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Charles Moreland
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« Reply #15 on: August 25, 2008, 09:58:20 AM » |
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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? |
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Animus
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« Reply #16 on: August 25, 2008, 10:56:10 AM » |
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Does that mean switching from wide arm to diamond or PPPUs or just shifting the feet?
The former. |
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Spencer B.
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« Reply #17 on: August 25, 2008, 05:01:09 PM » |
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Spinja, is that "b-up" any different from a jackknife?
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.   |
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WARNING: Prone to rambling on and on about stuff and completely destroying the potency of any words I may have by being to verboe.
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Animus
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« Reply #18 on: August 26, 2008, 05:09:16 AM » |
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Circuit training is a little different.
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Spencer B.
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« Reply #19 on: August 29, 2008, 04:17:02 PM » |
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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? |
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WARNING: Prone to rambling on and on about stuff and completely destroying the potency of any words I may have by being to verboe.
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Chris Salvato
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« Reply #20 on: August 29, 2008, 05:48:50 PM » |
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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
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TeddyO
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« Reply #21 on: August 31, 2008, 05:13:00 AM » |
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The key to Tabata's is the oxygen debt it creates to cause adaptations. These deplete the oxygen in a smaller number of probably smaller muscles. Although clearly full body exercises are better than isolated exercises... oxygen depletion is not the cause of body recomposition. 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? 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. [/quote] 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. |
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Chris Salvato
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« Reply #22 on: August 31, 2008, 07:42:30 AM » |
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Ah Geez...this was a biggie  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). 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.. 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? 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. 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. 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. 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? 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. 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.
Yes, but we don't always want an oxygen debt. We want the debt in fat loss and I explain why above. |
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Steve Low
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« Reply #23 on: August 31, 2008, 11:21:06 AM » |
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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..
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« Last Edit: August 31, 2008, 11:23:49 AM by Steve Low »
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Use the search function, please.
Any advice given is not to be taken as professional information either medical, training or nutritional.
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TeddyO
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« Reply #24 on: August 31, 2008, 01:05:16 PM » |
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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). Actually high intensity focuses more on aerobic pathways, which is the key to success in fat loss 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) 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. 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. You seem to really like GH but misunderstand its role. 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). Leptin is the main cause for body recomposition changes. 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. 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. 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. 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. Exactly you aren't taxing your body enough thats why speed and exercise selection becomes impotant. Yes, but we don't always want an oxygen debt. We want the debt in fat loss and I explain why above.
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? |
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Steve Low
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« Reply #25 on: August 31, 2008, 04:43:33 PM » |
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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... Really then what is the cause? High intensity stress causing changes in muscles and energy pathwaysI 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. As I said, oxygen debt is a bad way of stating it because it describes the state; it is not the underlying cause. Stress on the muscles and energy pathways causes the adaptations.
Of course, body recomposition changes can occur through purely changes in diet.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. See above. The key is stressing your body.. not oxygen debt.
Oxygen debt describes a particular stressor related to training (aka unsustainable high intensity intermittent training or tabata protocol)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). First, as I described in my paragraphs on theory, pushing into "lac threshold" is solely due to the inability of (1) the cardiovascular system to adequately provide oxygen to the muscles, OR (2) the muscles cannot use the oxygen available because of lack of mitochondria. Thus, net accumulation of NADH occurs.
Secondly, Lac is not related to GH. High intensity stress is related to GH. As you wrote (later), why do 100m sprinters have great body composition? It's sure as hell not because they are training intervals or anywhere NEAR lac thresholds. High intensity stress on the muscles.
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
Jacques B. IHO Urinary Growth Hormone – Clininal Value Applicatiions. International Health Organization. April 27, 2008. Available at: http://www.ihealthorg.com/iho_data.html.
Summary: In resistance training, serum human growth hormone tends to increase with intensity of exercise with the highest amounts being secreted with high work loads and low rest times
Kraemer WJ, Marchitelli L, Gordon SE, Harman E, Dziados JE, Mello R, Frykman P, McCurry D, Fleck SJ. Hormonal and growth factor responses to heavy resistance exercise protocols. J Appl Physiol 1990; 69: 1442-1450.
