Cardio

You should realize that you can not get rid of slow twitch muscle fibers, and certain muscles are like 80% slow twitch fibers. There's nothing wrong with that, either. Soleus is mostly slow twitch, gastrocnemius is mostly fast twitch.

Type II fibers are all fast twitch. You have two different types of those, and they can both perform nearly identically when trained for power. The real goal should be to strengthen everything enough that the slow twitch fibers alone can handle the low intensity cardio training. Most people are working too hard in this kind of work, your heart rate should be around 120. 130-140 is what most people think of as low intensity and that is not low intensity. That is moderate. You can't easily carry on a casual conversation at that rate, and that is the layman's way of judging how hard you are working.

Understand that low intensity runs, or any other low intensity activity... it doesn't have to be running... is going to have completely different training effects than high intensity intervals.

In all honesty, genetics probably play a bigger factor in gaining strength as opposed to adding the supplemental cardio training. But that's neither here or there.

Regardless, I'm more inclined to go with what slizzard is saying or what gymrob is saying

1. sub lac thershold running or near lac threshold running. E.g. in terms of the RPE scale (rate of perceived exertion) you should be able to carry on a convo while doing this type of running.

Aerobic base via Lydiard's stuff is trained through the sub lac threshold runs. While the slightly above lac threshold runs will generate somewhat quicker adaptations they particularly be a burden on training if coupled with other volume work. But again, it depends on the person's overall work capacity.

2. Tempo runs via Clyde Hart style can also work for what gymnasts are needing to do, which is more than enough for most of the amateurs here like us. However, they are a bit higher intensity than sub lac running so you need better conditioning to adequately perform these without burning out especially as a novice.

PHILIP said:

No one sees these runs causing adaptation in an unfavorable direction?

If you read my post I addressed that.

I said that the negative adaptations of stimulus of type I fiber adaptations is offset by the fact that things such as floor exercise require repetitive volume over the course of 75s in which the aerobic base will help out with recovery during so the athletes don't crash and burn. Also, the adaptations can also be somewhat offset by the fact they do strength and plyometric training much like 400m runners do despite having tempo runs.

However, I do agree in concept. If your goal is pure strength you don't really see any of the world class powerlifters or Oly lifters doing much cardio work at all (unless I've been living under a rock and haven't seen these implemented in their training programs which may be the case).

So yes, it may not be such a good idea if you want to maximize a particular facet of your training.

Thank you braindx that was what I was getting at. Thank you for that note there. Think I'll go hit some intervals now.

... However, I do agree in concept. If your goal is pure strength you don't really see any of the world class powerlifters or Oly lifters doing much cardio work at all (unless I've been living under a rock and haven't seen these implemented in their training programs which may be the case) ... So yes, it may not be such a good idea if you want to maximize a particular facet of your training ...

Until someone demonstrates that their method of developing high levels of gymnastics strength is as proficient as the top gymnastics programs in the world (through matching them in ring strength), then all other opinions to the contrary will remain merely unsupported supposition.

Rather than arguing on how this low volume of running could not possibly work (when it has already been demonstrated to do so), perhaps it would be wiser to implement it and find out personally if it has value within your own training.

Yours in Fitness,

Coach Sommer

Oh, I definitely agree with it being used for a competitive gymnastics program.

I could see how it could be argued the other way for someone whose goal was only strength though. That's all I'm saying.

slizzardman said:

... Type II fibers are all fast twitch ...

Oops. :oops: I thought I was getting something wrong...

braindx said:

If your goal is pure strength you don't really see any of the world class powerlifters or Oly lifters doing much cardio work at all (unless I've been living under a rock and haven't seen these implemented in their training programs which may be the case).

The Chinese Olympic lifters do the similar thing to the gymnasts of a light jog (I don't think it's longer than 20 minutes) a few times per week. I don't know what the rest of the Olympic lifters do.

Quite a few top powerlifters do GPP work with the goal of increased heart rate and muscle recover, became really popular through the work of Louie Simmons. Some do this just through walks and hill walks at a brisk pace, others push/pull sleds or the prowler, some do a complex of prehab movements with high repetitions (really popular with band work). Strongman implements such as farmers walks and other carries (not max strength the weight is greatly reduced and is done for longer distances) are pretty popular too.

Very informative post thanks Braindx and Coach Sommer.

braindx said:

Oh, I definitely agree with it being used for a competitive gymnastics program.

I could see how it could be argued the other way for someone whose goal was only strength though. That's all I'm saying.

That doesn't make sense when you think about the pace and the time frame for the low-level aerobic activity. If you can increase blood flow without causing undesirable training effects you are going to heal better and faster. Whether it is a really slow jog, elliptical machine training, easy sled work, walking, or whatever else doesn't matter. They are all interchangeable in terms of the training effect that low level cardio produces. I'm not saying they are all equal, but they are all interchangeable and all will do the job.

