FaCT testing

I recently had some FaCT testing done to find my weaknesses. Here are some pictures to give a idea of how versatile and portable the equipment is. 

It can not be seen in this picture but under my shirt I have EKG pads that have a wireless link to the  computer next to me. On my right thigh under the cycling short is a phone size device (NIRS) that gives the tissue saturation information which is also transmitted via a wireless live transfer to the computer next to me.

On the left computer screen is the live hemodynamic feedback, middle computer screen is live blood flow and tissue saturation information, the orange grey box leads to the mask on my face which gives live respiratory info, and finally the small blue device is for lactate info.

Testing is done where ever you want to do it.

The mobile sports laboratory, doing a roller ski to compare treadmill and road results. The equipment has enough range to pick up live blood flow and hemodynamic info from the car following close behind.

The respiratory info needs to be carried in a back pack and can be analysed later.

Here some screen shots from some of the testing where all the information is looked at as a whole, and a better understanding of how each of the systems influences each other. Instead of traditional testing where conclusions are sometimes made based on one system only. 

The aim is to find the Limiter which we can then train so that there is a performance improvement where as traditional testing tends to look at how good you are, comparing VO2 and statistics to other athletes, how much wattage you can push  or testing running economy, all the traditional type test which help you very little in training and finding your weakest system.

From this one FaCT test I now have a much clearer idea of what my body is doing and how to train it than any of the previous traditional tests done over the last 13 years.

I was tested by Duncan Clarke who does level V testing, contact information for him and other test centers can be found on the FaCT Canada website.

Understanding the weakest link and more ideas.

Some more ideas and thoughts, and why we find LBP and the weakest link. Read Athletes weakest link to get the background on this article.

This is the scenario: A pro cyclist has a well developed leg muscular system which has a good capillary network to delivery oxygen to mitochondria. The cyclist may have a vital organ as a limitation. Now move the cyclist to a rowing machine where his arms are poorly developed and utilisation of fuel to the muscle will be a problem even though he's vital organs are providing sufficient blood and oxygen to the upper body. Make the cyclist do cross country skiing, here will be another scenario where same as rowing the upper body is the limitation involved but coordination may be more of a problem.

In each of these cases LBP will be different and a different system will create LBP. Which is why LBP needs to be tested for every sport activity. To add to the previous paragraphs scenario, using tools such as NIRS and Phisio Flow, a coach can easily find out what system in the body is the weak link, muscular, respiratory or cardiac. Then adapt the training so that the weakest link will improve the LBP which will lead to a faster athlete.

Training the Weakest link if:

The heart is the weak link, then one could perhaps train the heart in a way so that the respiratory system will challenge the oxygen delivery so that the heart has to react. Using Pulmonary Endurance Training PET is a example. If we have a portable device to monitor heart hemodynamics we can monitor stroke volume training. Intervals may have the ability to improve Stroke volume but only if the interval intensity (rest and load) period is so fixed, that we do not create a 'storage of blood' or a occlusion in the working muscles but rather move as much blood back into the system and to the heart to increase circulatory blood volume.

It is muscular limitation where utilization is the problem then work needs to be done on capillarisation and mitochondria density.

The respiratory system is the the athletes limitation then keeping the heart rate low by using SpiroTiger to stimulate the respiratory system.

Blood system is the limitation, then it could be improved with nutrition and IHT (Intermittent Hypoxic Training) and PET.

If the limitation is coordination and stabilisation you might think swiss balls and sit ups! Worst choice, (see my last article why)! A better answer is once again specific diaphragm training. The diaphragm is a vital stabilisation muscle of the core, strengthening of the diaphragm with breathing training will strengthen the core indirectly and stop the 'falling apart' at the core when a athlete is fatigued. The dead lift and squat actively activates the core better than core exercises! Training with specific coordination training is the better answer.

Most of these ideas needs equipment to check respiratory information, heart hemodynamics, and the muscle situation. Even not having access to this type of equipment and just understanding what is happening to the body and why we need to look for certain biomarkers will improve our training programmes. Here is a very basic idea on how we can build training programmes around recovery instead of the recovery around training as the body adapts and becomes stronger when we recover: Test LBP, then do a session where we stress the LBP or a session where we go above LBP, then retest LBP to see if the body has recovered from the session. If LBP is lower the athlete has not yet recovered, if it is back to baseline we are ready to go again. This is the beauty of the LBP assessment over a standard Lactate Test in that the athlete doesn’t need to be pushed to maximum and a LBP assessment can be done before a session to see if a athlete is ready for the next push or needs to just go for a easy bimble.

