Study: 1 set vs 3

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(QuantumPositron @ Feb. 21 2008,16:40)</div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE"> <div></div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">This may not necessarily be the same as 90% 1 RM.  I posted this question at the Max-Stim forum and no one answered, which is unusual, so I can only presume no one knows.  </div></div>
Sorry I must have not seen the post there, I've been very very busy as of late.

Not neccessarily, as the speed and degree of movement may not match a true 1RM.
 
<div>
(colby2152 @ Feb. 29 2008,15:45)</div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">It looks like we have a new lab coat (nkl) in the arena!</div>
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Isn't that why we're here? Besides some social interaction.
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For myself I want my training to be effective and productive. So many have spent years going nowhere, so science is a means to an end.

Although I got an engineering degree and am a lecturer at an university, I'm not all theory and no practice.

You never stop learning. Thanks Dan, for your info. Everything isn't cast in solid stone, I know. One study isn't enough to base a practice on.
 
One final note on TTI is that although I belive in the premise one must consider it's original purpose and evolultion. It was a means of quantifying work in an environment with no measurable external work, ala isometrics. Granted the TTI and energentic hypothesis is sound and this TTI is absolutely tied to extent of activation, in dynamic movement it's usefulness is not only less dramatic but also less measurable. One can surmise though that the heavier load does cause heightened stimulation (recruitment, rate coding) and therefore heightened ATP turnover. But IMO this is a consequence of contraction and the two are intrinsically tied.

MS does not try to circumvent this process, as it simply can not, MS trys to allow increased force/volume, which I and many others have seen it does.

How important is force/volume? Very important IMO and this is backed up emperically with the likes of research by Dr. Kennith Baldwin's team, the newer research by Crewther et al, and of course the work by many others. Yet we still also have to consider the negative effects of too much force/volume as well and it's direct and indirect effects. Namely molecular signalling changes and recovery respectively.
 
I agree with you, Dan. I've believed for some time that MS is one of the more sound methods to get increased force/volume.

What I have been discussing here, is what to do to get sufficient stimulation when using a lesser load, such as in the 15s. Volume is one thing, but if the force is not that great, and if we want to cut the volume down, then we logically have to increase stimulation in another way, without increasing the load. In MS the volume stays the same throughout our weight progression, so there might be of interest to increase stimulus at lighter loads as well.

Functional isometrics (iso-concentric contrast) was measured to give more TUT than ordinary dynamic contractions, and from my understanding, isn't one of the goals of volume to get more TUT? MS cheats fatigue, but HST strives for lactate during the 15s to prepare the muscle environment for heavier loads, so there is a connection there. If we add an isometric contraction to each MS repetition with light loads, we add TUT, but with some additional fatigue.

But we do not want to high a tension stimulus when working with lighter loads as this may accelerate RBE, so we are left with one last option. Metabolic work have been shown to generate hypertrophy (whatever the pathways) with light loads as seen in some of the occlusion studies. Or is there another path to take?

The application is simple: As load progression continues, we decrease the length of our isometric pauses, until it's pure concentric-eccentric contractions. When we reach our maximum concentric capacity we might add isometrics and later on eccentrics to get more tension. We have to be careful so we do not get overtrained (excessive force/volume) so we might need to introduce drop sets. In simple words: we gradually shift between different kinds of stimulus throughout our cycle.

Am I repeating myself ad nauseam?  
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As for the relevance of ATP turnover, mTOR rebound effect, etc. we all have to wait and see what the scientists digs up. I have followed the thread on occlusion in the MS-forum with great interest. Perhaps, someday, we have a more solid foundation to stand on. In the meantime we can experiment, based on the findings so far (if we ever get any cohesion between them), and see what methodology produces most hypertrophy.
 
Don' take what I'm saying as I disagree with your quasi-isometric approach, I don't disagree at all. Occlusion interests me as well but I'm not yet sold on it's &quot;magic&quot; and instead look at it for what it actually does.......high metabolic demand that causes changes in the recruitment and activation strategies much akin to drop sets, static holds and so forth.
 
<div></div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">Occlusion... causes changes in the recruitment and activation strategies much akin to drop sets, static holds and so forth. </div>

Oh. Would those, ah, recruitment and activation strategies by chance maybe...increase ATP turnover? Could this be the &quot;man behind the curtain&quot;, to play on your magic analogy?

<div></div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">Yet we still also have to consider the negative effects of too much force/volume as well and it's direct and indirect effects.</div>

Do we have any guidelines for inducting how much is too much?
 