Active recovery is active recovery no matter what you use to accomplish it, and active recovery has been shown conclusively to produce better results than not having it in your program, pretty much regardless of what your program is.

So Slizzardman, could this also be super high rep prehab work to also get a similar effect? Such as lots of band series work?

This also makes me wonder because I train sometimes 3 times a day and my recovery never feels taxed. I also don't have a car and a lot of my day involves walking miles between jobs. Could that be increasing recovery?

I have been training super hard full body 3x a day for the past week or so, and I feel fine too. Of course, there are very specific things I am avoiding in order to do this, but volume can be "inhumanly" high if you know what you're doing. The next two days will just be active recovery, and yes you could do something like that, but it won't have as much a systemic effect.

Something as simple as a 15-20 minute brisk walk (just faster than you can comfortably walk, so slight exertion but nothing crazy... remember HR =120!) plus the band work would be ideal. You could also do a combination of locomotion stuff like crab walks and bear crawls and punctuate the sets with a round of the super light band work for 20-30 minutes. You might break a light sweat but you should not feel tired if you are doing it right. Doing more than a 1/4 mile of bear crawls and/or crab walks total is probably going to be too much for the shoulders, but I don't know. I guess that depends on each person. Heck, you could play a light game of tag or ultimate frisbee and get similar results!

Edit: I also have around a 1 mile run every day M-F with 25-35 lbs added, as I nearly always jog to school from the train station. Light job, no heavy breathing, I stop to walk when I feel like I'm going to do more than active recovery.

Your walking could definitely be helping your recovery, especially if you are eating before you walk. Not that you have to, but having your blood pumping while extra nutrients are in it is going to be really good. That's why I'm eating right now before I go on my slow jog.

Awesome post as always thank you! Before, I didn't see the point of distance work for cardio. But for recovery, I could see some use. Not so much for the heart but to get blood flowing. I will use a different tool to reach the goal but the end result of recovery is great. Thank you for clearing that up.

Sliiz mentions tag above. I find tag with my children to be a great recovery workout. There is a real mix of speeds, changing of directions, etc. Gets the heart going, but not too exhausting. (I also do some running workouts on non-strength days.)

Also, dancing is also a great cardio exercise. Too bad I look so bad doing it!

Me too Wolf, me too. :oops:

slizzardman said:

braindx said:

Oh, I definitely agree with it being used for a competitive gymnastics program.

I could see how it could be argued the other way for someone whose goal was only strength though. That's all I'm saying.

That doesn't make sense when you think about the pace and the time frame for the low-level aerobic activity. If you can increase blood flow without causing undesirable training effects you are going to heal better and faster. Whether it is a really slow jog, elliptical machine training, easy sled work, walking, or whatever else doesn't matter. They are all interchangeable in terms of the training effect that low level cardio produces. I'm not saying they are all equal, but they are all interchangeable and all will do the job.

Active recovery is active recovery no matter what you use to accomplish it, and active recovery has been shown conclusively to produce better results than not having it in your program, pretty much regardless of what your program is.

Aerobic base cardio is different from very light active recovery work (whatever type of active recovery work it is)

So yes, I think the point still applies.

But yes, in general, active recovery work is good. You can get this from just being up and around all day walking. I belive there is some recent research on how if you're sedentary besides you're workouts you're almost no more healthy than the general population, and those who actively move throughout the day are the healthiest overall which would make intuitive sense.

braindx said:

slizzardman said:

braindx said:

Oh, I definitely agree with it being used for a competitive gymnastics program.

I could see how it could be argued the other way for someone whose goal was only strength though. That's all I'm saying.

That doesn't make sense when you think about the pace and the time frame for the low-level aerobic activity. If you can increase blood flow without causing undesirable training effects you are going to heal better and faster. Whether it is a really slow jog, elliptical machine training, easy sled work, walking, or whatever else doesn't matter. They are all interchangeable in terms of the training effect that low level cardio produces. I'm not saying they are all equal, but they are all interchangeable and all will do the job.

Active recovery is active recovery no matter what you use to accomplish it, and active recovery has been shown conclusively to produce better results than not having it in your program, pretty much regardless of what your program is.

Aerobic base cardio is different from very light active recovery work (whatever type of active recovery work it is)

So yes, I think the point still applies.

But yes, in general, active recovery work is good. You can get this from just being up and around all day walking. I belive there is some recent research on how if you're sedentary besides you're workouts you're almost no more healthy than the general population, and those who actively move throughout the day are the healthiest overall which would make intuitive sense.

Excuse my interjection here, but I think you're both right in a sense.

In this case it's sementics whether it is called active recovery or low-level aerobic work.

Since running is leg work. and GB involves almost no legs, it is all recovery for the upper body and trunk regardless if it's aerobic to the CV and legs.

Phillip: Even if this small amount of running caused small endurance adaptation in the legs, it has no impact to strength. Running can be thought of as a continious series of one legged squats! It does strengthen the legs, this I can assure you. You will not end up with toothpicks for legs. I have run for years, combined with minimal leg strength work, and not noticed any loss. I can still leg press more than 400 pounds. (Know it's not a squat but haven't trained those - let's not go there :-) )

All who want to can enjoy a short run, without fear.