Summary: GH tends to increase linearly with exercise intensity as there is more GH secreted per pulse.
Pritzlaff CJ, Wideman Laurie, Weltman JY. Impact of acute exercise intensity on pulsatile growth hormone release in men. J Appl Physiol 1999; 87: 498-504.
P.S. Some brief summaries... there's generally more data if you want to look at the specifically.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? EPOC is failure. I hate having to go over this again, but I will since you seem to want to learn.
“Based on current knowledge and considering all variables related to resistance training, it is still not possible to determine the best exercise protocol in order to substantially increase energy expenditure in comparison of various studies on HIIT (high intensity interval/intermittent training) and ET (endurance training).”
Meirelles CM, Gomes, PSC. Acute effects of resistance exercise on energy expenditure: revisiting the impact of the training variables. Revista Brasileira de Medicina do Esporte, 2004; Vol. 10, No. 2: 122-130
“EPOC comprises only 6 - 15% of the net total oxygen cost of the exercise.”
Laforgia J, Withers RT, Gore, CJ. Effects of exercise intensity and duration on the excess post-exercise oxygen consumption. J Sports Sci. 2006 Dec ;24 (12):1247-64
Contrasting 60 minutes of HIIT comprised of 1 minute at 105% VO2max running with 2 minutes active recovery, and 30 minutes of ET was composed of 70% VO2max running where they determined that there was <100 kcal burned in EPOC. These values were 7.1% and 13.8% of net oxygen cost for ET and HIIT respectively.
Laforgia J, Withers RT, Shipp NJ, Gore CJ. Comparison of energy expenditure elevations after submaximal and supramaximal running. J Appl Physiol. 1997 Feb ;82 (2):661-6
65% VO2max pace sustained for 60 minutes will generate a similar EPOC to that of HIIT
Romijn JA, Coyle EF, Sidossis LS, Zhang XJ, Wolfe RR. Relationship between fatty acid delivery and fatty acid oxidation during strenuous exercise. J Appl Physiol. 1995 Dec;79(6):1939-45. 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.
As I described earlier, LAC has nothing to do with GH. It's the high intensity stress. Why else would resistance training which involve NO oxygen debt also increase GH production?
Glycogen depletion, however, is correlated to increases in GH secretion BUT BUT BUT this is because high intensity stress burns completely through glycogen stores much quicker than low intensity stress.
Enzymes are a product of the energy pathway stress as I have stated before.
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.
Incorrect. Since tabatas are both aerobic and anaerobic they will both work type I and type II fibers. As the body fatigues and speed slows, increases in type I recruitment occur. Also, if the load is not heavy enough even with acceleration, there is no increased preferential recruitment of type II motor units (aka high threshold motor units).
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.
Uh, your example(s) are good but as we already hashed through, high intensity stress (AKA muscle/energy pathway usage) is why this occurs. Not oxygen debt. ------------------------------------------------ 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.. High intensity stress does not necessarily focus on aerobic pathways. For example, heavy lifting.
The effectiveness of HIIT/tabata/metcon is due better nutrient partitioning because of the release of hormones namely catecholamines (adrenaline, noradrenaline), possibly cytokine IL-6, and GH/test (possibly a few others).
Fortunately (or maybe unfortunately for your guys' arguments), heavy lifting also encourages nutrient partitioning through raising of said anabolic hormones. In these cases on an isocaloric or slightly hypocaloric diet, for example, nutrient partitioning goes more into muscular hypertrophy (contractile proteins) rather than energy pathways/sarco hypertrophy..... as opposed to adipose tissue.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. Both are stressed heavily (although as you said anaerobic does not recovery fully). Majority aerobic is correct BUT the stress on the pathways/energy systems causes the beneficial adapations.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. Little less than that actually.. numbers as stated before are about 6-15% or so from the above studies. Session of HIIT of 500 kcals only gives an EPOC of 30-75 kcal.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. 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. Well, reading Lyle's stuff steered you a bit wrong. The hormones responsible for the most change are probably GH and testosterone. Both of which are strongly anabolic for muscle and catabolic for adipose tissue. AKA the best ever for body recomposition.
