What is Lactate and Lactate Threshold
Thursday, July 17, 2014 | By Iñigo San Millán, PhD
Lactate threshold has been a term used for many years across all sports
and it is one of the most daily pronounced terms in the world of
training by athletes and coaches worldwide. However, do we really know
what lactate threshold is? Furthermore, do we know what lactate is and
its role in performance and metabolism? The fact is that there is still
too much confusion regarding what lactate is as well as what lactate
threshold represents.
What is Lactate?
Lactate is a great unknown in human metabolism despite its key role in
regulating metabolism. For many years it has been thought that lactate
was just a waste product as a result of anaerobic exercise or even a
waste product of exercise that would crystalize resulting in muscle
soreness. Nevertheless, lactate has been subject of study for many years
and by important scientists including several Nobel Laureates. Lactate
studies date back from the 19th century when a Nobel Laureate, Louis
Pasteur in 1863 proposed that lactate was produced by lack of oxygen
during muscle contraction. Another Nobel Laureate, Otto Meyerhof
described in 1920 that glycogen was a precursor of lactate. He also
observed that muscle contraction produced lactate and loss of
excitability. In 1923 another Nobel Laureate, AV Hill and his colleague
Lupton described the term “O2 Debt” and linked it to anaerobic lactate
production.
However, it wasn’t until late in the 20th century when we have started
to understand about lactate and its key role in exercise and metabolism.
Dr. George Brooks, from the University of California at Berkeley, and
one of the best experts in metabolism of all times, has studied lactate
extensively for more than 40 years and most of everything we know about
lactate nowadays is thanks to his work. One of the things we know from
his work is that lactate formation can perfectly occur under plenty of
aerobic conditions and that lactate production is the result of glucose
utilization by muscle cells under aerobic conditions. From Brooks’ work
we also know that lactate is not a waste product and in fact it is the
most important gluconeogenic precursor (new glucose generator) in the
body.
"Lactate is not a waste product and in fact it is the most important
gluconeogenic precursor (new glucose generator) in the body."
As a matter of fact, about 30 percent of all glucose we use during
exercise is derived from lactate “recycling” to glucose. Lactate is also
a key regulator of intermediary metabolism, regulating substrate
utilization. Lactate decreases and even inhibits the breakdown of fat
for energy purposes (lipolysis) as well as it can also interfere and
decrease the rate of glucose utilization by cells (glucolysis). Also,
believe it or not, lactate is crucial for the brain as lactate is the
main fuel that neurons use and it is essential for long-term memory and
could even be involved Alzheimer’s disease. Some studies show that when
lactate uptake by neurons is suppressed, long-term memory is inhibited.
Lactate could also be involved in some chronic metabolic diseases like
type 2 diabetes as blood lactate levels in this population are 2-3 times
higher than in healthy physically active population and it could be a
major player in this disease. Cancer cells have a disrupted metabolism
utilizing too much glucose aerobically (Warburg effect) and producing
large amounts of lactate which could contribute to tumor growth and
progression. Therefore, lactate is not just a waste product of anaerobic
exercise but a major fuel and a key regulator of metabolism and its
role in the possible epicenter of different chronic diseases is starting
to be investigated.
Lactate and Performance
Lactate is the byproduct of glucose utilization by muscle cells. The
higher the glucose flux into the cell, the higher the lactate
production, independently of oxygen availability. During high intensity
exercise Type II-Fast Twitch muscle fibers are fully recruited due to
high contractile demands by skeletal muscle to produce energy (ATP).
Type II muscle fibers are highly glycolytic (they use lots of glucose)
which results, under plenty of aerobic conditions, in the production of
high amounts of lactate as a natural by-product of glucose utilization
by skeletal muscle cells. During intense exercise, lactate production is
many times higher than that of resting levels and the release of
hydrogen ions (H+) associated with lactate can cause an important
reduction of contractile muscle pH resulting in acidosis. This excessive
accumulation of H+, not only from lactate, but also from ATP breakdown
for muscle contraction (ATP hydrolysis), may interfere with muscle
contraction at different sites like competing with Calcium (Ca++) for
Troponin C binding site (a protein involved in muscle contraction
regulation). H+ may also inhibit calcium release and re-uptake from
sarcoplasmic reticulum both processes involved in muscle contraction.