It depends on what perspective you choose to take. I don't look at things from the same perspective as most do. To me, training has to be considered purely in terms of the training effect elicited and the impact on recovery. Everything exists on a sliding scale, but it is very possible to look at things and say 'Ah, these can be separated and worked on separately, and doing so will allow the same adaptation with less recovery."

High intensity work makes the heart beat significantly harder and acts like strength training for the heart. The strokes get more powerful and somewhat deeper. Low intensity has a different effect, the heart chambers themselves actually enlarge, allowing them to hold more blood. In turn, each stroke moves more blood. You don't need to work very hard to make this happen, and the threshold is in the active recovery heart rate range. So, proper use of active recovery is actually helping to enhance cardiac function quite specifically.The two training effects work in synergy.

Future: You can not change the fact that there are a certain amount of slow twitch fibers in the legs. Slow twitch muscle fiber can produce just as much force as fast twitch fiber when comparing identical volumes of each. There are only two major differences: Slow twitch fibers don't grow as big, because they need a high volume to surface area ration in order to efficiently process lactate (in fact, this helps explains the extraordinarily high muscle fiber counts observed in shoulder biopses of swimmers) and slow twitch fibers take 60 milliseconds to generate peak force. Fast twitch takes 20-25 milliseconds. The fastest movements in sports are right around 60 milliseconds. So for one thing, worrying about slow twitch development is silly just based on those numbers alone. After all, active recovery work by nature is essentially using nothing but slow twitch. If that was problematic we wouldn't get good results from it.

The loss of strength supposedly comes when you are giving your fast twitch glycolytic fibers a reason to shift towards a slow twitch function. At low enough intensity levels that won't happen for the simple reason that they don't have to help out. However, if you think about it even THAT doesn't matter for most sports. The real issue is simply that you can not expose the muscle to the same amount of instantaneous stress with aerobic training as you can with strength or speed training, and so you do not get the strength adaptation. That is by far the largest reason that endurance athletes can not compare with strength athletes in terms of peak force generation. They train their bodies to be efficient for long distances, which involves figuring out how to use the least possible amount of muscle to get the job done in a winning fashion. That's why you have ex-gymnasts like Coach who can go run a marathon for fun without training, while you don't have any marathon runners who can just do muscle ups or single leg squats for fun without training for them.

Mr. Slizz, I think I can agree with about everything you said above

I would add that the increase in SV occurs to a great degree due to the increase in blood volume.

The heart has to pump more blood - because it does the ventricular size and wall thickness accomodate this

so HR is reduced. Increased blood volume improves the ability of the blood to carry O2 which improves V02Max and other capacities.

The conversion from fast to slow twitch is still open to debate from what i have read and also what is noted in

http://en.wikipedia.org/wiki/Skeletal_muscle (muscle fibers). In any event type 2a fibers still retain most of their strength characteristcs but have additional mitochon which support endurance, so it's the best of both worlds. And what proportions of the 3 types you have in your body or legs, as you say, appears to be genitically determined (or epigenitically as you brought up before ).

One thing for sure is that aging results in an earlier selective death of type 2 fibrers. They lived too fast and hard apparently Mostly this begins to occur after 50. (Not sure if this applies to type 2A which is an interesting question), This is one reason why older people can't match their earlier strength feats, although it by no means that they (we) are doomed to be weak and feeble.

It's a balancing act for sure. It's difficult to really know what's going on at this level in our own body, so I tend

to focus on observable physical signs. Theory, and there is a lot of it, is nice to know and makes working out interesting at another level for sure though.

So in short, there should be no negative impact to modest running at aerboic intensity to upper body strength, which was the OP's implied concern, subject to incorporating it an approrpriate manner. And there is ancedotal evidence that it may improve uppper body strength through indirect means, at least in advanced athletes as per Coach's references. And as Coach Sommer noted, it's easy enough to find out if it helps, hurts or is neutral by performing it oneself, if one has this interest.

That's very true, it is impossible to say anything with 100% certainty. It's silly to put the disclaimer "This is just the best evidence-supported idea we have at the time, but we could have this bass-ackwards" in every statement, but it's definitely implied. We really don't know that much on a biochemical cause and effect level. We know tons of reactions but we aren't sure how they translate to body adaptation as a whole. In the end, for anyone who wants to perform at a high level you do have to take a pretty even look at anecdotal evidence and the scientific research. Research is generally way, way behind because funding is hard to come by, so just because there is no research does not mean there is no validity to an idea. The proof is always in the athlete's performance. The understanding is something else again.

That's also a good point about the blood volume. It is believed that the generation of new blood vessels along with the new blood to fill them is a large part of why 20-30 point blood pressure reductions are seen after 4-6 weeks of consistent resistance training in untrained individuals.

