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Another Look at Sarcoplasmic Hypertrophy

So the concept of sarcoplasmic hypertrophy is currently back in the limelight of the fitness industry.  This is due to an additional analysis of the Huan et. al. study that Mike Israetel was involved with.  I discussed the original study in detail in my series on Training Volume and Hypertrophy and will briefly re-examine it below for background context of the newer paper.

In fact, I was originally going to do a research review on the new paper but, honestly, it was going to be boring and overly detail oriented and it seemed more useful to look at the topic in a more general sense (while still being my own boring, neurotic detail oriented self).

Edit on June 6th, 2015: When I originally wrote this, the paper had not passed peer review but it has just been published officially.  As I knew it would.

Now, I have written about the concept of sarcoplasmic hypertrophy in the past, probably in my Ultimate Diet 2.0 but I imagine elsewhere.  And in doing so, I wrote in favor of it existing (this will make more sense when I define it).  Others have written similarly.  In contrast, some experts have dismissed the concept entirely/out of hand.

I want to first look at what sarcoplasmic hypertrophy represents to begin with, how it has usually been described or thought of in a training or adaptation sense before looking at not only the current Haun et. al. study but others that are relevant to the concept.  Much of what I write will come from the newer paper’s discussion.

What is Sarcoplasmic Hypertrophy?

Ok, so what is sarcoplasmic hypertrophy?  In the most simplistic sense you can think of muscle fibers as consisting of two things: the actual myofibrillar proteins (specifically myosin and actin) which generate force and everything else.  Where everything else represents fluid, glycogen, the intracellular machinery and probably a host of other stuff I’m forgetting in my old age.  It doesn’t particularly matter.  Just think of it as the actual contractile fibers and everything else.

A more specific definition was actually provided in an epic review paper on hypertrophy (also with Cody Haun in the author list) which was:

“…an increase in the volume of the sarcolemma and/or sarcoplasm accompanied by an increase in the volume of mitochondria, sarcoplasmic reticulum, t-tubules, and/or sarcoplasmic enzyme or substrate content”

Like I said, it’s just everything that’s not part of the actual force production machinery (the myofibrillar proteins) in the muscle.

For decades, bodybuilders have described this as pump growth which occurred in response to higher rep/shorter rest/high volume training.  You’d hear guys talk about how the pumpers would look big but not show any real density (presumably due to not having increased the size of the actual fibers) and who would lose a ton of size if they stopped training for any period of time. Presumably this was due to the relatively transient nature of the ‘pump growth’. Such bodybuilders often weren’t as strong as you’d expect for their size.  They were all show and no go.

In contrast, guys who trained heavily were said to look different.  They appeared to be muscularly denser (presumably due to increasing the actual fiber content) and maintained their size with longer layoffs because muscle fibers are going to stick around a lot longer than acute changes in the sarcoplasm or fluid in and around the muscle.

Coaches of athletes (usually Eastern European or Russian) sometimes described this as functional and non-functional hypertrophy.  Basically if you want to make an athlete actually get stronger and improve performance, you want to increase myofibrillar proteins and that would be functional hypertrophy.

In contrast, sarcoplasmic hypertrophy might make the athlete bigger visually but wouldn’t necessarily increase performance.  Hence non-functional hypertrophy.  Training was guided by this concept and hypertrophy training was performed in such a way as to generate myofibrillar hypertrophy.

You can conceptualize how myofibrillar/fucntional and sarcoplasmic/non-functional hypertrophy would differ by looking at the following graphic. This is from Zatsiorky’s Science and Practice of Strength training.

Myofibrillar versus Sarcoplasmic Hypertrophy


So what you can see is that there is the original muscle fiber with 6 actual myofibrils surrounded by sarcoplasm.    In the case of sarcoplasmic hypertrophy, the fiber increases in size but it is due to an increase in the sarcoplasm of the muscle with no change in myofibrillar number in an absolute sense: it starts at 6 and ends at 6.   Rather, there is a reduction in the relative amount (or concentration/density) of myofibrils within the muscle.  This distinction between changes in absolute and relative changes is important so let me try the following example:

Imagine that you have half a glass of water and you put 25 grams of table sugar in it.  Now you add another half glass of water to the mixture.  The same absolute 25 grams of sugar is still present but it’s concentration has been cut in half because you added more water so the relative amount has decreased.

Same thing here.  An increase in muscle size with no increase in myofibrils will decrease the relative concentration of those proteins even if their absolute number doesn’t’ change.  I hope that makes sense.

In the case of myofibrillar hypertrophy there is an increase in the number of myofibrils.  There would also appear to be an increase in the density/concentration of myofibrils although it’s hard to tell from the graphic if the total volume of sarcoplasm has gone up or down or remain unchanged from the original graphic.  And I won’t even attempt to work it out because this is just conceptual/schematic at this point.

A third possibility not shown would be that both the myofibrillar protein number and the sarcoplasmic components increase and this would lead to the largest overall size increase in fiber diameter (i.e. it would be larger than either case shown above).

Controversy Over Sarcoplasmic Hypertrophy

As I stated above, there has been some degree of disagreement in the field over whether or not sarcoplasmic hypertrophy occurs with some (including myself) thinking that it does and others that it does not.

