max-stimulation hypertrophy routine

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dont know if anyone has tried this but it has been developed by dan moore,through exstensive hypertrophy research.i can try and get a pdf up if i can download it but this explains alot.
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The goals are several fold but overall it's a means of increasing work while managing acute fatigue.

The trick is allowing M-Time to do it's purpose and not worry about if it's 2 secs or 30 secs, use whatever is needed to complete another repetition.

A quick test is take your known 8-10RM in a dumbell curl, load it on a DB and with your strongest arm do however many reps to failure you can, (should be around 8-10 reps or it's not your 8-10 RM) then with the other arm do a rep, set the DB down for a few seconds (taken completely out of your hands), do another, set it down, repeat adding a few seconds when needed to complete another rep. If you get to 30 secs in between reps and reach failure, how many reps where you able to perform?

The beuty is instead of increasing reps you should be able to substantially increase the load while maintaining the same number of reps throughout the entire cycle.

The Routine
M-Time – The Max Factor



M-Time is the time between each rep, after each rep the weight should be racked or set down and gotten completely out of your hands for the duration of the M-Time. This time can be manipulated as advancing fatigue ensues, IE first few reps use 3-5 seconds, next 5 to 10 - use 7 seconds, during the last 5 use 10 seconds. The starting time is usually going to be dictated by your own recovery from repetitive contractions and the intensity you are using. As the cycle progresses the M-Time may need to be increased to combat the effects of fatigue from heavier loading. The ideal starting time will vary and some experimentation will probably be needed to find the adequate time to use. In any case the M-Time should be used from the very first rep.

Frequency



As we’ve mentioned in the previous chapter once per week isn’t going to cut it when you are trying to build as much muscle tissue in the shortest amount of time possible. With that said the workout is set up in an alternating workout fashion, A&B routines, they are both full body workouts but may be split to upper/lower, push/pull or whatever you deem necessary to fit into your training schedule.



Each Body part should be hit at least 2 times per week with at least 1 set of the primary movement and if needed 1 set of the secondary.



A typical implementation would be-



Monday and Thursday A routine,

Tuesday and Friday B routine, this can be arranged in any fashion depending on your training level or schedule.



Other examples;

3X week

Week 1

Monday-A

Wends-B

Fri-A

Week 2

Monday-B

Wends-A

Fri-B



2X week

Monday-A

Thursday-B


Rep Cadence and Tempo



Each Compound movement IE the first movement for each exercise should have a cadence of as fast as possible concentric, a controlled eccentric. After each complete rep is performed the weight should be racked for the M-Time being used. (see M-Time above)



Each isolation or subsequent movement (if chosen to do so) should be performed with as fast as possible concentric and a controlled eccentric. Again after each rep the weight should be racked for the M-time being used.


Rest Between Sets



If choosing to do multiple sets, I only recommend one, the rest between sets should allow for enough strength recovery to successfully complete at least 80% of the same number of reps as the previous set.



Working in a circuit fashion may be advantageous as this may allow enough time between sets but if working in a gym where equipment availability is an issue then simply use a rest period as described in the previous paragraph.


Bicep and Tricep Work



Although direct bicep and tricep work may not be necessary since many of the pulling and pushing movements already activate these muscles many trainees simply can not have a successful workout without the addition of direct upper arm work. With this in mind you may add in any of your favorite bi and or tri work but I do not recommend doing this more than 1 or 2X week and I recommend the volume be kept low for each workout these are used. If you do I also recommend you use the same set up, a compound followed by an isolation exercise that concentrates on stretch, racking the weight between reps.



Bicep Recommendation-following your last set of Back exercises add 1 or 2 sets of incline DB curl, concentration curl, BB curl or whatever isolation exercise you choose to use.



Tricep Recommendation-following your last pressing/pushing movement for chest or shoulders add 1 or 2 sets of Tricep Extensions, pushdowns or whatever isolation exercise you choose to use.


Muscle Specific



This setup may also be used in conjunction with any individual muscle group in order to specifically induce growth to lagging muscle groups or address symmetry issues.


Progression and starting intensity.



The progression is set up in an undulating linear fashion. There are 3 phases to this program.



Phase 1- Using your 10 RM load 4 workouts per week

Phase 2- Using your 8 RM load 4 workouts per week

Phase 3- Using your 6 RM load 4 workouts per week



Each phase starts out at 75% of the RM for that phase and increases over the duration to a maximum of 110% of the RM.



Example.

10RM load = 100 lbs

Week 1

Workout 1, A routine- 20 Reps –75 lbs.

M-Time- 1 sec. Or whatever is needed to complete 20 reps without achieving any significant burn.

Workout 2, B routine- 20 reps –75 lbs.

M-Time- 1 sec. Or whatever is needed to complete 20 reps without achieving any significant burn.