That wiki is fraught with missing information and a lack of citations. For one thing, it claims that humans have fast twitch aerobic fibers. We do not. That is why we can not maintain high power outputs for long periods of time like birds can. That's why they can fly, aerobic fast twitch. That's what oxidative means. Human fast twitch muscle does not have the ability to utilize oxygen. That is why lactate gets transported outside of the fast twitch fibers and into the slow twitch fibers, because their mitochondria are different. They are able to process the lactate back into pyruvate, and are the only fibers that can. That is why high intensity intervals improve your aerobic ability: they literally overload the slow twitch fibers' ability to process lactate. In response you get an increase in mitochondrial density and capillarization.

The 2a fibers are able to shift along a wide spectrum of abilities, from highly glycolytic(like type 1 fibers, which is a gigantic error in that wiki) to highly CP. Their time to generate full force can be reduced to 25ms with training, which is almost identical to 2b's 20ms. More than fast enough for just about any human movement. After that it's all about coordination of activation, which is always the primary factor affecting external power output anyways.

There is aerobic glycolysis and anaerobic, but BOTH are glycolytic. They both utilize glycogen. Believe it or not, the primary function of slow twitch muscle in most sports, and even for the first half of a marathon, is not to be a direct source of propulsion but instead to be recycling lactate into pyruvate so that the other muscle fibers are able to use it. Of course with specific training you see a shift of the 2a fibers to a slow twitch function and an enlargement of existing type 1 fibers (and possible hyperplasia to increase surface area and thus the transmission of lactate and pyruvate between cells), but that's not to be confused with actual conversion of fundamental fiber TYPE. Muscle fiber types literally have different gene sequences. I do not believe there has ever been any observation of the genetic structure of a muscle fiber changing to the structure of a different type.

Sir Slizz: If the Wiki is in error you should attempt to correct it. I didn't see the errors you referred to, or perhaps they have been repaired since then. I didn't go over it with a fine toothed comb but I only see type I referred to as oxidative. Although type 2A does have more mictochondria which perhaps is why they are more resistant to fatigue...

Aerobic glycolosis just refers to using pruvate, the byproduct of initial anerobic gycolosis, as the substrate in mitochondrial (aerobic) celluar respiration, as opposed to lipds. I know that you know that, I'm just saying this so it's clear there there isn't yet another energy pathway. As you point out lactate processing in endurance fibers is one way that gymnasts probably would benefit from better aerobic conditioning. This is where aerobic condiioning and recovery merge!

Unfortunately, Type 1 fibres aren't subject to much hypertrophy, and hyperplasia (which would be entirely new fibres) is theortical hasn't been shown to occur in humans, from what I've read but otherwise I think we're in agreement Anyway this discussion has no bearing on topic at hand, and I don't want to detract from the main subject. You may be on the leading (bleeding) edge though and some of the things that are fancy today may be facts tommorow. Just not today :wink:

FutureisNow said:

Sir Slizz: If the Wiki is in error you should attempt to correct it. I didn't see the errors you referred to, or perhaps they have been repaired since then. I didn't go over it with a fine toothed comb but I only see type I referred to as oxidative. Although type 2A does have more mictochondria which perhaps is why they are more resistant to fatigue...

Aerobic glycolosis just refers to using pruvate, the byproduct of initial anerobic gycolosis, as the substrate in mitochondrial (aerobic) celluar respiration, as opposed to lipds. I know that you know that, I'm just saying this so it's clear there there isn't yet another energy pathway. As you point out lactate processing in endurance fibers is one way that gymnasts probably would benefit from better aerobic conditioning. This is where aerobic condiioning and recovery merge!

That isn't quite right. Aerobic lipolysis and aerobic glycolysis are both oxidative. They both happen in slow twitch oxidative muscle. Anaerobic glycolysis happens in type 2 fibers. That is why you have a lactate threshold that limits the time you can perform high intensity anaerobic exercise. You can perform low intensity anaerobic exercise pretty much until you run out of glycogen, at which point you shift over to aerobic lipolysis and your power output drops accordingly, unless you were already within your current lipolytic threshold. The limiting factor, and what causes the lactate threshold to exist, is the limited ability to transport fresh glycogen into the cells and pyruvate out. If glycogen can't be brought in as fast as it is being used, you're going to poop out. If glycogen can be brought in but lactate can't be moved as fast as it is being generated you run into the same problem: transportation failure. It is usually not a glycogen supply issue so much as a transportation issue. Glucose transport molecules increase 11 to 17-fold (1100% to 1700%, more or less) in response to anaerobic threshold work, so glucose transport quickly becomes a non-issue. Ability to process glucose becomes the next roadblock, which is dealt with both through increased mitochondrial count and by mitochondria migrating towards the cell membrane. Finally you are left with the inter-cellular transport of lactate as being an issue, along with the processing of lactate in aerobic fibers. Of course, the aerobic fibers are adapting in a similar manner as the anaerobic, so in the end you end up with lactate transport being the final limiting factor. This is also why you can achieve absolutely incredible increases in endurance over just 6 months of training.