Leptin, as Lyle describes, is mainly a regulator of appetite (along with ghrelin) and possibly some effect on metabolism. Indirectly playing a role in body recomposition HOWEVER as Lyle stated mainly the opposite effect (much like insulin downregulation is related to obesity and diabetes).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. This is wrong. Glycogen depletion is associated with high intensity exercise. Aerobic pathways are operating SIMULTANEOUSLY with increased rate of glycolysis.
Moderate/low intensity exercise is already aerobic in nature (hence why you're breathing.. and why it's sustainable). Glycogen depletion occurs very slowly in these cases -- hence marathoners running out around miles 20-22.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. As stated before.. both are used fairly extensively. Depending on the exercise you may not even get preferential recruitment of high threshold motor units.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. This doesn't even make sense...  Yes, but we don't always want an oxygen debt. We want the debt in fat loss and I explain why above. This depends on goals ONLY.------------------------------------------------ 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. Indeed. In all cases I have stated above (and all cases that you should be familiar with), high intensity exercise (universally) is known as inducing large amounts of stress on the CNS/muscles and/or energy pathways. This is what causes the adaptations, as you now know.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) Totally wrong. Aerobic operates ALL the time (hence why you are breathing).
When exercising, glycogen can be depleted extremely fast at high intensity exercise. Within about 30 seconds for elite 400m runners.
This study confirms approximately 40/60 ratio of aerobic/anaerobic energy ratio in trained 400m runners and 60/40 ratio for 800m (higher in women most likely due to smaller amount of musculature = less PCR/glycogen stores = more dependence on oxidative/aerobic metabolism for energy). For world class runners one would expect that there is a higher contribution of aerobic energy for these events because it is burned out more quickly at higher intensity. For those of us who are more novices or untrained, expect that the energy contribution is lower because the overall intensity is lower.
http://www.ingentaconnect.com/content/tandf/rjsp/2005/00000023/00000002/art00010Secondly, there ARE anaerobic improvements when looking at similar forms of intervals (aka HIIT). There aren't enough tabata studies out there to confirm the non-existance of anaerobic improvements as you stated.[/b] 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. Glycolytic and Oxidative ALWAYS overlap. However, if talking about when one provides the most energy as I stated it depends on the intensityI 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). Lac in the blood goes back to the liver for nearly immediate reprocessing. Thus, it contributes practically nothing (well, stress on lac transporters is about most of it) to adaptations occurring within the muscles and energy systems of the body.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. Manipulation of leptin with carb cycling, for example, is a way to trick your body into thinking that it doesn't need to eat more and keep it out of starvation mode on a hypocaloric diet.
No clue why you're mentioning ATP from fat stores. At all.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. 2 reps.. won't do anything. Not enough volume.
Though you're a bit off on these. 90-100% is maximal strength (~3 RM or 90% is maximal fiber recruitment). 40-50% of 1 RM is where most power is generated (and can be maximized for power workouts).Exactly you aren't taxing your body enough thats why speed and exercise selection becomes impotant. Sure..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? Uh, yeah.. oxygen debt.. doesn't mean anything! 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). |
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« Last Edit: August 31, 2008, 04:52:24 PM by Steve Low »
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TeddyO
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« Reply #26 on: September 01, 2008, 02:25:46 AM » |
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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. First off, your understanding is apparently marred by lactic acid threshold which has already been disproven. Lactic acid threshold is decent indicator (but not solely) that the anaerobic pathway is working heavily. 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. • Sustained high intensity work (such as HIIT, tabata, metcon) creates oxygen debt. 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. 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. 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). 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. Really then what is the cause?