A snippet from the MS-forum thread on occlusion, on why rate coding can be a link to more stimulation via p38 signaling:
<div></div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">Nwlifter wrote:
Hey and for the first time, a direct line between rate coding and a fibriliar hypertrophic pathway. This is another possible explanation with occlusion. We know P38 is rate coding dependent, reguardless of tension.

The p38 pathway regulates Akt both at the protein and transcriptional activation levels during myogenesis.
Candice Cabanea, Anne-Sophie Coldefya, Karen Yeowb and Benoît Dérijard

Abstract

The molecular signalling pathways governing skeletal muscle differentiation remain unclear. Recent work has demonstrated that both the phosphatidylinositol 3-kinase (PI3K)/Akt and p38 pathways play important roles in myogenesis. Here, we describe the interactions between these pathways in C2C12 cells. Overall, our results suggest that Akt acts downstream of p38 in myogenic cell differentiation. Activating the p38 pathway results in the concurrent activation of Akt; conversely, activating Akt does not affect p38. We have analysed Akt messenger RNA and protein levels in a C2C12 cell line stably expressing a dominant negative (DN) form of the p38 activator MKK3. Compared to control cells, this cell line exhibits reduced levels of Akt messenger RNA and total protein. In addition, blocking the p38 pathway during differentiation inhibits Akt activation. Our results show for the first time that p38 can directly affect Akt at the transcriptional level as well as at the protein activation level during myogenic differentiation.</div>
We know that occlusion stimulates higher activation of MUs and higher rate coding due to metabolic stress, even if the loads are light. Also high tension contractions with heavy loads also requires all MUs to fire and rate coding is high. It is believed that the Akt/mTOR pathway is a crucial regulator of skeletal muscle hypertrophy, so activation of Akt by p38 is good news. Of interest is also the link that if p38 is blocked, Akt is inhibited (Akt is usually activated by the IGF-I/PI3K pathway, triggered by increrased muscle loading, of wich the isoform IGF-1Ec appears to be activated by mechanical signals).

I believe that NWlifter might have referred to this finding, when rate coding is concerned:
<div></div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">Exp Physiol. 2006 Nov;91(6):957-66. Epub 2006 Jul 20.
Influence of activation frequency on cellular signalling pathways during fatiguing contractions in rat skeletal muscle.
Russ DW, Lovering RM.

Activation frequency as a regulator of physiological responses in skeletal muscle, independent of contractile force, has received little attention. Here, the length-tension and force-frequency relationships were employed to keep active contractile force equal, despite a twofold difference in stimulation frequency (15 versus 30 Hz). Rat tibialis anterior muscles were tested in situ using 15 Hz stimulation at optimal length (15 Hz) and 30 Hz stimulation at shortened and lengthened positions (30 Hz(sub) and 30 Hz(supra)). Muscles were subjected to 1, 15, 30 and 80 Hz stimulation trains before and after 2 min of fatiguing stimulation. The principal findings were that the two 30 Hz protocols produced greater 38 kDa MAPK (p38) phosphorylation than the 15 Hz protocol (1.4- to 1.5-fold versus 1.1-fold), as well as greater fatigue (65-78 versus 43% decline in contraction force). In contrast, c-jun amino terminal kinase (JNK) phosphorylation appeared most responsive to total (active plus passive) tension such that the changes followed the pattern: 30 Hz(supra) &gt; 15 Hz &gt; 30 Hz(sub), while 44 and 42 kDa extracellular regulated kinase (ERK1/2) phosphorylation was not significantly increased in response to any of the protocols studied. Neither glycogen depletion nor myofibre damage accounted for any of the findings, but a decline in muscle excitation (m-wave) may have contributed to the greater fatigue seen at higher frequencies. These data suggest that neuromuscular activation frequency can influence certain signalling pathways in skeletal muscle, independent of force production.

PMID: 16857718 [PubMed - indexed for MEDLINE]</div>
 
Interesting stuff. I'm starting to get into the cellular and biomolecular area of hypertrophy research. When searching on pubmed its easy to get lost.