Workout 3, A routine-20 reps – 80 Lbs

M-Time- 2 sec. Or whatever is needed to complete 20 reps without achieving any significant burn.

Workout 4, B routine- 20 reps –80 lbs.

M-Time- 2 sec. Or whatever is needed to complete 20 reps without achieving any significant burn.



Week 2

Workout 5, A routine-20 reps – 85 Lbs

M-Time- 3 sec. Or whatever is needed to complete 20 reps without achieving any significant burn.

Workout 6, B routine- 20 reps –85 lbs.

M-Time- 3 sec. Or whatever is needed to complete 20 reps without achieving any significant burn.



Workout 7, A routine-20 reps – 90 Lbs

M-Time- 4 sec. Or whatever is needed to complete 20 reps without achieving any significant burn.

Workout 8, B routine- 20 reps –90 lbs.

M-Time- 4 sec. Or whatever is needed to complete 20 reps without achieving any significant burn.



Week 3

Workout 9, A routine-20 reps – 95 Lbs

M-Time- 3 sec. Or whatever is needed to complete 20 reps without achieving any significant burn.

Workout 10, B routine- 20 reps –95 lbs.

M-Time- 3 sec. Or whatever is needed to complete 20 reps without achieving any significant burn.



Workout 11, A routine-20 reps – 100 Lbs

M-Time- 4 sec. Or whatever is needed to complete 20 reps without achieving any significant burn.

Workout 12, B routine- 20 reps –100 lbs.

M-Time- 4 sec. Or whatever is needed to complete 20 reps without achieving any significant burn.



Week 4

Workout 13, A routine-20 reps – 105 Lbs

M-Time- 5 sec. Or whatever is needed to complete 20 reps without achieving any significant burn.

Workout 14, B routine- 20 reps –105 lbs.

M-Time- 5 sec. Or whatever is needed to complete 20 reps without achieving any significant burn.



Workout 15, A routine-20 reps – 110 Lbs

M-Time- 6 sec. Or whatever is needed to complete 20 reps without achieving any significant burn.

Workout 16, B routine- 20 reps –110 lbs.

M-Time- 6 sec. Or whatever is needed to complete 20 reps without achieving any significant burn.



For planning your routine please download the Excel Spreadsheet here



Increasing the reps-The system is based on 20 reps throughout the cycle. This can be changed if desired. However I do recommend trying to stick to at least 15- 20 reps as it allows sufficient TUT and it is much easier than trying to identify varying reps when fatigue is manipulated in this way.



Decreasing the duration- to decrease the duration from 12 weeks to fewer simply remove the duplicate intensity workouts IE each or every other workout would increase in intensity.


Work Out A

Follow the Exercise order, thigh and calf work may be put last if you prefer

Thighs-

Squat or Leg Press

Super set with Leg Ext or Sissy Squat (if desired)

Leg Curl

Super Set with SLDL or Good Morning (if desired)

Calves-

Standing Calve Raise

Superset with Donkey Calve Raise on Blocks (if desired)

Back-

Wide Grip Pronated Pull Up/Down

Bent BB Row to Bottom of Rib Cage or similar

Chest-

Flat Bench BB/Dips or DB Bench Press

Superset with Fly (if desired)

Shoulder-

Military Press or Shoulder DB Press

Superset with DB Incline Lateral Raise (if desired)

Traps, Rear Deltoid-

BB Laying Chin Row or Seated High Row

Superset with Prone or Bent Shoulder Lateral (if desired)


Workout B

Thigh-

Squat or Leg Press

Super set with Leg Ext or Sissy Squat (if desired)

Leg Curl

Super Set with SLDL or Good Morning (if desired)

Calves-

Standing Calve Raise

Superset with Donkey Calve Raise on Blocks (if desired)

Back-

Narrow Grip Supinated Pull Up/Down

Bent BB Row narrow grip to beltline

Chest-

20 Degree BB or DB Bench Press

Superset with Incline Fly (if desired)

Shoulder-

Primary-Upright Row

Secondary-Superset with Upright Lateral Raise (if desired)

Traps, Rear Deltoid-

DB or BB Shrugs Seated or Standing

Superset with Laying or Bent Shoulder Lateral (if desired)



If knees, shoulders or back is of concern then substitution of exercises can be done as long as plane of movement and degree of stretch is relatively equal for the substitutions. Whether done on free weight or machine should not make a difference. Machines will make this program inherently easier as the racking movement is already accommodated for in most machines. When substituting exercises always keep safety as your top priority.
 
interesting concept. I have been wondering about this myself in the past. You're basically doing rest pause sets on every set? Do you have to use your 10RM? Would be cool to try this on the bench press, loading it up with something like your 3RM and get maybe like 6-8 reps out of it.. I think I'm gonna try that on one of my bench press days.
 
Yea it's interesting stuff. I need to stop living in my comfort zone and actually try something new like this!

Or like kark said, it would be interesting on say the bench press.
 
