This is probably the single topic in this blog series on determining training intensity zones which is going to stir up the most controversy. I’ll start with a quick summary so you know where I’m headed with this, and then I’ll go into some more details. First a quick reminder: I’m an engineer trying to learn exercise physiology. As such, I don’t claim to be an expert, just an interested outsider.
Quick Summary: The concept of Lactate Threshold is based on wrong information.
What is Lactate Threshold?
There are many different formulations for the exact definition of Lactate Threshold. Generally, they all refer to a certain intensity level in a graded exercise test that causes some type of change in blood lactate levels. An old definition, now mostly discarded, is that Lactate Threshold is the exercise intensity that causes arterial blood lactate levels to exceed 4 mmol/l; this was the original “threshold.” More sophisticated definitions have since emerged that don’t place a fixed value on blood lactate, but rather attempt to find the point where blood lactate is produced faster than it is cleared.
Blood lactate is measured by doing a small blood draw from the fingertip or earlobe during exercise. Typically, one or two measurements are made at every load step during a graded exercise test. Portable blood lactate meters exist that allow readings to be taken outside of a lab setting.
Generally, Lactate Threshold is correlated with the heart rate of the athlete or the power they are putting out at the time the threshold is identified. From there, the remaining training zones are calculated as a percentage of the Lactate Threshold value.
Background on the Controversy
There are a couple of points about lactate that seem to be widely accepted:
- More lactate is produced at high intensity than at low intensity,
- Blood tends to get more acidic at higher intensity,
- Lactate is a product of oxygen-independent metabolism in the muscle.
Additionally, there are other ideas about lactate that have a lot of evidence supporting them but are in conflict with widely accepted historical assumptions. This is where the controversy stems from:
- Lactate does NOT cause fatigue or muscle pain,
- Lactate is a fuel source that can be used for producing more energy,
- Lactate actually helps buffer acid in the muscle.
These latter points are an almost complete opposition to the historical thinking on Lactate. If this seems an outrageous assertion to you, please don’t take my word for it. Jump on Google and check it out. Here are a few really good articles, but there are many more.
The reason that these are such controversial assertions is that lactate and lactic acid were historically believed to be the source of muscle fatigue and soreness. The origin of this idea comes from some studies in the 1920s on resected frog muscles that were electrically stimulated until they fatigued. The researchers noticed a significant increase in lactate and acidity at this point. They mistook correlation for causation and concluded that lactic acid was the cause of fatigue.
The mistake stuck around for a while and got written into physiology text books. It was a nice tidy theory in that it was simple to explain without going into a lot of deep biochemistry or neurology. Many physiologists were taught for many years that lactic acid is the cause of muscle fatigue.
“It ain't what you don't know that gets you into trouble.
It's what you know for sure that just ain't so.”
But science is science and some researchers were unwilling to live with the contradictions they saw between the prevailing lactic acid theories for muscle fatigue and their own test data. This started in about the 1970s and continues through today (Three cheers for skeptical scientists everywhere).
Now that the effects of lactate are more clearly understood, significant doubt has been cast on the efficacy of Lactate Threshold testing. If lactate actually helps prevent fatigue rather than cause it, why measure when it starts to accumulate in the blood? Why is shifting the curve to the right better?
One uncomfortable result of the improved understanding of lactate is that no one has yet come up with a theory for muscle fatigue to replace the existing lactate theory that is nearly as tidy. The Central Governor Model as described by Timothy Noakes seems to be consistent with a lot of observed data, but it’s more complicated to understand.
Is Lactate Threshold Useful for Setting Training Intensity Zones Anyway?
Existing Lactate Threshold testing protocols have been inspired by the belief that lactate impedes performance and that it can be readily measured. The idea that lactate is a bad thing is clearly incorrect, however it raises an important question - is Lactate Threshold a useful method for setting training intensity zones even though its origins are misguided?
I see several factors that make this question interesting:
- Many races have been won by athletes whose training was based on Lactate Threshold,
- Lactate levels often rise in correlation with fatigue-related factors such as acidity,
- Lactate Threshold testing typically defines training intensity zones based on an intensity that is close to whatever sport will actually be performed rather than an all-out intensity like Maximum Heart Rate or VO2 Max.
It is a difficult question to answer because most athletes improve performance no matter what they base their training on; only elite athletes run the risk of getting worse if their training intensity zones aren’t accurate. Everyone else merely gets better slower than they could have, which is difficult to measure.
This issue is further complicated by the elaborate efforts that have been taken to make Lactate Threshold testing work. Definitions and test methods have been refined over many years with the very practical goal of making the tests produce useful data rather than adhering rigidly to the notion that Lactic Acid causes fatigue. Some of the tests, like Onset of Blood Lactate Accumulation (OBLA), Maximal Lactate Steady State (MLSS) or Lactate Balance Point, may have developed usefulness through an evolutionary process of natural selection of what worked most of the time rather than from a solid theoretical basis.
Given these (and doubtless other) confounding factors, I’m going to have to leave this question with an “I don’t know.” Certainly, having feedback about lactate levels could be helpful to a knowledgeable trainer to better understand what is going on in an athlete’s body, but this is different than saying that Lactate Threshold is a useful method for setting training intensity zones.
There are a few other practical factors associated with Blood Lactate testing that should be taken into consideration. First, it requires a blood draw, which raises some safety concerns. Second, it provides one data point every several minutes rather than a continuous stream of data; looking for changes in the slopes of lines or break points when you only have 5 to 20 data points introduces some mathematical uncertainty.
Third, blood lactate is measured at the fingertip or earlobe, both of which are a minute or two away from the working muscle via the circulatory system; this means the data is delayed from the work that caused it, making interpreting the data a bit more challenging. Moreover, it’s also challenging to interpret the data because lactate can be produced in one muscle cell and consumed somewhere else; the fingertip measurement only shows the net result rather than what is going on locally.
Here’s the bottom line. If setting training intensity zones based on Lactate Threshold works, it’s only because the methods have been tweaked over time to make them work in spite of being based on an incorrect theory.
My next blog post in this series will take a closer look at a method for setting training intensity zones that was also developed based on the idea of a Lactate Threshold, however, it’s been tweaked so much that it doesn’t rely on lactate at all in practice. This method is called Functional Threshold Power.