ditto[b said:
A New and Unique Training Method is Here
- Thread starter Sub7
- Start date
I appreciate the kind words guys.
I just (theoretically) graduated with a BS in Biology finally! About dang time
Applying for grad school in physical therapy next fall, as it seems to coincide the best with my interests in exercise related matters.
Speaking of which, I need to harass a professor or two for a letter of recommendation. Want to write me a letter of recommendation Bryan? =0 *cackles*
Bear in mind that while I haven't contributed to discussion as much, I always check back on here for messages, goings on etc. To date, this is one of the best quality boards on the net for discussion of exercise physiology, particularly in its tone and mutual respect, something SO lacking at most other places.
P.S. Wish me luck as I'm about to take the GRE in a couple of hours :-x
I just (theoretically) graduated with a BS in Biology finally! About dang time
Applying for grad school in physical therapy next fall, as it seems to coincide the best with my interests in exercise related matters.
Speaking of which, I need to harass a professor or two for a letter of recommendation. Want to write me a letter of recommendation Bryan? =0 *cackles*
Bear in mind that while I haven't contributed to discussion as much, I always check back on here for messages, goings on etc. To date, this is one of the best quality boards on the net for discussion of exercise physiology, particularly in its tone and mutual respect, something SO lacking at most other places.
P.S. Wish me luck as I'm about to take the GRE in a couple of hours :-x
I
imported_dkm1987
Guest
Big Congrats
and
Good Luck
You can DO IT.
and
Good Luck
Fausto
HST Expert
Mikey
And we all know BS does not stand for bull-####
specially where you are concerned!
Big congrats, and good luck for the next phase
That is the truth! What a site we are! Kudus to Bryan for strating it up and to all the guys for keeping it just so...we'll just ignore the very few hicups that somtimes happen, they are indeed few and far between.
A bigger, BETTER Christmas and a prosperous new year to y'all, you're a great bunch of people!
[b said:
And we all know BS does not stand for bull-####
Big congrats, and good luck for the next phase
[b said:
That is the truth! What a site we are! Kudus to Bryan for strating it up and to all the guys for keeping it just so...we'll just ignore the very few hicups that somtimes happen, they are indeed few and far between.
A bigger, BETTER Christmas and a prosperous new year to y'all, you're a great bunch of people!
I
imported_dkm1987
Guest
Thanks a lot for the link. However please keep in mind that the first discussion of ACIT goes back further than that to Val's HIT forums. Those threads are a bit messy because the discussion veered off-topic numerous times. The link given by Dan is certainly useful, but may be better sutied to tracking the history of ACIT's development than to get the most important information about the method as quickly as possible. For that I definitely suggest[b said:
www.acit-training.com
The ACIT site was put together by Ron and I and, without trying to win a Noble prize with its scientific precision, tries to explain the method as clearly as possible.
Suby
NWlifter
Active Member
[b said:Quote[/b] ]I'm a fan of the Ron, if you could point me towards any in-depth discussions of all of this at some forum(s), I'd enjoy playing too
Hey I'm flattered, thanks dude!
Congrats on the graduation, great job!
Quick comments on 'the tension thing'.....
Occlusion training: Hypoxia induces full recruitment and rate coding (aka fiber activity) with lighter weights. Gains were similar (sometimes a bit less, sometimes a bit more) than training with 80%+ minus occlusion.
Why go through all this just to replicate? Safety? or maybe a reduction in CNS stress. Peak CNS output would be the same, but the duration of high CNS output might be lower. Most studies show time rather than peak output, as the fatiguing factor concerning the CNS.
Fiber activity vs. whole muscle tension: Most of the studies out there that equalize ATP turnover, TTI, ect. find no difference in MPS between whole muscle tension levels as long as the fiber activity was the same. This points to tension being a means to an end, rather than an 'end'.
Further, why do we even perform more than 'one rep' with each RM? The peak tension is the same with each rep?
Answering, 'metabolic conditioning' won't completely answer the question. Even if we received zero benefit to glycogen stores, mitochondria or capillaries, we would still need repeated efforts to stimulate hypertrophy.
(think ATP turnover --->mTOR, Calcium accumulation --> mechanical remodeling, calcineurin, etc.)
Don't know if that helps for confounds!
Cheers!