Karky said:
interesting concept. I have been wondering about this myself in the past. You're basically doing rest pause sets on every set? Do you have to use your 10RM? Would be cool to try this on the bench press, loading it up with something like your 3RM and get maybe like 6-8 reps out of it.. I think I'm gonna try that on one of my bench press days.
Click to expand...

actualy karky 3reps is the maximum recomended to go,any less than that and it isnt managing fatigue enough,but guys who have done it for a long period have actualy done there three rep max for 20 reps.
you start of on 10rm untill you reach 20reps then increase the load untill you reach you 5rm or 3rm for 20 reps.
some guys just do it for one bodypart as you suggested,if your on a platue on bench its a great way of pushing your strength up on that,but some guys have done fullbody workouts using this method,coach hale who has his own site has used it on some of his athletes,he posted a thread on it if i can find it i'll post it on here.
 
posted by coach hale

recently advised one of my female clients to use Max-stim. So her boyfriend decided to try it also. Her boyfriend is Steve Maxwell
Bjj black belt, Kettlebell instructor, author and sprorts conditioning coach. Maxwell and I ate dinner together in April and we had an in-depth discussion about the Max-stim protocol. He was very pleased to find something that increased his strength levels especially after training over thirty years. Steve's report on MaxStim appears below:

I placed 5 people on MaxStim protocol.

I saw the biggest results with the Chin-Up.
One, a middle-aged guy (mid 50's) (John) went from 4 reps to 12 reps. Another (mid 30's) (Chris) could get 5 reps. He went up to 15 reps One woman (T) averaged 3-4 reps and now gets 6. Tommy went from 7 reps to 12-13 reps

I see the Chin-Up as a de facto body composition machine and the ultimate upper body strength-to-weight ratio test, ie.,you are greatly penalized for carrying any excess body fat and greatly rewarded for extra upper body muscle mass and low body fat levels.

It's impossible to pull your body weight up without greatly improved upper body composition changes.

Everyone who followed the MaxStim protocol significantly increased upper body strength-to-weight pulling ability and reported feeling "energized", "energetic", and overall "good" from their workouts.

Other exercises performed on the MaxStim protocol were:

Military Press
Dip
Deadlift--both Sumo and regular
Dbl KB Front Squat
In their weekly training logs, everyone reported significant strength increases in all exercises.
The exercise I was most interested in and therefore, I most closely monitored, was Chin-Up ability, because everyone in this particular group was Pull-Up challenged.

I was unable to produce results in one additional individual but I chalk that up to a case of overtraining, as he was on a very high-volume program over 9 months or so in prep for a 2-week strength-endurance test.

Because I couldn't monitor each individual's form, particularly the weight-training exercises, the Pull-Up data is most reliable because after close questioning, I was satisfied everyone was going from dead-hang to throat-over-the-bar and I'm confident MaxStim increases pulling strength-to-weight ratio in the upper body.

There were 3 additional people reporting positive results with MaxStim as far as feeling "good" and improved body composition, but because they don't routinely turn in training logs and rep counts, I can only go with their subjective comments.


I have personally had great results with MS and most of my clients have also reported benefits. I think I have had only 1-2 clients that didn't seem to reap the rewards and they really didn't follow the protocol as was suggested.

thanks,
Coach Hale
 
this is the pdf it explains the science of it and everything else hope it downloads ok
 
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I actually tried this yesterday on front squats and bench. I waited for a count of 6 (probably around 6 secs) on the front squats I used 105kg and got 6 reps on the first set and 5 on the next.. it was weird, as I have done that without the resting before.

On the bench press I also used 100kg, which is something around my 3-5 RM (for those following my log, I'm at a different gym now, the benches are lower so my RM goes down for the bench) I got 3 reps, then I tried a straight set, and I got 3 reps way easier. It was weird. I figured maybe I lost my set up and tightness while laying there counting to 6, so I did another one where I sat up, counted to 10 and layed back down again and set up all over, again it was worse! It was really weird.

I'm gonna try it with the chins next time. I'm thinking that for the front squats, just walking the weight in and out takes some energy, then you gotta set up with your foot positioning, etc, I think all that just makes you tired so the extra few seconds of rest is not worth it. For the bench press, the whole set up thing and unracking is kind of demanding aswell.

I'll let you know how it goes for pullups or chins on friday!
 
your starting of to heavy,you should start with your 10rm and do 1x20 then build it up every wk,,one set should be enough especialy when you get to the 5s 3s etc.
it helps if you have a partner also but deadlifts leg-press etc are easy enough.
 
I know, but 10RM if way too light for me, I wanted to try this strength wise to see what happened. It's still kinda weird that I get more tired from the resting..
 
10rm might be light if your only doing 10 but if your doing 20 thats different,also basicly its a hypertrophy routine so a gradual progression is needed,but it has shown great results for strength,the thing is you cant rush it.
 
