Athletes weakest link - MCL

“Maintainer Compensator Limiter-MCL”, these terms are something that most people are unfamiliar with and most physiologists don't want to accept or understand yet.  (MCL is something that is well researched by FaCT and still ongoing.) So here is a deeper insight into understanding the body which was touched in one of my previous articles, "The FaCT way of looking at the body".

MCL

If you have read my previous article then you might understand that the body has three trainable systems, cardiac, respiratory and muscle. Traditional physiologist would disagree but if you look at the research done (FaCT) these three systems are perfectly trainable. What stops an athlete from performing at his best and going faster or harder is his weakest system called the Limitation, knowing what the Limitation is would thus make sense to improve. But it goes deeper than this. Where there is a Limiter there is a Compensator and a Maintainer. In well trained athletes when the Limitation is reached one of the other systems in the body will compensate for the weak link to keep pushing the body. In most cases an athlete will have one very strong system (Maintainer) which will not be a Limiter or Compensator and just happily keep on going without getting stressed.

What does this basic understanding of the body mean to us? This is where we go deeper into understanding what is going on and you may start to understand why it is perhaps not always the best idea to finish a preplanned interval when you are unable to maintain the time or heart rate. And why, objective intervals are just that, objective. Let's look at the physiology from a new angle and why you should stick to your training zones.

The weakest system, cardiac, respiratory, muscle, will reach its weakest state at LBP aka lactate threshold, of which lactate is the indicator. The body will have a Compensator to compensate for the Limiter which will happen most times in a race situation. which you may think is great, so training above LBP is good to a point, as you improve your Compensator but it does not matter how strong the Maintainer and Compensator is, the athlete WILL ONLY GO AS FAST AS HE'S WEAKEST LINK (Limiter).

If you always push on or slightly above LBP you will ALWAYS overload the Limiter 'who' creates LBP (threshold). If the Limiter is always overloaded severely it will get weaker (UPS underperforming syndrome and LBP will drop) and in turn the Compensator will get overloaded also! If there is no Compensator, overtraining may take place if the Limiter is pushed too often which will create a breakdown of the system overall. Thus you need to know which is the Limiter and Compensator and you have to know which one needs what amount of recovery to be pushed again. This does not mean that you should not go to max heart rate and push over the LBP, you just need to know how long to stay there and give the recovery before the next rep. Do you think it is still a great idea to guess your threshold and that speed and watts is the best idea for intensity?

Here is a picture from a portable hemodynamic cardiac machine showing stroke volume on the left. This example is from a triathlete doing a brick workout having gone from the bike transition to the run. The stroke volume shows a ''collapse'' as the body has been stressed too far in a normal intensity workout.

LOOKING AT THE SYSTEMS MORE CLOSELY

Here are three easy ideas to think about

a. Who is the Limiter?

b. Who is the Compensator?

c. What muscle fibre type and how strong?

If your cardiac and or respiratory (vital organs) are a clear limiter, than you will have a problem going above LBP and maintain the performance. You will be able to go above LBP with the Heart Rate but you will always loose performance. The reason is the CGM (cardio reflex and metaboreflex). When a vital system reaches its limitation, then the CGM will actually reduce the blood flow or recruitment pattern to the working muscles. This will either rescue O2 supply to the muscles and/or increase intramuscular tension (less fibres have to produce the same performance). So we have either a reduction in O2 delivery due to less blood flow and/or due to increase mechanical pressure on the blood vessels.

In both cases the muscle has to move to a better ATP delivery than O2 can be, and that's why we see an increase in lactate. So when the cardiac system (Noakes) is reducing the recruitment pattern, we will see as a reduction in performance. If we try to push harder then the situation will get worse, as the cardiac system really will 'blow up'. Same is the case with the pulmonary system (Metaboreflex = breathless legs)

Now if the muscles are the limiter (Mitochondria density and or capillarization) then you can move only so much energy to reproduce ATP and that's it.

So you can go to a certain intensity. As you go higher you will create somewhat more CO2 (respiration will go up) and if the respiration is not a limiter but a compensator you will simply increase respiration rate and if it is a very good compensator even Tidal Volume. This does not help to increase ATP production but it will help to maintain the Tissue Saturation Index (TSI %) and the ability to produce ATP with O2. The increased work in the respiratory system will increase your heart rate as the respiratory system itself will need more O2 as well. As the heart is not a limiter the cardiac output will go up with increased heart rate and if the heart is a very good compensator the stroke volume will go up as well. Now we have a higher demand on O2 for the heart as well, but it still can be delivered.

All this increased activity by the vital organs will not improve performance but can MAINTAIN it but - your HR will be higher than at LBP and your performance will stay stable. What we see in this case is higher VO2 as well.

This shows why some people with a lower VO2 can be faster than people with a higher VO2. It is all a question on who uses the O2 and who can do what with the O2. In running, the running economy may be one of the major factor why people with a relative lower VO2 max still run faster than people with a higher VO2 max. We have this situation in the history over and over again but despite this clear info, the majority of physiologists still use VO2 max for research and groups to compare.

