Recovery and adaptation, or is it?

Here are a few ideas on recovery.  When we train we break our bodies down, and we become stronger by adaptation when we recover.  As athletes and coaches we advise a variety of ideas to have a faster recovery so that we can adapt faster and complete the next session sooner but, little do we think, do we hinder adaptation? sometimes there are faster ways to recovery than we already think we know?  Here is a summary.

Antioxidants:  Antioxidant refers to the group of substances which includes vitamins E, C, A, and carotenoids.  When our body cells use oxygen, the body naturally produce free radicals which can cause damage, thus used in sport and general health to prevent cellular damage from free radicals.

The adaptation to stress caused by training is the reactive Oxygen.  So by using antioxidants you are getting rid of the stress trigger before your body can adapt.  So use antioxidants sparingly as the body has its own antioxidant defences.  Eating fruit after training will probably be ok as the antioxidant concentrations are low compared to that of supplements.

Ice baths:  Ice baths are the new in thing, and research although not conclusive generally support its use as a recovery method.  But the body when under stress has a secretion of hormones that aid in muscle repair.  By taking a ice bath the cooling of the muscle is stopping this recovery cycle which will most likely reduce adaptation.  As with antioxidants it is the timing of the ice bath that is important, that it does not interfere with the bodies natural adaptation cycle.  Taking a ice bath directly after a hard interval session would be a bad idea as where if you take it the day after would be better.

Finishing a race:  We get told after we collapse on the finishing line or hard session to stand up even though the natural reaction was to collapse! Perhaps it is our bodies natural response that it is easier for the cardiac system to pump blood laying down than against gravity, thus getting blood round your body quicker.  Makes sense huh?


Stretching:  Stretching has its place in sport when done at the right time and for the right reason, but certain people are naturally more flexible than others and need to stretch less.  It is a proven fact that stretching too much has a negative effect on running economy as the muscle tends too loose its springiness. Think of the muscle as a coiled spring, the more it is stretched the less power it will have and the more energy it requires to produce the same power. We get told too easily for every little thing that we need to stretch. A perfect example is a ITB muscle injury that comes from running where the muscle rubs agains the side of the knee. Every body says, stretch it and let it rest. Well The reverse is actually true the ITB muscle needs to be strengthened! The ITB is rubbing because it is compensating by shortening for its lack of strength! 

Cooling down:  Saving the best topic for last,  it has taken some decades to find and accept that lactate is the indicator of fatigue and not the cause of it, and that lactate helps to delay acidosis.  Any physiologist or coach worth he's pay will know that lactate is the preferred fuel used by the heart.  So if we test lactate we should look at it as a biomaker of fatigue and a indication of energy stores in the same way that we test glucose for fuel stores.

So if we get told to cool down after a hard session what is the first answer when we ask why? "Get rid of lactate"!  Here is another question, would you cool down to get rid of glucose? No! So why get rid of lactate if it is a fuel. Would it not be better to keep the lactate in our system so that the heart and brain can use the fuel.  Our kidneys get rid of the wastes in our body so if we cool down we take blood away from the kidneys and to the muscle, thus slowing down even more the clearing proces of the supposedly bad stuff. 

Here is a reply you might get for not cooling down.  "The next interval session was slower because lactate was still so high".  Answer: perhaps lactate is a indication that the body needs lactate, and the body has not recovered fully because rather the respiratory, muscular or cardiac system is still fatigued from the last session.

Think through some of these ideas, I am not saying that we should not use antioxidants or ice baths or cool down, simply have a think of how our bodies react, and not do something just because everyone else does it. Be a sheep or be a pioneer.

Many of these thoughts come from FaCT Canada who look at physiology from a different angle and make sense of everything.  More on ice baths and antioxidants read these two articles:  Antioxidant supplements are they needed  and When damage is a good thing.

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.

The case against stability training (throw away the swiss ball?)