I don't mean light like not challenging, I just like doing lower reps. And I get that the routine says 10RM and 20 reps. What I usually do when I see stuff like this is that I take the idea and adapt it to myself. He says resting for 5 sec between reps on 10RM, I think "why not try it with a 3RM?".. I just find it weird that it didn't work. Anyways, I'll be trying with BW pullups on friday, I can do about 10 reps of BW pullups, so it should be interesting to see. I bet I'll get a lot of reps with pullups, since the first rep of every set is usually dead easy, but then I get tired fast because of stability issues. If I hit the floor between each rep, I don't have to control my body's swing so much.
 
the science behind it.

Introduction

"cheat fatigue, enhance strain, increase the translational response to weight training and grow"

Have you ever wondered how you can increase your growth?

Do you want to lift heavy but can't get enough reps in?

Now you can, Max-Stimulation is a developed training system that can be easily incorporated into your existing routine, used exclusively or used just for lagging body parts. The immediate effects are decreased fatigue, increased Time Under Tension and the ability to work with heavier loads.

There are no supplements to buy, tricks or gimmicks just a simple way of manipulating the bodies fatigue response to repetitive high force contractions.

What I present is a unique method for combating the inhibitory signals that accompany highly energetic workouts starting with a brief review of the science and a subsequent training system that can be utilized no matter the current level of your training expertise.

Daniel Moore
Founder and Creator of Hypertrophy-Research.com and now presenting Max-Stimulation.


The Science

When I first decided to write about this method one of the particpants trying it asked me "Dan, what's there to write about? I mean I don't think anyone needs an instruction manual to do this, it's so simple"

Well he is definitely correct, it is simple but the reason it works is much more complicated.

Science has made some decent progress in identifying what may and I stress, may, be occuring during skeletal muscle hypertrophy and it's causes. Even though there are gaps in the total process, the foundations appear to be rather solid. It is these foundations that I will briefly touch on over the next few pages.


Translation, Protein Synthesis and Hypertrophy


Increases in skeletal muscle mass are mediated via protein turnover, the balance between protein synthesis and protein breakdown also known as "protein accretion" (1).

There are many controls that govern changes in protein synthesis and eventual gain in muscle mass.

Incorporation of both transcriptional and translational inputs can influence the protein synthetic rate (2). Generally, alterations in protein synthesis associated with altered gene transcription generally occur over a period of days to weeks (3), whereas increased mRNA translation (i.e. the process of synthesizing a protein based on the information encoded by the mRNA) can be manifested within minutes to hours (4).

Transcription and translation each contain three distinct steps (initiation, elongation, termination) with the predominant influence belonging to the initiation phase (5,6). However, translation is different and unique because mRNA is summoned and recruited rather than produced and this process is responsive to acute mechanical, metabolic, nutritional alterations (7).

Translation initiation essentially revolves around two main components mediated by eukaryotic initiation factors (eIFs) that control protein synthesis rate-limiting events. The first of the two components allows the ribosome to bind to the mRNA (eIF4F complex), the second brings the ribosome to the site on the mRNA where translation begins (eIF2/eIF2B). An essential mechanism for regulating growth within translation initiation involves the mammalian ‘target of rapamycin’ (mTOR) protein. Two common downstream targets of mTOR are the 70-kDa ribosomal proteins S6 kinase (S6K1) and the eIF4E-binding protein-1 (4E-BP1)(8).






A common misconception regarding changes in translation initiation is that activation of any protein in this pathway corresponds with increases in protein synthesis. For our purposes, after resistance exercise, elevations in protein synthesis have shown to be delayed for several hours yet mTOR controlled events can be rapidly upregulated during this very same period (9). Later, increases in protein synthesis appear to coincide with eIF2B changes (10). It’s becoming indisputable that chronic mTOR signalling is very valuable for increasing cell size and therefore increased muscle mass as blocking this pathway almost completely blocks the response (11). The downstream mTOR target, S6K1, strongly linked with muscle hypertrophy (12), is also crucial.

Currently it is safe to propose that both components of translation initiation are essential to increased muscle mass. Events linked with eIF2B regulation appear to regulate the acute changes in protein synthesis following resistance exercise, whereas activation of mTOR/4E-BP1/S6K1 pathways appears to result in synthesis of proteins necessary to "enhance" the translational process, creating an optimal environment for increases in translational capacity and hence the capacity for protein synthesis with long-term training.

Chronic vs. Acute-Once is not enough


Recent studies designed to better understand the regulation of translation initiation show us that following an acute bout of resistance exercise distinct eIF proteins are rapidly phosphorylated (13). Intermittent and transient activation of these proteins may provide better control for the modulation of a growth response. Or simply, the responses appear to be temporal and the acute impact of resistance exercise on mRNA translation likely becomes cumulative with each successive bout performed; it therefore appears that this pathway is intermittently turned on with repetitive resistance exercise and distinct mRNAs (ribosomal proteins, etc.) may accumulate to a point where an increase in the amount of specific proteins occurs (14). These responses highlight the chronic and acute more rapid control mechanisms associated with transcription and translation, that contribute to achieving muscle hypertrophy (Fig. 2).



