Thanks Dan ,
Here a try to give some feedback and some even may be actual answers .
Sorry but I write a lot ans sometimes it may be smart sometimes more confusing.
so here your question where I need some help:
I read on the forum or in the pdf's that training at the highest point of SmO2 would be valuable
I am nor sure but I can't remember nor would I have the courage top give an answer on how coaches out there with much more experience suppose to train vascularisation and mitochondria density.
This is up to the coaches to do that. We simply supply a tool so coaches can see what is limiter and what is compensator. In the past they did not had this now they know after a test what has to be improved and now they can create a training plan based on this directions and goals rather than on % of something.. But again can you show me what the heck I may have written in a pdf or on the forum. on how to stimulate mitochondria density and capillarisation.
2. Now the dropping FEI zone would indicate an increased demand for O2 but decrease in ability to supply it (via cardiac or respiratory or maybe the delivery men?)...
I am not sure whether we can do this that simple and that is the risk when going too basic. So here my take.
A dropping SmO2 .where we use to make the ideas, that this is in FEI, can have different reasons.
a) Same O2 demand but less supply than before so SmO2 drops.. Could be seen in tHb reaction. So same CO perhaps even same HR and Same SV but more muscle compression. Or Same CO but lower SV and higher HR and more muscle compression and many more options.
b) Higher O2 demand and higher O2 delivery, but the demand is higher than the even increased delivery can handle so SmO2 is dropping as well as well.
c) your suggestion as a decrease in delivery and an increase in demand so SmO2 drops.
d) same delivery but higher demand so SmO2 drops.
This options will help you do get more feedback on limiter and compensator.
So that would lead to some thoughts on your last part
however can this dropping Sm02 be a result of poor capillarization?mitochondrial density.
poor capillarisation could be a part of poor delivery ability or as capillarisation is a part of the delivery system .
SmO2 is a part of the energy delivery idea so O2 % of the tHb.. Whether we have a great loaded Hb depends mainly on the exchange area in the lungs to the blood. Once it is in the blood it will be somehow delivered.
. If we have a great CO and a good respiration ( CO2 balanced than we have a good loaded blood SpO2. Now the delivery is no dependent on the blood vessels and as such on the ability to utilize it in the mitochondria..
So a poor capillarisation and a low mitochondria density would not change the amount of O2 I have loaded , in fact it may be that I have a great CO and optimal loading, and I load so much , that I not or barely will see a dent in the utilization if there is a poor mitochondria density.
. That is the reason why we have in many cases a very interesting situation. A top endurance athlete and I work for the moment with a 100 - 150 mile runner, barely shows a drop in SmO2 and he can go long and long relative fast long meaning over 10 plus hours and fast meaning 5 min / km and faster for that duration.
His deliver when we test him is incredible and his ability to move on FFA and using O2 as well but he is in complete balance after " warm up where he is " fully moving O2 and his is balanced in his race speed. Interestingly enough barely can handle changes in speed otherwise , he runs into trouble.
On the other side we have very healthy but very untrained people. Their delivery system is not great but healthy an good enough to delver far more than they can utilize or turn around. So same picture as we see an increase in SmO2 an than minimal sometimes no drop in SmO2 even in an all out intensity.
Like poor CO is a part of poor or lets put it more positive not optimal delivery. Sop the question is, whether when I have a low mitochondria density , whether SmO2 drops really as I simply turn around what i get delivered. As O2 only can drop or possibly only can drop if it is used it seems to me it depends on mitochondria activity and as well density.
. So low density no drop of O2 as it is not utilized.
Hmm does that makes sense.
.The other interesting part is as well that mitochondria density is directly connected with capillarisation. The ability to use O2 can be dependent on the mitochondrial activity.
So to create in simple terms more mitochondria I have to develop first more blood vessels.
But I can improve mitochondrial utilization without more mitochondria and than I can turn more energy , around as well.
That is the every 15 years new discussion between HIT and LSD.
A very high intensity training and much research shows that over 6 - 8 weeks is more successful in using O2 than a LSD for 6 - 8 weeks.
So the conclusion we than learn is HIT is better than LSD and it is used as a great fitness PR for centers.
Go short and hard an you will have the same end result as when you go long or slow actually even better as you do not " waste " time. Than EPOC moves in it an you have a very Gospel like group of people running for that.
LSD over 6 - 8 weeks shows limited changes as it is an intensity, where a lot of structural changes take place like for example vascularisation or numbers of mitochondria.
. There are ample of research done showing this
BUT you have to look at studies over 3 -5 and more years. If you go all out HIT and this is the only traininig your do you see great and fast improvement for 6 - 8 Weeks. Do the same for 16 - 18 weeks and than for 3 - 4 years and compared with the once who do a lot of LSD ( and see, how they stake up now.
Problme : I can not find , so please help. A HIT research. where they did the HIT over a 3 -4 years duration and than compared with the LSD idea. On the other side we have even longer studies on LSD from cross counrty skiing and rowing, where in this sports 80 +0- % of the time invested is done in a LSD or they use lactate as a no show for their LSD as it is still produced but it is turned around and does not show up in the finger or ear. If and just IF we can do a 20 min HIT and than go and win a 50 km cross country skii or a Tour de france, may allow to ask the question, why all this pros train so much and so long and so slow. Will try to fond ome stduie s who show tweh ratio of LSD to HIT in endurance sport.
This discussion may answer Dan's first question on STEI and intensity versus high SmO2.
What is your goal :
Functional versus structural ?
Here a little bit more to start.
Structural and functional adaptations of the cardiovascular system by training.
Huonker M, Halle M, Keul J.
Department of Rehabilitation, Prevention and Sports Medicine, Freiburg University Hospital, Germany.