When we know what the athletes limitation is for each sport activity, then we need to decide what will improve the limitation, and not just do a set of exercises because everyone else is doing that exercise (i.e. sit up for core instead of diaphragm strengthening), once we understand what will improve the limitation then we can focus on structural training rather than functional training.

Overload:

We strive to push our selves to the limit in every training session and sometimes athletes will push so hard that they may see God for a brief few seconds. The question during such hard intensities where overload and stress takes place, is there any point in stressing the system further with more repetition to over stress it? A session that stressed the respiratory system, would it be a good idea to complete another respiratory session with the SpiroTiger so that we have a drop in performance and LBP when we want to do another session the next day? Probably not until the respiratory system has recovered, what if the cardiac system was overloaded then followed by something that challenges coordination or the respiratory system? That would be a smarter idea as you are challenging something which has not yet been stressed. This idea comes from the Austrian researcher, Hans Selye. Except that most coaches will take his idea too literally and push the athlete so that the athlete has to complete the predetermined set of intervals to get the most out of the session, even though (ie cardiac workout) with the same perceived exertion the heart rate can not be maintained, lap times are getting slower and the Central Governor Model (CGM) is kicking in because the body is more interested in survival than performance, the athlete systems is now in overstress mode. The Coach missed the point where the athletes system reached its overload point and the session should have been done for the day. What Hans Selye meant with overload is perhaps not overload but simply change the way we stimulate and challenge the systems. i.e. today we challenge the respiratory system, then the cardiac system which is still fresh, coordination or technique, once a system has recovered it can be challenged again.

Example of listening to the body:

Here is a picture where we follow physiological reactions rather than set intervals, this is a profile from NIRS. Green line is total blood flow (tHB), red oxygenated blood which tell you how much blood is loaded with O2, blue deoxygenated blood. The time frame from 0 to 1400 is where the athlete warmed up to get get blood flow into the working muscle (rise in green line) upto the point (900) where the intensity increased and the blood volume started dropping and deoxygenated blood (blue line) increased as a sign of O2 usage. From line A the the intervals start, blood volume rises dramatically as there is more blood in muscle during the recovery and drops during intensity as muscle tension and occlusion takes place, the last interval by 2400 was stopped due to not reaching the recovery Tisue Saturation Index (TSI%) which was also indicated by a slower rise in the green line, so the session was over. The interval before already, the tHb (Green line) did not drop to the same level as the previous intervals. The athlete ran into ATP delivery problems due to increased intramuscular tension and thus a reduction in blood flow. (The feeling of 'blown up legs' due to a occlusion situation in the muscles).

We will always have a overall programme with a idea of what we are going to do in a session, but a perfect training session will be where, neither coach nor athlete has any idea of the sessions outcome. They do not know how many reps or how long the recovery will be, as this will be decided by biomarkers such as heart rate, glucose, lactate, breathing frequency, tissue saturation etc. instead of a paced workout where we complete 10x400m meters, after the second interval we know how to pace the session and by knowing this we have changed the physiological end result. What if we followed some of the pre mentioned biomarkers and were able to achieved more physiologically in 6 reps than the planned 10 by rather stopping when we reach the same physiological stress as the first interval? Why train for 60min when you can achieve the same result in a shorter period, or perhaps you need longer for the overload, but you will not know unless you start to understand the physiology and look at the biomarkers that is available to you. This is where we start training smart versus being sheep following a cook book.

Lactate Balance Point – LBP

The majority of physiologist and athletes reading this article will think these ideas are crazy, if you think so come back in 10 or 15 years and read these ideas again. Read this article and the links, understand why, and you may have found a better tool for threshold testing.

DIFFERENCES BETWEEN A LT TEST AND LBP TEST: 

At first it may look similar to a normal Lactate Threshold (LT) test, ventilatory test or anaerobic threshold. But it is different. LBP is a assessment for fitness training levels. The LBP is simply lactate in balance at a certain level, there is no increase in the lactate level and no decrease. It is the area where the body if the ECGM (CGM) is correct reaches its weakest point. LBP, originally developed over 20 years ago has been researched and field tested over the last several years by FaCT with hundreds of repeatable results.

