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.

Compression Socks, just a trend?

Paula Radcliffe was one of the first well known people to make use of compression socks. Now days they have become very popular in most sport although I have not yet seen them used by cyclist in the pro peloton? Although cyclist tend to wear them for recovery. Compressions are also popular with pole vaulters, long and high jumpers.

Compression garments and socks have a place in the medical world for patients who suffer with deep vein thrombosis, bed ridden patients that can not move or people that have to sit for long periods of time such as traveling in aircraft.

The theory behind compression socks are that the compression helps to improve blood circulation. The graduated compression from the ankle to the calf helps blood that tends to pool in the lower limbs fight gravity and thus improve circulation. This then could move dexoygenated blood quicker away from the limbs with oxygenated blood flow back.

Another theory is and this will explain why long jumpers and pole vaulters use the socks where blood circulation is perhaps not a major issue is muscle vibration. Every time the foot strikes the ground the force of the impact send vibrations through the lower leg. These vibrations caused by impact are thought to be a contribution to muscle fatigue and delayed muscle soreness. There is research which has shown compression socks to increase leg power (Kraemer et al., 1996, 1998).

Research on compression socks whether they work has had mixed results. Knowing whether the socks improve blood flow during activity has been hard to research compared to using the socks for recovery which is probably why cyclist are not using them yet for racing. Although a portable NIRS could be a future option for testing something like this during exercise.

There have been research that show improvement in performance and economy while other research has shown no improvement in performance but a reduction in muscle soreness. (Kremmier et al. 2009 and Ali et al. 2007). Some research has looked at how compression socks influence lactate (blood lactate is measured not muscle lactate) and has found the socks seem to help lower blood lactate . Why this occurs is open for discussion as there are different theories what happens to the lactate. But perhaps with the increased blood circulation the blood helps transport the lactate to other muscles that need the lactate so improves the lactate shuttle?

Studies from (Byrne & Easton, 2010, Ali 2007), found decreases in muscle soreness from plyometrics and running. It is thought that the compression helps to alleviate inflammation and swelling. Once again why compression socks help with this is not known and there are several theory's.

Overall most research found decreases in muscle soreness but there is mixed results on the improvement in blood flow more so during intense exercise which is hard to study. The variations in research could be because of the wide variety of socks used from different manufacturers. The use of graduated compression to constant pressure compression socks. There is a certain amount of correct compression needed at different parts of the lower leg for a compression sock to work. It seems that a graduated compression sock running tighter at the ankles and less up to the calf would improve blood flow better than the same pressure in the case of constant compression sock. But also there is a individual element as different people could have a different reaction. People with circulation problems will likely see bigger results.

I own three different brands of compression socks and pants. It is impossible to say if they actually work without having some form of tests done. If someone feels like they work it may be psychological. But wearing the socks does feel very comfortable, and most of the research although perhaps it can not explain why the socks work indicate some form of benefit most of which shows reduced muscle soreness and improved blood flow at least during recovery use. Compression socks are just another small thing that makes a small improvement in recovery which could add up with all the other small tools that we add to our training. For now I will continue to wear my socks during hard session, or where there is high impact. And when the fashion catches on in cycling I might wear it during a Sunday coffee ride.

Altitude training, IHT, Hypercapnia recovery and the benefits.

Many athletes now days have some sort of altitude camp or Intermittent Hypoxic Training (IHT). There are various combinations of Living high training high or living high training low etc. With living high and training low (which could be done using a altitude tent) a athlete can avoid reduced muscle recruitment found when training high so have a better training session at lower altitude with the benefit of increased red blood cells.  A more common practice now days is IHT which has shown to be more effective than altitude tents. Depending on the protocol the body will adapt to the hypoxia effect and increase red blood cell production so there is more oxygen carrying blood going to the working muscles.

If you have read the post FaCT way of looking at the body you might understand why there could be altitude responders and non-responders. Example: If your muscles are the limitation before the altitude camp, then after e.g. three weeks at altitude  they may not have changed at all but in fact the muscle "may" be worse from the camp due to a reduced muscle recruitment at altitude. If that is so and we have better oxygen transportation with more Oxygenated blood (higher red blood cell count) it is much easier for the heart to keep the vital organs happy. Pumping more blood to the muscle will make no sense, as the limitation of muscle can't take more oxygen in anyway (muscle recruitment/utilization). This would be a non-responder and the same holds true when athletes use EPO and in some cases there are also non-responders. So once again knowing what each individual athletes limitation is through testing and not guessing will help one to understand the effects of training at altitude.