More accurately the people who deny the existence of sarcoplasmic hypertrophy argue that you can’t get preferential increases in the sarcoplasm versus the myofibrils.   That is, that whatever the starting ratio of those proteins was, they would both increase at relatively the same pace.  Let me try to show this by example.

Imagine a situation where a muscle fiber has 10 myofibrillar and 10 sarcoplasmic proteins (these are totally made up numbers) and the ratio is 1:1 to begin.  Now consider the three potential outcomes from training.

Outcome 1: You get an increase of myofibrillar proteins to 12 with no change in sarcoplasmic proteins (stays at 10).  The ratio is now 1.2:1.  Both the absolute number and density of myofibrillar proteins has gone up.

Outcome 2: You get an increase of sarcoplasmic proteins from 10 to 12 with no change in myofibrillar proteins (it stays at 10).  Now the ratio is 1:1.2 and the concentration (but not absolute number) of myobfibrillar proteins has gone down.

Outcome 3: Finally imagine a situation where you train and increase both myofibrillar and sarcoplasmic proteins to 12 each.  The ratio remains at 1:1 (12:12) but the number of both has gone up, simply in equivalent amounts.

With a given outcome presumably being dependent on the type of training being done. So high volume “pump” style training (higher reps and/or shorter rest) would be generating more sarcoplasmic growth while higher intensity ‘strength/power’ type training would generate more myofibrillar growth.  Potentially some middle ground might in fact increase both equally.

Note: The above are not the only possibilities.  You might train and get an increase in myofibrils from 10 to 13 and sarcoplasm from 10 to 11 or vice versa where both the absolute number and concentration are changing at the same time but the ratio is still changing in one direction or the other.

That is, the idea isn’t necessarily that you’re only getting changes in one or the other, simply that the relative amount of growth in one component or the other differs or that training is generating preferential increases in one or the other.

In premise I suppose, it might be possible for one component to go up in absolute terms while the other goes down in absolute terms.  So for some reason you were training in such a way that myofibrillar proteins went from 10 to 8 while sarcoplasmic went from 10 to 12 or something and you got both a reduction in absolute and relative concentrations of myofibrillar proteins.  Moving on.

Those of who argue for preferential sarcoplasmic or myofibrillar hypertropy (again, depending on the type of training) are saying that Outcome 1 or 2 can possibly occur depending on the training being done.  Those who say that sarcoplasmic (or preferential myofibrillar hypertrophy) doesn’t occur are saying it’s always Outcome 3: that both increase in relatively equal proportions and that training can’t impact or generate preferential growth in one component or the other.

So who appears to be right?  Guess.

The Original Haun et al. Study

So as noted above, the current Haun et al. paper I’m looking at is actually a further analysis of a previously published study and I want to run through it in brief first.  In it, 31 trained males (at least 1 year of resistance training and back squat of 1.5Xbodyweight 1RM) were put on an identical training program.  To whit they did sets of 10 at 60% of their 1RM and trained three times per week.

Note: the study had an additional nutritional component involving protein and carbohydrates but this appears to have had zero impact on the outcomes so everybody was grouped together in terms of their results and I won’t mention it again.

The workout appears below.

Haun Workout Design

Let me note that the exercises were not done in sequence, that is all sets of squats in a row before moving onto bench press.  Rather, one set of each exercise was done before moving to the next one after a rest (90-120 seconds if I recall) and the next one finally coming back around to the first exercise.

With 4 exercises and up to a 2′ rest interval between individual sets, this means a rest interval of 8-10′ between work sets.  I have no clue why they choose this approach as it’s not representative of any training style I am aware of.  Well certainly no training aimed at growth.  If it’s anything, it’s a long rest interval sort of circuit training I suppose.

As well, the reported reps in reserve (RIR, the number of reps to hit failure) stayed at about 4 across the individual workouts and study.   Basically it was all a lot of non-fatigue submaximal work and nobody got tired across the series of sets since RIR didn’t drop across the workouts.  There was no cumulative fatigue at all.

And while some have tried to defend this as being challenging, I assert that anybody even decently trained could probably do repeat sets of 10 at 60% of 1RM with a 10 minute rest interval for as long as they wanted until they went nuts from boredom.

It was low tension (60% of max) and low fatigue because the rest interval was stupid long.   It was just a bunch of submaximal work that might as well amount to a bunch of warm-ups so far as I’m concerned (yes, I know about the paper that found growth on a 4RIR but it also didn’t use 10′ rest so there would have been cumulative fatigue across the sets).

Now, do those sets sequentially it on a 90 second rest interval and fatigue will accumulate across the sets with RIR dropping with each set.   Do sets of 10 at 70-75% of max (a near RM load) and it’ll be hard(er) even with a 10′ rest.  But as written, it’s a ton of junk/warm-up sets so far as I’m concerned because 60% of max is more or less a warm-up weight unless you take it to failure.  And they didn’t.

And if you still disagree let me remind you that the RIR didn’t change at all across all the sets.  It stayed at 4.  That means there was no cumulative fatigue.   End of argument.

Methodologically the study was very thorough measuring changes in muscle size three different ways before the study and at the 3 and 6 week mark.  Total LBM change was measured with DEXA while muscle growth in the biceps and quadriceps were measured by Ultrasound.

