Shownotes

VLamax background

03:25 -

• VLamax attempts to measure maximum lactate flux through glycolysis.
• The method to obtain it is to take a blood sample at rest, perform a 15-20s sprint and take more samples after.
• You take the maximum lactate concentration obtained and calculate the rate of increased lactate. (measurement of the glycolytic flux)
• It comes from a Mader, 2003 paper, which described adequately cellular energetics.
• One of the topics was the rate at which phosphorylation was happening, the breakdown rate of phosphocreatine, and the blood rate of glycolysis.
• One method of evaluating this parameter is with the rate of lactate accumulation.
• This model is good, as long as lactate is not "disappearing" simultaneously. If we look at a whole-body level (you measure lactate remotely from the ear lobe or fingertip), to obtain lactate there, it has to exit the muscle, reach the bloodstream and the point where you are measuring.
• At that point, the lactate concentration relationship and the flux in the muscle do not coincide.
• VLamax comes from the assumption of taking a lactate sample after a maximal sprint and estimating the lactate accumulation rate.
• Lactate is a dynamic molecule concerning its use and value.
• Lactate concentration is a balance between the accumulation and clearance rates. It is not a direct measure of glycolytic flux.
• Therefore, the VLamax model is limited for me. It does not mean it is not applicable, but it is something I will be using.
• For me, there are too many steps in the process.

The scientific knowledge of VLamax

07:35 -

• Academically, it has not gained much traction. There are 3-5 papers where you will find it defined as VLamax.
• I do not find these papers convincing, and from a mainstream physiological perspective, there are many "academic battles" over the lactate concepts.
• In the early 1980s, there were significant debates between laboratories over the anaerobic threshold concepts.
• In the 1990s, there were many debates about the maximum lactate steady-state and different lactate threshold measurements.
• From a biochemical and physiological view, lactate is a controversial parameter. For that reason, physiologists avoid these topics.
• Unless you can link it to a physiological process, which is robust and defendable, you will not convince the academic community of its worth.
• Now, we have the lactate shuttle model as the central paradigm in which we interpret lactate concentration in the blood, and VLamax will be against this model and mechanism of lactate shuttle.
• There is lactate accumulation and clearance all around the body, which will affect the exercise you do and the lactate you produce.

The reason for VLamax gaining popularity

09:55 -

•  From a coaching perspective, if you can make a short sprint, measure something physiological and conclude something about your training, it is a powerful tool.
• If you believe that it has physiological robustness and a physiological parameter, it is an easy sell if you can measure your lactate and sprint power.
• We can give your VLamax and some software that you have to pay to understand your training and other parameters that derive from it.
• If you are going to use it, it is suitable as an absolute comparison of values before and after training; however, if you use it to predict VO2max and your training zones, I think that is too far.
• If you have a sprinter and they have a high VLamax, it makes sense.
• If you have an ultra-endurance athlete, they will have a low VLamax.
• These two things make sense. Then, if you want to measure minor changes between those two individuals, VLamax is not suitable.
• It will depend on the fluxes and the point where we take lactate samples. Trying to make conclusions from that is doing too much speculation.
• People use it much because it is easy to measure and you can compare it to other people. (that does not make it physiological meaningful)

Potential for future VLamax studies?

12:20 -

• It is something that I would read more about to understand the concept better. However, I would use it as an interesting undergraduate project, and it would not be something I would be investing in an entire research project.
• By looking at the measurements, you can already understand some limitations of this parameter. 
• I do not think it will get much mechanistic interest from that perspective.
• It is already evident that taking a lactate sample after a sprint is not necessarily telling you what is happening inside the body.
• You might want to look at doing biopsy samples and comparing the values to the ones obtained with fingertip or ear lobe samples.
• You might find some traction in those individuals that want to destroy VLamax entirely. If there were something I devoted my time to, it would be in this area.
• I would be trying to demonstrate why the model is wrong.
• I am not sure that performing a maximal sprint and showing the maximal anaerobic capacity adds much value to our current knowledge of lactate threshold.

