American Parkour

I just finished a Tabata workout, and I have not sweted like this in a long time. But I was wondering if I did it wrong because I switched up all of my exercises to give me a full body workout.

For the first twenty seconds I did push-ups, and the rest is as follows:
2nd, set of twenty sec; Squats
3rd; Lunges
4th; Cruches, Leg-Lifts, and Russian twists
5th; Pushups
6th; Squats
7th; Russian Twists
8th; Pushups

Were Tabata workout meant to allow the ability to get a full-body workout like this, or were they meant to be focuses on one pat of the body?

It's the same exercise over and over.  :-X  Do 8 rounds of pushups or w/e.

http://media.crossfit.com/cf-video/sample2tabata.wmv wfs


You did all three exercises in 20 seconds? 

Good point corey...maybe he alternated them one rep at a time? ???

And corey is right.  One exercise.  8 times.

The reason for this is to push those muscles well into their lactate threshold and into fatigue.  By doing alternating exercises you are not pushing your muscles and CV system where it needs to be.

What you did is actually pretty useless...

8 rounds of 20 seconds. For **EACH** exercise.

Not one round of each exercise! :) You'll know when you did a good tabata set... after the squats you'll feel like you wanna puke probably. And then you have 7 more exercises to go.

I think I understand what you are talking about, just about an hour ago, I did another similar to this, because I could still do the exercise. I am pretty wiped out, but I think that I could better on, so I will try with just one exercise next time.

On the three exercises in 20 seconds, I was scrambling because I forgot which exercise I had set for this time, so I just chose abs, and did them as they came. Got about 8 Crunches, 4 Leg lifts, and 6-7 Russian Twists.

i tried Tabata for the first time today.

(http://i35.tinypic.com/535oc3.gif)

If you want a full body tabata...do thrusters and add weight. Good luck breathing.

Charlie u just gave me a great idea:

Dual tabatas - thrusters and pullups.

Now THATS a full body workout!

Jesus fucking Christ...

... Tabata Fran ???  Sounds like fun.

Did it right this time, well, kinda. I decided that I was going to do a new exercise that I learned in wight training class. They call it B-Ups. It's like a completed leg lift with your legs raised in the air, and then you crunch into it touching your hands to your toes. I made about five 20 sec. reps before I started to lose form, after which I had to constantly correct and ensure I was doing the exercise right. Don't think I pushed it as far as I could have because of my loss of form.

A few hours later when I went outside to practice climbups, and yes my abs were hurting after the Tabata, but I go to do my climbup, and I stop half-way through gasping for breath and drop the two feet I was up. I go to do a double kong and it feels like my core is ripping apart. Try and do a pullup, and legs feel like they are trying to rip me in two at my abs. So... yeah GREAT workout.  ;D

I guess it depends on your reason for doing Tabata's.

Tabata's research was on cyclists, so it was on a large muscle groups(Legs/ glute) with some intensity carry over to the upper body, something had to hold them there.

For Body composition changing (Fat loss) and anaerobic conditioning the more whole body the exercise the better. The key to Tabata's is the oxygen debt it creates to cause adaptations.

1 exercise light weight(empty Olympic bar = 45lbs) to start.

Overhead squat with pressout is good, Snatch from hanging just below the knees is another, these deplete the oxygen through a large number of large muscles

curls not so good, abs not so good, leg extensions and calf raises not so good. These deplete the oxygen in a smaller number of probably smaller muscles.

Sprints with a sled, kettlebell or dumbbell swings are other good choices. With the sprints add about 10% of your body weight.

Pick your poison, then it's 20 secs all out(with good form), rest 10 secs and repeat.

Spinja, is that "b-up" any different from a jackknife?

Although clearly full body exercises are better than isolated exercises... oxygen depletion is not the cause of body recomposition.

Hormonal response (GH/test/etc.) + high intensity stress (see glycogen depletion and energy pathway stress) make the muscles undergo rapid changes such as increasing enzymes for glycolysis and oxidative phosphorylation, perhaps increases in contractile proteins if you're weak, hypertrophy of type I and possibly some type II fibers, etc.

Quick question..  If I were to run through a tabata push-up session, would it be all right to change stances each cycle?

Does that mean switching from wide arm to diamond or PPPUs or just shifting the feet?

The former.

I doubt it. My school actually uses a lot of the exercises that I've learned about on this site to train their athletes, mostly wrestlers. For example, Tabatas are known as Circuit Training in my school, like muscleups are known, only by some, as super pullups.  ??? ::)

Circuit training is a little different.

Really? I explained Tabatas completely, and he still said that it is circuit training, but if I've been mis-informed then what is the dfference?

who is this "he"?

"he" sounds like he has no idea what he is talking about

circuit training is where you cycle through several different exercises one right after the other....

tabatas mean doing the same workout over and over -- its a form of INTERVAL training, not CIRCUIT training

Really then what is the cause?