All this can result in a decrease muscle contraction capacity which can
cause an important decrease in peak twitch force, a decrease in maximum
muscle shortening velocity and performance.
We know very well that the better the competitive and training level of
an athlete is, the less blood lactate accumulation that is observed. In
table-1 we can observe blood lactate levels of different cycling
categories at different exercise intensities (watts/kg) that I have
collected over the years during physiological tests. We can clearly see
that the higher the competitive level of a cyclist, the lower the blood
lactate and the higher the power output and performance.
Workload |
Junior Cyclist |
Top Amateurs |
Avg. Pro-Tour |
World Class |
w/kg |
Blood La (mmol/L) |
Blood La (mmol/L) |
Blood La (mmol/L) |
Blood La (mmol/L) |
3 |
1.3 |
1.1 |
1.1 |
0.8 |
3.5 |
1.8 |
1.3 |
1.2 |
0.8 |
4 |
3 |
2.3 |
2 |
0.96 |
4.5 |
6.6 |
3.5 |
3.2 |
1.8 |
5 |
10 |
7.6 |
5.8 |
3.1 |
5.5 |
|
9.2 |
8.2 |
5.2 |
6 |
|
|
|
8.9 |
Table 1. Differences in Blood Lactate levels (mmol/L)between
competitive cyclists of different levels. Table Modified from San Millán
et al, 2009
This lower blood lactate levels observed in the top athletes is due to
an enhanced lactate clearance capacity. Lactate can be exported to the
blood for clearance and energy purposes in pretty much every organ in
the body. However, this process takes time (minutes) while lactate is
produced continuously during exercise. Well trained athletes are very
efficient and export less lactate to the blood as they clear it in
higher amounts right in the lactate producing muscle which takes seconds
or milliseconds. This is very advantageous as it allows contractile
muscles a faster H+ removal as well as a faster lactate “recycling” for
extra energy (ATP) within that contractile muscle. During exercise,
lactate is mainly produced in fast twitch muscle fibers which use lots
of glucose for energy purposes and it is cleared mainly by slow twitch
muscle fibers. This is a complex process involving different
lactate-specific transporters and enzymes. Fast twitch fibers have a
high content of one transporter called MCT-4 (Monocarboxylate-4) which
transports lactate away from these fibers and slow twitch fibers possess
a transporter called MCT-1 which takes lactate inside these fibers
which is then converted to pyruvate in slow twitch fibers mitochondria
by an enzyme called mLDH (mitochondrial lactate dehydrogenase), to then
finally synthesize ATP (energy). Endurance training (Zone 2) has the
purpose of improving lactate clearance capacity by increasing the number
of mitochondria to clear lactate mainly in slow twitch muscle fibers as
well as by increasing the number of MCT-1 and mLDH. Both high intensity
and endurance training increases the number of MCT-4 to increase
lactate transport away from fast twitch fibers.
As shown in table-1 lactate is probably the parameter that
discriminates the most between different levels of athletic performance.
Lactate analysis can give us a lot of information on muscle metabolism
during exercise where we can indirectly assess mitochondria density,
oxidative and substrate utilization status or muscle fiber recruitment
patterns. Lactate testing is probably the best way to assess muscle
metabolic stress and performance, especially in endurance athletes. It
is also probably the best method that we have to predict performance in
endurance events as well as an excellent parameter to prescribe
individual exercise training zones for athletes. Among those training
zones “lactate threshold” is that special training zone we all want to
train and improve. The only way though to directly measure lactate
threshold is by doing lactate testing.
What is Lactate Threshold?
