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Lactate – shrouded in mystery?

Our Perspective on Human Performance

Lactate – shrouded in mystery?

Lactate – shrouded in mystery?

Why the confusion?

Up until recently, the name ‘lactic acid’ has been the subject of much confusion in sports science, and for good reason. Measurements taken during studies designed to understand the onset of fatigue and exhaustion in athletes performing maximal exercise had previously and wrongly associated ‘lactic acid’ with the abrupt fatigue at intensities approaching maximal.

Even though lactate  is associated with a drop in blood and muscle pH at maximal exercise, at sub-maximal levels, lactate itself is a fuel which enters metabolism when glucose has been inefficiently (plundered) converted to pyruvate, which cannot then enter normal mitochondrial respiration (Krebs cycle and oxidative phosphorylation) due to an insufficiency in available oxygen. In this scenario, pyruvate is shunted to form Lactate which can be used elsewhere or reconverted to glucose (and hence glycogen in the liver) reducing localised blood lactate concentrations and bringing much needed fuel to muscles that require it.

Brooks’ Lactate Shuttle

The acid theory held sway from an early ‘frog’s-legs’ experiment before the First World War. Current was applied to detached frog’s legs, and pH measurements were taken until the muscles fatigued (tetany). The pH at the end of the experiment was much lower than at the start, showing what was presumed as ‘lactic acidosis’.

The conclusion was that lactic acid caused the fatigue, and the acid present was due to the lack of oxygen to metabolise it to ATP. The lack of oxygen was probably due to the legs not having any circulation. Since then, it has taken the work of George Brooks and the understanding of the Brooks Lactate shuttle and his discoveries from the 1970’s up until present day, to change the world’s understanding of lactate physiology. Luckily for us, valid peer reviewed scientific research now presides over popular opinion.


Carl and Gerty ‘Cori Cycle’

The reason for ‘carbo-loading’ before a big race is so we can saturate our liver and muscles with abundant glycogen to provide us with energy for higher intensities experienced during racing. Whether these are anaerobic or aerobic efforts depending on the relative intensity will dictate how long the finite amount of glycogen stored in your body will last. Aerobic glucose oxidation is much more efficient than anaerobic glycolysis in the absence of sufficient oxygen to produce the necessary ATP  for muscle contraction.

The multi-functional liver (through the Cori Cycle) is capable of supplying glycogen, via the bloodstream, to wherever it’s needed within the body. Individual muscles, however, can only use the glycogen that is embedded within that particular muscle. Once it’s in the muscle it can not leave to go anywhere else. Lactate is different and works in a different way.

Special transporter proteins or ‘shuttles’ (Mono Carboxylate Transporters, MCTs) exist which allow lactate to enter the blood and distribute to other muscles around the body.

Once in the liver, the lactate is converted to glucose, then to glycogen through a process called gluconeogenesis. The blood is then used to transport the glucose back to the muscles. Once in the muscle it is metabolised back to glycogen to store as fuel when the athlete is recovering, or if the athlete is still going flat out, that glucose is converted straight back to lactate!

This supplementary muscle fuelling happens very quickly, and is an important part of maintaining the associated lactate threshold, although this process cannot be sustained indefinitely. Re-fuelling with carbohydrate will help reconstitute depleted energy levels once the intensity has lowered, albeit much more slowly.

The liver expends 2 ATP molecules changing lactate to outgoing glycogen. But it costs the liver 6 ATP molecules from fatty acid metabolism to be able to do this. So the liver suffers a 4 ATP deficit for each ‘upgrade’ it carries out. Sooner or later (around 30 minutes depending on pre-event hydration and fuelling levels) the energy giving stocks of glycogen will be exhausted. When that happens, you run out of glycogen and bonk!

The only way to reconstitute ATP is to back-off the intensity until you reach a level of positive balance. At this point you need to remain at a lower lactate balance if you want to get to the end of the day before the time cut-off.

