Lactate - Villian or Hero?
For over 100 years lactate has been considered a “waste product” and the enemy of cyclists. Nothing could be further from the truth!
Under heavy exercise, the concentration of lactate rises in the blood, leading people to associate it with fatigue, pain and reduced performance. It is not lactate that causes you to stop exercise. More likely it’s the hydrogen ions (acid) that is transported along with lactate that causes this.
Historically lactate was thought to be produced by muscles when there wasn’t enough oxygen to meet the energy demand of intense exercise.
It turns out that lactate is produced at all exercise intensities, even at rest and under fully aerobic conditions.
Lactate is produced in very high quantities when exercise reaches extreme intensities, and under conditions of high stress such as suffering a major injury or illness (Brooks 2022). The mistake was associating the high levels of lactate with lactate being the cause of other associated symptoms like fatigue, pain and performance loss.
Lactate production is better thought of a stress response. In response to stress, be it exercise or injury, the body activates the sympathetic nervous system which will trigger increased lactate production. Lactate is then available as a fuel source for exercise or tissue repair.
Yes, you read that right – lactate is a fuel! Not a waste product!
Lactate is currently thought to have at least 3 major roles in the body (Brooks 2022):
1. Fuel source.
2. Supports blood glucose levels.
3. Powerful signalling molecule for adaptation to metabolic stress (i.e. lactate production is important in training if you want to improve and adapt!).
Muscles constantly produce lactate and it is considered the preferred fuel for multiple organs in the body.
The brain and heart both run more efficiently and strongly when fuelled by lactate compared to glucose, both of which circulate through the blood.
It is very easy to think of lactate as a fuel – it is a carbohydrate after all. Most cyclists know the primary form of carbohydrate stored in muscle cells is called glycogen, which is a glucose polymer. Glycogen can be broken down into glucose when needed for energy. Glucose is a sugar with 6 carbon atoms. Lactate (and its close relation pyruvate) are essentially half a glucose molecule – they are formed from 3 carbon atoms.
It’s very easy to see how the body would love lactate as a fuel – it is already half-digested compared to glucose.
Lactate is the major fuel the heart uses once you start exercising (Brooks 2021).
It is used as a fuel by muscles and the brain, and any unused lactate is converted back into glucose by the liver for storage.
As the intensity of exercise increases, muscles create an increasing percentage of their energy via glycolysis, which is using glucose as a fuel without needing oxygen (otherwise known as anaerobic energy production) (learn more about glycolytic power production here). Lactate is the mandatory by-product of glycolysis. In other words, once you start breaking down glucose without using oxygen, you will always produce lactate.
Lactate in Cycling: MLSS & FTP
Of interest to cyclists is that lactate is produced faster than the body can consume it during high intensity exercise above a certain threshold of intensity known by various names including the (second) lactate threshold (LT2) or the Maximal Lactate Steady State (MLSS). Exercise above the lactate threshold will cause the concentration of lactate in the blood to rise and keep on rising. This is what functional threshold power (FTP) attempts to estimate.
For a steady state effort if you ride at a higher power level than your FTP, blood lactate levels will keep on rising, along with acid levels, until you are forced to stop. The actual threshold above which lactate will keep on rising is thus more appropriately called the Lactate Threshold (LT2) or Maximal Lactate Steady State (MLSS), not FTP which is just an estimate of MLSS. Exercise below the MLSS will see lactate levels stabilise; exercise at higher intensities will see lactate (and H+) levels continue to rise until eventually you are forced to slow down and are unable to maintain the same power output.
How Does the Body Cope with High Levels of Lactate?
When your muscle cells produce high levels of lactate it is transported into the blood via monocarboxylate transporters (MCTs), and as it exits the muscle cell a hydrogen ion (H+, or acid) is transported out at the same time. This is why both lactate and acid levels rise and fall together as the two different substances are transported together – the MCT’s will not transport one without the other (Juel & Halestrap 1999). There are several types of MCT’s, and in skeletal muscle the main ones are MCT1 and MCT4.
Why does this matter? In general terms, muscle cells which use glycolysis to produce energy such as type 2 fast twitch fibres need a lot of MCT4 transporters to transport lactate out of the cell. Slow twitch oxidative fibres (type 1) have a lot of MCT1 transporters which love to take transport lactate into the muscle cells where it is consumed aerobically as a fuel.
One positive adaptation to training is muscle fibres building more transporters to facilitate lactate shuttling in and out of the cells and bloodstream as required. This makes it easier to control the fuel supply and acid levels in your body as you get fitter.
The ability to produce higher power for longer is one of the determinants of success in cycling, so managing lactate delivery and acidosis is critical.
Having more MCT’s allows you to do this better, which is why this is one of the adaptations we are seeking when creating a training plan for an athlete.
Now think about racing: if your slow twitch oxidative fibres are well trained (meaning that you have a very well-developed oxidative system and lots of MCT1 transporters) then you can burn a lot more lactate than someone whose aerobic system is weak. This well-developed aerobic system prevents lactate / acid levels rising as rapidly as someone who, all other things being equal, has a weaker oxidative system. This is one of the most important keys to winning endurance races!
If your glycolytic system is overly well developed in relation to your oxidative system, then you will produce more lactate (and acid!) at a given power level and your oxidative system will be unable to burn this lactate at a fast enough rate to keep you in the front group. However, a well-developed glycolytic system might be required for certain types of races that require very high-power outputs to win, so working out how to optimise the balance of each system is a critical calculation for your coach to incorporate into your program. This is a complex topic beyond the scope of this post.
The modern view on lactate has evolved. It is now seen more as a “universal fuel” used by many of the body’s tissues under periods of stress, often being the preferred fuel.
The ability to “shuttle” lactate in and out of cells and the bloodstream to distribute it where it’s needed make it an ideal substrate for oxidative metabolism (energy production).
Lactate testing is widely regarded as the best method of tracking progress for endurance athletes, which is why it’s part of the regular testing protocols for Cycle Physio Coaching athletes who are focussed on performance.
Perhaps a rethink of the role of lactate in your training and/or racing regimen might be in order!
Brooks G (2021): Role of the Heart in Lactate Shuttling. Front. Nutr 8: article 663560.
Brooks G et al (2022): Lactate in contemporary biology: a phoenix risen. J Physiol 600:1229–1251
Juel C & Halestrap A (1999): Lactate transport in skeletal muscle — role and regulation of the monocarboxylate transporter. J Physiol 15:633-642.
Pallares JG et al (2016): Validity and Reliability of Ventilatory and Blood Lactate Thresholds in Well-Trained Cyclists. PLOS ONE | DOI:10.1371/journal.pone.0163389.
Rabinowitz JD & Enerbäck E (2020): Lactate: the ugly duckling of energy metabolism. Nat Metab. 2(7): 566–571