Bryan, What Are Your Thoughts On Higher Frequency Training?

[NWlifter]

I agree, I believe DOMS can be an indicator, and might provide some insight to RBE. Most studies that look at RBE look at DOMS and 'damage', and how once RBE is in effect, DOMS doesn't occur. Yet, hypertrophy still can occur. In fact, I'd venture to say that DOMS might prevent hypertrophy as post PS is more about repair and alterations than it is about hypertrophy that leads to CSA gains.

Increasing load while maintaining volume: That yes, for sure. When you do that, you are increasing work and the TTI of the work. Same number of contractions with a heavier load is more work. Now if load was key, by itself, then just using more load, even with less volume would increase the stimulus.
ie, in reverse order of stimulation. 12 reps with 12RM least, 8 with 8 RM more stimulus, 6 with 6 RM even more stimulation, 1 rep with 1RM would be highest stimulation.

 

[Old and Grey]

https://www.strongerbyscience.com/hypertrophy-range-fact-fiction/

 

[NWlifter]

That's a great article, I've read that before, seems pretty much accurate IMO.

 

[Bryan Haycock]

Wow, great thread!

I just wanted to add one thing. When thinking about load vs work, it should not be overlooked that mechanical strain triggers anabolic signaling whether the muscle is actively contracting or not. Cellular components such as membrane and extracellular matrix bound proteins like costameres, intregrins, G protein-coupled receptors have all been shown to be activated in response to being mechanically distorted (i.e. stretched). This does not negate anything that anybody has said to this point, I just wanted to point out that mechanical loading of the the tissue (i.e. stretch) does initiate anabolic signaling pathways independent of the work the tissue is doing. Furthermore, these "mechanosensors" do become less sensitive to mechanical distortion as part of the adaptive process of the muscle cell to mechanical strain.

 

[Old and Grey]

Furthermore, these "mechanosensors" do become less sensitive to mechanical distortion as part of the adaptive process of the muscle cell to mechanical strain.

Ergo the problem. The longer we work out, the tougher any sort of gains.

 

[NWlifter]

Wow, great thread!

I just wanted to add one thing. When thinking about load vs work, it should not be overlooked that mechanical strain triggers anabolic signaling whether the muscle is actively contracting or not. Cellular components such as membrane and extracellular matrix bound proteins like costameres, intregrins, G protein-coupled receptors have all been shown to be activated in response to being mechanically distorted (i.e. stretched). This does not negate anything that anybody has said to this point, I just wanted to point out that mechanical loading of the the tissue (i.e. stretch) does initiate anabolic signaling pathways independent of the work the tissue is doing. Furthermore, these "mechanosensors" do become less sensitive to mechanical distortion as part of the adaptive process of the muscle cell to mechanical strain.

Good post Bryan!

Here is the thing that has bothered me for many years..... really think about this, maybe you have some thoughts on it.
People tend to think we 'put a load' on a muscle fiber, but we don't. It 'creates tension'.
So a fresh fiber in tetany can 'create some exact' tension (sum of cross bridges in parallel)
I've read that almost all human movement, especially under load, is tetanic contracts. Force is varied by rate coding and synchronization of the motor units. Almost like the lights blinking on a Christmas tree.
That means, if I lift a 5Rm or an 8Rm anytime a fiber 'is active', it's in tetany and putting out it's tetanic force. The same force. The 5Rm just has more motor units 'on' at the same time, more often to sum up to a higher total muscle force.
You can see what bothers me then, if all that physiology is true, then each muscle fiber 'creates/feels' the same absolute tension with different loads, they are just creating it more often or 'on' for longer blinks of time.

IF that is true, it would be like having 100 digital people, each with a rope, all the ropes attached to a load. If the load was 1000 lbs, you might need 60 our of 100 pulling with full force at any point in time to support it. If the load was 1500 lbs, you might need 75 people, pulling with that same full force at any point in time to support it. Either way, each person still only would pull and 'feel' the same individual 'part' of the load. Does that make sense?

