Lactate Fuels the Human Brain During Exercise

Physical activity, using our muscles, requires energy in order to allow the muscles to repeatedly contract as they do during movement.  If we were to go for a walk, most of the energy that our muscles use can be replaced through aerobic metabolism, which means that we are using oxygen to produce energy from substrates such as carbohydrate or fat.  Since this is a relatively low intensity movement, the energy requirements to perform the activity are relatively low, and we would have little problem supplying the energy required to sustain it.

As the intensity of our movement increases, the requirement for energy does as well.  Move faster, and you need more energy.  But if intensity continues to increase there becomes a point at which we cannot supply our muscles with the energy they require at the speed they require it through the same process, aerobic metabolism.  This is because through aerobic metabolism we are using oxygen to produce energy, and as hard as we may try by increasing our heart rate and breathing speed, there is a limited amount of oxygen we can supply for this energy production.  But fear not: anaerobic energy production will take over!

As the name implies, this process of anaerobic metabolism is not aerobic, which means it does not use oxygen.  This is fantastic if we just can’t quite manage to shuttle enough oxygen into our muscle cell as it allows us to still make some energy.  This different process for energy production uses a slightly different chemical pathway and has limits itself just like aerobic metabolism does.

Let’s use solely carbohydrate for simplicity in the following example.

In order to make energy, our muscle cells will use their store of glycogen by breaking it down to glucose, which will be metabolized via the glycolysis pathway for energy production. The end products of this pathway are a molecule called pyruvate, ATP which is what our cells use for energy, and another molecule called NADH.

Normally, this pyruvate enters the citric acid cycle (an aerobic process) and this pathway regenerates NAD+ from NADH so that glycolysis can continue.  When we are working at too high an intensity, as was mentioned in the above scenario, and cannot supply enough oxygen for this aerobic chemical process to occur, pyruvate will simply accumulate in our muscle cells because it cannot enter the citric acid cycle.

When there is inadequate oxygen and pyruvate begins to accumulate, (now anaerobic) the pyruvate is converted to lactate in order to generate more NAD+ so that glycolysis can continue.

Lacate! The “evil” molecule that causes our muscles to burn when we exercise too hard?!  Not quite the case.

Lactate acts as an intermediate link between aerobic and anaerobic energy production, and can be converted back into pyruvate or into glucose.

Long ago it was thought that this lactate was responsible for causing muscle soreness, but this belief has not held up as our understanding of the process has increased, and in fact lactate is used by our muscles for fuel.  One of the things known now to contribute to muscle soreness during exercise is an accumulation of H+ molecules from energy production, and lactate actually helps to stop this accumulation of H+. That we use lactate for fuel in our muscles is now rather well-understood, and having more and better mitochondria helps with using up the lactate.

brain metabolism

What’s not as well-understood though is what our brain does with lactate as it leaks into our blood.  We do know that it enters our brain, and that it doesn’t leave our brain after doing so, and so it’s assumed to be used for energy in some sense.  I’ve come across a paper titled “Lactate fuels the human brain during exercise” (hence the name of this blog post) that provides some insight into this process.

For something like this to occur in the first place lactate must be of some use to our brain.  Glucose is the predominant fuel source for our brain, but it turns out that during exercise this energy-guzzling organ can take in lactate as well in order to use it for ATP production.  Using another fuel substrate in our brain during intense exercise would no doubt spare glucose, and this may even be the sole purpose for our brain allowing the lactate to enter.

This idea of lactate sparing glucose may even support the strategic use of more intense bursts of effort during a race in order to generate some lactate!

One of the thoughts on why we feel tired after exerting ourselves during physical activity is that the blood-glucose supply for the brain decreases, and although we’re not actually out of energy, the brain attempts to save us from a perceived lack of energy and so initiates central fatigue.  Just like the effects of ketones in our brain, however, having lactate in there for use as a fuel source will likely help to stop our brain from running out of its perceived energy reserves (glucose) as fast which may delay the onset of feelings of fatigue.

Perhaps the brain’s use of lactate as a fuel can even be improved as well, inreasing the threshold before which central fatigue sets in during intense activity.  This was an interesting quote from the paper from which I stole the name for this post, “…during exhaustive physical exercise with intense activation of large muscle groups, during which anaerobic metabolism prevails and arterial lactate is elevated, the brain takes up lactate in amounts that may supersede the uptake of glucose.” (emphasis mine)

If it’s taking in more lactate than glucose, there’s either something horribly wrong with the way our brain has evolved to function during intense physical exercise, or we can use this in place of glucose during intense exercise.

Maybe the continuous exposure of our brain to elevated levels of this fuel source during exercise is one of the physiological mechanisms through which high intensity training might decrease the rating of perceived exertion of subsequent less intense exercise.  We expose our brain to lactate during exercise, become better at metabolising lactate for energy production in our brain, use lactate more effectively and thus spare glucose, and allow for our brain not to run out of glucose as quickly so that it will not cause us to feel fatigue as abruptly.

Another quote from the paper:

“In summary, cerebral lactate uptake becomes significant when arterial lactate is elevated and the brain is activated, as during intense exercise.  The brain should be added to the list of organs that contribute to the elimination of plasma lactate, thus taking advantage of accidental availability of additional chemical energy and thereby sparing glucose.”

One of the things that fascinates me the most about endurance performance is the many adaptations of our brain, in both the sense of psychological changes and physiological changes.  The brain very obviously plays a major role in performance, and obviously some of this governance is due to thoughts and psychological states.  But as much as I’m interested in that, I also like to understand underlying physiological mechanisms behind this stuff.  As I stated in my training philosophy: Some training sessions should be for psychological improvements.  This also means creating a favourable physiological environment wherein “improved” psychological states can occur.  As we know, chemicals in our brain affect our thoughts and our thoughts will affect chemicals in our brain, so focussing solely on one is only half of the puzzle solved!

Making our brain better at using energy during exercise (potentially via lactate exposure during training) seems like a helpful way to prevent fatigue and maintain a positive psychological state.

Train your brain!

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One response to “Lactate Fuels the Human Brain During Exercise

  1. There is one important function of the brain that has been entirely forgotten: REM sleep.
    Every single day, every single person goes to sleep and at one point during the resting stage the process of rapid eye movement takes place. This stage of sleep is characterized by a slow respiratory function, low oxigen intake (apnea) and an increased brain activity accompanied by a fast twitching of the eye’s muscles. Could it be this process also mediated by a switch from glucose to lactate as main fuel substrate? As the sleeping process goes through the night the number of apnoea related events increase too. Is it possible to interpret this feature as the result of a lacking supply of glucose to the brain due to hours of fasting and the attempts of the brain to stimulate lactate intake from cells within the brain capable of producing and delivering lactate for energy?
    I’d like to hear from the experts on this topic.

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