Ron
"Peak CNS output would be the same, but the duration of high CNS output might be lower."[b said:Quote[/b] (NWlifter @ Dec. 26 2005,12:54)]Hey I'm flattered, thanks dude![b said:Quote[/b] ]I'm a fan of the Ron, if you could point me towards any in-depth discussions of all of this at some forum(s), I'd enjoy playing too
Congrats on the graduation, great job!
Quick comments on 'the tension thing'.....
Occlusion training: Hypoxia induces full recruitment and rate coding (aka fiber activity) with lighter weights. Gains were similar (sometimes a bit less, sometimes a bit more) than training with 80%+ minus occlusion.
Why go through all this just to replicate? Safety? or maybe a reduction in CNS stress. Peak CNS output would be the same, but the duration of high CNS output might be lower. Most studies show time rather than peak output, as the fatiguing factor concerning the CNS.
Fiber activity vs. whole muscle tension: Most of the studies out there that equalize ATP turnover, TTI, ect. find no difference in MPS between whole muscle tension levels as long as the fiber activity was the same. This points to tension being a means to an end, rather than an 'end'.
Further, why do we even perform more than 'one rep' with each RM? The peak tension is the same with each rep?
Answering, 'metabolic conditioning' won't completely answer the question. Even if we received zero benefit to glycogen stores, mitochondria or capillaries, we would still need repeated efforts to stimulate hypertrophy.
(think ATP turnover --->mTOR, Calcium accumulation --> mechanical remodeling, calcineurin, etc.)
Don't know if that helps for confounds!
Cheers!
Ron
Wouldn't mind hearing more of an elaboration on that.
And as far as tension vs. fiber activity goes, I dunno. Obviously, if the occlusion studies are indicating similar gains at substantially reduced tension by virtue of getting more recruitment, that implies that recruitment itself is the factor and, as you said, that 'tension is a means to an end and not an end unto itself.'
That said, I'm still curious how that relates to the RBE. It seems the limiting factor over time is still progressive tension overload. If you're not lifting heavier stuff over time, regardless of the means, it still seems you're dead in the water. I would imagine in the occlusion studies that if they carried them out for a longer period of time, you'd still see the same old trend of increasing tension over time being necessary to keep inducing gains.
Also, I recall Bryan commenting in the past that the rate limiting step in hypertrophy was the activation of satellite cells and the donation of their nuclei to muscle, and that even though lighter weights were capable of generating as much MPS as heavier weights in some cases, it was the heavier weights which allowed that process to occur in the first place as a product of mechanical strain.
So fine, I am still fuzzy on how "increase in weight" translates to "increase in mechanical strain." If you or anybody else has any new thoughts on that, I'd like to hear it.
Btw, read around the hypertrophy research forums to reacquaint myself with some of this stuff as I haven't 'seriously' looked into hypertrophy research with any frequency in probably 2 years.
I'm now starting to put together the picture you and Dan are laying out better.
Let me know if this sounds like your perspective:
* Comparatively heavier loads involve muscle fibers experiencing their peak tension more often than comparatively lighter loads, and 'tension per fiber' never increases in absolute magnitude above what that fiber itself produces. However, the frequency at which a muscle fiber displays that maximum tension increases with heavier loads. So if there's a heavier load = increased strain logic, I'm guessing that's it.
* It looks like you guys are questioning the 'damage as a prerequisite to hypertrophy' angle. As per the post above, I'd be really curious to know your thoughts on the contribution of satellite cells to the big picture, then. Afaik, it is damage/strain that is a necessary step in initiating that whole process.
* Tension time integral seems to be a key factor to look at for hypertrophy, seems to correlate well with some of the MAPK's and is something I totally don't understand as I haven't seen an explanation for it anywhere. lol
I guess right now I'm trying to integrate this information into 'hypertrophy over a longer period of time' scenario. In an acute sense, (muscle) hypertrophy is any net accretion in muscle protein. Understanding what needs to change in terms of loading/exercise parameters from your perspective seems fuzzy to me.
Anecdotally, it seems to me that progressive tension overload still rules and is fundamental to every successful weight training system ever. But I'm having trouble understanding how you'd relate that to your present understanding of hypertrophy.
I'm now starting to put together the picture you and Dan are laying out better.