High intensity stress causing changes in muscles and energy pathways 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. As I said, oxygen debt is a bad way of stating it because it describes the state; it is not the underlying cause. Stress on the muscles and energy pathways causes the adaptations. 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. Of course, body recomposition changes can occur through purely changes in diet. true but they are not the same and they are not as great as exercise and neither alone compare to diet and exercise combined. Lac is not related to GH. High intensity stress is related to GH. Exercise scientists have noted that these dramatic muscle changes accompany growth hormone secretion (GH). And maximum GH levels are augmented directly through blood-lactate increases. Lactate and GH sound related to me. “Based on current knowledge and considering all variables related to resistance training, it is still not possible to determine the best exercise protocol in order to substantially increase energy expenditure in comparison of various studies on HIIT (high intensity interval/intermittent training) and ET (endurance training).” 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. As I described earlier, LAC has nothing to do with GH. It's the high intensity stress. And as Don Alessi points out in his article it does. |
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Zachary Cohn
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« Reply #27 on: September 01, 2008, 07:40:25 AM » |
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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: 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. and 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. 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. |
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TeddyO
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« Reply #28 on: September 01, 2008, 03:26:03 PM » |
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You (TeddyO) are operating under a logical fallacy, and I think these two quotes demonstrate it best: 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. 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. and 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. 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. 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. That's fine in academia, but in the real world, people are satisfied with accepting that if they understand it better. 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. 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. |
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Steve Low
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« Reply #29 on: September 01, 2008, 05:40:50 PM » |
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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. If you meant the ignorant comment, I stand by that. It didn't appear that you did much research; however, if you did I apologize.First off, your understanding is apparently marred by lactic acid threshold which has already been disproven. Lactic acid threshold is decent indicator (but not solely) that the anaerobic pathway is working heavily. 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. Lac has nothing at all to do with limiting muscular failure (aka muscular acidosis).
It is a decent indicator of how much glycolytic activity there is. As I said, can be used as an indicator of high intensity, BUT is not the cause of anything related to slowing/failure of the muscles themselves. Probably slightly off topic on my part.
Instead of saying "oxygen debt" use "max intensity" (which is more accurate by the way). It's not that hard to think of examples either such as sprinting. Oxygen debt is too vague as it applies specifically only to certain types of trainingFirst 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. Unsustainable pace (100% intensity such as 100m sprint) is unsustainable for 400m.
Sustained high intensity work is SPECIFIC to relative intensity. For example, in intervals if I am able to run a 400m in 50s, this is 100% intensity for 400m; however, IF after 4 intervals I am only able to run 400m in 60s, this is still 100% intensity (again, relative intensity). This is what is meant by sustained high intensity -- working at 100% (or close to it) for your relative intensity for a certain distance or workout.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. No, this is not semantics. Again, oxygen debt can describe a certain type of exercise, but it does not describe all exercise intensity.
This is like me saying that "tabata is a form of exercise" and you saying that "exercise is a form of tabata." Not true in all causes. Like Zach (happydud) said... A -> B is not always B -> A.
"Max intensity of during XXXX" is much more descriptive and accurate. Saying "oxygen debt" makes it seem like you're trying to just use fancy words.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. Yeah, like I said above about the tabata and Zach said... A->B is not B->A. It describes a certain form of exercise, but it is not universal to all exercise.Lactate and GH sound related to me. No, you said Lac/oxygen is responsible for stress. High intensity is responsible for the stress which causes the adaptations.
This is like me saying that:
1. Children learn to speak around age 1-2.
2. Children also eat more at ages 1-2.
3. Therefore, children eating more causes them to speak more.
Bad causation/correlation.“Based on current knowledge and considering all variables related to resistance training, it is still not possible to determine the best exercise protocol in order to substantially increase energy expenditure in comparison of various studies on HIIT (high intensity interval/intermittent training) and ET (endurance training).” 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. Wow, are you serious? You said EPOC was significant. This quote directly contradicts that.“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. For a year, you serious? Look at study summary:
http://www.exrx.net/FatLoss/HIITvsET.html
This directly refutes EPOC as well.As I described earlier, LAC has nothing to do with GH. It's the high intensity stress. And as Don Alessi points out in his article it does. As I said before, just because LAC increases and GH increases doesn't mean LAC is causing GH increase. This should be obvious.
If a researcher is claiming that then he is flat out WRONG. You can use LAC to predict GH release, but you can't say it causes it (aka your oxygen debt/LAC hypothesis). |
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« Last Edit: September 01, 2008, 05:43:38 PM by Steve Low »
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