Muscular training induces structural and functional adaptations within the cardiovascular system which vary according to type, intensity and duration of muscular exertion. Dynamic muscular training for more than 5 h a week involving more than 1/6th of the skeletal muscle mass causes an increase in parasympathetic tone and an eccentric myocardial hypertrophy. The dimensions of all cardiac chambers enlarge up to 20% and the cardiac muscle mass may increase by 70%-80%. Static muscular training does not induce any change in the parasympathetic heart regulation, nor does it lead to any disproportional increase in cardiac muscle mass relative to skeletal muscle mass. However, a tendency towards a concentric myocardial hypertrophy can be observed. The effects of regular muscular training on the arteries are the subject of current scientific investigation. To explain the acute and chronic adaptations of the arterial vasculature to exercise, a "shear stress" hypothesis has been proposed. During dynamic muscular exercise the regional arterial blood flow is enhanced. This leads to an acute increase in intraluminal shear forces, which stimulates the vascular endothelium with a reactive flow-dependent regional vasodilation mediated by endothelial-derived relaxing factors (EDRF, EDNO). Chronic enhancement of shear forces induces endothelial cell-mediated alterations in gene expression (endothelin, growth factors, regulators of fibrinolysis) and chronic structural adaptations of the vascular wall (cytoskeletal redistribution, cell shape change). Recent duplex sonographic studies in humans have revealed a significant lumen increase of muscular type arteries induced by dynamic, predominantly aerobic muscular training, but not by static muscular training. These structural adaptations are confined to those arteries supplying exercising muscle groups, whereas functional adaptations with an improvement of regional compliance are found in all arteries.
and some more I put together
Functional vs Structural changes through training
This blog is about making athletes think about their training, why do certain things and what happens when we try to adapt training programmes to our physiology instead of following the normal cookie cutter approach of just doing. Understanding what functional and structural changes are helps with this understanding of why we see certain changes through training. There is no official definition and these ideas come from FaCT so I have made my own version of the definition here plus given a few examples so you can get a idea of what functional and structural training is.
Don't confuse the definitions of functional training (or functional strength training) which Wiki writes it as, training the body for activities of daily life, which in short is transferring the strengths from one movement with resistance to a sport or activity.
Functional change definition: This is normally a short term result of training and is where the initial changes in the body is seen. Functional changes are often temporary and is gained and lost quickly.
Structural change definition: This is a long term change in the body that results from starting as a functional change and through months and sometimes years of specific training to develop that specific system may see the development of a structural change which supports the human body.
So when the two definition are combined then functional and structural training implies to the development of the human body through specific training which will normally start with functional change, and through specific stresses and adaptions lead to a structural change which will improve athletic performance. The development of the structure of the body which broadly speaking will include the respiratory system, cardiac system, muscular system, hormones, blood system etc.
Here are some simple examples: A professional cyclist who has been cycling for years, has a higher amount of mitochondria growth and capillarization compared to a amateur. Using the same trained cyclist, his muscles have developed from being a amateur cyclist being functionally good to adjusting the muscle fibres structurally so that they can better perform the required activity.
Athletes thus in general have a higher ability to utilise oxygen and pump a higher volume of blood which is developed through training.
You say so what, this is obvious. Here are some more examples to think through: A novice cross country skier will have problems initially learning to ski and use a huge amount of energy learning to balance, after a few days he has learned to balance and found the needed coordination and he will be skiing faster simply by having made a functional change. Now you did some tests as he started skiing and a few weeks later the skier has shown an improvement and you think, great he is fitter, but most likely due to the improved balance and coordination the skier is able to use more muscle to ski faster, which may show a higher VO2, instead of using muscle to balance. The Skier will initially very quickly develop the utilisation ability through capillarization and mitochondria density and the before mentioned improved balance and co-ordination. This is often the big improvements seen in research studies which last only a few weeks versus trained athletes where changes are small as there is very little room for functional changes. To make structural changes which will strengthen the athletes respiratory system, improve cardiac output and stroke volume may take months or even years.
Another type of example: A athlete goes to altitude or sleeps in a altitude tent and is able to raise his blood values, now he goes back to a lower altitude to compete and if he is a responder to altitude, he/her body is simply utilising the extra oxygen available to the body. To make a real altitude adaption takes many years of IHT and altitude training where the body learns to adapt, and to better utilize and deliver.
Some individuals can improve Stroke Volume (SV) through certain training protocols or even exercise which can be due to a plasma volume increase. This again is a very functional change which is temporary. Repeating this functional training over several weeks, sometimes months should (if the correct stimulus is used with the correct timing to stress the limitation) see a structural change in End Diastolic Volume (EDV) as a change in heart size, thus a higher volume ability to pump blood (stroke volume) and a lower heart rate (CO=SVxHR).
So in any system that you are training you need to think, is it development or just utilisation, i.e. capillarization or capillary utilisation, SV through plasma expansion or SV through EDV improvement, mitochondria density or mitochondria enzyme reaction. Is the sudden improvement weather related, (hot=warmer tarmac=different reactions on bicycle/skate wheels resistance.) or is it true structural adaptation. Another improvement which has not even been mentioned is on the mental side. Once you have done lets say a performance test, you know how it feels, so next time in most cases without any physical improvement you know how to pace it better. Changes in nutrition can make functional changes to blood (e.g. beet root) certain supplements which may buffer H+. Respiratory training with specific devices will initially show great improvements as coordination and general conditioning improves (similar to the idea with the skier) but long term diaphragm strength and transfer of training to sport specific activity may take months.
The key to train structure, you need to find what is the limitation which is creating the weak link in athletic performance.
If I make a short summary in a picture than it looks like this below.