LT and Vo2 max concept question

[gonzalovilaseca]

There is somethig I just dont understand about this two concepts.
VO2 max is the maximum volume of oxygen one can consume, and LT is expresed as a % of VO2 max, but if LT means that your body switches from burning fat and O2, to producing energy without using oxygen, how can it be that after reaching LT threshold your still can consume more oxygen? Shouldn't it stay steady as once you are above your LT you are not consumig more oxygen because you produce energy without 'burning' O2?
TIA,
Gonzalo

 

[2LAP]

Originally posted by gonzalovilaseca
There is somethig I just dont understand about this two concepts.
VO2 max is the maximum volume of oxygen one can consume, and LT is expresed as a % of VO2 max, but if LT means that your body switches from burning fat and O2, to producing energy without using oxygen, how can it be that after reaching LT threshold your still can consume more oxygen? Shouldn't it stay steady as once you are above your LT you are not consumig more oxygen because you produce energy without 'burning' O2?
TIA,
Gonzalo

You are correct about VO2 max being the maximum volume of oxygen that can be consumed... this is directly related to the maximum amount of energy released during aerobic metabolism as each L of oxygen used 'releases' roughly 5 kcal.

LT is simply where the body starts to produce more lactate than can be 'processed' by the body and as a result lactate starts accumulating in the blood. Obviously, this sets you on the road to fatigue as lactate accumulates over time and at a faster rate with increased intensity. As it has nothing to do with starting or stopping to burn oxygen, it can occur as a percentage of VO2 max and training is able to raise the % it occurs at.

Anaerobic energy is used all the time to some extent and there is always some circulating LT. As intenisty increases so does aerobic and anaerobic metabolism.

Hope that makes sense?

 

[gonzalovilaseca]

Originally posted by 2LAP
You are correct about VO2 max being the maximum volume of oxygen that can be consumed... this is directly related to the maximum amount of energy released during aerobic metabolism as each L of oxygen used 'releases' roughly 5 kcal.

LT is simply where the body starts to produce more lactate than can be 'processed' by the body and as a result lactate starts accumulating in the blood. Obviously, this sets you on the road to fatigue as lactate accumulates over time and at a faster rate with increased intensity. As it has nothing to do with starting or stopping to burn oxygen, it can occur as a percentage of VO2 max and training is able to raise the % it occurs at.

Anaerobic energy is used all the time to some extent and there is always some circulating LT. As intenisty increases so does aerobic and anaerobic metabolism.

Hope that makes sense?

It does, thankyou very much.

 

[2LAP]

Also check out this thread...
http://www.cyclingforums.com/t38627.html
I made it sticky for you!

 

[dot]

VO2max mostly is your potential maximum and defined by the cardiovascular system capabilities. That's is how much oxigen your heart can pump when working at maximum.
LT is a point where accumulation of lactic acid starts to grow because of oxidative capacity of whole body cannot catch up lactate production. Massive lactate production is due to work of glycolytic part of muscle. The more glycolitic fibers you have in working muscles the lower your LT and the more lactic acid you produce.
All training techniques aim to increase oxidative capacity of glycolytic fibers to reduce lactic acid production and hence to increase LT.

E.g. at HR=170 your heart has some reserve for supplying oxigen to muscles but muscles cannot consume it because all oxidative fibers already recruted and cannot consume more O2.

 

[2LAP]

Sorry, not sure I agree with all that...

Originally posted by dot
VO2max mostly is your potential maximum and defined by the cardiovascular system capabilities. That's is how much oxigen your heart can pump when working at maximum.

Its also to do with how much oxygen can be extracted by the muscles (i.e. the a-vO2 part of the VO2 max equation). In people who are poorly trained their ability to extract oxygen from the muscles may be less than the ability of their heart to deliver oxygen and so oxygen extraction of the muscles may limit VO2 max. However with trained people the muscle has the potential to extract more oxygen than can be delivered to them by the heart, in which case the heart becomes the limiting factor.

Originally posted by dot
(1) LT is a point where accumulation of lactic acid starts to grow because of oxidative capacity of whole body cannot catch up lactate production. (2) Massive lactate production is due to work of glycolytic part of muscle. (3) The more glycolitic fibers you have in working muscles the lower your LT and the more lactic acid you produce.

