Physiology of Lactate Threshold and Practical Applications to Training
All right, now that we've briefly covered the basics of
lactate metabolism, let’s move on to training for lactate production, transportation and oxidation.

As for completing longer 40+ minute LT runs - I do not believe these are appropriate for 800/1500m runners because they are not specific in terms of pace or energy demands. No, 40:00 LT runs should not be difficult for 1500m runners, but that does not mean they should do them. Running 40:00 at a pace near LT, you get relatively low lactate values (maybe 4-6 mmol/L) - which do not replicate the >10 mmol/L that will be seen during 1500m running. Additionally, during the relatively prolonged slower pace 40:00 run, the athlete will not be recruiting the faster twitching glycolytic fibers to the same degree that will be called upon during a 1500m race. This is not to say that 1500m runners should never complete 20-40 minute LT runs. But these types of workouts should be saved for recovery cycles, or early introductory periods.
Cairns Simon P. Lactic Acid and Exercise Performance Culprit or Friend? Sports Med 2006.
Janssen, Peter. Lactate Threshold Training. 2001. Human Kinetics.
Juel C., Halestrap AP. Lactate transport in skeletal muscle – role and regulation of monocarboxylate transporter. J Physiol 1999;517;633-642
Morris DM, Shafer RS. Comparison of power outputs during time trialing and power outputs eliciting metabolic variables in cycle ergometry. Int J Sports Nutr Exerc Metab 2010; 20(2):115-21
Production, of course, refers to the creation of lactate
through glycolysis. And remember, to be able to create lactate, glucose must be
present (from blood glucose or cleaved from glycogen) to run glycolysis. So to
create lactate, an athlete needs to engage in training that relies on
glycolysis for ATP production, in turn creating H+ and lactate. Again, lactate
is not the molecule we need to buffer or transport out of the cell. It is the
H+ that accompanies lactate that disrupts glycolysis and muscle contraction. H+ must be transported out of the muscle cells by monocarboxylate
transporters (MCTs). These are H+-Lactate co-transporters, meaning H+ and
lactate must be present before they are both pumped out of the cell together
into extracellular space. Then the lactate and H+ may diffuse into the
bloodstream.
When the H+ and lactate diffuse into the bloodstream,
the H+ will be buffered by phosphates and bicarbonate. See below:

Reading the equation from right to left, increasing [H+] in
the plasma will consume a proton to create carbonic acid (H2CO3). Applying Le
Chatelier's principle, we know that decreasing [CO2] will enable this reaction
to proceed to the left. That is one reason why ventilation increases
dramatically (ventilatory threshold) near lactate threshold (to purge the blood of CO2 to buffer the H+
created from very high rates of glycolysis).
Because of this buffering mechanism, we see relatively constant plasma pH values with increasing intensities, and increasing [lactate]. But eventually, with high enough intensities, the buffering mechanisms
become overwhelmed and plasma pH drops. This is known as acidosis. It has been argued that pH threshold is a better indicator of
performance than lactate threshold (Morris and Shafer, 2010). Here you can see,
the difference in power outputs at the two different thresholds:
pH is indicated by magenta markers, [Lactate] is indicated
by the blue. Notice, the pH threshold in these subjects (240W) falls long after
the lactate threshold is met (200W). This further demonstrates that it is not the accumulation of
lactate that contributes to acidosis, rather it is H+. Morris did, however, find that pH threshold and lactate threshold are
significantly correlated to 20 km time trial performance; meaning, the higher power
output at lactate threshold (LT) or pH threshold, the faster the time trial
performance. The same can be said for running performance – the faster an
athlete can run before lactate accumulates,
the faster that athlete will be able to complete a bout – indicating a need for
high lactate thresholds, or high work rates with less reliance on glycolysis.
To raise an athlete’s LT, training can be approached from a multitude of angles, but two of the most utilized workouts are tempo runs and intervals. Tempo runs or lactate threshold runs are generally done at paces/workrates just slower than or equivalent
to LT – often referred to as maximal lactate steady state (MLSS), or just LT. Sometimes you will hear coaches talk about anaerobic lactate threshold runs - these are just sustained 10-20:00 runs done just above lactate threshold pace. Training at paces/workrates greater than LT – also
called supramaximal or intensive intervals are shorter bouts of higher intensity training separated by bouts of recovery.
An example of the first workout is a steady 40:00-60:00 @
LT pace, whereas an example of a supramaximal session would be something like 8-12
x 1:00-3:00 at >100% LT with 1:00-3:00 recovery. Physiologically, the responses
to the two workouts are very different from one another – blood lactate
concentration during the 40:00-60:00 LT run may remain relatively constant
between 3 – 6 mmol/L, whereas lactate values during the supramaximal intervals
may be as high as 20+ mmol/L.