I didn't say "Oxygen debt causes body comp changes" I said it causes the adaptaions [to occur] - you listed more adaptations than I was thinking of but you also listed all the adaptations I was thinking of does that make me wrong? No oxygen debt, no adaptations.

There seems to be some misconceptions about what the "Tabata Method" is and that's what I was trying to address. So I focused on what is the fundemental knowledge one needs to understand Tabata's(all lactic acid interval training for that matter). Really it is the concept of oxygen debt. Not small focused oxygen debt (say in the arms or calves) but real body impacting full body oxygen debt. Get the biggest bang for your buck instead of picking up pennies. So I didn't explain all that goes on, but the key is creating an oxygen debt.

How do you get into creating lactic acid and pushing the lactic acid threshold IF you don't create an oxygen debt? You can't, lactic acid is formed in the absense of oxygen, ie oxygen debt and since cells are full of oxygen we need to deplete it is much as we are able. The Lactic acid Level with regards to training is what stimulates the hormonal changes esp impacting GH release, so limit the rest intervals and it goes up more than "normal" training. That's also why High intensity (speed) is needed because it really focusses on the anaerobic pathways again an adaptation that I was aware of(but didn't figure I needed to overload people with).

If Oxygen debt doesn't cause body comp changes, Why is it worth studying? Why is there a term EPOC? Why do they say that in the 12 - 36 hours after HIIT the metabolism is still up and the total calories burn is greater than longer duration lower intensity aerobic training? Why has HIIT found to have a bigger impact on subcutaneous fat? Why, because creating oxygen debt/ EPOC cause a cascade or responses for the body to adapt to one of which is a higher metabolism over a 24 hr period...you don't think burning more calories while resting affects body comp?

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So if you don't create an oxygen debt, you limit the amount of lactic acid build-up which limits the impact on any hormonal changes (esp GH). If you limit the oxygen debt, and have a longer rest(aside from not being able to call them Tabata's - which is what this thread was about) you limit the glycogen depletion and limit how much enzymes the body needs ot create to compensate because the body naturally slowly replenishes the cell and a 3-5 minute rest allows for about a 90% replenishing.

And with this type of training the fibre impact is more likely going to be with type 2a and b fibres not type 1 since the time under tension and speed aren't there to stimulate the type 1's as effectively.

So take for example a guy that follows the Tabata protocol using only curls and some one that follows Tabata protocol using power snatches...Which will cause the greater total oxygen debt? (I can tell you from experience the focussed burn in my biceps beat the overal burn of the power snatches -but it didn't illicit the same overall response.)Which will illicit the great body comp changes?

Now suppose we take that person and they only do 2 resp of power snatches instead say 10 in each 20 sec rep for 6-8 weeks (even though the person knows they can do 10 reps, and then follows that with 6-8 weeks of Tabata using power snatches but does 10-12 reps each set. Now which has the greater oxygen debt? Which is most likely to have the most body comp changes? Which one will have illicited the most Hormaonal changes? Which will have taxed their energy systems more?

If you are not going to train with speed, intensity, minimal rest and use larger muscle groups you are not going to create an oxygen debt worth adapting to.

Ah Geez...this was a biggie :P


Actually high intensity focuses more on aerobic pathways, which is the key to its success in fat loss.  The primary source of ATP in the aerobic pathways is fat.  By doing high intensity you quickly deplete all sources of energy aside from oxygen and fat, thus making your body turn to these sources for assistance.  There is more to it obviously, but the effectiveness of HIIT is due to the aerobic nature of the training..


Oxygen debt is important -- its a fundamental component of exercise physiology.  Going into an oxygen debt causes the anaerobic components to pick up the pace but these pathways only last 45 second max.  A tabata workout is 4 minutes and the 10 second recovery is not enough for your anaerobic pathways to recover.  This is where the aerobic pathways come in.  A Tabata set is actually most like 60-80% aerobic depending on your level of conditioning.

EPOC is also a joke these days, pretty much.  While it exists, its effects are negligible.   A high intensity interval may accumulate something like 80 extra calories per day burned due to EPOC where the HIIT bout burned well over 400-500.  This is relatively insignificant in the grand scheme of thing.

Subcutaneous fat loss is mostly related to a lack of insulin and an increase in leptin caused by a caloric deficit.  HIIT is mostly effective due to the fact that you can burn shittons of calories in a short period of time...and the calories generated are mostly from fat stores due to the highly aerobic nature of the exercise.

I wouldn't rely on EPOC here.


You seem to really like GH but misunderstand its role.

GH is an active hormone in increasing muscle mass and promoting growth throughout the body in most tissues (connective and muscular mostly -- bone as well).

Leptin is the main cause for body recomposition changes.

Glycogen depletion is important for calling your aerobic pathways into the forefront, less to do with the effects on hormonal/enzymatic levels.  This is why the minimal rest is important.

And with this type of training the fibre impact is more likely going to be with type 2a and b fibres not type 1 since the time under tension and speed aren't there to stimulate the type 1's as effectively.