The other day I was sifting through T-nation and came across an article that mentioned Eric Heiden. If you don't recall or don't know, he was an Olympic skater. In 1980 he won 5 gold medals in 5 skating events: 500m, 1000m, 1500m, 5000m, and 10,000m. He also set 15 world records during his career. He had 28 inch thighs. When asked about his routine in an interview he said he never squated more than 300lbs, but that he did a lot of repetitions. The T-nation article states that he once did 205lbs for 300 reps. He mentioned elsewhere doing leg presses for 600 reps (I don't recall the weight). Its perfectly legit to call genetic endowment on Heiden as he calls it on himself. But I don't think that marginalizes the effect his training had on his legs. In fact, I've looked up pictures of other Olympic skaters on Google Images and they all have very large, well developed thighs. Clearly talent is necessary to be an Olympic athlete. But to forestall any potential detractors I must say that their physiques are in large part due to their training regimen, the same as it is for bodybuilders.

Its interesting that such hypertrophy can develop without the high tension we associate with mass building.

Links:

Interview with Heiden at US Olympics website. Mentions training.

T-Nation article (scroll down some).
 
Interesting QP. For a natty lifter, I think that squatting with 300lb produces quite a bit of tension and then you have the time that he used it for; if he did a lot of reps that's a lot of TUT with a pretty heavy weight and a lot of work done. Plus there are the occlusion effects from the high rep sets. All this mounts up to being a pretty good stimulus for hypertrophy.

Eric obviously could have squatted heavier but he didn't need to grow his thighs any more for the job they had to do; five gold medals testify to that. If he had wanted to be an Oly lifter he would have had to have lifted heavier and would no doubt have achieved more hypertrophy depending on his weight class. He definitely had great genetics.

EricHeiden.jpg
 
<div></div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">I believe that NWlifter might have referred to this finding, when rate coding is concerned:</div>

That's the one
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<div>
(nkl @ Mar. 03 2008,09:23)</div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">A snippet from the MS-forum thread on occlusion, on why rate coding can be a link to more stimulation via p38 signaling:
<div></div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">Nwlifter wrote:
Hey and for the first time, a direct line between rate coding and a fibriliar hypertrophic pathway. This is another possible explanation with occlusion. We know P38 is rate coding dependent, reguardless of tension.

The p38 pathway regulates Akt both at the protein and transcriptional activation levels during myogenesis.
Candice Cabanea, Anne-Sophie Coldefya, Karen Yeowb and Benoît Dérijard

Abstract

The molecular signalling pathways governing skeletal muscle differentiation remain unclear. Recent work has demonstrated that both the phosphatidylinositol 3-kinase (PI3K)/Akt and p38 pathways play important roles in myogenesis. Here, we describe the interactions between these pathways in C2C12 cells. Overall, our results suggest that Akt acts downstream of p38 in myogenic cell differentiation. Activating the p38 pathway results in the concurrent activation of Akt; conversely, activating Akt does not affect p38. We have analysed Akt messenger RNA and protein levels in a C2C12 cell line stably expressing a dominant negative (DN) form of the p38 activator MKK3. Compared to control cells, this cell line exhibits reduced levels of Akt messenger RNA and total protein. In addition, blocking the p38 pathway during differentiation inhibits Akt activation. Our results show for the first time that p38 can directly affect Akt at the transcriptional level as well as at the protein activation level during myogenic differentiation.</div>
We know that occlusion stimulates higher activation of MUs and higher rate coding due to metabolic stress, even if the loads are light. Also high tension contractions with heavy loads also requires all MUs to fire and rate coding is high. It is believed that the Akt/mTOR pathway is a crucial regulator of skeletal muscle hypertrophy, so activation of Akt by p38 is good news. Of interest is also the link that if p38 is blocked, Akt is inhibited (Akt is usually activated by the IGF-I/PI3K pathway, triggered by increrased muscle loading, of wich the isoform IGF-1Ec appears to be activated by mechanical signals).

I believe that NWlifter might have referred to this finding, when rate coding is concerned:
<div></div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">Exp Physiol. 2006 Nov;91(6):957-66. Epub 2006 Jul 20.
Influence of activation frequency on cellular signalling pathways during fatiguing contractions in rat skeletal muscle.
Russ DW, Lovering RM.

