prof. Noakes beliefs about the role of muscle in endurance performance were modified with the introduction of the central governor model. In the updated 2003 edition of his book, Lore of Running, Prof. Noakes first introduces the running community to his newly formulated central governor model. He articulates the integration of the muscle power and central governor this way, "I interpret these findings to indicate that muscle and neural (brain) factors contribute to running performance at any distance." (3) Prof. Noakes has clearly modified his beliefs about the role of muscle power in performance and integrated the muscle power model into his central governor model .

Training Implications

What are the practical implications of the integration of these two models? First, in order to perform at your maximum your training will need to improve both the total power output of your muscles and re-set your central governor so that it allows greater power output prior to kicking in.

To increase muscle power, recall our power formula from the “power running” series.

Power = strength + contraction speed + muscular fatigue resistance + metabolic fitness

We can substitute “central governor” for the term “metabolic fitness” in our power formula since they are basically the same thing, leaving us with the following:

Power = strength + contraction speed + muscular fatigue resistance + central governor

Improve any of the first three factors – muscle strength, muscle fiber contraction speed, muscular resistance to fatigue - and the overall power output of your muscles will increase. Using our motorcycle example, an increase in any of these three factors will result in an increase in the total horsepower of your muscles. Review the series “power running” and “muscle contractility” for recommendations on how to increase any of these three factors.

Re-setting the central governor so that it allows a higher power output before it is tripped is best accomplished by training specificity and intensity. The more specific your training the more precise your central governor will be in determining the most effective power output for that activity. For example, if you are going to be competing in heat or on hills, then you should strive to train in the heat or hills. Specificity means that you should conduct some of your training at a similar distance and pace as you will be competing. Each time you do this, your central governor becomes more precise at determining the proper power output for your particular event.

High intensity training also powerfully affects the central governor, re-setting it so that it allows increasingly higher power outputs before being tripped. One of the reasons that high intensity training causes immediate performance improvements, improvements that have been shown to occur in the absence of physiological changes (i.e. no changes in lactate production, mitochondrial density, heart size, capillary density, muscle fiber size, etc), is from the re-setting of the central governor at a higher level. High intensity training helps re-set the central governor so that it allows a greater mass of muscle fiber to be activated at one time, resulting in a higher total power output.

Summary

The muscle power model of performance and the central governor model of performance are complimentary models. Integrating these two models allows us to more accurately describe the physiological processes occurring in the body and helps us design more effective training programs. In order to improve your performance you will need to increase your power output. This is best done by increasing the power capacity of the muscle fibers and by re-setting the central governor to allow a higher power output before it is activated.

References:

1.

Noakes, T, Lore of Running, 3rd edition, 1991, Human Kinetics, pg 21
2.

Noakes, T, Lore of Running, 3rd edition, 1991, Human Kinetics, pg 38
3.

Noakes, T, Lore of Running, 4rd edition, 2003, Human Kinetics, pg 64

Source http://www.powerrunning.com

[Toks]

interesting post Rob, thanks for sharing

[Robh]

[quote="Toks"]interesting post Rob, thanks for sharing

[mrP(Boonen)VT]

[quote]Re-setting the central governor so that it allows a higher power output before it is tripped is best accomplished by training specificity and intensity. The more specific your training the more precise your central governor will be in determining the most effective power output for that activity. For example, if you are going to be competing in heat or on hills, then you should strive to train in the heat or hills. Specificity means that you should conduct some of your training at a similar distance and pace as you will be competing. Each time you do this, your central governor becomes more precise at determining the proper power output for your particular event.

[Robh]

Some comments from Dan Zucconi Level 1 certified :-

Hello everyone...I was hoping to verify my understanding regarding the ECGM and then post some thoughts/questions with regards to training...like Juerg and Andrew have written in the past, the information is sometimes overwhelming, but maybe I can clarify my own thoughts...the basis of the ECGM is that the body will protect the vital organs heart, resp. system and brain by maintain the needed O2 at teh expense of working muscle so there will be vasoconstriction therefore less blood going to muscle or shut down (maybe not best word) of muscle fibres and possible increase in use of oxygen independent means etc....if this is so, should a new approach to training come from this perspective:
1 - ensure adequate O2 to heart, respiratory muscles through specific training...is this possible?...these have traditionally been thought of as "aerobic machines" in the past, but the implementation of the spiro for the resp. muscles has challenged this...can the same be done with the heart?...or maybe simply improve the efficiency so that you recruit fewer resp. muscle fibres thereby reducing their demand for O2...can the same be done for the heart (I don't think so in this exact context but perhaps by decreasing HR at a given intensity this is what we are doing)...
2 - increase the efficiency of working muscle so that we recruit fewer muscle fibres at the same intensity again decreasing the demand for O2

So protect the heart/resp. muscles first so train them first.

Perhaps this is what Juerg and others have been talking about all the time but the blocks are just falling into place now in my mind...

Andrew made a comment in the thread regarding functional/structural changes:

"This would then bring up the second problem we discussed in J.Tree. Do you want a higher VO2 at race pace, or a lower VO2? For all you just shaking your head, and saying "higher of course". Consider that if you race at a higher VO2, you will need to supply oxygen faster to working muscles, meaning deeper or faster respirations, and stronger or faster heart rate. If you can go the same speed with less oxygen being utilized, would that not be an indication of "better" physiological preparation?"

Looking at the old VO2 numbers that are thrown around, perhaps that was the key to Frank Shorter's success...it's often quoted how his VO2 numbers are so much lower but he was one of the premier marathon runners of his time...

I had even written down what I had wanted to say, but now reading it over it seems like just a mash of ideas tumbling over each other...time to rest brain and body...

[huw williams]

[quote="mrP(Boonen)VT"] This aligns with the more old fashioned theory of training and goes against modern theory of short sharp intensity training is all that is required to improve endurance - as per Huw.