Lactate threshold is probably the most used training term by coaches
and athletes worldwide. However, there is wide controversy as of what
lactate threshold really means as well as to what is the exercise
intensity that elicits it. Lactate threshold is commonly known as the
exercise intensity or blood lactate concentration at the one we can only
sustain a high intensity effort for a specific period of time. However
this is where the controversy is: What is that period of time? What is
that blood lactate concentration at? How long can we sustain that given
exercise intensity for before we crack down?
Many authors and coaches have been trying to answer these questions for
a very long time. The first description of a blood lactate threshold
dates back from 1930 and it was named by W Harding Owles, the “Owles
Point”. In 1964 Waserman and Mcilroy proposed the term “anaerobic
threshold” based on the belief that lactate accumulation was due to a
lack of muscle oxygen availability and therefore anaerobic muscle
metabolism was necessary for the continuation of muscle contraction.
Mader and co-workers determined in 1976 that “anaerobic threshold” was
reached at the blood lactate concentration of 4 mmol/L (milimol per
liter) which was in 1981 named by Sjödin and Jacobs “Onset of Blood
Lactate Accumulation” (OBLA) occurring at the blood lactate
concentration of 4 mmol/L as well. Farrel and co-workers proposed in
1979 the term Onset of Plasma Lactate Accumulation (OPLA) which was the
exercise intensity that elicited a blood lactate concentration of 1
mmol/L greater than baseline. Another term proposed in 1981 by
LaFontaine and co-workers was the “Maximal Steady State” which in theory
happens at a blood lactate concentration of 2.2 mmol/L. In 1983 Coyle
and co-workers proposed the term “Lactate Threshold” which was a
non-linear increase in blood lactate of at least 1 mmol/L. Another term,
“Maximal Steady-State Workload” (MSSW) was proposed by Borch and
co-workers in 1993 and was established at the fixed [La-] of 3 mmol/L.
Veronique Billat in 2003 proposed the term Maximal Lactate Steady State
(MLSS) as the exercise intensity at the one blood lactate can be
sustainable.
Confusing, isn’t it? There are multiple theories and hypothesis among
the scientific community and not a common consensus of what “lactate
threshold” is. The bottom line to understand what lactate threshold
means is that as muscles get more metabolically stressed there is a
higher lactate accumulation and H+. Mitochondria in contractile muscles
become more stressed to clear lactate in a timely manner and at some
point, if the exercise intensity continues, contractile muscle
mitochondria become saturated and therefore cannot keep up with lactate
clearance, then exporting it to the blood and this is when we see a rise
in blood lactate levels which correspond to the metabolic event when it
is not possible to maintain that given exercise intensity.
In my opinion it is important to look at the lactate threshold concept
from a different angle. In the first place unfortunately, many athletes
and coaches don’t perform lactate testing so they can never find out
about their lactate metabolism despite they still talk about lactate
threshold training.
"Many athletes and coaches don’t perform lactate testing so they can
never find out about their lactate metabolism despite they still talk
about lactate threshold training."
Furthermore, we tend to describe lactate threshold efforts to those
high exercise intensities we can sustain for relatively short periods of
times without “blowing up” and this is where there is a lot of
confusion. Where do we define that exercise intensity and period of time
at the one we can sustain a high effort?. Is it 5, 10, 30 or 300 min?
Is it at 3, 4 or 6 mmol/L of blood lactate concentration? Climbing a 5km
Cat-1 climb during 25 minutes without getting dropped requires a
specific “lactate threshold”/maximal steady state which could represent a
blood lactate concentration of 4-6mmol/L and a specific individual
power output (or fractional threshold power/FTP). This intensity however
is different than climbing a 10km Cat-2 climb without getting dropped,
which may take 40 minutes and therefore a different threshold/maximal
steady state which could represent a blood lactate concentration of 3-5
mmol/L and a different FTP which at the same time is different than that
threshold or maximal steady state of a 40km TT. Running a marathon at
goal pace requires a very important effort at maintaining a maximal
steady state which is actually a truly lactate threshold for the entire
marathon which elicits a blood lactate concentration of ~2-2.5 mmol/L.