Activation frequency as a regulator of physiological responses in skeletal muscle, independent of contractile force, has received little attention. Here, the length-tension and force-frequency relationships were employed to keep active contractile force equal, despite a twofold difference in stimulation frequency (15 versus 30 Hz). Rat tibialis anterior muscles were tested in situ using 15 Hz stimulation at optimal length (15 Hz) and 30 Hz stimulation at shortened and lengthened positions (30 Hz(sub) and 30 Hz(supra)). Muscles were subjected to 1, 15, 30 and 80 Hz stimulation trains before and after 2 min of fatiguing stimulation. The principal findings were that the two 30 Hz protocols produced greater 38 kDa MAPK (p38) phosphorylation than the 15 Hz protocol (1.4- to 1.5-fold versus 1.1-fold), as well as greater fatigue (65-78 versus 43% decline in contraction force). In contrast, c-jun amino terminal kinase (JNK) phosphorylation appeared most responsive to total (active plus passive) tension such that the changes followed the pattern: 30 Hz(supra) &gt; 15 Hz &gt; 30 Hz(sub), while 44 and 42 kDa extracellular regulated kinase (ERK1/2) phosphorylation was not significantly increased in response to any of the protocols studied. Neither glycogen depletion nor myofibre damage accounted for any of the findings, but a decline in muscle excitation (m-wave) may have contributed to the greater fatigue seen at higher frequencies. These data suggest that neuromuscular activation frequency can influence certain signalling pathways in skeletal muscle, independent of force production.

PMID: 16857718 [PubMed - indexed for MEDLINE]</div></div>
First that study does not tie a link to rate coding and fibrillar trophic paths, it does point to a link between P38 and myogenic differentiation but, we also have studies that point out that actual hypertrophy can and does occur without additional satellite cell donation, so this study's true importance lies in the realm of sat cell activity not hypertrophy per se.

Secondly the idea that AKT is a crucial regulator is questionable as well. It is obviously one path and a very important path with respect to IGF but mTOR phosphorlyation is not dependant on it and in fact has been shown to be independant of AKT and growth factor release.

Even more importantly, IMHO, is p70S6K1. This has been shown to be &quot;directly&quot; implicated in the amount of hypertrophy observed. In both occlusion/ischemic trials and non occlusion/ischemic trials p70 is increased. So whether or not the high rating and subsequent high ATP turnover has anything to do with the actual CSA change is still in the air. Perhaps it's just a matter of similar paths through seperate means, again making the human body much smarter than thought and leaving us genetically prepared for various circumstances.

This is what makes it all so interesting.
 
All that is true, but so much of this stuff is speculation, like ampk and PS inhibition but we gotta do our best to hypothesize. I know my article and posts aren't 100%, if we could get research that was 100% and non-conflicting it would sure help.....
 
<div>
(NWlifter @ Mar. 04 2008,14:30)</div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">but so much of this stuff is speculation, like  ampk and PS inhibition but we gotta do our best to hypothesize.</div>
That has been directly observed so it's not speculatory at all.

Resistance exercise increases AMPK activity and reduces 4E-BP1 phosphorylation and protein synthesis in human skeletal muscle.J Physiol. 2006 Oct 15;576(Pt 2):613-24.

AMPK Activation Attenuates S6K1, 4E-BP1, and eEF2 Signaling Responses to High-frequency Electrically Stimulated Skeletal Muscle Contractions.J Appl Physiol. 2008 Jan 10;

AMP-activated protein kinase suppresses protein synthesis in rat skeletal muscle through down-regulated mammalian target of rapamycin (mTOR) signaling.J Biol Chem. 2002 Jul 5;277(27):23977-80.

Activation of AMP-activated protein kinase leads to the phosphorylation of elongation factor 2 and an inhibition of protein synthesis.Curr Biol. 2002 Aug 20;12(16):1419-23.

What is speculatory is whether it truly impacts hypertrophy or not in a trained person. Now that's speculation
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I do think the rate coding hypothesis is interesting and it may prove to be correct but the cited study doesn't support it. Russ' future work also points back to tension (active and passive, but mostly active) as a significant inducer of AKT irrespective of activation frequency. So if AKT is crucial for hypertrophy then one would hypothsize, based on this study, that tension and not stimulation frequency would prove more useful.

Med Sci Sports Exerc. 2008 Jan;40(1):88-95.

Active and passive tension interact to promote Akt signaling with muscle
contraction.

Russ DW.

