The Ultimate Performance-Limiting Factor

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Have you ever wondered what it is that doesn’t let you keep on exercising? Is it your muscles? Is it your thoughts? Your brain? What is the real performance-limiting factor that makes us stop exercising?

Welcome back to Endur Science! I couldn’t wait any longer to talk about what is one of the mysteries within exercise physiology. One of the unresolved questions. One of the most discussed topics among sport physiologists. A current hot topic. And it looks like it will be hot for pretty long…

I am talking about the physiological limits of athletic performance.

As most physiologists that are interested in the molecular basis of sport performance, I am also hugely interested in understanding the origin of fatigue and what limits our performance. I have spent hours and hours digging into that and reading related papers. However, it seems that there isn’t a clear understanding of it and a clash between two models exist: the currently accepted and taught peripheral fatigue, by Archibald Vivian Hill and colleagues, and the new-coming model of the central governor, by Timothy Noakes.

Let’s see if we pull apart and understand each model!

Peripheral fatigue model

The peripheral fatigue model, also called cardiovascular/anaerobic/catastrophic model, holds that exercise is limited by metabolic changes in the peripheral muscles, which impair skeletal muscle contractility, independent of any regulation by the central nervous system (CNS).

This is the currently accepted model for fatigue and athletic performance limitation, and it is the model that is taught in schools and universities.

It was originally postulated by Archibald Vivian Hill in 1923 influenced by the earlier findings of Frederick Gowland Hopkins and Walter Morley Fletcher in 1907. They showed higher lactate concentrations in frog excised skeletal muscle (previously stimulated to contract until they no longer responded to stimulation) and its disappearance in presence of oxygen and concluded that “the accumulation of lactic acid in muscle occurs only in the conditions of anaerobiosis” and that “fatigue due to contractions is accompanied by an increase in lactic acid”.

Hill believed that lactic stimulated muscle contraction (we now know this is not correct), and its accumulation caused a failure in muscle relaxation, which ultimately led to sustained contraction or muscle rigor, resulting in involuntary termination of exercise.

Hill and his colleagues also believed that the maximum cardiac output was limited by the development of myocardial ischaemia caused by a limiting oxygen delivery to the heart. Accordingly, he placed the heart as the cause for skeletal muscle anaerobiosis, and thus the cause of skeletal muscle fatigue.

Hill’s model was taking shape. He put everything together and theorised that an inadequate supply of oxygen to the heart caused myocardial ischaemia that limits cardiac output. This made skeletal muscle blood flow be inadequate to match the high skeletal muscle oxygen demands during maximal exercise. A resulting skeletal muscle anaerobiosis then caused lactic acid to accumulate, which impaired skeletal muscle relaxation, ultimately terminating exercise.

Peripheral fatigue model
Peripheral fatigue model by A. V. Hill. Adapted from: Noakes 2011

Thus, this popular model of exercise physiology involves a catastrophic failure of homeostasis leading to skeletal muscle dysfunction (called peripheral fatigue) usually as a result of either an inadequate oxygen supply to the exercising muscles or a total energy depletion in the exhausted muscles (as it has been established later).

Central governor model

Timothy Noakes then argued that the peripheral fatigue model is unable to explain how exercise can terminate even though there is a population of fresh muscle fibres waiting to be recruited by the brain. This argument was based on his belief that if exercise is regulated purely by changes in the ability of exercising skeletal muscles to produce force, then this fatigue can only occur after all the available motor units have been activated.

Noakes then found out that the scientific community missed out a crucial detail from Hill’s model. His complete model included an anticipatory mechanism that, even though it was activated only when the catastrophe had already begun, acted to ensure that a worse catastrophe, irreversible myocardial damage, was prevented.

We suggest that… either in the heart muscle itself or in the nervous system, there is some mechanism (a governor) which causes a slowing of the circulation as soon as a serious degree of unsaturation occurs

Hill et al. 1924

This is when Noakes started to look into this “governor” and ended up developing the idea that “the central nervous system can ensure that homeostasis is maintained in all bodily systems, not just the heart, by regulating the motor units recruited in the exercising muscles by the brain in a feed-forward manner on a moment-to-moment basis”. This is now the basis of the Central Governor Model (CGM).