Figure 2

Contractions, Stretch and Strain-Negatives vs. Positives, how about both


Over time the world of body building has seen many routines come and go and all had their own dogma on how to perform the reps. Many have touted slow or fast reps, full or diminished range of motion, static or isotonic. But again there was some commonality in them all, strain. It has been shown that strain is a potent stimulator of hypertrophy (15).

What hasn’t been so pronounced is which mode of contraction produces the most hypertrophic response (16-20). The debate still rages as to whether eccentrics (negatives) are better, worse or the same as concentric (positives).

What can be seen is that the issue of contraction mode isn’t much of an issue at all. Most human in vivo movement uses both and resistance training is the same. We raise the weight, we lower the weight, we do it again. Lending the tissue to the extremes of both contraction modes. The extent of muscle fiber strain is dependant on the compliance of the series elastic elements that not only tie the muscle fibers to our bones but also hold the fibers in their respective place. These elastic series elements take a large amount of force before stretching to a point where the force is then transmitted to the fibers themselves. What this means to a person moving an object is; even when stretching the entire muscle tendon complex the degree of stretch needed before actual strain is felt on the fiber depends on many things but there is hope. Looking into the mechanics of muscle tendon units (21) it’s been seen that two things predominantly affect the level of fiber strain, the length of the muscle when the stretch shortening begins and the number of stretch shortening cycles themselves.

If a muscle is pre-stretched in vivo the series elastic elements are already stretched and become stiffened, allowing a greater amount of force to be directly applied to the fiber. Using the other means it’s apparent that repetitive stretch shortening cycles stiffen the series elastic elements as well, again allowing more force to be directly applied to the muscle fibers (22).

How this ties into translation is two fold.

Fiber strain acts on the Mechanotransduction (23) mechanisms within the cell itself. This is a term used which denotes the bodies ability to turn a mechanical signal into a chemical signal. When cells are stretched the stretch is picked up by a couple notable elements. One of these is the Focal Adhesion Complex (24). The FAC, as it’s known, are sites where the extracellular matrix is physically coupled to the cytoskeleton within the cell. In skeletal muscle FAC can be found at the myotendinous junctions, neuromuscular junctions and in structures that lie above the z-bands named costameres. The FAC are protein dense regions and most of the molecules in the FA contain multiple domains that can interact with a variety of molecular partners. One of the major constituents of the FA is the family of cell surface receptors termed integrins (24). As the cell wall is stretched these integrins then transmit the stretch to the cell nucleus, which in turn up-regulates or down-regulates translational mechanisms. Another stretch sensor is the Stretch Activated Channel (25) or SAC. As a cell is stretched these channels are opened allowing ion flow in or out of the cell, the increased flux of ions can then increase translation items relevant to protein synthesis, metabolism or other cellular functions.

Much of the work on translational events revolved around the autocrine and or paracrine release of growth factors. It is proposed that the PI3K/Akt-1 pathway and subsequent mTOR pathway was dependant on the growth factor input. However it’s been shown (26) that mechanical stimuli are indeed similar to growth factors in that they require signalling through both PI3K and mTOR to promote an increase in protein synthesis but, unlike growth factors, mechanical stimuli activate mTOR-dependent signalling events through a PI3K/Akt1-independent mechanism and the release of locally acting factors is not needed for the induction of this pathway. Since PI3K is indispensable for growth factor-based signalling through mTOR, it appears that mechanical stimuli and growth factors provide their own distinct inputs through which mTOR co-ordinates an increase in the translational upregulation and efficiency.

Amino Acids-The building blocks


Over the last 25 years numerous studies on protein metabolism involving oxidation, synthesis and breakdown have been performed (27). It’s is this body of evidence that makes it abundantly clear that amino acids are a critical component to building muscle mass. It’s also become convincingly clear that the exogenous amounts of available AA are critical to signalling chains (28). Of the EAA’s made available through the infusion or oral dosing studies, the importance of the Branch Chain Amino Acid Leucine is coming to the forefront (29-31). Not so much in its role during energy expenditure but because of it’s prominence in signalling anabolic translational events leading to increased protein synthesis (32).