Thoughts about that?

 

[_Simon_]

...mechanical strain triggers anabolic signaling whether the muscle is actively contracting or not.

Ah interesting, could you please elaborate on that thanks Bryan? Are you saying that simply undergoing sufficient resistance itself (the body's structure as a generality, even if the muscle tissue isn't contracting much or at all) is sufficient? Because all the surrounding ligaments, cellular structures etc are undergoing stress, that it still brings about the anabolic signalling?
This sort of a ties in with the other thread I just brought up.

But I'm confused what you mean.. I'm trying to understand it in a more direct application I guess hehe. I did think that the muscle had to be contracting to oppose the load for there to be any mechanical strain and therefore anabolic growth..

This does not negate anything that anybody has said to this point, I just wanted to point out that mechanical loading of the the tissue (i.e. stretch) does initiate anabolic signaling pathways independent of the work the tissue is doing.

And that it's moreso important that the tissue undergoes something (just resistance with enough frequency, then obviously adaption will occur hence the need to progress), and not so important the amount of work done? Sort of makes sense, what's important is just that something/mechanical strain is occurring, and that it's a sliding scale as to what that something is (depending on current training adaptions).

I'm just throwing around ideas, happy to be corrected haha. Thanks Bryan

 

[Bryan Haycock]

Hey NWlifter. I understand your thinking. I may not be able to answer this question fully, but I think I can shed some light on what really happening to relieve you of some stress.

Does a fiber generate its own "load"?

Yes, but its more complicated than that. Keep in mind that all the fibers are connected. So when one fiber contracts, all of the fibers around it are pulled and stretched by virtue of their connectedness both at the level of the extracellular matrix, and connective fascia. So, even if a fiber is not actively contracting, it is experiencing passive stretch (and distortion of its membrane) when loads are applied to the tissue. The mechanosensors in the cell membrane are then activated turning on anabolic signaling pathways.

Is a contracting fiber in tetany?

No, not unless you are dead. Let’s use the tug-o-war example. In a normal tug-o-war, each “puller” grabs the rope and pulls continuously until the war is over. They may reposition their grip occasionally but it is not the rule. Actin/Myosin interactions are similar but different enough that it matters when using tug-o-war as an analogy. Actin/myosin cross bridging occurs in a cyclic manner many many times per second (i.e. the speed of a chemical reaction). I have to speak in generalities here. As long as ATP is available at the site of the cross bridge, the myosin head will immediately “let go” of the actin once its power stroke occurs. Again, this occurs in a tiny fraction of a second. So each myosin head is grabbing the actin, pulling on it for a millisecond, then letting go, and grabbing it again, etc until the waves of action potentials stop coming into the t-tubules releasing pulses of Ca2+. The amount of force the fiber develops depends on how many crossbridge cycles are occurring simultaneously. Here is a super slo-mo video http://www.sci.sdsu.edu/movies/actin_myosin_gif.html

Fiber experiences same load whether lifting 5RM or 8RM?

Yes, to some extent this is true and for the reason you explained (i.e. more motor units + more force). However, you must then add the actual mechanical load imposed on the tissue, in addition the force the tissue is generating. This increases the physical distortion that occurs in the tissue and increases mechanotransduction signaling in all fibers. So the fiber may create the same tension, but it does not “feel” the same load when going from 8RM to 5RM.

 

[Bryan Haycock]

_Simon_ yes, all you have to do is stretch a muscle and it will turn on anabolic signaling including the activation of satellite cells. As mentioned in the other thread, mechanosensors in the cell membrane sense stretch and distortion of the cell membrane and they respond by activating anabolic signaling pathways in the cell.

 

[NWlifter]

Hey NWlifter. I understand your thinking. I may not be able to answer this question fully, but I think I can shed some light on what really happening to relieve you of some stress.