Pyruvate is the actual compound that is used to generate ATP. Glygocen, lipids and proteins can all be (and are) broken down into pyruvate when used for energy. That is what energy metabolism is. The rate at which these can happen is limited by number of mitochondria, type of mitochondria, location of mitochondria within the cell and enzyme availability. Mitochondrial respiration in type 2 fibers is anaerobic. This is where people get tripped up, and where things are kind of weird.

Gymnasts actually most likely have exceptional lactate processing in type 1 fibers, particularly in the lower legs and shoulder girdle. Extensive bouts of circles, handstands, tumbling, and everything else builds up quite a bit of lactate, which in turn stimulates extremely high mitochondrial density in all muscle fiber types. Now, they WOULD benefit from having more blood flowing and larger heart chambers, which is part of the science behind why Coach's recovery jogs work. Not only do they utilize the muscles that a gymnast depends on the least, thus mitigating any small amount of fiber conversion or proliferation that may occur, but the body sends fresh nutrients all over the body and the heart chambers slowly expand.

Unfortunately, Type 1 fibres aren't subject to much hypertrophy, and hyperplasia (which would be entirely new fibres) is theortical hasn't been shown to occur in humans, from what I've read but otherwise I think we're in agreement Anyway this discussion has no bearing on topic at hand, and I don't want to detract from the main subject. You may be on the leading (bleeding) edge though and some of the things that are fancy today may be facts tommorow. Just not today :wink:

Hyperplasia has in fact been heavily suggested to occur in humans through tissue biopses and has been conclusively proven to occur in many different lab animals. Do you know why we can't conclusively probe hyperplasia in humans? To conclusively prove hyperplasia you need to train one side of the body and not the other, and then completely remove the muscle and count fibers. You do that by digesting the connective tissue with nitric acid. You can not ethically do that to humans. Therefore you can not conclusively prove hyperplasia. This is what I mean by science being limited. Not only is funding an issue, ethics are too. However, we can use biopses and biopses show significant increases in fiber count across a cross-sectional biopsy after various types of training. It is ridiculous, in my personal opinion, to not take into account the increasingly heavy evidence we have that supports hyperplasia. There is no significant detraction from these studies, and they are quite recent. None will claim hyperplasia as fact, because as I stated above that can't be done with biopses alone. Anyways, google scholar will show you to these studies. They are good reads.

Now, I do have to alter what I said about muscle fiber conversion. Stain tests show an 8% conversion from white to red types with inactivity, and a similar conversion from red to white with aerobic activity. This is a staining technique and not a myosin chain comparison or a motor unit comparison. Keep that in mind. That is from a 2008 study. The participants have Stable Cardiac Failure, which makes them really crappy at oxidation. This, in turn, leads to more type 2 fibers forming since they do not require oxidation. So, as the oxidative ability of the patients increased they saw a shift in fiber distribution. I have been unable to find good recent studies that demonstrate type 2 to type 1 conversion. From a chemical perspective it isn't entirely necessary, as type 2A fibers can take on characteristics of type 1 fibers without becoming type 1. I do not know if they can acquire oxidative mitochondria in significant numbers. This goes beyond my memory and as far as I know what I have read as well. Something is tickling my brain, but I think it's just hunger.

Here is what a very good 2001 study has said, and this should be read in full by everyone who is interested in this stuff.

This plasticity in contractile and metabolic properties in response to stimuli (eg, training and rehabilitation) allows for adaptation to different functional demands.2 Fiber conversions between type IIB and type IIA are the most common, but type I to type II conversions are possible in cases of severe deconditioning or spinal cord injury (SCI).2,20

Less evidence exists for the conversion of type II to type I fibers with training or rehabilitation, because only studies that use denervated muscle that is chronically activated with electrical stimulation have consistently demonstrated that such a conversion is possible.21

Full text: http://ptjournal.apta.org/content/81/11/1810.full

This goes into the mis-classification of muscle fiber types and why it happens, and what they really are and what they mean. There are currently 7 known human muscle fiber types. Furthermore, humans do not express the fastest myosin chain type, which is 2b. What we have, and what is referred to wrongly as 2b, is 2x/d. That's the fastest stuff we've got. It's a big difference too, with 2b generating peak force in something crazy like 6ms as opposed to our 20-25ms.

Anyhow, the only significant type 2 to type 1 conversion seems to happen with full immobilization, and the conversion reverses as soon as mobilization is restored. In healthy subjects, and that

slizzardman said:

FutureisNow said:

Sir Slizz: If the Wiki is in error you should attempt to correct it. I didn't see the errors you referred to, or perhaps they have been repaired since then. I didn't go over it with a fine toothed comb but I only see type I referred to as oxidative. Although type 2A does have more mictochondria which perhaps is why they are more resistant to fatigue...