Then, the CGM model theorises that exercise performance is limited by the brain. It determines the number of motor units recruited in a feed-forward manner by integrating both physiological and psychological inputs, such as the athlete’s physiological state at the start of the exercise, the athlete’s motivation, etc. It also allows continuous feedback during exercise from all the organs in the body (like hydrations state, fuel reserves, etc.) to regulate the exercise behaviour by continuously modifying the number of motor units recruited during exercise.

Central governor model
Central governor model by Timothy Noakes

Thus, this model guarantees that homeostasis is maintained under all conditions by modulating the demands of the exercising muscles through the number of motor units that are being recruited by the brain, and it ensures that exercise is ceased even though homeostasis is still maintained. A catastrophic outcome is prevented, unlike in the peripheral fatigue model where a catastrophe is a prerequisite for a reduction in performance.

Noakes defends his model by bringing up, among others, a really interesting yet not completely understood phenomenon: the “end spur”. How can the peripheral fatigue model can explain that athletes achieve their higher power outputs during the last minutes of the competition, if it is at the end of the race when physiological situations that impair exercise are at their highest? We are definitely missing something here, that may be explain by Noakes’ model.

Personal point of view

It should be clear that neither the peripheral fatigue model nor the central governor model are absolute true facts about what happens within our body when exercising, they are just theories about it. Only about 30% of human physiology is understood, which makes it hard to reach a conclusion about it. Thus, I would like to leave my humble opinion about it (which may change over time).

My understanding of fatigue goes further than a simple organ such as the heart. It looks more like an integrated network of signals that allow communication between and within cells.

The central governor model developed by Timothy Noakes seems totally plausible since it helps to explain many phenomena that are currently not understood. For example, if you have ever participated in a competition (let’s say running competition), you have probably experienced the sudden and involuntary increase in pace during those seconds you are being cheered up by your family and friends, even though you were already almost collapsed before noticing they were there. Or the ergogenic effect of the mouth rinse, that helps you keep a high pace by acting only in your brain, since no sugar (or a negligible amount of sugar) enters your digestive tract.

However, I believe that it is the metabolites that signal the brain (in case they do) which are the main point here and set the power output through the modulation of the energy systems and ATP regeneration. The brain, in my view, acts as an intermediate of the physiological signals and the responses, and it also integrates psychological inputs that can modulate the response.

The human physiology will never stop surprising us, and I don’t think this time will be an exception. Our body is highly complex, and we are still very far away from understanding it. I do not know how this debate will evolve. Even so, this is amazingly interesting!

Wrap up

The model for athletic performance limitation that dominates teaching and research in this field is the one developed by Hill and colleagues, called the peripheral fatigue. It is a brainless model which states that exercise is limited by metabolic changes in the peripheral muscle that disrupt homeostasis and impair muscle contractility, independent to any regulation by the central nervous system.

On the other side, we’ve got Timothy Noakes who, by claiming (among many other things) that motor unit recruitment is not maximal at the end of exercise or that the previous model does not explain the “end spur” phenomenon, redesigned a new model that spins around the brain. This is called the central governor model and holds that the brain determines the number of motor unit recruited, and thus the power output, through a feed-forward control and in response to afferent feedback from multiple central and peripheral sensors in order to ensure that the planned activity is completed without any loss of cellular homeostasis.

While none of them may describe perfectly what actually happens within our body, they both help us build up knowledge and adjust beliefs to get closer to the understanding of bodily function.

I don’t know where this debate will bring us, but I am eager to see it!

Main references

  1. Noakes, Timothy David. 2011. “Time to Move beyond a Brainless Exercise Physiology: The Evidence for Complex Regulation of Human Exercise Performance.” Applied Physiology, Nutrition and Metabolism 36 (1): 23–35.

Additional references

  1. Noakes, T D, and A St Clair Gibson. 2004. “Logical Limitations to the ‘“Catastrophe”’ Models of Fatigue during Exercise in Humans T.” British Journal of Sports Medicine 38 (1): 648–49.
  2. Lambert, E. V., A. St. Clair Gibson, and T. D. Noakes. 2005. “Complex Systems Model of Fatigue: Integrative Homoeostatic Control of Peripheral Physiological Systems during Exercise in Humans.” British Journal of Sports Medicine 39 (1): 648–49.
  3. Noakes, T. D., A. St. Clair Gibson, and E. V. Lambert. 2005. “From Catastrophe to Complexity: A Novel Model of Integrative Central Neural Regulation of Effort and Fatigue during Exercise in Humans: Summary and Conclusions.” British Journal of Sports Medicine 39 (2): 120–24.

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