2 reps is a focus for strength.  Even over an 8 set block thats only 10 reps, which is a focus of hypertrophy.  Something like 10-12/round would be well over 30 reps which is the zone for pain tolerance, fat loss and endurance building.  They both elicit hormonal changes, just different ones.

If you are doing 2 reps with a weight that you can do 10, though, you are just wasting your time because you are not taxing your body enough.


Yes, but we don't always want an oxygen debt.  We want the debt in fat loss and I explain why above.

Er, both of you are kind of off on some points... some more than others. I will post in a couple hours (with studies) -- and by couple I mean about 4-5 hours as I need to go out now..

How many fat/obese sprinters do you know? How Aerobic are they? Perhaps defining some terms is important High intensity can mean many things, High intensity can equal percent of 1 rep max, it can mean perception of effort, it can mean bar speed it can mean many things.

In 4 minutes you are barely breaking into the Aerobic cycle, The Tabata study showed that moderate intensity AEROBIC training did nothing for improving your ANAEROBIC threshold. So there is something more going on here than just aerobic something else is improving. Vern Gambetta calls this efficiency, the LA energy system is becoming more efficient(yeah theres probably even more going on but I had no idea this was going to become a university level thesis support session)

Thank-you for acknowledging it is important. If it is a fundamental component what is the issue. Actually the LA system and aerobic system are still over lapping around the 2-3 minute mark.


I wasn't the one that initially mentioned GH, I'm indifferent to it. Sure it is naturally released in the body but more is released when training causes a high level of lactic acid in the blood(one of the adaptations that occur with this type of training).

I thought the main cause was the use of ATP from fat stores in the areobic cycle you mentioned above. My understanding is that Low levels of leptin slow the metabolism. People with lower body fat also have lower levels of leptin that people with higher body fat levels(weird paradox eh?!). So manipulation of this hormone through proper eating(not dieting) and combining with exercise definitely has an impact if you can keep them elevated.


This is where more definition is needed. 2 reps at 30-40% of your 1 rep max is going to help explosive strength, 2 reps of 50-60 % of 1 rep max with a 4 second pause in the stretch position will work your starting strength, 2 reps in 60-80% of 1 rep max will I guess work submax strength and 2 reps of 80-90% of your 1 rep max will hit maximal strength. Each of those ranges will stimulate greatly different changes.


Exactly you aren't taxing your body enough thats why speed and exercise selection becomes impotant.


I have never said "we always want oxygen debt" but here we are talking about doing Tabata method. Show me how you can do Tabata's without creating an oxygen debt?

First off, your understanding is apparently marred by lactic acid threshold which has already been disproven.

Muscular acidosis is caused by ATP -> ADP + P dephosphorylation (hydrogen ions are released when this occurs) AND is a by product of carbon chain oxidation. Glycolysis as well as the Kreb's cycle themselves produce production of hydrogen ions. To be clear [ATP] drops, [ADP] and [H+] increase. H+ has been speculated to interfere with both Ca2+ interaction in muscles as well as instigate membrane disruption. This is at the very least one of the causes of fatigue.

Lactic acid threshold is decent indicator (but not solely) that the anaerobic pathway is working heavily. Oxygen debt occurs because there is not enough O2 to accept electrons from the electron transport chain. As you may well know, this causes a backup of NADH from glycolysis and kreb's enzymatic processing. To counteract this the body converts pyruvate/pyruvic acid to lactate/lactic acid (NO acid is produced from this reaction since BOTH are carboxylic acids at body pH and are thus already depronated) thus consuming NADH converting it back to NAD+. During this time, the aerobic pathway is still working at full capacity and thus being stressed as such HENCE why short bout efforts such as tabata protocol, HIIT and metabolic conditioning ALL are aerobically taxing.

• NON-sustained high intensity work stresses glycolytic pathways (aerobic is still working at this time). Primarily the work is intense enough (for example, sprinting) to cause increases in glycolytic enzymes, increases in contractile proteins (generally type II fiber hypertrophy) as well as other characteristics such as increased glycogen storage to a point.
• Sustained high intensity work (such as HIIT, tabata, metcon) creates oxygen debt. As a result from what we have already discussed we know it makes largescale aerobic changes (increases in Vo2max, cardiovascular endurance, etc.). In accordance with high intensity sustained work, it also induces glycolytic changes as well. Thus, as I said before you all of these occurring at the same time: "high intensity stress (see glycogen depletion and energy pathway stress) make the muscles undergo rapid changes such as increasing enzymes for glycolysis and oxidative phosphorylation, perhaps increases in contractile proteins if you're weak, hypertrophy of type I and possibly some type II fibers, etc."