Does a fiber generate its own "load"?

Yes, but its more complicated than that. Keep in mind that all the fibers are connected. So when one fiber contracts, all of the fibers around it are pulled and stretched by virtue of their connectedness both at the level of the extracellular matrix, and connective fascia. So, even if a fiber is not actively contracting, it is experiencing passive stretch (and distortion of its membrane) when loads are applied to the tissue. The mechanosensors in the cell membrane are then activated turning on anabolic signaling pathways.

Is a contracting fiber in tetany?

No, not unless you are dead. Let’s use the tug-o-war example. In a normal tug-o-war, each “puller” grabs the rope and pulls continuously until the war is over. They may reposition their grip occasionally but it is not the rule. Actin/Myosin interactions are similar but different enough that it matters when using tug-o-war as an analogy. Actin/myosin cross bridging occurs in a cyclic manner many many times per second (i.e. the speed of a chemical reaction). I have to speak in generalities here. As long as ATP is available at the site of the cross bridge, the myosin head will immediately “let go” of the actin once its power stroke occurs. Again, this occurs in a tiny fraction of a second. So each myosin head is grabbing the actin, pulling on it for a millisecond, then letting go, and grabbing it again, etc until the waves of action potentials stop coming into the t-tubules releasing pulses of Ca2+. The amount of force the fiber develops depends on how many crossbridge cycles are occurring simultaneously. Here is a super slo-mo video http://www.sci.sdsu.edu/movies/actin_myosin_gif.html

Fiber experiences same load whether lifting 5RM or 8RM?

Yes, to some extent this is true and for the reason you explained (i.e. more motor units + more force). However, you must then add the actual mechanical load imposed on the tissue, in addition the force the tissue is generating. This increases the physical distortion that occurs in the tissue and increases mechanotransduction signaling in all fibers. So the fiber may create the same tension, but it does not “feel” the same load when going from 8RM to 5RM.

Ah ha, ok now that is one area I hadn't considered, that the whole muscle tension could pull and distort 'tissue'. That the summation of fiber force is a factor. i guess I was thinking too much on the 'per fiber' basis and what a fiber 'sees/feels/generates'.

Tetany- This throws me? So many texts refer to 'max rate coding being synonymous with 'fused tetany', and one online physiology text I had read said basically, all human movement involves tetanic contractions? That anytime calcium floods the cell fully, (with max neural input) we have fused tetany?

Thanks a TON for the great information! you gotta post here more, inquiring minds wanna know stuff! lol

 

[_Simon_]

_Simon_ yes, all you have to do is stretch a muscle and it will turn on anabolic signaling including the activation of satellite cells. As mentioned in the other thread, mechanosensors in the cell membrane sense stretch and distortion of the cell membrane and they respond by activating anabolic signaling pathways in the cell.

Ahh I see, makes sense, but I did think it was moreso stretch under tension resulted in that, that the muscle had to still be contracting under load.. unless we're talking about a different type of stretch here hehe. Really appreciate it

 

[NWlifter]

Hey Bryan,
When you have time a few questions/thoughts...

All great replies. I'll just add a couple comments.
With resistance training, there are two underlying stimuli for muscle growth, mechanical load, and metabolic stress. Each has distinct recovery requirements.


Recovery from metabolic stress does not take very long, on the order of hours. Research using blood flow restriction (maximizing metabolic stress while minimizing mechanical stress) has shown that the muscle can be trained twice per day every day and grow quite dramatically.

This got me thinking about a couple things....

1) Is RBE a factor in the metabolic path? It 'kinda' seems like it might be. Even though DOMS isn't required for hypertrophy, I think it clues us into an idea, it seems DOMS appears when RBE is highly exceeded. I've had DOMS from doing something very 'metabolic' with really light loads.Then when I got used to it, no more DOMS. So even with way less load, but way higher fatigue, same movement, DOMS showed up and once adapted, it quit happening. So metabolic must be part of the RBE, adaptation areas too?