It wasn’t blinded which is odd since the lab usually does that.  However, since it wasn’t comparing different groups (all 31 subjects got the same training), there’s no real need to blind.  Everybody did the same training.   Still, I’d be remiss to not mention it (Hi Mike!).  Also, DEXA doesn’t need to be blinded since it’s a machine doing the measurement and there is no subjective component.

A biopsy of the quadriceps was also taken.  Here a chunk of muscle is cut out to be analyzed directly.  Of some interest, extracellular water (ECW) was measured and this was used to “correct” the measurement of LBM via DEXA.

The results were interesting to be sure.   By DEXA, the subjects gained roughly 1.35 kg/3 ish pounds of lean body mass from week 1-3 (10->20 sets) with an additional 0.85 kg/2 ish pounds from week 3 to week 6 (20->32 sets).

When this was corrected for ECW, the values dropped to 1.18 kg/2.6 lbs from weeks 1-3 and an insignificant 0.25 kg/0.55 lbs (0.18 lbs/week) from weeks 4-6.   Basically once the volume got over 20 sets, most of the “growth/LBM” was just water with the researchers concluding:

However, if accounting for ECW changes during RT does indeed better reflect changes in functional muscle mass, then it is apparent participants were approaching a maximal adaptable volume at ~20 sets per exercise per week.

Which is identical to the conclusion I drew in my 3-part series (specifically I felt that the studies supported 10-20 sets per muscle per week as roughly optimal).

The Ultrasound results were a bit weird and triceps appeared to go up to week 3 (20 sets) and then decrease by week 6 suggesting that excessive volumes are detrimental for the upper body.  In contrast quads seemed to shrink at week 3 and then go up at week 6

This might suggest that the legs detrain with too little volume and need more to grow (consistent with empirical belief).  This needs more systematic study and I’d note that the Week 6 quad value was no different than the pre-study value so it was a shitload of submaximal squatting for zero gains over 6 weeks.

This odd quad data is supported by the biopsy data where size went down from pre-study to week 3 and then back up to baseline.   If the study had only measured before the study and at Week 6, they would have measured zero growth.  That’s a lot of squatting for zero change.

And with that background.

The Current Haun et al. Study

Which brings me to the current study, another analysis of the original study, specifically the quadricep muscle biopsies.  This isn’t uncommon and frequently a single study will generate multiple papers as different aspects of the original research are examined in detail.

Toward this goal, the researchers examined the biopsy of 15 subjects (of the 31 total) who’s growth was above a certain point (basically sufficient to clear the error in measurement). This is actually interesting in its own right.   Here is the graph showing the actual changes in quadriceps CSA during the study.

Responders and Non-Responders in Muscle Fiber CSA Increase

You might note that roughly equal numbers of subjects showed increases as losses in muscle size (I do wish the study had biopsied the triceps as that would have been informative data to have had).   Certainly the average gain in the responders is higher (I’m eyeballing this) than the average loss in the losers but the guy who lost the most lost way more than the amount the largest gainer gained (2500 vs. 1500 of whatever the units say).

I don’t recall this individual variation being mentioned in the original paper but I always think it’s worth considering (and future work would help to identify who gains and who loses in response to any given training intervention).   Even if the higher volume generates some amount of growth ‘on average’, it’s clear that for about half of everyone it not only didn’t cause gains but caused size loss.  Just something to keep in mind.

Note: while I was working on this piece, Haun et. al. released ANOTHER analysis of this data set, examining the predictors of both high and low responders to the training.  While the associations were moderate at best, they found that subjects starting with the smallest fibers got the most growth and vice versa.

This makes logical sense: the less size you’ve gained, the more room you have to grow and vice versa.  Having more Type II fibers was also helpful which is not surprising in the least given the relatively greater growth tendency/potential for those fibers.  Ok, moving on.

Of those 15, an additional 7 came back 8 days later for another biopsy measurement to see what if anything had changed with “detraining” (I put that in quotes since 8 days is a fairly short time period) and only select measurements were done on them.

This is apparently due to financial limitations (studies get expensive fast).  So the sample size was small to be sure and the study itself is described as exploratory.  Basically a smaller examination to see if larger studies are warranted.

What the researchers wanted to examine is what was actually changing within the muscle during growth.  Basically what was growing.    This meant examining three components: the concentrations of actin and myosin (the actual myofibrillar proteins that generate force), citrate synthase (an aerobic enzyme used as a proxy for mitochondrial density) and sarcoplasmic proteins (representing a host of stuff).

They also measured intracellular water content to check for edema (swelling) and glycogen concentration along with a host of other stuff including markers of protein breakdown and such.  Basically, like the original study, this was thorough as hell but this lab actually seems to have their act together.

The Hypothesis Being Tested

Based on previous studies that I will discuss below, their hypothesis was:

Per the supporting literature above, we hypothesized that individuals experiencing notable fCSA increases would experience a decrease in myosin and actin concentrations, a decrease in citrate synthase activity (indicative of decreased mitochondrial content), and either no change or an increase in sarcoplasmic protein and glycogen concentrations.