These changes are not caused by oxygen debt; they are caused by stressing your muscles and energy pathways beyond what they are capable of. Oxygen debt is one way to say you are working both anaerobically and aerobically over a pace that is unsustainable. If there was enough available oxygen, for example, your body may still be unable to process it as you may not have enough mitochondria. IF you did, then the work primarily becomes a combination of glycolytic and oxidative stress much like you would get with non-sustained high intensity work. That is to say the stress is decidedly different. For example, this would be comparable to a 100% 400m run from you that takes 50s. However, since an elite 400m runner has a large capacity (VO2max, glycogen, etc.) if he were to run a 50s 400m it would clearly not be a 100% effort for him and thus not as stressful on the muscles/energy pathways and thus will not elicit the same changes. However, a 100% effort would (although with diminishing returns).

That said...





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Ugh, this was a pain in the butt to type out.......

Please do some research before you criticize any (if any) of the points I made. I don't like having to type out counter-arguments, and it tends to make you look ignorant (no offense).

Thanks for the list of articles to read. Wow and a little name calling too. I speak from my knowledge base, if you choose to interject to teach and correct me that is up to you but then don't go telling me not to waste your time.

This seems confusing, you're telling me it has been disproven but it is a decent indicator(but not soley)? How does that happen?

Vern Gambetta in Athletic development addresses Lactate Threshold, and utilizes research by Veronique Billet that talks about the improvement of Lactate Threshold. Sorry they are published and probably more experienced than you...I think I'll believe them.

I can agree to disagree with you, I use "creating an Oxygen debt" to roughly represent intensity. You don't want to agree with it, thats fine. Is it text book? No but I am okay with that. And when I explain it to the average joe it helps them understand well enough.
 



First you say "sustained High Intensity work creates oxygen debt"(I agree, never disputed it) But then you say that Oxygen debt is one way to say you are working at an unsustainable pace. I may need to read more but please communicate more clearly.


Really I read this and it seems to me we are dealing with semantics, I use oxygen debt to represent intensity, the more intense the greater the oxygen debt, the less intense the less the oxygen debt, and you don't agree with this use...and that's fine, I can agree to disagree. We both agree that the changes are different from high intensity to even moderate intensity. So you don't agree with my definitions I can accept that.


I agree with you. It seems you want something 100% empirical, something measureable. Define intensity, Vern Gambetta, Gerard Mach and Mihaly Igloi(I'm sure others) prefer to teach their athletes to use a scale of perceived exertion(as opposed to heart rate based). That perception is the "state created by the intensity" and it will be different from athlete to athlete...they seem okay with it. Perhaps you just need to deal with it.


I can agree with you that I refer to the state, but I use the condition of the state to define the intensity to create that state, again if you don't want to agree with me that is okay. I look at it like this, drinking alcohol is like intensity(the underlying cause) and oxygen debt is like being drunk(the state created), the more you drink the more drunk you are, the higher the intensity, the more oxygen debt there is, the less you drink the less drunk you are.

true but they are not the same and they are not as great as exercise and neither alone compare to diet and exercise combined.

Lactate and GH sound related to me.
Agreed, just as it is not possible to determine the "best exercise protocol" many definitions get argued too. So provide some leaway when peoples definitions don't jive with yours or when people don't go into the same detail as you do.

“EPOC comprises only 6 - 15% of the net total oxygen cost of the exercise.”
So meet halfway10% and figure out the impact after a full year of workouts.

And as Don Alessi points out in his article it does.

So I've been reading this thread, and it's very interesting. I don't know enough to contribute to the scientific side of the argument one way or another, but I do think I've identified the major problem here. You (TeddyO) are operating under a logical fallacy, and I think these two quotes demonstrate it best:


and


Classic logical fallacy: If A --> B, then B --> A. If A is the cause, and B is the state, when talking about the cause of something you MUST use A. You CANNOT use B. I'm going to make a silly analogy here to demonstrate the point: If A is jumping out of an airlock, and B is death, then you can say "Jumping out of an airlock, A, will result in Death, B." You cannot, however, say that "Death, B, is jumping out of an airlock, A."

You can refer to the state of oxygen deprivation as a byproduct of intensity (or whatever the consensus is, I'm studying these topics but this is still over my head), but you can not say that it is the same.

A lot of what you're saying is right, but your overall idea, how you put it all together, is wrong. Even disregarding all of the science, what you are saying is still, logically, wrong.

If that's what you want to call it. Ask yourself...hmmmm why would he choose to describe it this way? Well when I would write up a program for a soccer mom or coworker, when ever I get technical, their eyes glass over and they don't understand what I am telling them, then I try another way and they still don't get it(they have a hard enough time tensing their forearms because they don't have great control over their muscles yet), then I describe the perception, the state desired the heavy breathing and drained feeling (not always and to varying degree's I realize)that accompanies oxygen debt and suddenly the lights go on. Do it enough times and that's what you use. Again this didn't seem like an academic forum, so I figured laymans terms would suffice...evidently that is NOT the case.


and


Classic logical fallacy: If A --> B, then B --> A. If A is the cause, and B is the state, when talking about the cause of something you MUST use A. You CANNOT use B. I'm going to make a silly analogy here to demonstrate the point: If A is jumping out of an airlock, and B is death, then you can say "Jumping out of an airlock, A, will result in Death, B." You cannot, however, say that "Death, B, is jumping out of an airlock, A."