Finding the wattage/heart rate where this shuttle is working at its optimum efficiency is important to every athlete. It could be the difference between a top ten and a podium place in your target event.

Threshold fallacies…

For quite some time the Lactate Threshold (better technically described as a turning point) has been regarded as the Anaerobic threshold, this point is the first rise in blood lactate when it is thought that anaerobic metabolism starts to overwhelm energy production. Confusion between the technical definitions on the important turning points has existed for sometime, and still does to some extent, even in the world of applied exercise physiology.

Although physiologically rationale, the sliding scale of aerobic and anaerobic metabolism is not as clear cut as that.  Even now, the more widely accepted threshold definitions;  onset of blood lactate accumulation (OBLA) and maximum lactate steady state (MLSS) are considerably more representative of the physiological situation. The OBLA is the point where muscles start producing lactate quicker than the body can use it or remove it.

To add even more confusion, there is Functional Threshold Power (FTP) to consider. This effort, by definition, lasts for an hour, so it must occur at less power than OBLA. A 20 minute field FTP test is a good estimation of an athlete’s threshold power, although it is not an accurate representation of the point at which an athlete’s body balances blood lactate accumulation and clearance. Athletes are able to over-reach themselves to exhaustion to set the highest average power output. After all that is the goal, but crucial pacing always proves difficult during the field test. Typical FTP data from multiple athletes in different states of training suggest that blood lactate concentrations are significantly higher at the end of the 20 minute period than during the initial minutes of the test. This suggests that the true lactate threshold or MLSS has been breached as pacing has not been constant, and so a FTP value would not be representative or a consistent indicator of performance. In other words, athletes train too hard using power based training intensities set with a 20 minute field test.

Effectively, if you want to improve as an athlete, you need to find the level just before the lactate balance point. This turning point is now referred to as your Maximal Lactate Steady State. Which is the highest speed/power/heart rate at which you can ride where your body makes best use of the lactate you are producing. At this magical concentration, lactate works for you not against you. Depending on how well we process it determines at what point the associated acidosis overwhelms our muscles. At submaximal levels of exercise it’s a fuel. At maximal levels it’s a hindrance.

The optimal rate at which lactate is produced, metabolised and re-distributed is regarded as the lactate threshold. Further confusion has resulted from the definition of this point, when the balance is disrupted and lactate starts to accumulate. Sustaining low concentrations of a balanced lactate concentration at your highest sustainable power/ speed is every cyclists ideal performance goal, ultimately improving their efficiency.

Armed with this information, you can now train to improve your power output at MLSS and drive your self-limiting OBLA turning point closer to your genetically gifted VO2max level.

On the level? 

By measuring lactate accumulation, an athlete can establish their current point of exercise excellence. The point at which they can just sit there and, potentially cruise all day. If athlete As’ MLSS level is at a higher wattage than athlete B then athlete A will be performing significantly better than athlete B, depending on the event. Once you have pinpointed the level of effort that is right at the edge of your maximum lactate steady state production/utilization you can go about improving it.

Top marathon runners and ironman athletes run right on the edge of their MLSS, remaining aerobic, using predominantly fat for fuel especially in the liver, helping to recycle lactate, saving glycogen and recycling their pyruvate to get their race winning fuel for free.


To break this down to a simpler form: when we attain greater intensities during exercise, more work is done in the absence of oxygen (anaerobic). The fuel that provides the energy for this exertion is glucose and when used in this anaerobic state, the return on the investment (food intake) is less (we get far more energy for glucose when broken down in the presence of oxygen, aerobic). Lactate allows for the system to gain some returns by replenishing the glucose supply that the muscle will use to continue the intensity. Lactate at this point is not the evil byproduct that slows your performance, but the component that prolongs your ability. Training will improve your ability to be more aerobic at higher intensities and produce less lactate while also becoming more efficient with your use of lactate as a fuel source.

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