Unstable surface training UST is used to improve trunk muscle strength and core activation. But, there is enough research and an excellent article at Science of Running that debunks this idea, here is a summary.

When working with stability exercises on devices such as the swiss ball, bosu balls, wobble boards etc. we will have agonist and antagonist muscles involved. For a positive improvement the agonist muscle needs to be engaged and the antagonist involvement decreased. What research is showing is that UST is doing the opposite. Most of the research has been done by Behm (2002) and the research has shown significant activation in antagonistic muscle when performing exercises with UST which has led to greater reduction in peak power output and a reduction in agonist muscle activation. Thus a negative adaptation.

One of the biggest 'side effects' of UST training seems to be a reduction in force which eliminates the effect of adaptation, as much as 59.6% force reduction. Willardson, 2004, showed that UST will lead to improper muscle recruitment patterns, so UST has no place in sport specific skills. Stanton et al. (2004) found that runners were unable to improve running performance or posture using UST devices compared to non UST runners.

NCAA Division I soccer players performed their normal strength and conditioning programs, except that one group performed the final exercise of each training session on an unstable surface (Cressey et al., 2007). After ten weeks of training, the UST group saw performance decrements in bounce drop jump, countermovement jump, 10- and 40-yard sprint times compared to the group which did the same exact workout except for the last exercise (Cressey et al., 2007).

The core is activated more during a stable floor exercise such as a squat or any other stable floor exercise than druring the same exercise performed on a UST device (Drake et al., 2006). A study done by Kavcic, found that of 8 exercises that focus on the muscles that stabilize the spine. The least effective exercise done was also the only exercise using UST.

The idea that replacing a chair with a swiss ball and that it will improve posture has been proved wrong.

Other research has been conducted by researchers (Anderson & Behm, 2004; Cressey et al., 2007; Drake et al., 2006; Hamlyn et al., 2007; Kavcic et al 2004; McBride, 2006; McBride et al., 2006; McBride et al., 2009; Nuzzo et al., 2008) have found similar results from the combination of UST and traditional resistance training exercise.

The one thing that stability training seems to do positively is that using UST is the only thing that we will become good at using! We may improve our balance but from the research done, core activation and force output is found to be negatively influenced using stabilization devices. If you want to effectively improve the core it seems a squat is still the best option, you may not get a six pack from squatting, but then do you really need a six pack for performance? If you want stability and balance, sport specific is still the best sensible option. Often overlooked is the diaphragm which is a major core stabilization muscle which if weak will lead to quickly 'falling' apart when fatigued. Specifically strengthening the diaphragm with breathing work focused on strength, will do more core activation and core stabilization than traditional core stability exercises performed on UST and dare I say even traditional core exercises.

We are so focused on finding the magic session that will improve us that we so often forget to do our own research into why and how a new activity, training session or device will influence or outcome on performance and that we seem to be happy just to follow the crowd, just because we accept that it is the right thing to do.

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.

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.

Latest in fancy kit vs testing. Part 2

(This follows from Latest in fancy kit vs testing. Part 1) Testing is seen as a way to assess how good a athlete has become. If any improvements have been made, to see how long and hard a athlete can push themselves.  We are told we pushed a bigger wattage, we have a better power to weight ratio, we have reached a higher max heart rate, we need to improve on lactate threshold. Would it not be better to look at fitness testing to find a athletes weakest link in the trainable system (Physiology from a different angle) and if the weakest link has become stronger? Thus looking at the individual systems in the body.  To do this we have to change the philosophy, that power and speed and time are objective tools to see a result towards the physiology, that individual physiological reactions are the tool for success.