Agreed.


That's fine in academia, but in the real world, people are satisfied with accepting that if they understand it better.


I am not disregarding the science, I am willing to accept less than perfect definitions. If it helps my clients understand a little better but piss you guys off because I am willing to be more accepting of concepts...so be it.

"It is the point at which lactate removal by the muscles cannot keep up with lactate production, so lactate levels in the blood rise. The resulting high lactate levels in the blood impede muscle action, so the ability to keep working at a significantly high level drops significantly. This can be seen at the end of a 400m race when an athlete ties up." Athletic development, by Vern Gambetta, pg 124.

This from a published book by a compaby called Human Kinetics, I'm guessing they'll have a good editing dept, and fact verification. This is the Vern Gambetta, that has been a trainer for many profession sport teams, and was one of the founders and the first director of the USA Track and field Coaching Education Program.

If you read the little bit from above, I guess you can figure I disagree with you.


I never said "oxygen debt" sescribes all exercise intensities, I made many comments that I was refering to the Tabata protocol. If you can show me a way to follow Tabata protocol and not create an oxygen debt, I would like to know.

I would also use max inensity when it applies, however as I have stated when I talk with my clients about XX% of your 1 rep max, or focusing on this type of fiber or energy system, their eyes glaze over, it's too technical, they want laymans terms, so I put it in terms they can understand. Had I realized this was a university level academic forum I would have used different terms...maybe.



Ouch you won't like this if 50s 400m and a 60s 400m are still considered 100% the an 11s 100 and a 48s 400 are 100% 11s X 4 = 44s a 4 s difference much less that the 10s difference of your example.


I never said it applies to ALL forms of exercise, If I did please quote me and I will stand corrected.



I don't recall stating that Lactate causes Gh release, The article I provided said that Lactate augments GH sectretion(the body secretes more) not that it causes it, The Body naturally has GH bursts, it just so happens Lactate creates conditions were the body seems to respond by releasing more.

Even one of your articles seems to agree with this(I have not found access to read it yet though)
Summary: Anaerobic exercise also tends to lead to the production of more GH compared to aerobic training and is related to the intensity of the exercise

I don't know how I contradict my view on EPOC. The comment quoted from you basically states there are so many variables in resistance training that to find the "best" protocols or criteria is too difficult to compare HIIT and ET conclusively...it doesn't say anything about negating results found so far.

How does that refute EPOC? In only 20 weeks HIIT group(creates more EPOC) lost almost 3 times as much fat, now that is in mm, and I couldn't find any conversions for mm to lbs. Sounds like HIIT and EPOC are supported.

And as Don Alessi points out in his article it does.

You seem to read into what I type and or read words that aren't there. Neither Don Alessi nor myself said lactate was the cause of GH release, just that for some reason more GH is released in the presense of Lactate.

You live in the past.  Book was written in 2006 (probably with antiquated data then, as well).  Recent findings pretty much blow the whole notion that lactic acid causes musculature failure and fatigue leading to reduced capacity.

The general consensus (which is always open to change, much as the lactic acid theory was, since this is SCIENCE afterall) is that the stress causes calcium channels to become "leaky" and not function properly as we fatigue.  This is on the molecular level.  CNS stresses also cause fatigue due to things like neurotransmitter depletion...

Remodeling of ryanodine receptor complex causes “leaky” channels: A molecular mechanism for decreased exercise capacity Bellinger,  Reiken, Dura, Murphy, Deng, Landry, David Nieman, Lehnart, Samaru, LaCampagne, Marks; PNAS, Nov 2007; http://www.pnas.org/content/105/6/2198.abstract

If you prefer lighter reading that summarizes this study:http://www.nytimes.com/2008/02/12/health/research/12musc.html?ex=1360472400&en=550537e3a9cdb3eb&ei=5088&partner=rssnyt&emc=rss



If your clients do not understand what 80% of their Max means, then there is a big problem with them.  If they DON'T understand this for some reason it literally takes 3 seconds to explain -- but that is neither here or there.

Max intensity does apply here...as this is the whole purpose of tabata.  NOW we are talking semantics as you are using terms improperly.  You cannot say that oxygen debt is intensity.  That is like saying that "A person is a baby" because a "baby is a person".  It just doesn't work like that. 

And if you are telling this to your clients you are confusing them further and educating them improperly-- i know it took ME a long time to figure out what the hell you were talking about and i have coached people and studied Ex phys, neurophys, anatomy and physiology and sell medical research equipment -- so what the hell is a plumber or electrician going to think?  Probably nothing and wind up ignoring you, no offense


You totally ignored his point on RELATIVE intensity.  The point of tabatas and all high intensity intervals is to perform at your maximum at that time no matter what.  The reason the 400m is superior to the 100m is because the 100m takes 11s and you can hold your breath the whole way through if you like.  The 400m will stress EVERY bioenergetic pathway to a high degree.