Aerobic glycolosis just refers to using pruvate, the byproduct of initial anerobic gycolosis, as the substrate in mitochondrial (aerobic) celluar respiration, as opposed to lipds. I know that you know that, I'm just saying this so it's clear there there isn't yet another energy pathway. As you point out lactate processing in endurance fibers is one way that gymnasts probably would benefit from better aerobic conditioning. This is where aerobic condiioning and recovery merge!

That isn't quite right. Aerobic lipolysis and aerobic glycolysis are both oxidative. They both happen in slow twitch oxidative muscle. Anaerobic glycolysis happens in type 2 fibers. That is why you have a lactate threshold that limits the time you can perform high intensity anaerobic exercise. You can perform low intensity anaerobic exercise pretty much until you run out of glycogen, at which point you shift over to aerobic lipolysis and your power output drops accordingly, unless you were already within your current lipolytic threshold. The limiting factor, and what causes the lactate threshold to exist, is the limited ability to transport fresh glycogen into the cells and pyruvate out. If glycogen can't be brought in as fast as it is being used, you're going to poop out. If glycogen can be brought in but lactate can't be moved as fast as it is being generated you run into the same problem: transportation failure. It is usually not a glycogen supply issue so much as a transportation issue. Glucose transport molecules increase 11 to 17-fold (1100% to 1700%, more or less) in response to anaerobic threshold work, so glucose transport quickly becomes a non-issue. Ability to process glucose becomes the next roadblock, which is dealt with both through increased mitochondrial count and by mitochondria migrating towards the cell membrane. Finally you are left with the inter-cellular transport of lactate as being an issue, along with the processing of lactate in aerobic fibers. Of course, the aerobic fibers are adapting in a similar manner as the anaerobic, so in the end you end up with lactate transport being the final limiting factor. This is also why you can achieve absolutely incredible increases in endurance over just 6 months of training.

Pyruvate is the actual compound that is used to generate ATP. Glygocen, lipids and proteins can all be (and are) broken down into pyruvate when used for energy. That is what energy metabolism is. The rate at which these can happen is limited by number of mitochondria, type of mitochondria, location of mitochondria within the cell and enzyme availability. Mitochondrial respiration in type 2 fibers is anaerobic. This is where people get tripped up, and where things are kind of weird.

Gymnasts actually most likely have exceptional lactate processing in type 1 fibers, particularly in the lower legs and shoulder girdle. Extensive bouts of circles, handstands, tumbling, and everything else builds up quite a bit of lactate, which in turn stimulates extremely high mitochondrial density in all muscle fiber types. Now, they WOULD benefit from having more blood flowing and larger heart chambers, which is part of the science behind why Coach's recovery jogs work. Not only do they utilize the muscles that a gymnast depends on the least, thus mitigating any small amount of fiber conversion or proliferation that may occur, but the body sends fresh nutrients all over the body and the heart chambers slowly expand.

Unfortunately, Type 1 fibres aren't subject to much hypertrophy, and hyperplasia (which would be entirely new fibres) is theortical hasn't been shown to occur in humans, from what I've read but otherwise I think we're in agreement Anyway this discussion has no bearing on topic at hand, and I don't want to detract from the main subject. You may be on the leading (bleeding) edge though and some of the things that are fancy today may be facts tommorow. Just not today :wink:

Hyperplasia has in fact been heavily suggested to occur in humans through tissue biopses and has been conclusively proven to occur in many different lab animals. Do you know why we can't conclusively probe hyperplasia in humans? To conclusively prove hyperplasia you need to train one side of the body and not the other, and then completely remove the muscle and count fibers. You do that by digesting the connective tissue with nitric acid. You can not ethically do that to humans. Therefore you can not conclusively prove hyperplasia. This is what I mean by science being limited. Not only is funding an issue, ethics are too. However, we can use biopses and biopses show significant increases in fiber count across a cross-sectional biopsy after various types of training. It is ridiculous, in my personal opinion, to not take into account the increasingly heavy evidence we have that supports hyperplasia. There is no significant detraction from these studies, and they are quite recent. None will claim hyperplasia as fact, because as I stated above that can't be done with biopses alone. Anyways, google scholar will show you to these studies. They are good reads.

Now, I do have to alter what I said about muscle fiber conversion. Stain tests show an 8% conversion from white to red types with inactivity, and a similar conversion from red to white with aerobic activity. This is a staining technique and not a myosin chain comparison or a motor unit comparison. Keep that in mind. That is from a 2008 study. The participants have Stable Cardiac Failure, which makes them really crappy at oxidation. This, in turn, leads to more type 2 fibers forming since they do not require oxidation. So, as the oxidative ability of the patients increased they saw a shift in fiber distribution. I have been unable to find good recent studies that demonstrate type 2 to type 1 conversion. From a chemical perspective it isn't entirely necessary, as type 2A fibers can take on characteristics of type 1 fibers without becoming type 1. I do not know if they can acquire oxidative mitochondria in significant numbers. This goes beyond my memory and as far as I know what I have read as well. Something is tickling my brain, but I think it's just hunger.