Looking at these values, one might assume that “more is
better” and supramaximal intervals must stress the system more because they invoke
higher lactate values. But consider the time of the bouts – keeping in mind
recoveries after the shorter supramaximal intervals. While the shorter
intensive intervals may cause higher spikes in blood lactate, they are short
lived. And by completing extensive intervals or steady runs near LT, blood lactate concentrations will remain relatively low, but over a longer period of time. So, which will make you faster? Arguably, both. But which is best? Well, it depends.
Graph 96, from Peter Janssen’s book Lactate Threshold Training, demonstrates lactate responses to the respective types of training. Admittedly, this graph is a bit over simplified – but it gets the point across. Intensive (supramaximal) intervals elicit high [lactate] but can only last so long (1:00 - 3:00). Whereas longer extensive repetitions (3:00 - 10:00) elicit lower [lactate], but an athlete can sustain them over longer period of time. And finally, intensive endurance (MLSS, marathon pace) runs elicits even lower [lactate], but can be sustained for a substantially longer period of time (20:00 - 60:00).
Graph 96, from Peter Janssen’s book Lactate Threshold Training, demonstrates lactate responses to the respective types of training. Admittedly, this graph is a bit over simplified – but it gets the point across. Intensive (supramaximal) intervals elicit high [lactate] but can only last so long (1:00 - 3:00). Whereas longer extensive repetitions (3:00 - 10:00) elicit lower [lactate], but an athlete can sustain them over longer period of time. And finally, intensive endurance (MLSS, marathon pace) runs elicits even lower [lactate], but can be sustained for a substantially longer period of time (20:00 - 60:00).
Training to maximize lactate threshold or pH threshold is no
easy task. There are multiple ways to
approach the issue when it comes to types of workouts and timing of workouts in
preparation for a season or championship race.
First, a coach or athlete must recognize the specific
demands of the goal race because specificity is important when choosing the types of workouts an athlete should run. A 1500m is much different in terms of energy demands from
a half marathon. Lactate values during a 4:00 1500m may reach
>15 mmol/L whereas lactate values during a 65:00 half marathon may be closer
to 4-6 mmol/L. And since lactate threshold has been found to be closely
correlated with pH threshold (Morris and Shafer, 2010), it’s safe to assume
that intramuscular/plasma pH falls lower during 1500m running than it does
during a half marathon.
With that said, and with the rule of specificity in mind –
training for the respective events should mimic their demands. 1500m runners
should engage in high-intensity training to create large amounts of
lactate. But if exercise continues (without recovery periods or rest) the athlete will experience a decrease in intramuscular pH and eventually the exercise will cease. Remember Table I from Cairns
(2006):
In this review, Cairns demonstrates that short high
intensity exercises do indeed elicit the greatest decrease in muscle pH. The
lowest values found here were after 20 minutes of 30-40s repeated sprints, and
during maximal exercise lasting from 1.5 to 11 minutes. Unfortunately, I
cannot access reference 21 to look up the repeated sprint exercise protocol.
It’s nothing profound, but this data indicates that these
exercises best mimic the demands of the 1500m run – and a 1500m runner would be
wise to run intervals of 30s to 11 minutes. But wait, 11 minutes? That’s a long
interval. And remember, these were maximal efforts – running a workout
consisting of multiple 11 minute intervals at a maximal effort just isn’t feasible. That’s because a drop in pH (acidosis) inhibits glycolysis, inhibiting ATP production in subsequent
bouts. Therefore, a 1500m runner is better off completing 2 sets of 6-8 x 60s
with 60-75s recovery and 3:00-4:00 active recovery between sets.
By incorporating active recovery into the workout, lactate is transported out of the glycolytic muscle cells along with those hydrogen ions (by the MCT co-transporters). The H+ ions will be buffered by bicarbonate, and lactate can either be transported to the liver to be converted back into glucose, or transported by MCT1 into oxidative (slower twitching) muscle fibers and utilized for ATP production in the Krebs cycle and then oxidative phosphorylation. So, what you see with recovery is a decrease in lactate, and increase or maintenance of intramuscular/plasma pH. Because intramuscular pH is maintained with adequate recovery, glycolysis is not inhibited and the athlete can complete more work: more sets or reps. In this case, instead of completing 11 minutes in one bout, the athlete can complete 12-16 minutes of work at or near the same workrate or pace.
By incorporating active recovery into the workout, lactate is transported out of the glycolytic muscle cells along with those hydrogen ions (by the MCT co-transporters). The H+ ions will be buffered by bicarbonate, and lactate can either be transported to the liver to be converted back into glucose, or transported by MCT1 into oxidative (slower twitching) muscle fibers and utilized for ATP production in the Krebs cycle and then oxidative phosphorylation. So, what you see with recovery is a decrease in lactate, and increase or maintenance of intramuscular/plasma pH. Because intramuscular pH is maintained with adequate recovery, glycolysis is not inhibited and the athlete can complete more work: more sets or reps. In this case, instead of completing 11 minutes in one bout, the athlete can complete 12-16 minutes of work at or near the same workrate or pace.