The LBP assessment is different, in that the bodies Lactate Balance Point is more easily and accurately found than using traditional sometimes misinterpreted Threshold Tests.

Diet influence on traditional LT test

Diet influence on LBP test

We need to look at lactate as a bio marker of fatigue and an indicator of energy stores. Lactate is highly influenced by what you eat, as lactate responds to glucose which will affect lactate levels. The LBP assesment is hardly affected by what is eaten but glycogen stores can mess up the traditional LT step test curve. This can be proven completing a traditional LT test carbo loaded and then repeated being carbo depleted (protein loaded). So the theory that (Mader) 4 mmol is anaerobic threshold is blown out of the water with this in mind. It would be like saying every person has a max heart rate of 220 minus their age. So looking for 4 mmol will not be accurate as there are other factors involved. Just because you had x mmol of lactate at x heart rate in a test does not mean that x mmol will always indicate threshold. 

The traditional LT test is based on a objective protocol based upon wattage normally 20 watt step increases, for some people 20 watts is to much at some point which will lead to a too big jump in heart rate which will mean a large part of the heart rate range may be missed, this big jump will also lead to a 'jump' in lactate which will falsely indicate threshold. Lactate is always present in the human body even at rest and will increase linear as heart rate increase (Connet et al circa 1984). The LBP assessment follows physiological parameters where heart rate is increases by 5 to 10 beat and the balance point is not missed. LBP will normally be lower than what you get from a LT test and this is because LBP test give you the point of the weakest link, with a LT test you are getting the point where the test has overstepped the bodies (weakest point) limit and the bodies ability to handle the metabolic process in the muscle.

Anaerobic threshold does not exist! There is no proof or evidence that muscle would go anaerobic during intense or max workouts. Research is showing that oxygen may actually be higher during all out exercise than lower intensity’s (Connett, Gayeski, Saltin). Lactate is used as a fuel and may especially at higher intensity be a preferred fuel source (Brooks and Dubouchaud).

The above were some of the reasons for the development of the Lactate Balance Point assessment.

THE LBP ASSESSMENT:

A brief explanation of the test. The body is warmed up gradually with a step increase of 10 to 20 watts every 3 minutes upto a perceived exertion (Pe) of 7 to 8 (about 15 min). No lactate is taken during the step test, only at the end of the 3 min where Pe 7/8 is found, SpO2 is also taken (oxymeter). This is the only part that resembles a traditional step test and is only done to warm the body up and get lactate raised, ready for the actual assessment. There is absolutely no need to take lactate before Pe 7/8 or any need to take the athlete to max which will tell you nothing about his LBP (or threshold if you really wanted to call it that).

Now drop the wattage by 50% and continue without rest. This is where protocol stops and physiology reaction assessment starts. Take lactate and SpO2 after 3 min at 50% wattage, continue at 50% until you have the lactate reading and decide if or how fast the lactate and heart rate has dropped from the Pe 8 reading, whether to continue on 50% for another minute.

LBP test with LBP at 155 bpm

If there was a big drop go to the next step immediately if a slow drop in lactate and heart rate stay another minute. To go to the next step increase wattage until HEART RATE increases by 5 to 10 beats, after 3 minutes take lactate and SpO2 again stay at the current HR and wait for the Lactate result, if not dropping wait another minute if lactate is dropping increase HR by 5 to 10 beat again, continue this until lactate stops dropping and there is a increase in lactate. When there is a increase you have your balance point.

Using this method less lactate strips are used. (to know how much to increase wattage for the 5 to 10 beat increase use the initial step test to Pe 8 as a guide on wattage/hr increases). What a lot of coaches and physiologist find hard to accept with this test is that there is no protocol, that steps can be be prolonged, and that the test follows physiological parameters, we have to look at how the body reacts and have to think during the test. Read the articles on FaCT test system and what is LBP test.

Instead of wattage perceived exertion or speed can be used as a guide for increasing HR.  The SpO2 reading is used to get information on the blood situation and can be used as a guide for finding LBP in combination with lactate. This is the basic assessment to find the LBP, for zoning a later article will be written.

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.