(1) Agree.
(2) Whats the 'glycolytic part of muscle'? Surely almost all of the cells in the body have a capacity to metabolise using all of the energy systems (although at different rates) and as a result have the potential to produce lactate?
(3) Are you sure its that simple? So how do you account for changes in LT given that muscle fibre type is far less changable than LT?

Originally posted by dot

All training techniques aim to increase oxidative capacity of glycolytic fibers to reduce lactic acid production and hence to increase LT.

What even psychological interventions, weight training, sprint training, etc.?

Originally posted by dot

E.g. at HR=170 your heart has some reserve for supplying oxigen to muscles but muscles cannot consume it because all oxidative fibers already recruted and cannot consume more O2.

Thought you said that the performance of the heart limits O2 consumption and why don't fast twitch fibres use oxygen?

 

[dot]

Originally posted by 2LAP
Sorry, not sure I agree with all that...

Its also to do with how much oxygen can be extracted by the muscles (i.e. the a-vO2 part of the VO2 max equation). In people who are poorly trained their ability to extract oxygen from the muscles may be less than the ability of their heart to deliver oxygen and so oxygen extraction of the muscles may limit VO2 max. However with trained people the muscle has the potential to extract more oxygen than can be delivered to them by the heart, in which case the heart becomes the limiting factor.

I agree. v-aO2 plays a role. But it trained as a side effect. Pros have higher a-vO2 at high load than sedentary ones but do they specific training?

(1) Agree.
(2) Whats the 'glycolytic part of muscle'? Surely almost all of the cells in the body have a capacity to metabolise using all of the energy systems (although at different rates) and as a result have the potential to produce lactate?

Muscle fibers has two types: mostly oxidative with a lot of mitochondia and mostly glycolytic with low mitochondria concentration and high amount of glycolytic enzymes. When first fibers work they metabolize fat and CHO without lacate buildup. When second fibers work (they are high threshold motor units) they produce lactate.
To metabolize lactate there should be mitochondrias in fibers. To produce lactate there should be glycolysis. Glycolysis occurs mostly in fibers with high glycolytic enzymes activity and these fibers are high-threshold motor units. They work under heavy load only.
That's why lactate accumulation builds up after very intensive work. Low intensity recruites only highly trained
motor units. They have a lot of oxidative capacity just because of their low threshold and always constant training
at any intensity.

(3) Are you sure its that simple? So how do you account for changes in LT given that muscle fibre type is far less changable than LT?

No. it's not simple. But it's impossible to write books on biochemistry and physiology here. It's better to read books offline if one is curious. Fiber type doesn't change. It just grow up mitochondrias as a response on regular cyclic load and becomes more oxidative.

What even psychological interventions, weight training, sprint training, etc.?
Thought you said that the performance of the heart limits O2 consumption and why don't fast twitch fibres use oxygen?

Not fast fibers, but glycolitic fibers. Slow fiber can be glycolytic too. Just stay in bed for 50 days without any motion and your muscles will be completely glycolytic.

 

[2LAP]

Originally posted by dot
I agree. v-aO2 plays a role. But it trained as a side effect. Pros have higher a-vO2 at high load than sedentary ones but do they specific training?

Of course trained athletes have a larger a-vO2 difference due to greater oxidative capacity of the muscle; but I'm not sure that this is a side effect. It is a specific adaptation that results from training to increase VO2 max or LT specificaly. As this thread isn't about pros or highly trained individuals the factors that limit a-vO2 difference remain very important.

Originally posted by dot
Muscle fibers has two types: mostly oxidative with a lot of mitochondia and mostly glycolytic with low mitochondria concentration and high amount of glycolytic enzymes. When first fibers work they metabolize fat and CHO without lacate buildup. When second fibers work (they are high threshold motor units) they produce lactate.
To metabolize lactate there should be mitochondrias in fibers. To produce lactate there should be glycolysis. Glycolysis occurs mostly in fibers with high glycolytic enzymes activity and these fibers are high-threshold motor units. They work under heavy load only.
That's why lactate accumulation builds up after very intensive work. Low intensity recruites only highly trained
motor units. They have a lot of oxidative capacity just because of their low threshold and always constant training
at any intensity.

Actualy, it is common to describe muscles as having three types of fibre types (although in reality the situation is much more complex). These are fast twitch (split into type IIa or fast oxidative and IIb or fast glycolytic) and slow twitch (type I or slow oxidative).