Basically they were assuming that the muscle ‘growth’ that occurred was NOT due to increases in myofibrillar concentrations and, quite in fact, they expected a decrease in those components based on previous work I’ll mention below.  And to examine this they did some seriously technical stuff that I will not even attempt to describe or examine.

I don’t have the background, wouldn’t know what I was talking about and would fuck up trying to describe it and I’ll have to take at face value that they did it right.  It’s Western blotting and proteomics and a host of super technical molecular shit.  Read the paper if you want to have your eyes glaze over.

The Results

And what they essentially found was this: over the 6 week duration of the study, there was no change in glycogen or edema (this is water within the muscle, not extracellular so don’t confuse this with the argument over systemic edema impacting on Ultrasound measurements).

There was no indication that protein breakdown occurred either although this was based on a very indirect measure (protein breakdown is really hard to measure technically).  This can be more or less ignored.

They found a decrease in citrate synthase (an enzyme involved in aerobic metabolism) but don’t take this as an absolute decrease.   Rather, the concentration of the enzyme went down, suggesting a dilution of mitochondria within the muscle fiber.  This has been found by previous studies as well where weight training caused increased muscle size at the expense of mitochondrial concentration.

Which brings us to the big finding which is that there was a decrease in the concentration of myosin and actin, the myofibrillar proteins that actually generate force.  As above, this doesn’t mean that they necessarily went down in absolute terms (i.e. muscle was lost) but simply that that relative concentrations decreased.

Yes, this could have been caused by a loss of those proteins but it could also be caused by growth in a non-myofibrillar component.  Which wasn’t glycogen or edema.  Which really leaves only one thing: an increase in sarcoplasmic content.  That is, sarcoplasmic hypertrophy occurred.

Based on one of their analyses, they found that:

Of the 157 sarcoplasmic proteins detected, 40 proteins were significantly upregulated (p<0.05; Figure 4a), and 1 protein was significantly down-regulated from PRE to W6 (tropomyosin beta chain, 0.29-fold relative to PRE; data not shown on Figure 4).

Oh yeah, basically none of this changed with 8 days of detraining although fiber fluid content went down (which I think raises questions about when Ultrasound is measured since fiber fluid content might impact on this).  But myofibrillar protein concentration was still significantly lower with sarcoplasmic protein content being significantly higher than at the start of the study.

This led them to conclude that

Collectively, these data suggest that: a) sarcoplasmic expansion (i.e., sarcoplasmic hypertrophy) was the primary mode through which muscle hypertrophy occurred from PRE to W6, and b) this effect seemed to persist up to 8 days following the last training bout in the subset of participants that were analyzed at the W7 time point.

Which couldn’t be clearer.  Basically in response to this massive volume of low-intensity/low-fatigue training (increasing from 10->32 sets over 6 weeks), there was an increase in lean body mass (DEXA) at least some of which was water when the volume got stupid, an increase in muscle thickness (Ultrasound) and an increase in quadriceps cross sectional area (biopsy) and it was primarily driven by sarcoplasmic hypertrophy rather than actual increase of the contractile proteins themselves.

Of some interest was that many of those sarcoplasmic proteins are involved in energy production both for glycolysis and ATP.  Presumably this is due to the metabolic stress that occurs from high volume training.  In this vein, I recall a much older study (cited in my original Ketogenic Diet book that I’m too lazy to look up) where the muscles of bodybuilders were found to be physiologically more like that of endurance athletes than strength/power athletes.

Mind you, the study was in the 80’s when the style of training was higher reps and short rest and this makes total logical sense: training that is more of a metabolic than tension stimulus is going to generate metabolic adaptations rather than myofibrillar ones.

Let me note that it was unclear from reading the paper whether or not the concentrations of contractile proteins went down in absolute or relative terms.  The verbiage is dense and I don’t have the background to parse it since it’s a lot of molecular stuff. Several online exchanges I saw indicated that I wasn’t the only confused one.  So I emailed one of the researchers (MDR who appears to run the lab) who replied:

What we think is going on is [sarcoplasmic] expansion outpaces the laying down of actin and myosin with really high volume training.  However, this does not indicate that the absolute amount of actin and myosin is decreasing (i.e., a loss of these proteins).  As a matter of fact, that is HIGHLY unlikely (just doesn’t make sense).

Which I will take a the end of the story on the issue.  Simply, there was no loss of myofibrillar proteins with training but there was either no increase OR that increase was outstripped by the increases in sarcoplasmic content.  Thus the relative concentration of myofibrillar proteins went down.  I hope that makes sense.

Just One Study on Sarcoplasmic Hypertrophy

For reasons that are abundantly clear to me, the findings of this study are not being happily accepted by at least one member of a certain guru brain trust that I’ve been going on and on about (his name rhymes with Tad Broenfeld).

Among his general mis-understanding (he’s under the impression that myofibrillar proteins did go down in absolute terms), he’s fallen back on the classic “Well it’s just one study.”  Probably because if the results of this paper are correct, it has implications for ALL HIGH VOLUME studies (ahem, 45 sets/week) to date in terms of what is happening in terms of “growth” (i.e. it’s just a bunch of sarcoplasmic growth).  And he doesn’t want to admit that his paper didn’t show what he claims it showed.