Lactate fuel or foe?

Myth:  Lactate causes fatigue. Fact:  It corresponds with fatigue but does not cause it. In fact it is a mechanism to help delay fatigue. I will try to explain what lactate is and let you navigate to the links to understand how lactate is formed. Lactate has had a bad wrap over the years and even though it is proved that it is not the cause of fatigue people still believe that the burn is associated to lactate!  Or on TV a commentator might comment "look at that cyclist he's unclipped his foot from the pedal and shaking the lactate out of his legs" Wow! there must be a stream of lactate on the asphalt to sweep up!

Lactate is part of the Cori Cyle.  Lactate is hugely affected by the amount of glucose in the body.  A carbo low diet will have a lower lactate level than for the same intensity when the body is carbo loaded.  So lactate is rather a indication of fuel in the body. 

• Lactate gets produced to help to retard acidosis.  (Acidosis is thought to be the cause of the burn).  
• Lactate goes through the Cori Cyle and is converted back to pyruvate and then glucose  where it is used as a fuel again.
• The heart and brain prefers lactate as a fuel!!!

So based on the current research lactate is essential to fuel the body. Still doubting if it is so bad?

Traditionally athletes cool down after a hard session to get rid of lactate.  If lactate is such a important fuel in the body is it wise to cool down after or between hard session when the heart and brain needs this fuel and you are using more glucose to go for the cool down which could be used for recovery? Perhaps what the body is rather doing during a cool down is to get rid of excess CO2, pumps oxygenated blood back to the muscle and simply metabolises lactate back in to fuel! I don't know the full answer to not cooling down, its a question that was discussed by FaCT  see the discussion here! but once you understand the inter functions of the body one can start challenging traditional ideas.

Here is a easy to read article on lactic acid.

Here is a in depth look at the Biochemistry of Lactate Metabolism

It will help to have a chemistry back ground to fully understand and appreciate the article but reading past the formulas one will still understand the article.

You can find many more on this and other topics in the FaCT Canada discussion.

The FaCT way of looking at the body!

I have a keen interest in the FACT - Feldmann and Chlebek Testing System, mainly their way of looking at the athletes body from a alternative angle to the usual University text book answer.  Instead of only looking at lactate as a marker of performance/fatigue one should look at the process that is going to lead to the "lactate threshold point" or as FaCT test it LBP (lactate balance point).

The body has three trainable systems: The heart, the lungs, the muscle. Did I just say lungs? yes the lungs are trainable in the same way the heart and muscle is.  More on that topic in another post.  Each person has a weak link in their body. Some have strong lungs but weak muscle system, others strong heart weak lung system etc.   FaCT calls this weak link the limitation or limiter.

Your body will only go as fast as the weakest link, at some point your body is going to have one of the other two main systems that is going to compensate for this limiter.  So if your respiratory system is weak then there could be a poor gas exchange, the diaphragm is weak then you could for e.g. start having a lower TV (tidal volume) and a increased breathing rate.  The heart might compensate by increasing the cardiac output which will increase heart rate to compensate for the loss in incoming oxygen or not getting rid of the CO2 in the gas exchange.  At the LBP your CGM (Central Governor Model, Noake's) is going to "kick in" to save the body's vital organs.  Similar will happen if you have a muscular limitation.  Either there isn't enough capillarization, mitochondria etc which could affect muscle utilization of the oxygenated blood to the muscle. once again there will/should be a compensator such as lungs or heart.

The body can only go as hard and fast as it's weakest link before the CGM or ECGM, metaboreflex etc "kicks in".

Each athlete will have a different limiter, and the same workout for two athletes will have a different training effect based on the above.  This is why some training programs will work for some athletes and not for others, as the coach hopes that he's workout is training VO2 meanwhile athlete 'A' has a muscle utilisation problem so will never stress his VO2 while athlete 'B' has great utilisation but a VO2 weak link so will benefit from the VO2 session.  Are you starting to see the picture?  The coach has 5 athletes but only 2 improve and he wonders why!

The FaCT solution to this problem is to test the body for the three trainable systems the FaCT way  and then to train the weak link without guessing and hoping hopelessly that a programme that has worked for 60% of athletes over the past 20 years will work again.  Here is a short article on the limitation subject from another athlete Rethinking current exercise physiology.