PURPOSE: The extent to which factors associated with muscle contraction activate Akt remains unclear. This study examined the influences of mechanical (active and
passive tension), neural (activation frequency), and metabolic (glycogen depletion) factors on Akt activation during in situ contractions. METHODS: Muscle length was modified to produce comparable active contractile forces in three protocols, despite a twofold difference in stimulation frequency (15 vs 30 Hz); a fourth protocol used 30-Hz stimulation at optimal length to produce greater active forces. Two protocols were performed at optimal length, using 15- or 30-Hz stimulation (15 Hz opt and 30 H zopt, respectively). Two other protocols used 30-Hz stimulation at shortened or lengthened positions (30 Hz sub and 30 Hz supra, respectively). RESULTS: The principal finding was that the 30-Hz opt
protocol induced significantly greater Akt hosphorylation (approximately threefold relative to control) than did the other protocols, suggesting that activation of this signaling pathway is most sensitive to active tension. This result could not be attributed to differences in glycogen depletion, stimulation frequency, or fatigue. Despite producing the lowest force-time integral, the
30-Hz supra protocol, which had the greatest passive tension, exhibited a greater degree of Akt phosphorylation than did the 15-Hz opt and 30-Hz sub protocols. Although these differences were not significant, they suggest a possible secondary role for passive tension, which may interact with active tension in activating the Akt signaling pathway. CONCLUSION: Akt activation seems more sensitive to active contractile tension than to passive tension. <u>Activation
frequency seems to play no role in the phosphorylation of Akt.</u>
 
<div></div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">What is speculatory is whether it truly impacts hypertrophy or not in a trained person. Now that's speculation</div>

Yes, that's what I meant by that
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all that stuff being quoted from your board was when we were speculating on just how occlusion training does work, since it does induce hypertrophy with such low tensions. Being that in humans, FT's and ST's have almost identical fatigue times and fatigue is related to tension and time rather than fiber type, it's hard to figure how such low tensions can induce PS increases. (occlusion causes full recruitment very early so most fibers would fatigue at very similar rates)
 
<div>
(NWlifter @ Mar. 04 2008,19:43)</div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">just how occlusion training does work, since it does induce hypertrophy with such low tensions. Being that in humans, FT's and ST's have almost identical fatigue times and fatigue is related to tension and time rather than fiber type, it's hard to figure how such low tensions can induce PS increases. (occlusion causes full recruitment very early so most fibers would fatigue at very similar rates)</div>
It's really not that hard Ron and you and I have discussed it a myriad of times and you hit upon it in your post above.... recruitment and once recruited the fibers are generating tension and therefore experiencing tension.

The only way they will ever identify if there is something &quot;magical&quot; going on with ischemic training is to occlude flow during a period of blocked myosin binding as in the Dentel's paper (Am J Physiol Cell Physiol 288: C824–C830, 2005). Then carry this over a period of weeks and see if the muscle grows at all. If not then obviously it's not magical and simply a means to end in elliciting MU recruitment with low loads. Now if they did see growth, then that would be &quot;magical&quot;.
 
<div>
(QuantumPositron @ Mar. 02 2008,18:01)</div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE"></div>
<div></div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE"> <div></div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">Occlusion... causes changes in the recruitment and activation strategies much akin to drop sets, static holds and so forth. </div>

Oh. Would those, ah, recruitment and activation strategies by chance maybe...increase ATP turnover? Could this be the &quot;man behind the curtain&quot;, to play on your magic analogy?</div>Sure they'll increase ATP turnover as ATP turnover is simply a matter of work.

<div></div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE"> <div></div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">Yet we still also have to consider the negative effects of too much force/volume as well and it's direct and indirect effects.</div>

Do we have any guidelines for inducting how much is too much?</div> No not really but there are some studies which begin to point in that direction. The recent study on &quot;stacked&quot; training is one of them (Med Sci Sports Exerc. 2007 Dec;39(12):2135-44. Effect of high-frequency resistance exercise on adaptive responses in skeletal muscle). There are others as well that point out doing too much isn't any better than doing too little.
 
<div></div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">It's really not that hard Ron and you and I have discussed it a myriad of times and you hit upon it in your post above.... recruitment and once recruited the fibers are generating tension and therefore experiencing tension.</div>

Yeah, but I'm just learning to tie my shoes so this is really hard for me
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Seriously, it's not a 'hard to understand' thing like I can't comprehend. It's the idea that 20% of 1RM distributed between the entire motor unit pool induces hypertrophy . Yes, there 'is tension' but it's really low tension. If a person performs non occluded training with 20%, the tension is higher in the ST's for quite a while since they are bearing the entire load, but occlusion quickly induces full recruitment and distributes tension across the entire pool.
So it's the small level of tension I'm talking about. 20% of 1RM or even of MVC across the whole pool, is a lower per fiber tension than daily activities present, yet it induces strength and size gains.