Seems like you are just trying to argue for the sake of arguing now...


No.  The LAC bursts CORRELATE or are RELATED to the GH releases...they are not the cause.  They do not augment.  They just simply both happen at the same time.  This is the root of the disagreement here.

Even the source you cited does not support you.  It says ANAEROBIC exercise related to the INTENSITY of said exercise tends to lead to the production of more GH -- NOT the production of lactic acid.

If what you were saying is true, we wouldn't need to be worried about GH use as a performance enhancer -- people would just be injecting lactic acid into their blood so it would stimulate GH.  That makes no sense.


Well there is a "best exercise protocol" when you have a specific goal.  If your goal is weight loss, as the study steve provided shows, then Tabatas and HIIT is the best.  If your goal is a 400# DL...then HIIT will hinder your progress.

good chatting with you

My 2 cents on lactate threshold.   Like others have said, it has been disproven that lactate acid causes fatigue.  Even though there is tons of literature that refers to lactic acid being the cause of fatigue, it is not.  However, lactate threshold can  still be used as measure point for performance.  One way to think of it is like ventricle (sp?) threshold (the point in exercise when your breathing becomes faster).  If you get tired while breathing faster, does that mean that it is the breathing that makes you get tired? No.  Breathing faster is a side effect of increased intensity.  Likewise increase in lactate levels does not mean that lactic acid makes you tired, but it is a side effect of increased intensity.

Interestingly, LT has been found to be a more accurate predictor of performance in endurance events than VO2 max.  That is say for a group of people running a 10k, if you were to line them up in order of VO2 max, that order would have little correlation to there finishing order*.  However if you line them up in order to of their LT (measured by the pace at which their lactate level sharply increase) there would be a much stronger correlation to their finishing order.  It is because of this strong correlation that coaches and researchers for years have talked about lactic acid and its believed side effects.  But as has been pointed out, lactic acid is not  is not actually the cause of fatigue it is only the side effect of increased intensity.  However, I myself when speaking to people I know still talk in terms of lactic acid, because from a pragmatic point of view, it is just easier to talk about and understand even though in the back of my mind I not it is not quite true.

*This point about VO2 only holds true with people of somewhat similiar VO2 maxs.  Obviously if someone has a VO2 max that is twice that of someone else there is a very high probability that the first person will beat the other person.

Chris answered most of them for me. I am NOT arguing semantics TeddyO. This is fundamental underlying causes.


1. LAC may be correlated with GH spikes but not the cause.

If you read some of my links you'd see that increased body temperature is one of the proposed causes of increased GH release (hypothalamus regulation of pituitary). I can provide studies for this as well.

Like Chris said...
"If what you were saying is true, we wouldn't need to be worried about GH use as a performance enhancer -- people would just be injecting lactic acid into their blood so it would stimulate GH.  That makes no sense."


2. LAC is not the cause of muscular acidosis and failure. Your professor is wrong and the research is out there that proves it.


I can provide multiple studies showing LAC is not the cause of acidosis and fatigue. Your professor is behind the times.


3. Failure is proposed to be caused my multiple sources such as increased heat, Ca2+ disruption, sarcolemma/contractile protein disruption, etc. The one thing we are sure of is that LAC has nothing to do with failure of the muscles themselves. Search pub med.


4. EPOC is bullshit. There is no way around it. Look at the studies I post. Hell, look at this one study again which you said EPOC is supported.

http://www.exrx.net/FatLoss/HIITvsET.html


Hell, I'll even GIVE you 25 continuous sessions  (as says only half completed) + 19 sessions + 16 sessions = 60 sessions total over 20 weeks = 3x a week frequency.


60 sessions * 72.3 (maximum end 57.9 +14.4) = 4338 kcals

As we said before in those studies MAXIMUM EPOC = 6-15%. I'll GIVE you 15%.

4335 * .15 = 650.25 kcal

Now, you burned off a whopping 650 kcals on this program. However, 1 lbs of fat contains over 3500 kcals. This is less than 20% (specifically 18.5%) of 1 lbs of fat.

So you're telling me that subjects lost basically .2 lbs of fat... and that's even measurable? Especially to 13.5mm reduction in subcutaneous fat? Hahahahahaha....

Basically, you are wrong. EPOC is false. You cannot argue this. I have posted studies that say EPOC is a joke; you have given me no studies or proof that EPOC is significant (nor will you find any but you can try).


5. Again, A->B is not B->A. The point I made about relative intensity is basically that some normal joe who has a 100% intensity to complete at 400m run as fast as he can may only do it in 60s. However, someone who is elite may be able to complete it in 45s at 100% of their intensity. In addition, AS YOU FATIGUE 100% intensity may only be a 70s run because you cannot physical go faster.

This is why looking at max intensity and relative intensity are important... saying oxygen debt to describe multiple states like this is vague and misleading.