Here is what a very good 2001 study has said, and this should be read in full by everyone who is interested in this stuff.

This plasticity in contractile and metabolic properties in response to stimuli (eg, training and rehabilitation) allows for adaptation to different functional demands.2 Fiber conversions between type IIB and type IIA are the most common, but type I to type II conversions are possible in cases of severe deconditioning or spinal cord injury (SCI).2,20

Less evidence exists for the conversion of type II to type I fibers with training or rehabilitation, because only studies that use denervated muscle that is chronically activated with electrical stimulation have consistently demonstrated that such a conversion is possible.21

Full text: http://ptjournal.apta.org/content/81/11/1810.full

This goes into the mis-classification of muscle fiber types and why it happens, and what they really are and what they mean. There are currently 7 known human muscle fiber types. Furthermore, humans do not express the fastest myosin chain type, which is 2b. What we have, and what is referred to wrongly as 2b, is 2x/d. That's the fastest stuff we've got. It's a big difference too, with 2b generating peak force in something crazy like 6ms as opposed to our 20-25ms.

Anyhow, the only significant type 2 to type 1 conversion seems to happen with full immobilization, and the conversion reverses as soon as mobilization is restored. In healthy subjects, and that

Ok thanks that really clears things up

I don't have time to really examine this post as I'm off to a party sad to say. Hopefully I won't think about it, lol.

But I really think it should be in another thread, if it's possible for you to peel of these posts and create one?

Sidenote: Definitely we need that popcorn eating smiley for this post! and this post needs pics too! over.

That's also a good point about the blood volume. It is believed that the generation of new blood vessels along with the new blood to fill them is a large part of why 20-30 point blood pressure reductions are seen after 4-6 weeks of consistent resistance training in untrained individuals.

This is slightly incorrect. The reason why obesity is correlated strongly with hypertension is because of the total increase in vascular resistance (e.g. adding blood vessels in the added fat mass = more total area through which the heart has to pump blood = heart must pump harder to force blood through the extra area = blood pressure increases).

The real reason probably lies in the fact that the body has better hormonal regulation (via hormones that actually affect blood volume such as aldosterone, ANP, etc.) and overall metabolism with exercise.

Quite possible that a blood volume reduction according to the amount of total area is why there may be blood pressure decreas as well.

That isn't quite right. Aerobic lipolysis and aerobic glycolysis are both oxidative. They both happen in slow twitch oxidative muscle. Anaerobic glycolysis happens in type 2 fibers. That is why you have a lactate threshold that limits the time you can perform high intensity anaerobic exercise. You can perform low intensity anaerobic exercise pretty much until you run out of glycogen, at which point you shift over to aerobic lipolysis and your power output drops accordingly, unless you were already within your current lipolytic threshold. The limiting factor, and what causes the lactate threshold to exist, is the limited ability to transport fresh glycogen into the cells and pyruvate out. If glycogen can't be brought in as fast as it is being used, you're going to poop out. If glycogen can be brought in but lactate can't be moved as fast as it is being generated you run into the same problem: transportation failure. It is usually not a glycogen supply issue so much as a transportation issue. Glucose transport molecules increase 11 to 17-fold (1100% to 1700%, more or less) in response to anaerobic threshold work, so glucose transport quickly becomes a non-issue. Ability to process glucose becomes the next roadblock, which is dealt with both through increased mitochondrial count and by mitochondria migrating towards the cell membrane. Finally you are left with the inter-cellular transport of lactate as being an issue, along with the processing of lactate in aerobic fibers. Of course, the aerobic fibers are adapting in a similar manner as the anaerobic, so in the end you end up with lactate transport being the final limiting factor. This is also why you can achieve absolutely incredible increases in endurance over just 6 months of training.

Lactate transport is likely the limiting factor near lac threshold, but that is also blunted by hydrogen ions interfering with a lot of the intracellular metabolism and transport. So it's kind of a multifactorial type of thing.

Pyruvate is the actual compound that is used to generate ATP. Glygocen, lipids and proteins can all be (and are) broken down into pyruvate when used for energy. That is what energy metabolism is. The rate at which these can happen is limited by number of mitochondria, type of mitochondria, location of mitochondria within the cell and enzyme availability. Mitochondrial respiration in type 2 fibers is anaerobic. This is where people get tripped up, and where things are kind of weird.

Don't really like the wording here. Pyruvate itself does nothing. It's a common metabolic byproduct of energy metabolism, but not used itself to generate ATP at all.

Nucleic acids can be used for energy as well (via fructose pathway), and fatty acid metabolism actually goes through acetyl-CoA straight into the citric acid cycle (aside from glycerol) which is after the metabolism of pyruvate. Likewise, some proteins are metabolized straight into CAC rather than go through pyruvate metabolism.