And the “It’s just one study” is a convenient dismissal.  Except it’s not just this one study.  And saying it is either shows ignorance or deliberate misrepresentation.   I don’t know which it is in this case.

Rather, at least 4 other studies, some using admittedly older technology, have identified this same type of response to training: an increase in sarcoplasmic hypertrophy over that of myofibrillar.

In the introduction of the Haun paper, four are cited.  A very early study (1969) found a decrease in myofibrillar area in response to isotonic, isometric and run training.  A second paper found significant reductions in myofibrillar area and an increase in sarcoplasmic volume in untrained beginners trained for 6 months.  Of some interest this paper compared the untrained individuals to elite bodybuilders.   In the bodybuilders:

Myofibrillar volume density was significantly lower and cytoplasmic volume density significantly higher in the elite group than in the trained controls.

Which is interesting in its own regard.  The elite bodybuilders, presumably having spent years training had a lower myofibrillar density than the trained controls, suggesting that much more of a proportional increase in sarcoplasmic volume over their years of training.  Hmm…..

A third study found a 15% DECREASE in myofibrillar area in both heart failure patients and healthy controls who resistance trained for 18 weeks.

A fourth study not only supports the idea of sarcoplasmic hypertrophy but one of the early claims regarding it.  Kadi et. al. took 15 untrained men and put them through 30 or 90 days of high-volume resistance training (4-5 sets of 6-12RM in 4 leg exercises) who were then studied at day 3, 10, 30 and 90 during detraining (i.e. no training was done) with growth being measured by muscle biopsy.  After 90 days of training, quadriceps size had increased by 16% with a 3% further increase at day 3 (19% total).

By day 10, the values were not significantly different than before training.  Basically, the entirety of the size gain induced by high-volume training was lost in 10 days.  Maybe there was something to the idea that pump bodybuilders lost size rapidly if they didn’t train regularly, eh?

It seems pretty damn unlikely that trust muscle/contractile tissue was lost in that short of a time based on other detraining studies, shifts in fluid, glycogen and sarcoplasm are likely at work.  Which, once again raises some questions about the time point for measurements of muscle size increases.  Three days (cough cough) is unlikely to be long enough if we’re seeing short-term fluid shifts occurring.

Finally, I already mentioned their own recent study which found, surprisingly, that the subjects who started with the highest myofibrillar density to begin with saw the LARGEST decrease in myofibrillar concentrations with training.  This is interesting in its own right and I’ll come down to what this might suggest is going on below.

There is other indirect data in this regard that I will look at below.

Why Sarcoplasmic Hypertrophy?

It’s taken as a matter of faith that the goal and purpose of resistance training is to increase muscle fiber cross sectional area and, with it, myofibrillar proteins.  Why would this response be occurring?  There are a few possibilities and in their discussion Haun et. al. suggest 3:

  1. High-volume resistance training may promote sarcoplasmic expansion to spatially prime cells for the expansion of the myofibril pool.
  2. An increase in the expression of enzymes involved in ATP re-synthesis and metabolism is sensible considering that myofibrillar protein expansion requires large amounts of ATP due to the energetic costs of synthesizing and assimilating myofibrillar proteins.
  3. An upregulation in sarcoplasmic proteins related to ATP generation and excitation-contraction coupling may also occur in lieu of sarcoplasmic expansion due to the metabolic demands of high-volume training as well as the energetic demands of myofibrillar protein synthesis and assimilation.


Spatial Priming for Expansion of the Myofibrils

Basically this is saying that sarcoplasmic expansion is an early adaptation to increase the cell size/volume to allow for increases in the actual contractile proteins.  That is, go back and look at the graphic comparing sarcoplasmic and myofibrillar hypertrophy above.  In the far right example, the myofibrils are packed within the cell.  Perhaps the cell volume itself has to expand to make ‘room’ for more contractile elements to be laid down.

This would seem to be indirectly supported by the newer Haun et. al. study where those subjects with the highest starting myofibrillar concentration/density saw the largest dilution and vice versa.    Perhaps when myofibrillar density is high beyond a certain point, sarcoplasmic hypertrophy dominates to make room for further growth.  In contrast, when there is already sufficient room (i.e. low myofibrillar density), more myofibrillar hypertrophy occurs.

If true, this also has implications for training that I will discuss below.

Increased Energy Production Proteins

Protein synthesis is energetically costly so another possible explanation for sarcoplasmic hypertrtrophy is that the early adaptation to training occurs to increase the proteins to “prepare” for the myofibrillar growth down the road.

This seems unlikely to me given that study after study shows that protein synthesis turns on just fine from day 1 of training without this having to occur.  I suppose it’s possible that, in trained individuals, these energy producing proteins need to be upregulated to support even higher rates of myofibrillar protein synthesis.

As an interesting side-note in this vein, at least one study has shown that mitochondrial function is predictive of being a high-responder to resistance training.   The mitochondria are the powerhouse of the cell and being able to support energetically costly protein synthesis might be part of it.  It might also suggest that “hardgainers” or “low-responders” to training might benefit from aerobic work to increase mitochondrial function within their skeletal muscle.