This idea and the tools used with it will be in another 10 - 15 years time when it is hopefully better accepted by Sport Science in general. We now have great physiological testing tools, NIRS, PhisioFlow, Polar Heart Rate Monitors, Suunto Heart Rate Monitors that give information on EPOC and BioHarness which measures through a heart rate strap body temperature, breathing rate, ECG and pulse. But due to the development of flashy and high tech gadgets like SRM (which undeniably has had its successes) we are taking a step backwards from physiological information. We have rowing machines and spinning bikes that have wattage information and everybody is pushing for a target wattage and forgets to listen to the bodies response. We have new training devices like the SpiroTiger which is a brilliant training tool when used correctly but due to our own competitiveness we will try to push the biggest bag size and breathing frequency with only short term if little improvement.

We have to wait until people can see and understand physiology from a different angle and that absolute values and graphs are great tools but give limited information for the deeper assessment to the working body.

Latest in fancy kit vs testing. Part 1

This article and much of this blog is inspired by the forward thinking of FaCT Canada. 


Look at any one of the recent Olympics or World Championships for most sports, and one will see the amount of money spent on sport equipment rather than the athlete centered ideas.  Agreeably some equipment is essential but I am talking more about the latest in aerodynamic helmets, swimsuits, clothing design because image is everything.  Or we see professional cycling teams with bigger budgets than some low key Olympic sports that spends huge sums of money on doctors and drugs (this is a generalisation) i.e. the Festina afair 1998.

But then one sees these same things in general public sport where we see riders rather buy the latest deep section aero wheels to be faster (modern bicycles and cycling speeds, any relation? ), rather than get properly assessed and tested so that they can have real performance improvements by searching for the weakest link and looking for bio-markers.

Swimming is a example that has not changed a lot in the way we coach and train athletes. Despite the fact that we have Heart Rate monitors now for water use (Hosand) and even intramuscular Oxygenation testing (NIRS), we still plan programs on amounts of fingers on your hand and length of the pool and turns on a clock. 

Have a think about it.


Latest in fancy kit vs testing part 2

SpiroTiger

SpiroTiger:  Spiro what? sounds like a fuzzy little animal that lives in the woods!  Rather it is currently the only training device that can train your lungs effectively.  Sure there are other low cost devices such as Powerbreathe and PowerLung out there, but they will only allow one to train the respiratory muscles for about 30 seconds before one goes blue in the face and keels over panting.

The PowerLung is more like gym training for the lung where as the SpiroTiger was designed to train the endurance muscle of the lungs which will train the diaphragm, breathing co-ordination and the inter and intra muscles involved during breathing.

If used correctly will a athlete develop a larger VO2? Will you run/bike/ski/swim faster? Will you have more power? It all depends on what is limiting your performance... if you have a respiratory limitation and then strengthen this limiter then the answer to the previous questions is a possible yes. So for the same given heart rate, power output and effort your lungs could be more efficient.  Depending on how much you use and abuse the SpiroTiger (abuse because there is some unofficial protocols for hypoxia (IHT) training, disclaimer: The Spiro Tiger is not ( NOT ) build to be used as a IHT equipment but only as a diaphragmatic endurance training equipment the reason is the O2 and pCO2 reactions) you could improve the gas exchange in the lungs, improve muscle coordination of the muscles involved.  Example: If a athlete was tested to have a limitation of the respiratory system and strengthened the lungs he will likely be able to race or train longer before his diaphragm muscles starts to tire out, where upon his vT or TV (Tidal Volume) might likely drop (smaller TV), his breathing rate will increase and the body will have one of several reactions, one could be metaboreflex (here is another explanation, metaboreflex) or the ECGM (Extended Central Governor Model).   The better we can train our weakest system (which can be found through various tests) the better we can train the system before the ECGM or CGM "kicks in".

You may ask don't we train our lungs when doing normal exercise?  Yes and no!  How often can you stress your respiratory system to get the training effect you want for the lungs? If your lungs is not your weakest link and example your muscle utilisation is the limiter and you train just up to the point where the muscle is stressed (assume the other two systems do not compensating for it) then it is unlikely you will be able to efficiently and regularly train the respiratory system through normal exercise.