Lactate accumulates when the oxidative capacity of the muscle is no longer sufficent to produce ATP at the rate dictated by the exercise intensity; lactate is produced as a result of the incraesing anaerobic glycolysis after this point. My point in the previous post was that the oxidative capacity is not only due to proportion of any fibre type and as a result fibre type does not dicate LT as you suggest.

Originally posted by dot
No. it's not simple. But it's impossible to write books on biochemistry and physiology here. It's better to read books offline if one is curious. Fiber type doesn't change. It just grow up mitochondrias as a response on regular cyclic load and becomes more oxidative.

Obviously, you can't write a book here. However your post suggested that LT is only caused by muscle fibre composition. This is far too simple and misses pretty much all of the adaptations that occur from training that allow LT to change from 60% in untrained people to 90% in some trained people!

Originally posted by dot
Not fast fibers, but glycolitic fibers. Slow fiber can be glycolytic too. Just stay in bed for 50 days without any motion and your muscles will be completely glycolytic.

Not sure what 'completely glycolytic' means as muscle fibres will always have a level of oxidative capacity. Also, there is little evidence to suggest that type I fibres can become type II fibres with any level of training or detraining. Although type IIa fibres will become more like type IIb fibres with detraining and IIb will be more like IIa with training.

 

[dot]

Originally posted by 2LAP
Of course trained athletes have a larger a-vO2 difference due to greater oxidative capacity of the muscle; but I'm not sure that this is a side effect. It is a specific adaptation that results from training to increase VO2 max or LT specificaly. As this thread isn't about pros or highly trained individuals the factors that limit a-vO2 difference remain very important.

I read that greater a-v02 values are due to good capillarization and slower blood flow through muscle.

Actualy, it is common to describe muscles as having three types of fibre types (although in reality the situation is much more complex). These are fast twitch (split into type IIa or fast oxidative and IIb or fast glycolytic) and slow twitch (type I or slow oxidative).

It's just one of classifications. Fibers could be divided also by their oxidative activity.
Frequently used ones are oxidative (mostly slow, slow are low threshold motor units). Rarely used ones are glycolytic.

Lactate accumulates when the oxidative capacity of the muscle is no longer sufficent to produce ATP at the rate
dictated by the exercise intensity; lactate is produced as a result of the incraesing anaerobic glycolysis after this point. My point in the previous post was that the oxidative capacity is not only due to proportion of any fibre type and as a result fibre type does not dicate LT as you suggest.

This is old and not complete theory. Muscle consists of fibers. It doesn't consist of "blck box" energy sources that are forced to produce energy and power under certain loads. "Aerobic energy" produced in fiber energy factories - mitochondrias. If fiber has no mitochondrias it cannot use oxidative phosphorylation. If fiber has no glycolityc enzymes it cannot use glycolysis. It HAS NO required parts to do it! Oxidative fibers have a lot of mitochondrias
but low volume of glycolytic enzymes and glycolytic fibers vise versa.
It's simplification. In real world fibers have both enzyme types in different ratios.

Obviously, you can't write a book here. However your post suggested that LT is only caused by muscle fibre composition. This is far too simple and misses pretty much all of the adaptations that occur from training that allow LT to change from 60% in untrained people to 90% in some trained people!

Not by composition, just by oxidative capacity.
Please tell the other ones for complete picture

Not sure what 'completely glycolytic' means as muscle fibres will always have a level of oxidative capacity. Also, there is little evidence to suggest that type I fibres can become type II fibres with any level of training or detraining. Although type IIa fibres will become more like type IIb fibres with detraining and IIb will be more like IIa with training.

Yes. They have some oxidative capacity but it's very low if fiber is untrained and belongs to high-threshold motor unit. Oxidative/glycolytic activity domination in fiber is defined by SDH or LDH enzymes activity that comes from our genes. We can just to shift it significantly from one type to another but don't change it completely.

 

[dot]

2LAP, just take a look at any interval or continuous training investigation.
There is always strong correlation between increased working muscles' oxidative activy and LT upswing.
Any investigation I read about shows this corellation.
Only short sprint sessions (<15 sec) show no imrovements in oxidative capacity. But there are some little evidences that they can

PS Excuse me for my bad english and misprints. It's hard for me to write a lot in this languague.