An Adaptation to the Type of Training

A final possibility is that the increased sarcoplasmic protein was simply an adaptation to the training stimulus itself.  That is, it was simply a specific adaptation to the specific type of training that was done.  High volumes of training, as I stated above, are conceptually similar to an endurance type of training.

And this is especially true if the tension is low, which it was in the Haun et. al. high volume training study.  Again, argue all you want but shitpiles of work at 60% nowhere close to failure is not a major tension stimulus to myofibrillar components of the muscle.   The absolute load and fatigue are both too low and you need one or both present.  It had neither.

Now, this would be totally different if the sets were close to or reached failure.  In the low-load training studies, it’s clear that hitting failure is the key to making it “work”.  At failure, almost irrespective of load, the body will have to recruit all muscle fibers (I’ll be writing more about this before too long) so they will be exposed to a high-tension stimulus.  Blood flow restriction works similarly due to how it affects fiber recruitment.  With low loads, you get recruitment of the highest threshold muscle fibers.

The workout in Haun was simply too sub-maximal in both load and fatigue to cause this to occur.  The high threshold muscle fibers simply weren’t exposed to a high enough load or enough contractions under conditions of high tension to stimulate myofibrillar growth.  Rather, the metabolic aspects of the muscle were challenged, generating the specific adaptation that occurred.  In this vein, they state:

In this regard, some have argued that the utilization of high-volume training to volitional fatigue promotes skeletal muscle hypertrophy to a similar degree when compared to lower volume/higher load training [37].

This argument is supported by numerous studies which have determined that both training modalities similarly increase surrogates of skeletal muscle hypertrophy [1, 38-40].

However, these conclusions have primarily been drawn through the utilization of ultrasound to assess muscle thickness or fCSA assessments using histological staining techniques, and none of these studies have examined if the stoichiometric relationship between myofibrillar and sarcoplasmic protein concentrations are preserved relative to pre-training levels.

Stated differently, it is unclear in these studies the specific mode through which hypertrophy occurred (e.g., sarcoplasmic, myofibrillar, or connective tissue) and what the functional outcomes of these findings may be.

Basically, perhaps sets of 30 to failure and sets of 8 generate the same total growth but the sets of 30 were mostly sarcoplasmic and the sets of 8 or even lower mostly myofibrillar.  I could see this going either way to be honest so it’s speculative. 

On the one hand, sets of 30 or whatever to failure and BFR do result in high threshold muscle fibers being exposed to high mechanical load which would predict no difference in response.  On the other hand the sets of 30 are far more metabolically stressful which might lead to more sarcoplasmic growth (and there is super limited data that the sets of 30 might result in Type I fiber preferential growth).

As Haun et. al. state:

While speculative, it is possible that higher load training (e.g., 3-5 RM lifting) proportionally increases myofibrillar protein levels and fCSA, and this mode of ultrastructural hypertrophy promotes optimal strength gains.

Conversely, higher volume/lower load training (e.g., 8-12+ RM lifting) may increase fCSA predominantly through sarcoplasmic expansion and metabolic conditioning, thus leading to sub-optimal strength gains.

And I’d love to see this studied directly: take two groups, have one do a certain volume of 5RM lifts and another higher rep work of some sort (whether 12-15 or 25-30RM or whatever). Match the volume and frequency and stuff and measure not only growth but the underlying cause of that growth in terms of whether or not it is primarily myofibrillar or sarcoplasmic.   There is an older paper by Campos et. al. examining this to some degree but it was in untrained individuals over 8 weeks so I don’t think it’s safe to extrapolate the results to trained individuals.

And there is another point that suggests that the third point, a specific adaptation to training might be at the root of this sarcoplasmic increase.

Muscle Size and Strength

In general, there is an incredibly strong relationship between muscle fiber cross sectional area and force production, at least at the fiber level (this is impacted in the real world by mechanics, levers and everything else).  Hence increases in contractile components of muscle are expected to increase strength.

And this fact indirectly suggests that high volume, especially the low load stuff, training is generating a fundamentally different response in that it doesn’t increase strength to the same degree as heavier training (I’d note that it also doesn’t improve bone mineral density which is another big negative against it in my mind but that is a separate issue).

Now I had generally assumed that the lack of strength gains was due to the lack of a neural/practice effect with the lighter loads as I imagine most others had.  That is, strength production is impacted by a number of factors but muscle size and neural factors are two of the biggies that training can impact.

And lighter load training doesn’t impact neural factors in the same way (because you are not practicing heavy lifting with all that entails).  Without that adaptation you wouldn’t expect maximum strength to go up irrespective of increases in muscle size.

But it might also be that a preferential increase in sarcoplasmic fractions is part of the picture.  Only the actual myofibrils (actin and myosin) generate force.  If they don’t increase with muscle “growth” than muscle strength doesn’t go up either.    Or at the very least doesn’t go up in proportion to the growth response.  That is, nobody is saying that strength will increase 1:1 with increases in fiber size.  But you would expect a true increase in myofibrillar components to increase strength.

There is some indication that this might be the case.  Specifically is a recent study which compared the specific tension of single muscle fibers of bodybuilders to that of true strength/power athletes and recreationally active controls.  Specific tension here basically refers to the relations of fiber cross sectional area and force production. As I said above, there is generally an insanely strong relationship between the two.