As for completing longer 40+ minute LT runs - I do not believe these are appropriate for 800/1500m runners because they are not specific in terms of pace or energy demands. No, 40:00 LT runs should not be difficult for 1500m runners, but that does not mean they should do them. Running 40:00 at a pace near LT, you get relatively low lactate values (maybe 4-6 mmol/L) - which do not replicate the >10 mmol/L that will be seen during 1500m running. Additionally, during the relatively prolonged slower pace 40:00 run, the athlete will not be recruiting the faster twitching glycolytic fibers to the same degree that will be called upon during a 1500m race. This is not to say that 1500m runners should never complete 20-40 minute LT runs. But these types of workouts should be saved for recovery cycles, or early introductory periods.
The same goes for cyclists – except cyclists can generally
complete more extensive workouts than runners because of the absence of eccentric
muscle contractions.
Not only can you get more work out of your workouts with
adequate recovery, but the recovery can also train the MCT co-transporters and
slower twitching muscle fibers. Because high intensity exercise creates large amounts of lactate, it will also increase the number of MCT4
co-transporters so that more lactate and H+ can be transported out of the glycolytic
fibers. Further, high intensity exercise has also been shown to increase MCT1 (Juel and Halestrap, 1999). MCT1
transports lactate and H+ into slower twitching oxidative muscle fibers. Here, lactate
dehydrogenase can convert lactate back into pyruvate to be converted to acetyl Co-A and oxidized it in
the krebs cycle. So in a way, your slow twitching fibers become hydrogen buffers and lactate "recyclers."
But what about our half marathoner? The guy running for 65:00
at roughly lactate threshold. Could he also benefit from high intensity intervals?
You bet! By increasing lactate and H+ clearance from glycolytic fibers, they’ll
be able to function at a higher capacity for a longer period of time.
Additionally, by increasing the number MCT1 co-transporters, he’ll be better able
to buffer H+ and use it and lactate as fuel in his slower twitching oxidative
fibers. But, with that said it is still important to keep event specificity in
mind. High intensity intervals are not the be-all and end-all. A 65:00 half
marathoner likely does, and should do high intensity interval training, but he
may do them less frequently than the 800m, 1500m, or 5000m runner.
Additionally, his intervals should be longer and slower than those of the 1500m
runner to emphasize specificity. A main-set for this half marathoner may be 5-6
x 2k at 100-105% LT (5:00 – 4:45/mile) with 60-120 sec. recovery. The recovery
to work ratio here does not need to be as high as it would be for the 1500m
running his workout because running within 5% of LT should not cause an
accumulation of H+ that would inhibit glycolysis.
I’ve mentioned a couple of examples of workouts for middle
and long distance runners, but through the course of a season or build to an
important race we don’t want to have the athlete complete the same workout
again and again. I believe the athlete needs some variety, and a change in
training stimulus to continue to improve. And it can get complicated when developing a
training plan – depending on whose coaching methodology you follow, or what you
believe in terms of periodization and progression. A number of coaches (Jack
Daniels, David Morris, Brad Hudson, Joe Friel, and Arthur Lydiard) prescribe
shorter, higher intensity bouts early to midway through in the training phase – even for the marathon
runner or long distance cyclist.
These short high intensity intervals can work to raise LT by
increasing the number of MCT co-transporters while potentially building
strength and improving recruitment through faster running. These
high intensity interval workouts are not high in volume so that the short intensive
interval sessions can also serve as primers for longer more extensive workouts. After completing 6-8 weeks of training with a mix of high intensity intervals when our half marathoner goes to run his steady 40:00-60:00
LT run or 3-4 x 2 mile interval workout, he can actually maintain a higher pace (and still be running at LT) than he would if he had not completed the intensive training early in the
training period because he can transport, buffer H+ and utilize lactate. Late in the training phase, half marathoners and marathoners should incorporate more and more of the pure LT running with 40:00 - 60:00 @ LT or long broken LT intervals because they are more specific to their respective events.
And that's about all I have to say about that. I'm sure I'll think of something I left out later.
And that's about all I have to say about that. I'm sure I'll think of something I left out later.
References
Janssen, Peter. Lactate Threshold Training. 2001. Human Kinetics.
Juel C., Halestrap AP. Lactate transport in skeletal muscle – role and regulation of monocarboxylate transporter. J Physiol 1999;517;633-642
Morris DM, Shafer RS. Comparison of power outputs during time trialing and power outputs eliciting metabolic variables in cycle ergometry. Int J Sports Nutr Exerc Metab 2010; 20(2):115-21
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