Fatigue in Endurance Sport: Parallels with Pain Science

16th February 2012

I was involved in some research in 2003 into the phenomenon of ‘central fatigue’ in endurance exercise. Here i’ll briefly explain what this means, how sports science knowledge of fatigue has progressed during the last decade, and how these new sports science findings have paralleled pain science advances.

Central fatigue refers to supra-spinal mechanisms involved in producing fatigue. ‘Peripheral fatigue’ on the other hand, implies a reduction in the ability of muscle fibres to produce force due to changes in the peripheral biochemistry (for example the accumulation or depletion of critical substrates).

Recent advances in Sport Science demonstrate that a complex interaction of these mechanisms determines our exercise abilities and susceptibility to fatigue in different situations. We used to think that exercise fatigue was solely due to excess lactate in the muscles or depletion of glycogen (peripheral fatigue). This was a ‘brain-less’ model. However the importance of the central mechanisms i.e. the brain and spinal cord, has been increasingly demonstrated and has considerable implications for the way that we train and compete.

In 1923, Nobel Laureate Archibald V Hill developed the still popular model of exercise fatigue [1]. Hill proposed that exercise fatigue develops when the heart is no longer able to produce a cardiac output sufficient to cover the increased demands for oxygen from exercising muscles. If failure of oxygen delivery was the limiting factor, then it follows, that those with the largest VO2max values would be the most successful athletes. However, it has been known for at least 4 decades that the best athletes do not always have the highest VO2max values.

Hill’s model also suggests that measurement of blood lactate concentrations during exercise can be used to define both the precise exercise training intensities that will produce the greatest training benefits.

If lactic acid was the sole limiting factor, it was natural to presume that this molecule was also the regulator of the pace that athletes chose during exercise. But this interpretation was discounted when it was realised that there was considerable individual variability in the blood lactate response to exercise. This level of variability cannot explain why athletes start exercise at different paces depending on the expected exercise duration, nor why they speed up near the end of exercise. These common observations can be explained only by the presence of specific neural control mechanisms [2].


Studying the biology of exercise pacing has revealed some interesting findings. A recent study compared the best and worst 1500m time trial performances of a group of trained cyclists, and found that from the very start of exercise, experienced athletes adopt an optimum pacing strategy. It was also found that their chosen pace varied from test to test [3]. In other words, athletes begin their best performances at a faster pace and sustain a higher power output throughout the effort than when they perform less well.
These findings suggest that individuals are able to adjust their performance on a day-to-day basis via physiological and perhaps other cues interpreted even at the very start of the exercise bout.

We slow down or speed up in response to the brains interpretations and outputs. The brain generates all of the symptoms that we experience during exercise and the symptoms that you feel are likely to be unique to you. The primary goal of the brain is to protect us from harm- therefore it generates symptoms that stop us from overexerting ourselves and causing potentially serious (or even fatal) damage.

So the symptoms of discomfort we feel are illusionary and may have nothing to do with the actual state of the body at that time. They are based on the brains complete interpretation of the situation including past experience, beliefs, physiological and psychological factors (ring any bells with pain?!).

Feelings of discomfort arise in relation to how far you are from the finish explains Dr Timothy Noakes, Author of the Lore of running, “it’s not a matter of how far you’ve run, but rather how close you are to the finish” The best athletes are the ones’ who allow their illusory symptoms to interfere with their performance less. Greater athletes do not generate discomfort symptoms to the same extent.

The Sports Science world has been (and maybe still is) heavily focussed on peripheral biology and the Pain world has suffered from similar misconceptions, being distracted by structural-postural paradigms.

Pain science and Sports science advances, which demonstrate some uncanny resemblance, likely reflect our developing understanding of the complexity of the human species. The complex interaction between nature and nurture and top down (brain driven) and bottom-up (peripherally driven) mechanisms that determines our behaviours and experiences. Whilst some researchers are looking for specific chemicals or neurotransmitters, others are taking a more holistic approaches and looking at behaviours and experiences. Neither tells us the whole story, but perhaps everyone is just looking at the same truth from different angles. The truth is complex and multi-dimensional.

The last decade has gradually began to give the brain prize of place in terms of both Sports performance and Pain treatment, but we still have a long way to go and a lot of old, peripherally-centred paradigms to leave behind.

[1] Noakes TD. How did A V Hill understand the VO2max and the “plateau phenomenon”? Still no clarity? Br J Sports Med 2008;42:574–80.

[2] Noakes TD. The central governor model of exercise regulation applied to the marathon. Sports Med 2007;37:374–7.

[3] Hettinga FJ, De Koning JJ, Schmidt LJ, et al. Optimal pacing strategy: from theoretical modelling to reality in 1500-m speed skating. Br J Sports Med 2011;45:30–5.

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