Mark's work on polarised training

15:12 -

• I started working on this topic during lockdown around 2020. At this time, the only thing people could do was share their training diaries.
• There were many papers on how elite athletes were training during this period. 
• People consistently presented how the polarised training model is the prefered model for elite athletes.
• There was a second stage of papers to explain why polarised training works.
• "You need to do this many hours of low-intensity training for these reasons, and you need to do high-intensity training for these other reasons. And try to minimise the stuff in the middle."
• I texted Andy Jones in the middle of the lockdown, saying that this does not sound right and we should write something countering these publications.
• We believe there was much confirmation bias: we have an elite athlete doing polarised training, so polarised training is optimal.
• Every time people put a training distribution, it would look like a polarised training approach.
• Out of context, it did not make too much sense to us. If you are an elite athlete and train twice per day, you will do a lot of low-intensity training. (especially for ironman triathletes)
• On the other hand, 800m runners will do a lot of high-intensity sessions and a lot of low-intensity work because it is what they have to work. (sprint and anaerobic capacity)
• It does not make it optimal all the time. 
•  Andy and I did the Science of Ultra podcast, and we talked about polarised training. (the host view was similar to ours)
• Therefore, we decided to write something about this.
• We wanted it to be a comprehensive review when we started writing, and it seemed too negative. As we were going against this idea, it did not seem like a balanced review. (there was not the other side of the argument)
• Andy contacted "Medicine and Science in Sports and Exercise" about this idea. And we could do this paper.
• We had a more straightforward job. We only had to show it was not optimal, whereas the others had a more demanding task of presenting it as the best method.
• In the end, I think we all agreed on the same ideas.
• This paper stimulated much debate in social media and those using this approach.

Arguments for polarised training not being optimal for endurance athletes

19:51 -

• If you look at the time spent training, you do not select the parts where you are only working. Therefore, you have the whole package.
• You will cross the three zones in any training session when you do that. To say you are minimising one of those three (the one in the middle) seems strange.
• When you look at the time athletes spend working, athletes will do something that looks pyramidal.
• They will do much low intensity (most training), less volume of zone two work and a smaller zone three work.
• The previous training interventions on polarised training had often unfairly compared to threshold training. They have a situation where you do 80 % of your training in zone one and 20 % in zone three. (0% in zone two)
• The opposition is doing only zone two, a bit of zone one and no zone three.
• My argument is that I have yet to come across any athlete who does not do any training of the critical power.
• Threshold training also includes zone three. 
• If you are not an elite athlete, you will not do the same training volume so you will do less zone one work anyway.
• Thus, your training will gravitate more to threshold training. You do not have much time, and you want to use it efficiently.
• So, you tend to do higher intensity work.
• Moreover, some of the reasons for using polarised training did not make much sense. There is this argument that if you do a lot of zone two training, it will be autonomically stressful.
• You will increase adrenaline, and your markers of HRV will change. (overstress yourself) And it is why you might want to avoid zone two work. 
• The evidence comes from Stephen Seiler's paper demonstrating that they will have the same effect on these stress markers if you do zone two or three.
• You cannot sustain the argument that you should avoid zone two if zone three does the same thing.
• You might get the argument that if they are equally stressful, it will be better to do zone three work. However, you cannot use the argument to say you should not do zone two work.
• The third argument is that many people advocate moderate continuous training (a phrase used in the literature), which implies zone one. 
• But when you look at the literature, few training studies looked at the physiological adaptations to zone one training.
• Most training studies that evaluate moderate and continuous training are studies where athletes do zone two training.
• They exercise at 60-70 % of VO2max in their continuous training.
• For most people, this is zone two training.
• We use zone two adaptations to imply that we should use zone one and ignore zone two.
• Therefore, I realised the literature that supports polarised training is messy.
• The other argument is that if you do high-intensity exercise, you do less angiogenesis. (you get less capillarisation if you do high-intensity work)
• Much of that work is from single-leg exercises, which differs from whole-body exercises.
• Therefore, there is not much saying that zone one is what we should do most of the time.
• I would speculate that we have to understand how big zone one is for an elite athlete. (their lactate threshold will be higher than for other people) They have more type one fibres or trained their type 2a fibres to behave more as type one fibres.
• Their lactate threshold could be at 65-70 % of their VO2max. 
• The oxygen flux will be high when they do the upper hand of zone one training. It will lead to more angiogenesis compared to someone that does not have such high lactate threshold.
• We cannot gather elite athlete responses to training to infer what training is suitable for everyone. It ignores the training intensity distribution, which may differ for a recreational athlete.
• I believe there is much overinterpretation of the literature concerning polarised training.
• There is potential for future studies on how commonly training zones are not correct. Some papers used ramp tests and measured HR and gas exchange, and did not correct the ventilatory threshold to the ramp they performed. HR is non-steady-state in these tests, so we need to check these parameters better.
• After these corrections, we can have much of the zone one work is in zone two.
• Therefore, this would change the training distribution from a polarised to a pyramidal model.