Let me know if this sounds like your perspective:
* Comparatively heavier loads involve muscle fibers experiencing their peak tension more often than comparatively lighter loads, and 'tension per fiber' never increases in absolute magnitude above what that fiber itself produces. However, the frequency at which a muscle fiber displays that maximum tension increases with heavier loads. So if there's a heavier load = increased strain logic, I'm guessing that's it.
* It looks like you guys are questioning the 'damage as a prerequisite to hypertrophy' angle. As per the post above, I'd be really curious to know your thoughts on the contribution of satellite cells to the big picture, then. Afaik, it is damage/strain that is a necessary step in initiating that whole process.
* Tension time integral seems to be a key factor to look at for hypertrophy, seems to correlate well with some of the MAPK's and is something I totally don't understand as I haven't seen an explanation for it anywhere. lol
I guess right now I'm trying to integrate this information into 'hypertrophy over a longer period of time' scenario. In an acute sense, (muscle) hypertrophy is any net accretion in muscle protein. Understanding what needs to change in terms of loading/exercise parameters from your perspective seems fuzzy to me.
Anecdotally, it seems to me that progressive tension overload still rules and is fundamental to every successful weight training system ever. But I'm having trouble understanding how you'd relate that to your present understanding of hypertrophy.
NWlifter
Active Member
Hey Mike,
Yes, right on
That also goes along with a study Brian pointed out to us, that most of what we think is damage, is really a remodeling effect. (it peaks way after the initial tension. Damage would be highest at the time of injury)
TTI is kind of a mathematical summation of the 'contraction-relaxation' time of the fibers. This corrolates with ATP turnover rates. ATP turnover rates seem to track p70 and p70 is almost linear with MPS. (ATP seems to relate a lot to mTOR)
My thoughts are it's not the tension part of progressive tension, but the higher 'work per time' as we increase tension. ie we could 'stay ahead of the RBE' if you will, with more ways than just tension increases.
Hope that makes sense written as well as it does in me head
[b said:
Yes, right on
[b said:
That also goes along with a study Brian pointed out to us, that most of what we think is damage, is really a remodeling effect. (it peaks way after the initial tension. Damage would be highest at the time of injury)
[b said:
TTI is kind of a mathematical summation of the 'contraction-relaxation' time of the fibers. This corrolates with ATP turnover rates. ATP turnover rates seem to track p70 and p70 is almost linear with MPS. (ATP seems to relate a lot to mTOR)
[b said:
My thoughts are it's not the tension part of progressive tension, but the higher 'work per time' as we increase tension. ie we could 'stay ahead of the RBE' if you will, with more ways than just tension increases.
Hope that makes sense written as well as it does in me head
Sounds like pulsing and static holds.. HST customization[b said:
[b said:
Work per time, or power persay... would that also mean doing fast reps rather than slower ones? ..sounds like some Pete Sisco stuff. Maybe I oversimplified what I just read - still haven't looked through that ACIT website just yet.
-Colby
I
imported_dkm1987
Guest
I know I do, but so do many of the current researchers.[b said:
Remodeling occurs even without histological markers of damage. Now this could very easily translate into increases in PS that is seen.
I first saw indications of this when I read Crameri's study on satellite cell activity after drop jumps followed by two isokinetic leg extension exercises. Although they saw an increase in satellite cell number they saw no staining for fibronectin, no lessions or necrosis. But they also saw no donation of the nuclei to the existing fibers. They hypothesized that it wasn't so much the damage that was needed but a chronic application of stress.
Kadi furthered this work by looking at what occurs with training and detraining over a long duration. What he found was roughly the same, satellite cells increases in number but didn't contribute to the domain.
With both of these in mind it appears that satellite cell donation isn't really dependant only on strain, because both training protocols involved large enough loads, ( Crameri=fifty one legged ‘drop down’ jumps were performed from a stable platform of 45 cm, - eight sets of ten maximal eccentric knee extensions at -30°/s using an isokinetic dynamometer
and - eight sets of ten maximal eccentric knee extensions at -180°/s using an isokinetic dynamometer. Kadi=Hack squat, Leg Press, Leg Extensions, Leg Curl for 90 days 3X week @ 6-12RM) and neither of these showed large amounts of donation occuring. It may be that donation is an occurrance based on training status more so than acute damage. This is also backed up by what occurs with some of the mitogenic markers, Cyclin-D, Myo-D, Myostatin and Myogenin during prolonged chronic application of stress.