--------------------------------------

As I said earlier -- and you shouldn't take offense to this -- but you should back up your claims with proof as right now you are making a fool of yourself because you are not up to date on research (LAC) or have not done the research in some of these areas (GH, EPOC).

Well Steve you are correct, it is vague and over simplifiedthough I wasn't describing multiple states as you suggest - this thread was about Tabata method and that's what I was commenting on, I was describing the state you want to achieve in Tabata's I wasn't trying to describe any other protocol. Again I didn't realize you wanted University level academic answers.

I am accused of poor reasoning, but I will ask for what I think is the 3rd time, Tell me how you can do Tabata's without creating an oxygen debt(we are both well aware that compound exercises at high intensities are need otherwise how do you create the oxygen debt in the first place)? yep I was wrong typing that the debt causes the adaptations part of it was an over simplification and part if it was thinking one thing and typing another.

I figured I qualified this comment when I stated the exercise chosen should be done "all out" read Max Intensity in my very first post.


You read into what I say, I never said lactate causes GH release but it coincides with an increased lactate level, so if you train in a way to increase Lactate...there's a very good chance there will be an increase in the release of GH.

http://www.pnas.org/content/105/6/2198.abstract

A study published in Feb/ 08 not even published in an exercise and physio Journal,done on mice where the researchers push the mice into an overtrained state actually not just an overtrained state but an absolutely exhausted state twice daily 90 minute swimms and their once weekly treadmill test was to the point where they couldn't continue even with prodding) And then a minimal number of humans for three days for 3 hours at 70%. But they weren't really studying the conditions of exercising (definitely not under "normal" protocols) nor were they trying to disprove Lactate Threshold(never once mentioned that in the article)...they had to push them to this extreme state to study a drug they have found/created (which looks like it will work esp in heart attacks and Congestive Heart Failure and possibly COPD) to counteract such conditions.

Here are some of the researchers comments:

"Taken together, these data suggest a possible mechanism by which Ca2+ leak via calstabin1-depleted RyR1 channels leads to defective Ca2+ signaling, muscle damage, and impaired exercise capacity. "

"On the other hand, exhausting exercise, such as that performed by a marathon runner or a long-distance cyclist, results in significant muscle damage and can impair task performance for days or weeks (23–25), although the mechanisms underlying this impairment in exercise capacity are not understood.

"The role of PKA phosphorylation of RyR1 remains controversial, however, because other groups have found little or no effect on channel function (10)"

Here is a study from 07/08 that says "the molecular mechanism underlying its depressive effect on muscular performance remains unresolved." I guess these researchers aren't up to date yet either and it's from the American Journal of cellular physiology or something like that.
http://www.ncbi.nlm.nih.gov/pubmed/18480297?ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Again I have not said Lactate was THE(only) cause and evidently the lactate threshold theory and the thought that lactate contributes to muscular acidosis hasn't been disproven enough since there was a study published in May /07 and recently posted on 8/15/08 that will be republished in The European Journal of Applied Physiology, if it was truly, conclusively, beyond a shadow of a doubt disproven I don't think they would publish it.
http://www.ncbi.nlm.nih.gov/pubmed/18704482?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_Discovery_RA&linkpos=1&log$=relatedarticles&logdbfrom=pubmed

Heres another beauty mentioning Lactate Threshold from your esteemed pubmed
http://www.ncbi.nlm.nih.gov/pubmed/18762454?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum 8/30/08...wait that has yet to be printed.


Please don't as you can see I am not a scientist and don't really want to make this a priority.



You can provide many studies proving it wrong, the above studies say otherwise, they are recent and from pubmed;)

As I have said I can agree to disagree.



Usually research is stating HIIT is done in less time than ET too, I guess the idea is that this is a bonus and if you extrapolate the energy expenditure over the same time and figure in those weight loss differences the changes becomes bigger.

This study doesn't specifically mention EPOC but basically has the same results for weight loss.

http://www.ncbi.nlm.nih.gov/pubmed/8028502?ordinalpos=14&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Here's another one THAT DOES MENTION EPOC
http://www.ncbi.nlm.nih.gov/pubmed/18469249?ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
Published MAY /08 FROM YOUR CHERISHED PUBMED
very interesting
The Institute of Medicine proposed that 15% of energy expenditure (EE) as excess post-exercise oxygen consumption should be added to additional physical activity energy expenditure (DeltaPAEE) to estimate total EE.
Sure it says"These results suggest that EPEE has a small effect on 24-h EE" but is significant enough it is adding it to the 24 hr energy expediture.

If the Institute of medicine from a G8 nation says it's a significant, and a lot of others that read research(yeah some of it may be too old for your liking) say it's significant, I'm prone to believe it's significant, here's one of those guys
http://www.bodybuilding.com/fun/berardi29.htm (take a look at his credentials and he says it's huge - what is a nobody like me supposed to think with all these differing opinions flying around out there from people way more educated than I, you say one thing a PH.D Candidate says another thing - TeddyO shrugs)

I never said max and relative intensity weren't important, I was refering to Tabata method(never did I say multiple states), that's why I suggested compound movements, with a much lighter weight than a 100% max intensity(weight in relation to the 1 rep max) for the given exercise and do the reps with good form but "all out"(relative intensity)

If you would have asked a few questions to clarify my view BEFORE reading too far into what I wrote this probably could have been avoided.