Counter arguments in favour of polarised training

29:03 -

• They retold the story presented in the literature. 
• Elite athletes tend to do this type of training.
• They raised the autonomic argument, which we do not find convincing. 
• It surprised me that they would talk about "pyramidal/polarised training".
• We agreed that elite athletes do a lot of zone-one work.
• I believe there is work to do on confirming that elite athletes do most training below the lactate threshold and that it may reflect any physiological parameters.
• Twenty years ago, I did a session with some swimming coaches training junior swimmers.
• We talked about endurance training and connecting what cyclists and runners did with what swimmers do.
• Swimmers tend to do much high volume and low-intensity work because they want the feel for the stroke.
• Therefore, they do many sets at those intensities.
• We had a training plan from Paula Radcliffe from Andy Jones on what marathon runners do.
• We put that on a slide, and one of the coaches was surprised that she only did that training volume.
• His concern was that some of the juniors were training too much.
• We asked the coach what would happen if the swimmers did half of the sessions. He could not answer, but we could not answer it either.
• No one had researched this before. And to this day, the effects of doing high amounts of training volume at a moderate intensity, over bringing the training volume at that intensity and increasing the volume at higher intensities.
• No one will know what will happen because, from a molecular view, we need to stress AMP-kinase to "change the oxygen machinery". It will signal PGC1-alpha, which is the marker for aerobic adaptations.
• To do that, we need to have metabolic stress.
• We can do it by going very long and decreasing your glycogen stores. It works because ATP breaks down into APD, which can break down into AMP.
• When that happens, it activates AMP-kinase to signal the PGC1-alpha that the adaptation needs to occur.
• It is easy to do with high-intensity training, so zone three training is crucial.
• One of those studies comparing polarised vs threshold training without zone three will limit the threshold training approach.
• We do not know whether those long moderate training sessions produce the same effects of zone three training; we do not know.
• I look more at the perspective of how many zone-one work athletes need to get the same high-intensity training adaptations.

Takeaways from the polarised discussion

34:48 -

• There has been a fixation on training intensity distribution. And what we want to know is what the best training sessions are when they train.
• When we talk about training sessions, we talk about "meals". 
• When we talk about the training intensity distribution, we talk about the "food intake over one year".
• However, you would not base your meals based on those percentages. Therefore, you would not do every meal with the same carb, protein and fat intake.
• Therefore, we need to describe better how to train athletes properly. We focused too far on the overall intensity distribution across a year or periodisation block. And we did not focus on the training sessions themselves.
• We need to look at the "pennies" rather than the "euros".
• The second point is that there is no optimal training.
• If you are looking for an optimal intensity distribution, you will not find one. 
• I understand the idea of polarising training at specific points. 
• As you are tapering, you will polarise your training.
• You might do more sweet spot work in a build phase, and the intensity distribution will differ.
• We return to focus on the day to day training sessions rather than the overall training intensity distribution.

Fatigue mechanisms

38:32 -

• We have done some work on this area on the moderate, heavy and severe domains, but not on the extreme domain.
• The fatigue mechanisms are peripheral if you exercise above the critical power concerning metabolic depletion and accumulation and acidity in the muscle.
• The rate of peripheral fatigue occurs 4-5 times faster above critical power than below it.
• Below the critical power, we enter an energetic fatigue domain, in which glycogen depletion and heat storage are crucial mechanisms in the fatigue process. 
• We know now that there are various glycogen stores within the muscle. The glycogen store serves the triad junction, where calcium pumps out and in, which seems to be critical for muscle function.
• If we lose it, it may result in task failure and hitting the wall.
• We see peripheral fatigue in the heavy intensity domain, but it is in energy depletion rather than high energy phosphorate metabolism.
• In the moderate-intensity domain, glycogen depletion continues to be essential in that domain. As we approach lower intensities, central fatigue also has an impact.
• More extended duration exercise has a higher component of central fatigue than the shorter bounces of exercise.
• We do not have a continuum because there are thresholds, but the fatigue is peripheral at high intensities and high energy phosphate metabolism mediated. In the mid-intensity, we have glycogen depletion and heat tolerance. And at low intensities, the fatigue is central. (brain fatigue)
• Muscle damage and mechanical wear and tear will be significant if you run. The damage will cause pain and demotivate you by increasing the perception of effort.