Lastly, to cut this off and get out to the shop, let's look at Nosaka, in an obscure publication, International Journal of Sport and Health Science Vol 1 (1) 1-8, he even makes the statement that although eccentrics do cause damage, damage is not necessary for hypertrophy.
[b said:
Alright, my next question, then:
If damage is not a prerequisite for long-term hypertrophy (though, as an aside, do you still agree that the donation of nuclei from satellite cells IS a necessary prerequisite to long-term growth?), then why are eccentrics superior to concentrics for inducing hypertrophy?
As far as I know, the main difference between concentric and eccentric reps on the muscle tissue is the degree of strain that results from an eccentric being greater. In my mind, the damage before hypertrophy model justified the superiority of eccentrics. If damage isn't that important or a particular prerequisite, I would be curious to know WHY eccentrics do seem superior.
Or are you on the Ron bandwagon and now question that eccentrics are better for growth? :-x
I
imported_dkm1987
Guest
Well, let's see.
Yes, eccentrics generally produce more damage than concentrics, no doubt. But looking at hypertrophy does this equate to more hypertrophy?
Looking at work by Haddad, I would have to say no. Being that damage is the supposed cause to MGF leakage and eccentrics leading to damage should therefore induce a higher MGF elevation, yet in the the study by Haddad/Adams this wasn't the case. When looking at Iso, Con, Ecc, Concentric or shortening produced more MGF response than lengthening even though Lenghtening produced more torque over the torque time index they examined and therefore should have produced more strain. Granted their testing was after 10 training sessions whereas the results that Bamman saw where immediately after an acute bout and some of the immediate training stimulus may be changed in a chronic setting, but again this is what we are talking about, a chronic setting of resistance training over time and the hypertrophic response. In which, this study may give some insight into the relationship of responses and importance between eccentric vs concentric.
You can also look to the studies using a combined contraction and for the most part these would probably be the ones to use since most of the human training is done dynamically. Looking at these training status has a much larger part to play than training modality. For example DCER and DAER both show about roughly the same strength gains, albeit eccentrically biased may show a small bit more. But for hypertrophy ?? Not much of a difference, especially in resistance trained individuals.
So my bandwagon says this, since damage (if that's what you wish to call it) can be caused through either strain or metabolic stress and since most humans do not nor can not replicate the chronic extreme active stretch of the quail wing, it isn't worth worrying about the contraction mode or the progression mode. What's more important is progressing. As I've said in other posts I am a firm believer in that both tension and metabolic work must be included.
Bandwagon included
Yes, eccentrics generally produce more damage than concentrics, no doubt. But looking at hypertrophy does this equate to more hypertrophy?
Looking at work by Haddad, I would have to say no. Being that damage is the supposed cause to MGF leakage and eccentrics leading to damage should therefore induce a higher MGF elevation, yet in the the study by Haddad/Adams this wasn't the case. When looking at Iso, Con, Ecc, Concentric or shortening produced more MGF response than lengthening even though Lenghtening produced more torque over the torque time index they examined and therefore should have produced more strain. Granted their testing was after 10 training sessions whereas the results that Bamman saw where immediately after an acute bout and some of the immediate training stimulus may be changed in a chronic setting, but again this is what we are talking about, a chronic setting of resistance training over time and the hypertrophic response. In which, this study may give some insight into the relationship of responses and importance between eccentric vs concentric.
You can also look to the studies using a combined contraction and for the most part these would probably be the ones to use since most of the human training is done dynamically. Looking at these training status has a much larger part to play than training modality. For example DCER and DAER both show about roughly the same strength gains, albeit eccentrically biased may show a small bit more. But for hypertrophy ?? Not much of a difference, especially in resistance trained individuals.
So my bandwagon says this, since damage (if that's what you wish to call it) can be caused through either strain or metabolic stress and since most humans do not nor can not replicate the chronic extreme active stretch of the quail wing, it isn't worth worrying about the contraction mode or the progression mode. What's more important is progressing. As I've said in other posts I am a firm believer in that both tension and metabolic work must be included.
Bandwagon included