2) Based on that, it seems like there 'could' be a 'Metabolic HST' setup. Where instead of making load primary for the continual surpassing of RBE, you could make each workout exceed RBE via metabolic increases. It 'kinda' seems like metabolic is a multiplier with mechanical. Meaning mechanical x metabolic 'semi equals' MPS. The occlusion studies make me think that, really light load but super high fatigue equaled higher load with less fatigue.
Seems like one could do a 'fatigue step increase' over a cycle?
Reason I'm theorizing on that, is it might be a way for people like me (with injuries that prevent ever using heavy loads) to still do 'HST'.

Hey NWlifter. I understand your thinking. I may not be able to answer this question fully, but I think I can shed some light on what really happening to relieve you of some stress.

Does a fiber generate its own "load"?

Yes, but its more complicated than that. Keep in mind that all the fibers are connected. So when one fiber contracts, all of the fibers around it are pulled and stretched by virtue of their connectedness both at the level of the extracellular matrix, and connective fascia. So, even if a fiber is not actively contracting, it is experiencing passive stretch (and distortion of its membrane) when loads are applied to the tissue. The mechanosensors in the cell membrane are then activated turning on anabolic signaling pathways.



Yes, to some extent this is true and for the reason you explained (i.e. more motor units + more force). However, you must then add the actual mechanical load imposed on the tissue, in addition the force the tissue is generating. This increases the physical distortion that occurs in the tissue and increases mechanotransduction signaling in all fibers. So the fiber may create the same tension, but it does not “feel” the same load when going from 8RM to 5RM.

This info, gave me one more thought, I think that may very well explain 'Beginner gains'.
Beginners, once they get semi-coordinated, have so much room for neural improvements, they end up tossing more load on the bar almost every workout, so I bet they are blowing out past RBE every workout from those fast neural gains, getting a big nice rise in MPS after each. Then when those fast neural gains stop, they can't exceed RBE very much or very often so muscle gains naturally slow way down too.
Probably also why those HIT routines work so well the first time. You get a ton of neural improvements, keep adding weight like crazy while that short period of neural gains is occurring. Plus your getting a buttload of metabolic fatigue and really momentarily reducing ATP levels. Your hitting and exceeding mechanical, metabolic and energetic pathways every workout for a few weeks to a couple months until the neural gains peak.

Last thought/question , Re-RBE & SD

Here is another thing I've thought about over the years.
If take an SD, we take 2 weeks off, it makes the muscles more sensitive to load, enough so that lower the loads and going back to 15's, 'works again'. There really is no atrophy in healthy well fed humans in that time, so no losses, just re sensitization.

OK, so 2 weeks off slowly resets RBE without losses and makes us gain from loads lighter than we were doing 2 weeks before. So if a person were to train each muscle once a week, wouldn't there be a partial SD / RBE reset built into the lower frequency? So the muscle would be more sensitive and maybe get a larger effect each time? Could that be why some studies find only minor differences with training frequency when weekly volume is matched?
3x gives you 3 small 'bumps' in MPS and the conditioning limits the level and time course, where less often gives you a bigger 'bump' that lasts longer since RBE is kind of resetting more in between each workout, so long term the results are very similar?

 

[Renky]

Ergo the problem. The longer we work out, the tougher any sort of gains.

I agree... However, I have experimented a bit with taking longer and longer breaks from training. In my case, I have found that muscle loss was minimal and I feel that it paid dividends in spurring on new growth. I have experimented with 2 week breaks, 4 week breaks and even did a 6 week break.

 

[_Simon_]

I agree... However, I have experimented a bit with taking longer and longer breaks from training. In my case, I have found that muscle loss was minimal and I feel that it paid dividends in spurring on new growth. I have experimented with 2 week breaks, 4 week breaks and even did a 6 week break.

Ah nice, that's good to keep in mind, rest periods seem so important, never thought of taking that long a break!