Complexity measurements

42:20 -

• When I was collecting fatigue data, the way I set out the monitors, I could evaluate what the torque signal was doing within a contraction.
• When you do these tests, you push against a rigid bar, and you can see the torque rises and stays where the target is and drops again.
• The participants had continuous information on the torque they were producing and the target they had to achieve.
• It is different from an ergometer, where you set it at a specific power and people pedal along without caring how much torque they generate.
• Some people do, and torque in cycling is an important metric.
• In fatigues studies, participants need to know what torque is doing. And in the experiments, we can better understand what is happening as they hit the torque target.
• As they got more fatigue, they became more and more regular in their pattern. Participants start wavy and chaotic, and as they fatigue, you can see a pattern of a sin wave appearing.
• My wife was good at signal processing, and she did complexity work in her PhD.
• She understood that there were many metrics we could use to explain what was happening.
• We used measurements like approximate entropy and detrended fluctuation analysis (alpha exponent - the same concept used for HRV: DFA-alpha 1)
• Approximate entropy looks at the regularity of the signal. If a signal is a straight line, the approximate entropy is low. If we have a chaotic line, approximate entropy will be high.
• DFA concerns the noise colour. If you have uncorrelated noise, we have white noise. But if you have correlated noise, we will have red noise, and in the middle, there is "pink noise", where there is self-similarity.
• Self-similarity is like a fractal pattern in the output. It is not only a geometric pattern, but in a time series, you can see the fractal pattern. (clear relationship between the frequency and noise type you are seeing)
• We know that pink noise appears in all-natural forms. 
• An easy way to look at this is that if you contract against something, if you start to fatigue, by being adaptable, you can adjust.
• Fatigue causes that adaptability to be lost. (lose complexity as we fatigue)
• The approximate entropy starts high and gets lower as you fatigue.
• When you look at DFA, it tends to look like "pink noise", and it moves to "red noise". So it becomes less complex.
• When we look at complexity, there is no straight metric,s but we use these metrics combined to assess if the complexity is changing.
• As you fatigue, complexity goes down. 
• We think a nice contraction reflects on a smooth line against the target, but that is not the case.
• You want some waviness because it tells you that your neuromuscular system is adaptable.
• As you fatigue, you get less adaptable, and it gets harder to achieve the target. You get more waviness in the signal.
• This moment is where you have lost your complexity.
• We only see this occurring above the critical torque. There is something that seems to be peculiar to high-intensity exercise.
• The second thing is that these parameters relate to peripheral fatigue. (it is the main drive)
• Ultimately, we know we can analyse what is happening inside the muscle by using the high energy EMG electrodes to pick up what all motor units are doing.
• When you analyse how the motor units behave, you notice they are changing, and they become less complex in the way they put out their signal to the muscle.
• So, we believe this is a result of the change in motor unit behaviour because of the effect of peripheral fatigue.
• We can take these measurements easily now. (torque in cycling, and stride patterns in the running)
• As you age, your stride patterns become less complex.
• We believe that this may also happen with fatigue.
• So, if you have any wearable device that can pick up these signals, we might have a situation where we can use it to track fatigue in real-time.
• With complexity, you only need to measure a signal in the real world to evaluate fatigue in real-time.
• It is where I believe this knowledge will go in the future. We can use it to assess your fatigue during workouts or recovery status before a workout.

LINKS AND RESOURCES:

• Mark's Twitter, ResearchGate, and Youtube channel
• Lactate threshold with Mark Burnley, PhD | EP#330
• DFA alpha-1: A non-invasive, cheap option for estimating the aerobic threshold with Bruce Rogers, MD | EP#329
• Things you didn't know you didn't know: physiological complexity - video on All Out Physiology
• Polarized Training is Not Optimal for Endurance Athletes - Burnley et al. 2022
• Polarized Training is Optimal for Endurance Athletes - Foster et al. 2022