So to recap:

If CGM (Central Governor Model) has some merits than we would see in the case of a cardiac limitation reduced muscle recruitment at the critical level and less muscle fibres pushing the same of more wattage or load. This would lead to a restriction in the blood flow.

If the metaboreflex from R. Dempsey is somewhat true, than we have a direct reduction in blood volume due to vasoconstriction as a way of controlling the respiratory system for survival.

If the local muscles are the limitation, than we would have a reduction of blood flow as well but, with it also a reduction on tissue saturation as the muscle would take more and more O2 from the intracellular pool.

HOW TO TAKE THIS INFORMATION FURTHER

Here are two examples when we understand how to train the body with the above concepts. These two examples also highlight the importance of a 'correct' warm up.  This picture is from a portable NIRS (Near infrared Spectrometry) giving a live feed which measure tissue saturation. (Green line= (tHb) blood flow, blue line= (deox Hb) deoxygenated blood flow, red= (O2Hb) oxygenated blood)

The first example how we can use the above understood information with an explanation:

1. 5 mph 'warm up' even slow, you see the initial drop in O2hb (red line) due to the immediate need of ATP and the 'lag' of ATP supply over O2 dependent energy sources. The goal of this warm up; run until the O2Hb is back to base-line.
2. Short 15 sec sprint before up to 5mph; again a drop in O2Hb. The goal again wait until the tissue is 'loaded' with O2 Hb, followed by a set of very short 5-10 sec fast sprints.
3. Go to LBP speed of 8mph. See again initial drop and wait till back to base line.
4. Stop 1 min to get shoes ready and then start race on LBP speed 8 mph. See again short drop but less than at the beginning. Take lactate by half distance 3miles. Lactate 1.5 and stable HR.
5. Felt really great so increase speed to 8.5 mph which is above LBP speed. See the slow drop in O2Hb.
6. Felt neither great or loose. So lactate sample 3.2 and hr increase above 160. Nevertheless back to 8.5 mph.
7. Felt not good and reduced speed back to 8mph to 'recover'.
8. Try end sprint over 500m 10 mph.
9. HR 171+ Lactate 2.4
10. Cool down 5mph, HR 135 after 3min lactate 5.4

Second example of a controlled interval session:

This example shows a warm up similar to the previous example running O2Hb back to base line. The first interval (9 mph) was too fast (hard) dropping the O2Hb and tHb too low, the next interval was corrected. If the first interval was a planned part of the planned warm-up or in this case, if the athlete was to continue at 9 mph, he would have kept dropping O2Hb and tHb too low and probably not have had enough recovery in between reps to reload ATP. Here it was corrected to 8mph with recovery at 5mph.

HERE IS WHAT WE SHOULD DO

Assess the weak link: If it is the heart, than you have to assess, what would compensate for it and for how long. Perhaps the muscle is the compensator. Now once we have the limiter and the compensator from a very simple base test you now would do a set of generally used workouts with this athlete and his coach. You assess during a workout the same systems as you assessed in a base test. Now you have a base line for the next few weeks or month where you can use simple bio markers, when you do the same workout again. Biomarkers like HR, HR drop in the rest period. Respiratory frequency in combination with step frequency. Lactate and glucose if you like to go more invasive. Time if you go more for performance.

Now you will have from the initial interval the cardiac, respiratory and muscle info and this is then where you have the info from the BIO markers. Now if your HR reacts in certain way you know from the base line test that today, my heart was the limiter. If you have certain respiration changes with a certain SpO2 on the finger, you know from the base line that it's the muscle today which limits the performance and the respiratory compensates and vice versa.

This information will change as the weakest link gets stronger, so one test a year is not enough as you're back to guessing and hoping. Test, find the weak link, train it, come back in a few weeks and retest the weakest link (LBP)!

All this is information that can be tested and can be bought by a medium funded professional team. All you need is a portable VO2 machine (Cosmed) not for VO2 max assessment but to see the respiratory function with Tidal Volume, Fe02, Vital Capacity, Sp02 and compare from resting to LBP values. A portable Hemodynamic cardiac machine (Cosmed) to monitor live heomodynamics, and portable NIRS (Artinis) to view live blood flow to understand the muscle and plan intervals. There are few research labs with all this equipment or if they have would test for what has been explained here. Even not having this equipment, just having regular simple Lactate Balance Point test, will give you the bare basics to find the limitation point and hopefully from better understanding MCL why you should stay in your zones and know how long to be above LBP. An oximeter which measure (SpO2) blood saturation gives a bit more information. Zephyr makes a very affordable heart rate monitor with build in TV ECG skin temperature etc. It is all about what you have for testing and HOW YOU USE IT, then applying it.

Summary:

As you see, here is where we try not to speculate anymore based on a lot of theoretical info's we have from our education, but rather go test and see and have the correct answer instead of speculation.

Theories versus reality. Hoping versus testing. 


To expand you mind further read the discussions on FaCT.