With the SpiroTiger a athlete can effectively train his lungs every day, but within reason, I wouldn't use it the day before a race or hard session in case the breathing muscles involved has not recovered in time.

Abit more on the device and my own findings using the SpiroTiger: The device works with a hand held unit that can be programmed for breathing frequency and bag size.  The unit will also give information if you continue to breath incorrectly at the current breathing rate (inhaling more air than is being exhaled and vice versa) that you will start to hyperventilate or go hypercapnia in which case the machine will shut down as a safety precaution.  Apart from washing the device there is zero maintenance cost to it.  A Pulse Oximeter is used as part of my Spiro training to monitor blood oxygen saturation which is also vital when doing Hypercapnia workouts. 

Using it one will unlikely see any difference for some weeks. The main problem with the device is boredom, working out session which is interesting and fits in with my normal training programme.

Is it a training session?  Damn right, a average session is about 25 - 45 minutes. Sometimes after a session I am totally knackered, out of breath and my stomach muscles hurt!   Why my stomach muscles are hurting is probably because  I am using my diaphragm more than normal. The Diaphragm plays a big part in core stabilization.  So strengthening of the diaphragm with breathing training could prevent or slow the process of a athlete falling apart at the core. 

I have noticed huge differences in breathing using the SpiroTiger as part of a warm up before a race or hard training session. Yup breathing into a bag that resembles a over sized condom in front of your team mates does make one look like a plonker! But while they are lying on the floor from the last sprint session and I am already walking down the hill for the next rep who's laughing then!  Some differences I have notice both from daily use and as part of a warm up is, not gulping or gasping for air, I seem to recover (respiratory) quicker between intervals.  I don't have erratic breathing patterns in the early parts of a session and my lungs don't hurt as much anymore. A warm up may vary depending on what kind of race warm up a athlete needs respiratory wise.  One theory is a warm up of the diaphragm to give a metaboreflex reaction before the start of a race so you have pushed the respiratory rate into over drive so that when the race starts the body doesn't panic and the metaboreflex is delayed. Or you simply need to control the CO2 level, so you could go either hypercapnia or hypocapnia all dependent on your race start type. There is no specific protocol and it is very individual, I myself am still trying different variations to see what works. 

Another area that I have noticed differences compared to the past has been when training at altitude (IHT and Hypercapnia is not suported by the manufacturer, a athlete should work with a physiologist or doctor when planning to use the SpiroTiger for other than what the manufacturer recommends). With all of this there could be other factors also involved but I believe a lot has to do with how I have trained my lungs which was previously not possible. Another area I will summarise in a later blog is the use of hypercapnia for recovery which comes mainly from Russian studies.

SpiroTiger is not the solution to winning a race that will make you go from zero to hero, but it will add another tool to your training box. Keep in mind when training the respiratory system with this device that you are only training a part of the whole working system and the results are very individual. For further reading on SpiroTiger training visit the SpiroTiger FaCT, SpiroTiger Time to try harder.

Core exercises, are we sure we are activating the core?

Nearly every personal trainer, fitness advisor, coach advocates core work.  But once again do we understand what we are doing by following the trend!  We would like to think that what we are training with core exercises is the best way to activate the core muscle, and that it would improve posture, stability, balance etc. Do we understand the muscle involved when doing a core exercise?  I'm not goin to rewrite the following article as I don't think I can do it justice.  The summary is that traditional core exercises has its place for developing certain areas but a athlete can activates his core muscles more positively and directly with a simple squat, or dead lift exercise.  Here to read: rethinking-core-training-is-it-fad.

Also on FaCT Canada is a very long discussion that shifts away a bit from the above topic but from 9 post down the subject becomes of interest to the core topic and looks at it from a different angle, discussing the involvement of the diaphragm  as a major core stabilizer and follows to a interesting subject on its own on muscle activation during weight training.   (There is mention on a device called a SpiroTiger which I will discuss in a upcoming blog with my own experiences on the device which also has a effect on the core).