What I would like to give more in depth information on is the lesser known benefits of Hypoxia or Hypercapnia.  Many of the ideas come from the Russian school and one of the "leading" researchers is, Dr. Buteyko. Here is a abstract which might make you see the bigger picture.

• Oxygenation: Carbon dioxide (CO2) plays a large role in oxygen transport from the blood to the cells of the brain and body. A reduction in CO2 levels brings with it reduced oxygenation of tissue and vital organs (Verigo-Bohr Effect).
• Acid/Alkaline Balance and the Immune System: CO2, through its conversion to carbonic acid, is a primary regulator of the acid/alkaline balance of the body. 
• Vessels: CO2 helps to dilate smooth muscle tissue.
• The Cardiovascular System: CO2 helps regulate the cardiovascular system.
• The Digestive System: A direct relationship exists between the level of CO2 in the body and the functioning of the digestive glands.

Tatiana V. Serbrovskaya (High Altitude Medicine & Biology ( Department of hypoxic States, Bogomoletz Institute of physiology (Kiev Ukraine ) Volume 3, number 2 2002 @ Mary Ann Liebert Inc.

"Intermittent hypoxia research in the former Soviet Union and the Commonwealth of Independent States : History and review of the concept and selected applications. High Alt Med Biol 3:205-221,2002.- This review aims to summarize the basic research in the field of intermittent hypoxia in the Soviet Union and the Commonwealth of Independent States (cis) that scientists in other Western countries may not be familiar with, since Soviet scientists were essentially cut off from the global scientific community for about 60 years. In the 1930s the concept of repeated hypoxic training was developed and the following induction methods were utilized: repeat stays at high-mountain camps for several weeks, regular high altitude flights by plane, training in altitude chambers, and training by inhalation of low-oxygen-gas mixture. To the present day, intermittent hypoxic training (IHT) has been used extensively for altitude pre acclimatization; for the treatment of a variety of clinical disorders, including chronic lung diseases, bronchial asthma, hypertension, diabetes mellitus, Parkinson's disease, emotional disorders, and radiation toxicity, in prophylaxis of certain occupational diseases; and in sports. The basic mechanisms underlying the beneficial effects of IHT are mainly in three areas: regulation of respiration, free-radical production, and mitochondrial respiration. It was found that IHT induces increased ventilatory sensitivity to hypoxia, as well as other hypoxia-related physiological changes, such as increased hematopoiesis, alveolar ventilation and lung diffusion capacity, and alterations in the autonomic nervous system. Due to IHT, antioxidant defence mechanisms are stimulated, cellular membranes become more stable, Ca2+ elimination from the cytoplasm is increased, and O2 transport in tissue is improved. IHT induces changes within mitochondria , involving NAD-dependent metabolism, that increase the efficiency of oxygen utilization in ATP production. These effects are mediated partly by NO-dependent reactions. The marked individual variability both in animals and humans in the response to, and tolerance of, hypoxia is described. Studies from Soviet Union and the CIS significantly contributed to the understanding of intermittent hypoxia and its possible beneficial effects and should stimulate further research in this direction in other countries."

If you are still awake and have followed up to now well done!  So from these benefits one can summarise that IHT has many health benefits also.  Athletes are known to use Hypercapnia for recovery from day after day hard sessions or stage races but the protocol for this is hard to find and one would unlikely complete a full IHT course.  It is a matter of research and thinking how  and when to best apply it after ie a hard race.    

Here is another article to read. The lung and carbon dioxide:

There are many manufacturers of equipment that can be used for IHT and hypercapnia ie  AltiPower, the main disadvantage is maintenance cost of the CO2 filters, but also it can be hard to control SpO2 levels, the SpiroTiger  can be "abused" and allot more precisely control SpO2 levels through breathing alone. Disclaimer: SpiroTiger is NOT build to be used as IHT equipment but only as a diaphragmatic endurance training equipment. It is essential that with any IHT equipment a pCO2 and at the minimum a  Pulse Oximeter is used during IHT.  Dropping the blood saturation (SpO2)  to low, could lead to hospitalization or even death.