Leucine’s effect on protein synthesis is controlled through upregulation of the initiation of mRNA translation. As in the case of mechanical stimulation a number of differing mechanisms, including phosphorylation of ribosomal protein S6K, eIF4E BP1, and eIF4G, contribute to the effect of leucine on translation initiation. These mechanisms not only promote global translation of mRNA but also contribute to processes that mediate the selection of mRNA for translation. MTOR again is a key component in a signaling pathway controlling these phosphorylation-induced mechanisms. The activity of mTOR toward downstream targets is controlled in part through its interaction with the regulatory-associated protein of mTOR (known as raptor) and the G protein b-subunit-like protein. Upstream members of the pathway such as Rheb, a GTPase that activates mTOR, and TSC1 and 2, also known as hamartin and tuberin respectively, also control signaling through mTOR.

Let's move on and look at what inhibitors alter this process.

Inhibitory Signalling
With the advent of newer research putting light on the known mTOR/S6 chain it is becoming more and more clear that the AKT/mTOR/EIF4 chain is a very important regulatory mechanism in muscle growth (33). As with all signal chains in the human body there are signals that also combat the actions. Hypertrophy and increased protein synthesis via increased translation is no different.
 
The Switch
It has been noted by many researchers that protein synthesis does not occur for several hours after the exercise is completed (34-36). Recent work (37) has identified one possible mechanism that can be the cause. Called the “AMPK-AKT” switch (37), this switching of translational events leading to protein synthesis can be seen during the difference in exercise mode. Long duration endurance type activity causes increased activity in AMPK (5'AMP-activated protein kinase) this kinase then turns on events that switches off events that use ATP for anything other than fuel replenishment inside the cell, including the mTOR activated protein synthesis chain.

AMPK is another member of the heterotrimeric serine/threonine protein kinase. AMPK is composed of a catalytic alpha subunit and non-catalytic beta and gamma subunits (38, 39). The mammalian genome contains seven AMPK genes encoding two alpha, two beta, and three gamma isoforms. AMPK signaling is elicited by cellular stresses that deplete ATP (and consequently elevate AMP), the AMP/ATP ratio, by either inhibiting ATP or accelerating ATP consumption. Although AMP is produced in several cellular reactions, it most importantly appears to be the adenylate kinase reaction: 2ADP <> ATP + AMP. In healthy, resting muscle the ATP:ADP ratio is maintained at a high level, and therefore AMP is very low. However, if the cell experiences a stress that depletes ATP, the ATP:ADP ratio will fall (analogous to the battery becoming discharged), and a large increase in AMP will follow. These are exactly the conditions in which AMPK is activated.

Treatments that activate AMPK can either be stresses that interfere with ATP production, such as heat shock, metabolic poisons, glucose deprivation, hypoxia, or ischaemia (40,41) or stresses that increase ATP consumption, such as exercise in skeletal muscle (42). These findings led to the concept that the AMPK system acted as a “fuel gauge” or “cellular energy sensor” (41). This concept was reinforced by findings that AMPK was allosterically inhibited by physiologically adequate concentrations of phosphocreatine (43).

It has been shown that AMPK is a central mediator of insulin-independent glucose transport, which enables fuel-depleted muscle cells to take up glucose for ATP regeneration under conditions of metabolic stress (40). When rat epitrochlearis muscles were isolated and incubated in vitro under conditions that evoke metabolic stress accompanied by intracellular fuel depletion, rates of glucose transport in the isolated muscles were increased by all of these conditions, contraction (5-fold above basal), hypoxia (8-fold), and hyperosmolarity (8-fold) Fig. 3. All of these simultaneously increased both isoforms of AMPK, alpha1 and 2. There was close correlation between alpha1 and alpha2 AMPK activities and the rate of glucose transport, irrespective of the metabolic stress used, all of which compromised muscle fuel status as judged by ATP, phosphocreatine, and glycogen content.


Fig. 3 The fold increase in AMPK during differing metabolic stress

Fatigue-The TUT party crasher
During contractions, whether sustained static or repeated dynamic a big influence over the duration or number of contractions performed is fatigue. The overall cause of fatigue is still being debated as its effects on contraction are so pronounced in varying systems and no single consensus has been defined.

Muscle contraction increases muscle metabolism by an order of magnitude (44), this magnitude is influenced by type, intensity, duration and frequency of contraction and the fatigue rate in muscle falls in line with this magnitude. It has long been realized that the metabolic cost of muscle activation is a primary factor in fatigue (45), not necessarily the only factor but the buildup of metabolic byproducts (46-48) and depletion of substrate (49) have a large part to play. The results of many metabolic studies do not demonstrate, with any consistency, that it’s a matter of only one metabolite being the cause of fatigue, but they do show that several substances can alter force generation under varying conditions (50-52). In further support of a metabolic basis for fatigue, several studies have demonstrated that during short-duration, high-intensity exercise (both voluntary contraction and electrically evoked contraction), protocols that produce the greatest metabolic change also produce the greatest fatigue (53-57), although other factors, such as activation failure, are likely to be involved in the decline in force (58), but this factor goes far beyond the scope and intent of this brief.