This threshold is different and elicits a higher blood lactate
concentration for a ½ marathon, a 10K or a 5K race. It seems that each
endurance sport has different “lactate thresholds” which are key in
order to perform successfully.
Evolving Lactate Threshold
All this seems too confusing and for this reason I believe that it is
time to evolve the lactate threshold concept in a more pragmatic manner.
We may need to consider different terminologies like for example a
concept of a maximal metabolic stress that can be sustained for a given
amount of time (“maximal metabolic steady state”/MMSS). Depending on the
sport and event, there would be different MMSS which would represent
the maximal metabolic stress that we can sustain for a specific distance
and discipline like a marathon, 1500m, a 10k run, a 40km TT or a 5km
Cat-1 climb. Then we can translate this MMSS to a blood lactate
concentration to get our lactate threshold or to other different
parameters like heart rate, power output (FTP) or running pace. This is
not just a useful way to predict performance but also to track progress.
In a way this is already being done by many coaches and athletes who
use FTP or goal pace all the time.
Training Misconception Around Lactate Threshold
A typical training mistake that many athletes and coaches do is
training at “lactate threshold” in order to improve lactate clearance
capacity. This is not correct as we know that during exercise lactate is
mainly produced by glycolytic fibers (fast twitch) which are the ones
recruited at “lactate threshold”. However, lactate is mainly cleared by
adjacent slow twitch fibers that have a very high mitochondrial capacity
and a much higher amount of mLDH enzymes and MCT-1 transporters.
Therefore to improve lactate clearance capacity, and although totally
counterintuitive, it is key to train those slow twitch muscle fibers to
stimulate mitochondrial growth and function as well as increase MCT-1
and mLDH. Training at lactate threshold is essential to improve
glycolytic fibers and their machinery (our “Turbo”) and to upregulate
the number and function of glycolytic enzymes as well as to increase the
number of MCT-4 transporters necessary to transport lactate away from
fast twitch fibers to then be cleared by slow twitch fibers. Spending
too much time at lactate threshold is very tasking as well, as it is a
high effort and can lead to overtraining which is something we
constantly observe in our lab.
We constantly see in our lab athletes and coaches that have this
misconception and make this mistake leading to overtraining and not
improving lactate clearance capacity. With specific protocols we measure
lactate, fat and carbohydrate metabolism during all exercise
intensities to study the whole metabolic and physiological response to
exercise which allows us to predict performance as well as to define
individual training zones quite clearly, in particular Zone 2 (Z2) which
with the experience over the past 18 years it has shown to be the
training zone eliciting the best results to improve lactate clearance
capacity.
"Zone 2 (Z2) has shown to be the training zone eliciting the best results to improve lactate clearance capacity."
So many athletes come to our lab without knowing these concepts and
train too much at “lactate threshold” and by identifying their specific
training zones we turn their training programs completely upside and we
constantly see very important improvements in their lactate clearance
capacity and performance while at the same time we significantly
decrease the cases of overtraining.
To conclude, lactate threshold remains as the most used training term
worldwide and yet there is no consensus of what exactly it represents.
There is too much confusion not just regarding what lactate threshold is
but also what lactate per se is and what its role and importance in
exercise and metabolism is. I believe simply that after several decades
of discussion and controversy, it is time for the “lactate threshold”
concept to evolve and be named and defined differently so athletes and
coaches can use it in a more meaningful and understandable manner in
order to describe that “magic” exercise intensity that can only be
sustained for a specific amount of time which is crucial for performance
and success.
About the author
Dr. Iñigo San Millán, Ph.D., is the Director of the Exercise Physiology
and Human Performance Lab at the University of Colorado School of
Medicine and also Assistant Professor of Family Medicine and Sports
Medicine Departments at the University of Colorado School of
Medicine. Dr. San Millán is considered one of the most experienced
applied physiologists in the world. He has worked with many elite
athletes and teams in sports including track and field, running,
triathlon, rowing, basketball and cycling; including eight professional
cycling teams. Follow Iñigo on Twitter.