 

[Renky]

Ah nice, that's good to keep in mind, rest periods seem so important, never thought of taking that long a break!

I don't have any science on this... It is just something that I have played with to see what happens and I think that in my case it helped. What I have done the last few cycles (about a month out from taking a break) is to up frequency on my lagging muscle group to train the specific lagging muscle once a day, 5 days a week to twice a day, 5 days a week, to maybe even 3 times a day, 5 days a week. I keep adding frequency each week and adjust volume of course. Then I take a break, because I have learned that I cannot sustain that kind of frequency for too long. I definitely would not do this for the whole body either, just a specific muscle that I want to improve.
I do all this with HST and myo reps.

 

[Bryan Haycock]

I'll do my best to answer what I can...

Hey Bryan,
When you have time a few questions/thoughts...

1) Is RBE a factor in the metabolic path? It 'kinda' seems like it might be. Even though DOMS isn't required for hypertrophy, I think it clues us into an idea, it seems DOMS appears when RBE is highly exceeded. I've had DOMS from doing something very 'metabolic' with really light loads.Then when I got used to it, no more DOMS. So even with way less load, but way higher fatigue, same movement, DOMS showed up and once adapted, it quit happening. So metabolic must be part of the RBE, adaptation areas too?

The repeated bout effect (RBE) is an adaptive process that reduces the strength of the exercise stimulus (whatever it may be). So, with metabolic stress, the cell/body adapts by increasing its ability to both reduce inefficiency of energy delivery and metabolic by products. For example, metabolic stress causes a depletion of glycogen, and heavy demand on glycolytic/ATP energy producing systems. As a result you get increase H+, i-phosphates, ADP, and possibly reactive oxygen/nitrogen species (a recent study questions this one) to name a few. To adapt, the body will increase glycogen stores, beef up energy delivery pathways (i.e. glycolytic enzymes and creatineP), increase its buffering capacity (to export lactate and raise pH), and increase antioxidant enzymes. The end result is that the impact of an equivalent metabolically stressful workout is ultimately less stressful for the tissue/body, therefor, adaptation decreases/stops. This is the RBE in terms of metabolic stress (in a not very detailed nut shell).

Its highly likely that DOMS occurs as a result of increased oxidative stress, ecosenoid production, and/or nerve growth factor. Each of these serves to enhance afferent nerve sensitivity (hyperalgesia). Both metabolic and mechanical stress can induce these factors, thus people get sore from a variety of unaccustomed muscular activity including just higher fatigue.

2) Based on that, it seems like there 'could' be a 'Metabolic HST' setup. Where instead of making load primary for the continual surpassing of RBE, you could make each workout exceed RBE via metabolic increases. It 'kinda' seems like metabolic is a multiplier with mechanical. Meaning mechanical x metabolic 'semi equals' MPS. The occlusion studies make me think that, really light load but super high fatigue equaled higher load with less fatigue. Seems like one could do a 'fatigue step increase' over a cycle? Reason I'm theorizing on that, is it might be a way for people like me (with injuries that prevent ever using heavy loads) to still do 'HST'.

Absolutely! All you really have to do is raise the rep ranges to a point that your joints are no longer bothered by the loads themselves. Current thinking in academia is that load does not matter as long as sets are taken to failure. Although I've read the data, I still can't ignore years of experience showing me that at some point, increased mechanical load is the only way to trigger stalled gains. I don't have proof, only my own experience. I guess the question is, can a guy who lifts no more than 100 pounds to failure, ever get as big as a guy who lifts 200 pounds to failure. Personally I don't think you see a difference until both lifters have many years of lifting under their belts, but once they do, 200 pounds will get you bigger than 100 pounds even when training to failure.