Hydrogen ion gradient is used to generate ATP by ATP synthase. Hydrogen ions are pumped across the mitochondrial membrane through enzymatic pumps which utilize electrons as energy (hence "electron transport") through use of the carriers NADH+H and FADH2. The purpose of metabolism is to reduce (add electrons to) these metabolic carriers through the process of glycolysis and the citric acid cycle.

Anyway, other than that looks pretty good.

What mattered to me in this thread is whether the cardio hurts gymnastics or any other primarily anaerobic sport for that matter. I think slizz that we are in agreement that it shouldn't at the levels it's being recommended. Braindx was somewhat concerned that at higher intensities/durations it might. The idea was floated that it would benefit active recovery, and Brainx I believe wanted to differentiate that at low-levels this would be true, but at higher levels there was a potential issue.

The breaking point between recovery and low-level aerobic work is probably not a clear one.

I generally follow Lyle Mcdonald's thinking in these matters who is both an endurance (skater), strength athlete with science background. So he knows a lot about both aspects from a practical and theoretical viewpoint. Of course it varies by particular individual and situation, but he gives some general rules in http://www.bodyrecomposition.com/traini ... overy.html and also http://www.bodyrecomposition.com/muscle ... gains.html

... most of the problems with cardio training start to come into play when either the intensity or volume get excessive. As long as the amounts are kept moderate and the intensity is kept under control I think most of the concerns are mostly a non-issue.

So what defines moderate, reasonable, etc.?

At a bare minimum, 20-30 minutes of cardio performed three times per week will maintain some basic cardiovascular fitness, burn off a few calories, act as active recovery, and help to keep the fat burning pathways active so that the shift to dieting is a little bit easier; all of the good things that I mentioned. And it should do that without having any really major impact on progress in the weight room.

A higher frequency can be used but I wouldn’t see much point to more than five per week unless the intensity is kept very low (e.g. you can do brisk walking daily if desired). Going longer than the bare minimum of 20-30 minutes will burn a few more calories but there are limits to time availability (and people start to get bored) and I might set a reasonable limit of 40 minutes of moderate intensity cardio at the maximum; if the intensity is kept way down (again, think brisk walking), an hour is acceptable.

In terms of intensity, I think keeping things in the low to moderate range is going to be best. More specifically, a maximum intensity of 70% of maximum heart rate (140 beats per minute for someone with a maximum of 200 beats) or even lower should achieve some benefits without cutting into recovery or growth.

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HR needs to be taken in the context of what your MaxHR is. If you don't know this from testing, then it can be approximated with different age formulas. THe 220-age formula is usually way off, on the low-side for me, by 13 beats the last time I tested. So you may want to add 7 or 10 to it. (Seek and you will find).

It's alxo a little tricky because the GB isn't exaclty weights but but it can be interpolated. Coach's runs workouts are probably in this range (if they are a bit shorter, the HR could go a bit higher probably). The main thing is to feel better when you're done. That's the indicator of too much, too little, too hard or too easy as well. Point being, listen to what your body is telling you.

We also discussed recovery in terms of the body's ability to reprocess lacate. I think we're in agreement that the greater endurance potential a body has, the greater ability it will have to perform this conversion, thus extending mean time to failure.

In the event that someone went a bit too far with the cardio thing, I also referred to the fact that endurance adaptations in the legs should not impact upper body strength in any even, so concern about this is not warranted. I have not heard anything to contridict this so assume it addresses Braindx's concern.

When I referred to the term Aerobic glycolsis it was to differentiate it from fully anaerobic gycolosis Slizz. I said it "refers to using pruvate ... as the substrate in mitochondrial (aerobic) cellular respiration, as opposed to lipids." I think that is clear in this wording that both are used in aerobic (oxidative) respiration, but perhaps should have added "as opposed to lipids, which are always processed oxidatively". I assumed that this was understood and did not want to be pedantic about it. These posts will never appear in a text book. In any event you then went into a discussion of substrate transport and the like, which certainly is part of the big picture.

Responding with too much densly worded information can be perceived as a slapdown. You seem like a nice guy and real helpful, so you may just have a lot in your head that you want to share though it comes off as stream of consiousness / brain-dump. I would say that if someone doesn't know the subject, it will be difficult for them to understand it from this. And if they know it, then you are opening yourself up to critisim for getting this or that incorrect in haste. A full description is not needed to discuss the basic concept.

Hyperplasia in humans I mentioned because you described it as possible in an earlier post.

Perhaps it is possible. If it were to occur it would be a good thing. At this time I am just going with the consensus. I am aware that funding and ethics can be a problem for scientists (damn those pesky ethics!). Also the study's setup, size and repeatability can be a problem, but I'll take a look at those studies after I do what I have to do, later. Thanks.

As far as muscle fibre conversion goes you're saying it can happen given heart failure, rehabilitating spinal cord injuries or total immobilization. Well, these are not really conditions that we will be performing cardio or GB with are they :-) But thanks for the heads up.

Just keeping it real. Have a great day all!