You know me, I'm obsessed with recruitment issues
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<div></div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">The only way they will ever identify if there is something &quot;magical&quot; going on with ischemic training is to occlude flow during a period of blocked myosin binding as in the Dentel's paper (Am J Physiol Cell Physiol 288: C824–C830, 2005). Then carry this over a period of weeks and see if the muscle grows at all. If not then obviously it's not magical and simply a means to end in elliciting MU recruitment with low loads. Now if they did see growth, then that would be &quot;magical&quot;. </div>

and I agree, I highly doubt there is any magic going on either. I think I posted my views on your board, that it's not the ischemia, and it's not the fatigue, it's fatigue inducing full recruitment and ischemia making the myo-cells respond to lower tensions. (ie higher permiability, deformation, etc. )
 
<div></div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">Would those, ah, recruitment and activation strategies by chance maybe...increase ATP turnover?
Sure...</div>

I'm going to say no on this, that ATP turnover is tied to tension (which makes sense since ATP turnover in the contraction process is related to how many bridges are actually linking and re-linking), even fatigue seems to be proportional with tension, not stimulation frequency.

<div></div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">Tension-time index, fatigue, and energetics in isolated rat diaphragm: a new experimental model
Paul F. Klawitter1 and Thomas L. Clanton

The tension-time index (TTI) has been used to estimate mechanical load, energy utilization, blood flow, and susceptibility to fatigue in contracting muscle. The TTI can be defined, for a rhythmically contracting muscle, as the product of average force development divided by maximum tetanic force times duty cycle [contraction time ÷ (contraction + relaxation time)]. In this study, the TTI concept was applied to isolated diaphragm via a method that allowed TTI to be clamped at a predetermined value. The hypothesis tested was that, at constant TTI, muscle energetics and the extent of fatigue would vary with stimulation frequency. Isolated diaphragm strips were stimulated at 25, 50, 75, or 100 Hz for 4 min, one per second. Duty cycle was continuously adjusted to maintain TTI at 0.07, which was near the highest TTI tolerated for 4 min, at 20-Hz stimulation. At the end of the fatigue run, muscles were either immediately frozen for determination ATP, creatine, and creatine phosphate concentrations (n = 6) or stimulated for evaluation of low- and high-frequency fatigue (n = 5). Results demonstrated no difference in the extent of fatigue or in the final ATP and creatine phosphate concentrations between groups. Large within-run increases in duty cycle were required at low stimulation frequencies, but only small increases were required at the highest frequencies. The results demonstrate that, at a constant TTI, similar fatigue properties predominate at all stimulation frequencies with no clear distinction between high- and low-frequency fatigue. The method of clamping TTI during fatigue may be useful for evaluating energetics and contractile function between treatment groups in isolated muscle when treatment influences baseline contractile characteristics.</div>

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Larger view
http://jap.physiology.org/content....03.jpeg



Also,Hypoxia, doesn't appear to increase ATP turnover, rather it lessens.

<div></div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">Modeling the effects of hypoxia on ATP turnover in exercising muscle

P. G. Arthur, M. C. Hogan, D. E. Bebout, P. D. Wagner and P. W. Hochachka
Department of Zoology, University of British Columbia, Vancouver, Canada.

Most models of metabolic control concentrate on the regulation of ATP production and largely ignore the regulation of ATP demand. We describe a model, based on the results of Hogan et al. (J. Appl. Physiol. 73: 728-736, 1992), that incorporates the effects of ATP demand. The model is developed from the premise that a unique set of intracellular conditions can be measured at each level of ATP turnover and that this relationship is best described by energetic state. Current concepts suggest that cells are capable of maintaining oxygen consumption in the face of declines in the concentration of oxygen through compensatory changes in cellular metabolites. We show that these compensatory changes can cause significant declines in ATP demand and result in a decline in oxygen consumption and ATP turnover. Furthermore we find that hypoxia does not directly affect the rate of anaerobic ATP synthesis and associated lactate production. Rather, lactate production appears to be related to energetic state, whatever the PO2. The model is used to describe the interaction between ATP demand and ATP supply in determining final ATP turnover</div>
 
<div>
(NWlifter @ Mar. 05 2008,11:35)</div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE"> <div></div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">Would those, ah, recruitment and activation strategies by chance maybe...increase ATP turnover?
Sure...</div>

I'm going to say no on this, that ATP turnover is tied to tension (which makes sense since ATP turnover in the contraction process is related to how many bridges are actually linking and re-linking),</div>
I agree that rate coding isn't tied to ATP turnover but recruitment is for the same reason you elaborate on. So occlusion heightens MU recruitment. More MUs actively forming crossbridges means more ATP turnover.
 
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