The metabolic demand of muscle contraction is associated with the ATP hydrolysis occurring at three ATPases: 1) the sodium/potassium (Na+/K+) ATPase associated with maintaining the resting membrane potential of the sarcolemma, 2) the actin myosin (AM) ATPase associated with cross-bridge cycling and force production, and 3) the sarcoplasmic reticulum (SR) Ca2+ ATPase associated with Ca2+ reuptake at the SR.
The demand of the AM-ATPase is related to the force produced by a muscle (59), as ATP consumption increases proportionately with force during voluntary contractions. ATPase activity, however, is lower in fibers that have been chemically skinned to remove the SR, this eliminates the metabolic demand associated with the SR Ca2+ ATPase. This coincides with findings suggesting that between 20 and 40% of the ATP hydrolysis that occurs with muscle contraction is thought to result from noncontractile (i.e., non AM ATPase) ATPase activity (60). This indicates that with repeated contractions the ATP used for all three ATPases would be higher than what is seen during isometric exercises. The increased ATPase activity indicates that during repetitive contractions AMPK activity would also be higher especially if the AMP/ATP ratio is severely affected.

Now that we’ve reviewed how the metabolic fatigue induced during repetitive contractions can cause a diminished response through the AMPK-AKT switching event, lets look into how the lactic acid burn and the pump can also affect it through increased acidosis, hypoxia and hyperosmolarity.


Blood Flow and it’s Effects

Adequate perfusion, blood flow across the tissue bed, is vital to the health and proper functioning of skeletal muscle. In healthy tissue, the metabolic demands of the muscle will largely determine the degree of its perfusion. While blood flow through the arteries is important in determining how much blood can reach the muscle, the amount of blood that enters the muscle bed via the micro-vasculature will determine the degree of gas and nutrient exchange, profoundly impacting the contractile state of the tissue.

Blood flow during resistance exercise highly oscillates due to the high intra-muscular pressures that are generated during contractions. High intra-muscular pressures impede (occlude) muscle blood flow, with the result that blood flow approaches zero during contractions but is greatly elevated after contractions (62,63).

The extent of temporary occlusion is directly proportional to the intensity of contraction and this continues to about 60% MVC (64). At this point the muscle blood flow becomes completely occluded and remains occluded for the duration of the contraction phase regardless of any further increases of force (65,66).

The ischaemia that occurs during the occluded state causes an increase in non-oxidative metabolism via hypoxia a.k.a. ischeamic hypoxia (67). Hypoxia is a condition of lessened oxygenation. The reduced blood flow during ischaemia does not allow the blood to circulate and therefore it does not re-oxygenate.

Interestingly this is true also when contraction frequency is increased, or the contractions retain sufficient tension for a prolonged period. The expansion of the muscle blood volume, as contraction frequency increases, is a result of the muscle vascular bed being expanded by vasodilator processes that occur with an increased metabolic rate, and occurs even though the time between contractions (“filling” time) is decreased (68). One of the more interesting observations seen is that the volume of blood contained in the muscle is greater during these states. A greater volume of blood contained in the muscle allows for a greater ejection of blood for a given contraction during the relaxation phase. In the case of prolonged tension or insufficient relaxation times the pooling that occurs interferes with nutrient and gas exchange.

All of these blood flow responses to contraction have an impact on the internal environment and metabolic state of the muscle. Every time ATP is broken down to form ADP and Pi, a proton is released. When the ATP demand of muscle contraction is met by mitochondrial respiration, IE oxidative metabolism, there is no proton accumulation in the cell, as protons are used by the mitochondria for oxidative phosphorylation. When the exercise intensity increases beyond steady state or there is a reduction in oxygen availability that there is a need for greater reliance on ATP regeneration from glycolysis and the phosphagen system (69). The ATP that is supplied from these non-mitochondrial sources is eventually used to fuel muscle contraction, which increases proton release and causes the acidosis that accompanies intense exercise. Lactate production increases under these cellular conditions to prevent Pyruvate accumulation and supply the NAD + needed for the second phase of glycolysis. Thus increased lactate production coincides with cellular acidosis.

Secondarily to the energetic effects are the cross sectional area changes that occur within the cell itself. The shifting of water and pooling of blood is what is commonly referred too as the “pumped” look. Increased perfusion directly increases muscle CSA. Edema, water shifting caused by hyperosmolarity and fluid pressures can also cause this temporary increase (70-72).

The human body is composed of 50-60% water, which corresponds to ~70% of lean body mass being water. Skeletal muscle amounts to ~40% of body weight, of which in the resting state 75% is water, accounting for around one-half the body water. The distribution of total muscle water in muscle at rest is ~90% cellular, ~9% in interstitial spaces, and ~1% in plasma.

The fluid distribution volumes are substantially changed during muscular activity. During exercise, there is an acute uptakeof fluid by the active muscle cells; hyperosmolarity is one mechanism that explains this shift.