 

[2LAP]

Originally posted by dot
2LAP, just take a look at any interval or continuous training investigation.
There is always strong correlation between increased working muscles' oxidative activy and LT upswing.
Any investigation I read about shows this corellation.
Only short sprint sessions (<15 sec) show no imrovements in oxidative capacity. But there are some little evidences that they can

PS Excuse me for my bad english and misprints. It's hard for me to write a lot in this languague.

I absolutly agree.

My original issue with your first post was that you stated... "massive lactate production is due to work of glycolytic part of muscle. The more glycolitic fibers you have in working muscles the lower your LT and the more lactic acid you produce" and "at HR=170 your heart has some reserve for supplying oxygen to muscles but muscles cannot consume it because all oxidative fibers already recruted and cannot consume more O2".

This suggests that it is the 'glycolytic muscle fibres' only that dictate LT and the more of these fibres you have the lower your LT. I know that we both agree that this is not the case and perhaps I have been a bit picky given that English is not your first language. I think you have also miss understood some of my posts!!!!

Anyway...

Have you considered that imporving efficiency might increase the power output at which LT occurs at. Changes in efficiency will be large for a new cyclist and therefore a new cyclist could imporve power output at LT without getting any *fitter*.

 

[dot]

Originally posted by 2LAP
I absolutly agree.

My original issue with your first post was that you stated... "massive lactate production is due to work of glycolytic part of muscle. The more glycolitic fibers you have in working muscles the lower your LT and the more lactic acid you produce".

This suggests that it is the 'glycolytic muscle fibres' only that dictate LT and the more of these fibres you have the lower your LT.

I insist that glycolytic fibers dictate lactate buildup at high intensity.

Have you considered that imporving efficiency might increase the power output at which LT occurs at. Changes in efficiency will be large for a new cyclist and therefore a new cyclist could imporve power output at LT without getting any *fitter*.

Efficiency is not abstraction.
It just reflects changes in the whole body including a lot of parameters.

 

[2LAP]

Originally posted by dot
I insist that glycolytic fibers dictate lactate buildup at high intensity.

Again, I think there has been a big problem with language as this isn't the point you made in earlier posts which suggested that glycolytic fibers alone determined LT (i.e. % of glycolytic fibres = LT as %of VO2max).

I agree with your post in this instance as you are suggesting that glycolytic capacity dictates the rate of lactate build up. As glycolytic fibers have the greatest glycolytic capacity, they are important in determining the glycolytic capacity of a muscle or organism and therefore the rate of lactate accumulation.

Originally posted by dot
Efficiency is not abstraction. It just reflects changes in the whole body including a lot of parameters.

Sorry, I am wrong in this instance. I meant and should have typed 'improving efficiency via changes in technique' would alow a greater power output at LT. This would present an 'easy' avenue for improvement for the beginner and inexperianced.

You are obviously well read, whats you background?

 

[dot]

Originally posted by 2LAP
Again, I think there has been a big problem with language as this isn't the point you made in earlier posts which suggested that glycolytic fibers alone determined LT (i.e. % of glycolytic fibres = LT as %of VO2max).

Ok. I think this statement must look like this:
oxidative/glycolytic capacities ratio determines LT

Sorry, I am wrong in this instance. I meant and should have typed 'improving efficiency via changes in technique' would alow a greater power output at LT. This would present an 'easy' avenue for improvement for the beginner and inexperianced.

I agree.

You are obviously well read, whats you background?

Lots of reading. It's my hobby for last 3 years.

 

[2LAP]

Originally posted by dot
Lots of reading. It's my hobby for last 3 years.

Cool.

 

[cycleboy]

At the risk of wading in...

VO2 max is determined primarily by genetics. Hence , the expression "champions are made and then trained". Elite athletes rise to the top of their sport because they were born with a higher than normal VO2 max (if that's important to their sport i.e. endurance athletes).

Your lactate threshold is the point at which lactic acid reaches 4.0 mMoles/ml/kg. Research has shown that for most people this is the point at which lactic acid builds faster that one can remove it from cells. This is a trainable factor. Riding at just below your lactate threshold will raise it but only within the range that your genetics allow.

Tip: Have you ever noticed that you are riding along at a fast but steady pace and suddenly you are having to breath heavily? Check you heart rate monitor and this will give you an approximate LT. You are breathing heavily to expel the excess CO2 in your blood from processing lactic acid.