As it is you say it's all 100% beyond a shadow of a doubt conclusive, yet there is research out there that comes across as less conclusive, and others that should be "in the know" don't seem to agree it's 100% conclusive.



Are those claims backed up enough?

I guess neither one of us is as up to date on the research as we thought, or perhaps we both are and still choose to believe the articles we want. I am big enough to admit I don't know everything, are you? Can we call a truce?

Please stop using the excuse that you didn't realize this was a "university level discussion." Most threads aren't, but by reading most threads here you can see that when facts need to be pulled out, they are pulled out. When they need to be explained, they are explained.

You've complained that you didn't realize this was a university level discussion in almost every post. We get that. You can stop saying it.

Zac is right...especially when people come on here spreading what they think is fact.  These need to be corrected.

This brings me to my next point, Teddy.  You originally claimed that oxygen debt is the cause of body recomp...shall i remind you?



This is not true, and several facts have been presented that represent this very well.  Yet the argument continues and has grown into something quite silly now....below are explanations of the silliness.


OK great, we go into oxygen debt when we do tabatas.  Tabatas cause body recomposition.  But guess what, so does high intensity (meaning high weight compared with your 1RM with moderate volume) exercise that does not put you into an oxygen debt.

Saying oxygen debt is the cause is just plan, flat out WRONG.

The cause is the hormonal response that accompanies the oxygen debt, but is not caused by it.  If you are running in a race and win, did you win because someone else was running, or did you win while the other person was running?  IN this case, you just happened to win WHILE the other person was running.

Analogously, "winning the race" is the body recomp.  While oxygen debt was occurring, the hormonal response that is caused by OTHER factors (NOT the debt) is what causes the body recomp.

This is the third or fourth time we have said this.  Why is it so hard to grasp????


Again, 5th time at least.  You create the debt during tabatas but that is not the cause, sorry.


Yes, this is how you do tabatas.  Going "all out" will cause an oxygen debt due to intensity.  It will also create the stress required to stimulate body recomposition.  6th time.  Oxygen debt does NOT cause the body recomp.


The upsetting part here is that you ARE saying that Lactate causes GH releast and you don't even realize it.  Now, and ONLY now do you actually say that increased lactate accompanies GH release -- before you were saying it is the cause. You are not being careful with your words and confusing everyone, yourself included.


You know nothing of the publishing process, apparently.  I do, so maybe I should explain.

The reviewers and researchers do not always know what the hell they are talking about.  One of my customers had an ECG signal published as if it was an EMG signal.  No review board caught this and the researched honest to god thinks its an EMG signal.  If you look at the signal and know anything about physiology, this is clearly wrong and laughable.

Many studies are done by people with a poor grasp of science.  Its sad, but true.  This is why you need to read more than the Abstracts -- the methods must be clearly examined.  Hell, half of nutritional studies are done for less than 2 weeks in duration.  A human needs at least 3-5 weeks to adjust to a new diet.  These studies flood journals.

Hell, brother, I am published in 3 medical journals.  Honest to god, I don't even know the stuff that my name is on.  Being published, imho, means shit.  Read my article in this forum about "Common Mistakes" and I go into more detail on this.

Many of these publications lack PIs (Primary investigators) who have done an ample amount of literature review that can relate to other fields, many times.

PLUS, in addition to this, it doesn't make sense chemically as Steve pointed out.  Lactate production does not yield a free hydrogen ion which is what would dictate changes in pH levels.  Muscle acidosis is the factor that you are referencing and this is NOT caused by lactate -- it is simply not the chemical reaction that occurs in the body..


Yes.  While it correlates, it is not the cause.  Are we catching on here?  You need to understand correlation and causation.


Still no mention that LT is the cause.  No one is saying LT doesn't exist.  We are saying that increased LT is not a cause of fatigue.  Correlation vs. Causation.


I think you are in too deep now to avoid citations, esp if you are going to provide them....i just dont think steve wants to waste his time right now since digging up studies is time consuming...


You are being silly.  None of those studies say that LAC is the CAUSE of the fatigue.  They are saying it is present DURING fatigue.


God this is borderline annoying.

No one said EPOC doesn't exist.  We are simply saying that its contribution is negligible.  Sure, if you want to be complete, factor it into the caloric expenditure.  What you posted up here is consistent with what Steve said....the only thing you can't grasp is that in a 600 calorie bout, 15% is only 90 calories.  That's not even a whole banana, for christ's sake. 

Over the course of 5 months at 3 times per week, you burn something like 700 calories extra.  So in that whole time, you can attribute pretty much 1 meal to be burned off by EPOC.  In 5 months, you can eat well over 450 meals.  I hope you enjoy the 451st...