OK, so 2 weeks off slowly resets RBE without losses and makes us gain from loads lighter than we were doing 2 weeks before. So if a person were to train each muscle once a week, wouldn't there be a partial SD / RBE reset built into the lower frequency? So the muscle would be more sensitive and maybe get a larger effect each time? Could that be why some studies find only minor differences with training frequency when weekly volume is matched? 3x gives you 3 small 'bumps' in MPS and the conditioning limits the level and time course, where less often gives you a bigger 'bump' that lasts longer since RBE is kind of resetting more in between each workout, so long term the results are very similar?

For this we have to start with the fact that data exists showing that 2-3/week leads to faster growth than 1/week. The more time the muscle spends in an anabolic state (producing contractile proteins) the faster it will grow. You will still get RBE liftine once per week, especially since you will likely have to lift harder and longer if you are only training once per week. Total volume is important. So you end up squeezing a week's worth of training into a single session. RBE sets in a the window of anabolic activity following each workout shortens to a number of hours, rather than days. There is good reason to believe that you can grow training a muscle once per week (many lifters use a 3-day 1/week split), and given enough time, its possible they may end up at the same point had they trained more frequently (especially if added hormones are involved).

I hate to go back to anecdotal evidence, but its been my experience that the body is "more comfortable" for lack of a better phrase, with more frequent consistent stimuli than from an occasional highly damaging assault. Remember that protein synthesis only goes towards growth after all damage has been repaired. More frequent, less damaging training is a better way to go in the long term in my opinion.

 

[NWlifter]

I'll do my best to answer what I can...



The repeated bout effect (RBE) is an adaptive process that reduces the strength of the exercise stimulus (whatever it may be). So, with metabolic stress, the cell/body adapts by increasing its ability to both reduce inefficiency of energy delivery and metabolic by products. For example, metabolic stress causes a depletion of glycogen, and heavy demand on glycolytic/ATP energy producing systems. As a result you get increase H+, i-phosphates, ADP, and possibly reactive oxygen/nitrogen species (a recent study questions this one) to name a few. To adapt, the body will increase glycogen stores, beef up energy delivery pathways (i.e. glycolytic enzymes and creatineP), increase its buffering capacity (to export lactate and raise pH), and increase antioxidant enzymes. The end result is that the impact of an equivalent metabolically stressful workout is ultimately less stressful for the tissue/body, therefor, adaptation decreases/stops. This is the RBE in terms of metabolic stress (in a not very detailed nut shell).

Its highly likely that DOMS occurs as a result of increased oxidative stress, ecosenoid production, and/or nerve growth factor. Each of these serves to enhance afferent nerve sensitivity (hyperalgesia). Both metabolic and mechanical stress can induce these factors, thus people get sore from a variety of unaccustomed muscular activity including just higher fatigue.



Absolutely! All you really have to do is raise the rep ranges to a point that your joints are no longer bothered by the loads themselves. Current thinking in academia is that load does not matter as long as sets are taken to failure. Although I've read the data, I still can't ignore years of experience showing me that at some point, increased mechanical load is the only way to trigger stalled gains. I don't have proof, only my own experience. I guess the question is, can a guy who lifts no more than 100 pounds to failure, ever get as big as a guy who lifts 200 pounds to failure. Personally I don't think you see a difference until both lifters have many years of lifting under their belts, but once they do, 200 pounds will get you bigger than 100 pounds even when training to failure.



For this we have to start with the fact that data exists showing that 2-3/week leads to faster growth than 1/week. The more time the muscle spends in an anabolic state (producing contractile proteins) the faster it will grow. You will still get RBE liftine once per week, especially since you will likely have to lift harder and longer if you are only training once per week. Total volume is important. So you end up squeezing a week's worth of training into a single session. RBE sets in a the window of anabolic activity following each workout shortens to a number of hours, rather than days. There is good reason to believe that you can grow training a muscle once per week (many lifters use a 3-day 1/week split), and given enough time, its possible they may end up at the same point had they trained more frequently (especially if added hormones are involved).