Some of the osmolytes that may be responsible for this are lactate, potassium, sodium and chloride (73). Another osmolyte that appears to have a profound effect on cellular volume is CrP (Creatinephosphate) (74). During exercise CrP is broken down to 1 mol of Creatine and 1 mol of inorganic Phosphate, the new steady state level effect on osmolality of this breakdown may be considerable causing increased water shifting to occur (75).

Now that we have gone through several mechanisms that can contribute to the inhibitory signalling during resistance training let’s begin to peace it together and knit a plan of action to counter or at least diminish the effect.
Applying the Science

M-Time-Making fatigue look retarded


When I first began reviewing the translational mechanisms involved in hypertrophy my beliefs were pretty well in line with the norm. Do a set, rest, do another, rest, this has been established as the way to not only provide enough work but also provide enough metabolic influence to increase the metabolic signalling chain as well.
 
During all my research it’s rare to see human studies that tried to actually manipulate fatigue and strain in any way except for the conventional set/rest scheme. Although some bodybuilders have used anecdotal variations of a rep/rest scheme most of these revolved around either increasing the inroad to fatigue via continuation of a set after substantial fatigue or in the case of competitive lifters, the use of singles for neural conditioning and surpassing plateaus in strength.

Not that there is anything wrong with either of these situations but in essence they are not aimed at reducing the inhibitory effects of fatigue on force and subsequently strain or the inhibitory effects of increased AMPK elevations (76).

It wasn’t until I was reading a study I referred too in the contraction section dealing with strain by Butterfield and Herzog that I began to piece it together.

Delving into many studies that manipulated the time between reps to see how this influenced many signalling events and the force fatigue relationship. Several studies on rats by Booth and Wong, the group of Farrell, Kubica, Jefferson and Kimball gave me the information I was looking for (77-81).

Looking further on force reduction and fatigue I also began to see a pattern where AMPK and energetics where strictly tied (82). A drastic reduction in metabolites, mostly revolving around the phosphagen system, caused a dramatic elevation in AMPK and tying that to the earlier work I saw on hypertrophy and protein synthesis I began to see more than just a casual relationship emerge.

Taking into account that any type of repetitive contractions have a larger influence on energy metabolism and that increasing the intensity only compounds this, I tried a very simple experiment.

In my weak arm I used my known 8-10RM during dumb bell curls and used a 5 second rest between each rep (what I have termed M-Time), one where I tried to remove all tension by setting the weight down after each dumb bell curl, just to make sure there was no occlusionary effect by holding onto the weight. In my strong arm I used a conventional set of my 8-10 RM to failure. I was astonished when I finally stopped doing reps in my weak arm after the 20th rep, yes 20 reps with my 8-10 RM. I was amazed and suffice it to say my strong arm failed on cue, right on the 10th rep and I mean failed, no way could I have gotten another rep. Others who have participated in this experiment experienced similar or even more extraordinary results. One participant actually achieved 42 reps before hitting failure when using M-Time reps with his know 8RM.

For any readers who are reading this for the first time and would like to try a simple experiment then follow what I have mentioned above, try it and see for yourself how this can dramatically change your training.

Progressive Work Overload-Getting it done


Secondly much of my research has shown or actually proven what several well-known trainers, have said now for some time. In order to grow one must progressively increase the work that the muscle has been subjected too. Now since work is a product of load and distance moved, in our case reps, how we increase work is important. Increasing work via increasing the load has shown dramatic results in not only protein synthesis but also hypertrophy (77-81), yet increasing the number of reps has a much larger influence on the metabolic efficiency of the muscle cell. When trying to accommodate this into this training method this simplest solution is to keep a consistent number of reps throughout the entire cycle while periodically increasing the load.

Contraction Mode


Much has been said about which contraction mode (eccentric or concentric) contributes more to hypertrophy and even though I am mentioning this in this book I am not going to go into great detail. Suffice it to say that even though eccentrics appear to cause more micro trauma than concentrics the most important aspect of training is progressing the work via mechanisms I alluded to above. In the case of this book eccentrics may not be necessary as we will be able to increase the work with heavy enough loads that continually increase the translation efficiency, which is truly the most critical event in hypertrophy of skeletal muscle.
 
So he is basically saying not to let lactate build up, PC to deplete, etc, as all that causes an increase in AMPK, which inhibits protein synthesis? But AMPK inhibits synthesis during training to allow the muscle to focus on training, after training, protein synthesis goes up.

Also, what about the increases in growth factors seen with fatiguing training? (with high lactate buildup, etc)

It was a very interesting read, I just don't know if there really is a big point to reducing AMPK activation during training. Also, isn't activation of AMPK thought to contribute to benificial processes that cause muscle growth?
 
did you get the pdf download ok.
BTW dan moore has now got a max-stim Q&A on the HST board his own site has gone down,he is a really nice guy and very well informed on strength/hypertrophy,he will answer anything you want to know.
 
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