In this study, the bodybuilders had fiber cross sectional areas that were 67% larger than the strength power athletes and 88% larger than the untrained controls (bizarrely the strength/power athletes fiber size was no larger than the controls).   So the bodybuilders had by far and away the biggest fibers. No shocker there since that is what bodybuilders specifically train for.

And, as it turned out, the strength/power athletes fibers had a specific tension that was 63% higher than the bodybuilders.  So for their actual muscle size they were much stronger.   Now this might just be a practice thing.  Strength/power athletes practice generating maximum strength and bodybuilders don’t.

However, this is argued against by the fact that the recreational controls had a specific tension that was 41% HIGHER than the bodybuilders.    This doesn’t mean that the bodybuilders were weaker than the controls per se, their fibers generated more absolute force to be sure.  But relative to their cross sectional area, the specific tension was lower than the controls subjects.

This led the researchers to conclude that

hypertrophy has a detrimental effect on specific tension

Noting that:

myofibril dilution through higher volume body building-style training may have been a driving factor for their observations.

Basically, despite being much larger, the bodybuilders muscles were relatively much weaker relative to the size increase.  And presumably this occurred through myofibrillar dilution which is caused by, duh duh duh, increased sarcoplasmic volume.

This would tie in directly with the idea of functional versus non-functional hypertrophy: clearly the strength/power athletes got strong without gaining much size while the bodybuilders got big without gaining proportional amounts of strength. Perhaps the all show no go idea isn’t too far off, eh?  Not that bodybuilders give a shit.

It is critically important for me to note that 9 of the 12 bodybuilders in the study admitted to using anabolics and it is completely possible that that is part of the equation here, that the impact on anabolics growth of muscle fibers is part of what threw off the numbers.  Mind you, it’s not as if strength/power athletes don’t use as well but it was not mentioned if those athletes admitted to using steroids.

Tangentially: this might also explain why the supposed “differences in growth” seen in Tad Broenfeld’s high-volume study didn’t show any differences in strength gains.  To whit, there wasn’t actual myofibrillar hypertrophy occurring (this is along with the fact that there were only differences in size gains between the low and moderate/high groups to begin with).  Because as I’ve stated 5X15RM on 90 seconds rest even “to failure” ends up being metabolic training since you can’t use any decent weight by the end of it.  Even if you use “form failure” as you metric (and they did), on squats that will mean stopping far from muscular failure.

And that’s probably why he played the “only one study” card above.  Despite his “not being biased” (hahaha, hi Mike), he has to dismiss any study that questions his own results (that’s without getting into the timing of the Ultrasound measurements yet again).  Mind you, his results are above criticism.  It’s only other results he doesn’t like that have to stand up to criticism.  I digress.

The Above Explanations are Not Mutally Exclusive

I want to make the point that I don’t necessarily think the above explanations are mutually exclusive or that only one or the other must be the case. There’s no reason that all three explanations couldn’t be partially true or true in a given context.

This is especially the case since the original study being reanalyzed only used one type of training, which makes it impossible to know for sure what the driver on the results were. Until two distinctly different types of training are compared head to head in a similar fashion, no truly strong conclusions can be made.  That paper, when done, will be fascinating.

But it might very well be that once myofibrillar density has reached a certain point, the body’s preferential adaptation would be to increase sarcoplasmic volume to make room for more myofibrillar growth.  A similar argument might also be made for the increase in energy production components..

Perhaps a limit is reached where skeletal muscle protein synthesis has reached the maximum rate for the cell’s ability to provide energy.  In this case increasing energy producing proteins within the cell might be the only way to even allow for further myofibrillar growth.

This would be conceptually similar to what we know about satellite cells and how a limit is reached for how much muscle a given SC can support. At that point, increasing SC proliferation appears to become required for more growth to occur.

In fact, it might well be that this holds for many other components of growth.  Mitochdondrial function, capillary density to bring in nutrients, ribosomal activity, etc.  Whatever is limiting for growth might need to preferentially adapt first before more growth can occur.  Basically, the limiting component should be addressed.

But that would tie in with the potentiality of specific types of training to generate those specific adaptations.  So consider a situation where sarcoplasmic volume and/or energy production is limiting for growth.  Perhaps at that point, the type of training that Haun just happened to do would be the best type of training to do.   This might also support the whole idea of ‘switching it up’ in terms of training style, a point I’ll come back to below.

Conclusions and Implications

Ok, so let’s see if I can reach a point.  I’m not sure what my favorite bit about the Haun et. al study is. Actually that’s not true.  My favorite bit is the smug sense of self-satisfaction I get from having been correct in my belief in sarcoplasmic hypertrophy when others said it didn’t happen.

But what other reasons do we really do this than for the smug self satisfaction of being right?

Clearly under some conditions, it’s clear that sarcoplasmic fractions within the muscle can expand out of proportion to myofibrillar fractions and there are now 5 direct studies on the topic along with some indirect data supporting the idea.  So clearly it happens. And it’s not “just one study”, Tad.

Your high volume study is “just one study” because Haun found a clear cutoff for volume above which the gains were mostly water and Raedelli was a trash fire because in NO world does growth in beginners not even start until 27-45 sets per week or whatever it was.