I hate to go back to anecdotal evidence, but its been my experience that the body is "more comfortable" for lack of a better phrase, with more frequent consistent stimuli than from an occasional highly damaging assault. Remember that protein synthesis only goes towards growth after all damage has been repaired. More frequent, less damaging training is a better way to go in the long term in my opinion.

Cool, awesome info, thanks a ton for that!
Only one thing perplexes me...
If 1x a week induces an RBE would you then need a really long SD to reset? Or would the 2 week SD still 'do the trick'? I was thinking in my mind, if 2 week SD resets RBE enough, then 1x a week training would have almost a 1/2 SD built in since it's a week between sessions, that you'd reset some before you trained again. Does that make sense?

 

[Bryan Haycock]

Rather than thinking of RBE as something you want to avoid, understand that muscle hypertrophy is part of the RBE! Trying to reduce the frequency to reduce RBE is the same as reducing frequency to reduce growth. The muscle grows larger in order to better withstand the stress of resistance exercise. To maximize growth, you must present the muscle with a new environment that is held constant for an adequate amount of time. Then, give it time to fully adapt as far as its going to go before thinking of SD.

 

[NWlifter]

Rather than thinking of RBE as something you want to avoid, understand that muscle hypertrophy is part of the RBE! Trying to reduce the frequency to reduce RBE is the same as reducing frequency to reduce growth. The muscle grows larger in order to better withstand the stress of resistance exercise. To maximize growth, you must present the muscle with a new environment that is held constant for an adequate amount of time. Then, give it time to fully adapt as far as its going to go before thinking of SD.

See, now you went and threw a monkey wrench into my theory lol
OK man... so moreso, exceeding RBE is the key, not avoiding it.

Now I have some killer questions for you, next time you have time (VERY much appreciate your responses when you have time).
* WHAT is RBE? I mean, physically?
* How can an SD 'reset it', yet 'keep' the physical adaptations? Seems like RBE would lower as adaptations regressed? 'What' is reset that leaves the good adaptations but yet lowers RBE making the muscle is more sensitive yet still larger? If RBE is good, and exceeding RBE is good, then resetting it would be regression?

hope that makes sense and you see where I'm struggling on RBE/ SD?

A post by Brad S. on facebook recently struck up some conversation on RBE, so thought I'd post something interesting, someone posted this study.
https://www.ncbi.nlm.nih.gov/pubmed/23372143

mTOR signaling response to resistance exercise is altered by chronic resistance training and detraining in skeletal muscle.
Ogasawara R1, Kobayashi K, Tsutaki A, Lee K, Abe T, Fujita S, Nakazato K, Ishii N.
Author information
Abstract
Resistance training-induced muscle anabolism and subsequent hypertrophy occur most rapidly during the early phase of training and become progressively slower over time. Currently, little is known about the intracellular signaling mechanisms underlying changes in the sensitivity of muscles to training stimuli. We investigated the changes in the exercise-induced phosphorylation of hypertrophic signaling proteins during chronic resistance training and subsequent detraining. Male rats were divided into four groups: 1 bout (1B), 12 bouts (12B), 18 bouts (18B), and detraining (DT). In the DT group, rats were subjected to 12 exercise sessions, detrained for 12 days, and then were subjected to 1 exercise session before being killed. Isometric training consisted of maximum isometric contraction, which was produced by percutaneous electrical stimulation of the gastrocnemius muscle every other day. Muscles were removed 24 h after the final exercise session. Levels of total and phosphorylated p70S6K, 4E-BP1, rpS6, and p90RSK levels were measured, and phosphorylation of p70S6K, rpS6, and p90RSK was elevated in the 1B group compared with control muscle (CON) after acute resistance exercise, whereas repeated bouts of exercise suppressed those phosphorylation in both 12B and 18B groups. Interestingly, these phosphorylation levels were restored after 12 days of detraining in the DT group. On the contrary, phosphorylation of 4E-BP1 was not altered with chronic training and detraining, indicating that, with chronic resistance training, anabolic signaling becomes less sensitive to resistance exercise stimuli but is restored after a short detraining period.

 

[Blade]

Awesome to see Bryan posting here again - long time, no see buddy! And also good to see many of the veterans still active here. I check in from time to time to see if there are any good discussions going, and haven’t been disappointed so far It’s a shame that "everyone" is on Facebook, as it is an extremely poor and messy platform for following discussions and quickly finding information.

Ok, so years have passed since the inception of HST, and it is pretty cool to see that what relevant research has been posted since then have validated the original format again and again.

We now have various studies showing that a rest period of 10 days-3 weeks does indeed resensitize the muscle to a growth stimulus, as per Strategic Deconditioning. What we still don’t know is whether that provides and advantage in the long term, i.e. so far it only seems as if we get "catch-up" growth - so it’s not hurting growth over 3-6 months but it doesn’t seem to provide an advantage either. Well, at least wrt muscle growth - there are obvious benefits when it comes to recovery and connective tissue health - and closing in on 44 years of age I can now say that I regret not following this principle throughout my training career.

We also now have good reason to believe that we can go all the way down into the 40-50% of 1RM range and get significant muscle growth, especially when combined with occlusion - or in my honest opinion, with Myo-reps

At these lighter loads, growth seems to stagnate faster, though - as Bryan also alluded to here - so progressive resistance is essential for any muscle growth beyond 1-2 weeks of this type of training.

The range of 60-80% of 1RM seems to work for much longer, though - so a suggested modification to the original HST format could be to prolong cycles by incrementing every 2-3 workouts instead of every workout. It is still difficult to say exactly how long one could (or should) extend a cycle, given the crude measurement methods we have available (even DEXA is too inaccurate to measure a difference of a few hundred grams of lean tissue growth), but I also think we should consider the connective tissue and joint health - we all know that full-body training 3x/week does take its toll on the body after 8-12 weeks.

Then we have the issue of volume. Bryan’s recommendation of 30 total reps for upper body in someone more advanced make a lot of sense, but there is also good research to suggest that due to the time-tension integral - and the enhanced mechano-transduction at higher relative loads - we can instead provide recommendations for "hard" sets. "Hard" meaning close to - but not necessarily to failure, so the submax periods when working within the next rep range should still be respected IMO.

So I think: 2 sets at 60% of 1RM (15-20 reps) or 1 Myo-rep set = 3 sets of 70-75% of 1RM (10-12 reps) = 4 sets of 80-85% of 1RM (5-8 reps).

This is also a conservative estimate given that 6 sets of 5 reps in a full-body workout 3x/week would for sure kill me, too

Keeping the stimulus "pure" also seems to make sense, and although there are a couple of cool studies where adding a high rep set either right before or right after heavy sets increase hypertrophy - this could simply be temporary swelling or caused by the added volume (since the groups weren’t volume matched).

I have a feeling that heavy, low-rep training provides a type of deconditioning and resensitizing effect to high-rep metabolic work, so not having the dropsets during the 5s phase makes sense from that perspective. Then you go into SD followed by high rep training and this deconditions the tissue to the heavy, low-rep training.

And the cycle repeats.

Also, considering the increased connective tissue stress at heavier loads - one *could* make a case for reducing frequency when you get to 5s - but as Bryan said, but I also think that reducing volume will take care of most of that.

Another thing to consider for advanced lifters is to start figuring out individual volume per muscle group, where some muscle groups and lifts just seem to respond better to higher reps and/or volumes, and vice versa.

Example, which I thought was pretty cool, was this study showing how higher volume/lower intensity leg training improved upper body gains:
https://www.ncbi.nlm.nih.gov/pubmed/29257792

This was also suggested in this article, although I don’t agree with everything the author said it is still food for thought that resonated with my own experience:
https://www.t-nation.com/training/the-best-training-split-youve-never-tried