A remaining question is exactly why it happens.  Because the why kind of determines what relevance all of this has.

Spatial Expansion/Energy Production

Let’s first assume that it occurs either to spatially prime the cell or provide sufficient energy production for actual myofibrillar growth.  If this is the case, then it’s semi-irrlevant in the sense that whatever adaptation is easiest or necessary is gonna happen no matter what you do.  If you’ve already packed the muscle tight with myofibrils, the body might simply “choose” to adapt by increasing sarcoplasmic components before you can get another myofibrillar increase.

You would expect to see some sort of staggered response in the different elements in this case.  So you’re doing your training and, depending on your starting point you see one or the other occurring.

So imagine you’re one of those high responders above with relatively smaller myofibrillar concentrations.  You train and since there’s “room” and “energy” your training stimulates myofibrillar growth.  Now you start to reach a maximum concentration where growth is limited and now the body has to increase sarcoplasmic components to provide more room and energy.    Or if you’re in a situation where your myofibrillar density is low so training causes an adaptation in that system first.  At which point you switch to sarcoplasmic, etc.  Maybe.

Determining this would take a seriously long term study taking serial biopsies to see if there is some time point where the body switches from developing primarily one component to the other.  So maybe for the first few months you get myofibrillar hypertrophy which maxes and then sarcoplasmic components come up preferentially and then myofibrillar catches up, rinse and repeat.

I’ll be honest that I find this one tough to accept (possibly/probably reflecting my own biases).  In studies looking at such, training induces increases in myofibrillar protein synthesis from the get-go and it’s hard to see how this wouldn’t lead to growth in those proteins over time regardless of any other factor (yes, this could be offset with increased protein breakdown).

But it’s critical to realize that those studies are based on exposing fibers to high-tension loading.  For example, Burd compared 1 and 3 sets to failure at 70% of max and saw higher protein synthesis in 3 sets.  In another study he compared high load to low load training TO FAILURE (the key aspect since this ultimately exposes fibers to high tension loads) and actually saw greater increases in protein synthesis with the low load training.

Mind you both increased myofibrillar protein synthesis.  Yes, I am aware that sometimes studies see increases in both myofibrillar and sarcoplasmic or mitochondrial proteins which is probably where the idea that you can’t get preferential growth in one or the other comes from.

And the simple fact is that the original Haun et. al study being examined did NOT do this.  It was just a shitpile of low load, low-fatigue volume far from failure.  But as I said, with only the one training type, it’s impossible to draw strong conclusions until two types are compared head to head.

It would have been fascinating to have had a second group doing lower volumes of heavier tension loading (i.e. sets of 10 close to failure or shorter rest intervals or something to make the workout actually stress the muscle fibers) so that comparative data could have been obtained.

There is also the single study on high-level bodybuilders who clearly did NOT see a proportional increase in both components fo the muscle.  This would suggest that they simply got preferential increases in sarcoplasmic components over their career.  Whether this was due to their training or the use of anabolics is impossible to determine at this point. Another study possibility: see if the same holds for provably natural bodybuilders.

I’m not saying that increases in sarcoplasmic hypertrophy or energy producing components isn’t important or doesn’t occur, just that I tend to doubt that it is some type of staggered alternating response to training where one occurs and then the other, etc.

It just doesn’t seem to fit what is known from every other training study to date, where high tension loads reliably increase strength and myofibrillar density whereas other studies using higher volume training seems to be increasing sarcoplasmic components preferentially.  Outside of rank beginners where neural adaptations predominate, any study using heavy training which finds an increase in maximal strength is, indirectly at least, suggesting an actual increase in myofibrillar proteins.

Bringing us to…

Specific Adaptation to Imposed Demands

But what if it’s just a specific adaptation to the type of training done? That is that high-volume training generates primarily sarcoplasmic growth and heavier tension based training (i.e. heavier weights, lower reps) generates myofibrillar growth.  The specific tension study on bodybuilders and strength/power athletes seems to support that and I tend to think this is what is at least primarily going on.

A recent study by Vann et al. found that heavy loading (sets of 4) specifically increased proteins involved in myofibrillar growth.  That lends support to this idea.

That very high volume training such as what was done in Haun are stressing metabolic components and generating sarcoplasmic growth while high tension loading (whether heavier low rep work ot high rep work TO FAILURE) are stimulating myofibrillar growth.  Again, this needs to be tested directly, I await said test and I’ll be happy to be wrong if I am.  But I’m not to worried about that happening.

So working from that assumption, what implications does that have?  Well first we might consider the population in question.   For performance athletes it’s pretty clear cut.

Gaining muscle size per se at the expense of training proportional amounts of strength would tend to be somewhat misguided.  Improving performance means improving strength and power.  If size gains come from “non-functional” hypertrophy, that’s not helpful to performance.

I’ve told the story about how my little post-college graduate mind was blown when I was told that Ol’ers do lots of sets of 5 to gain muscle size but this would be consistent with the idea that the growth from higher volume bodybuilding type training is not beneficial to performance in the aggregate.  Unless some performance athlete just needs to be big for the sake of being big, it just doesn’t serve any real purpose.

For bodybuilders, size is size and I doubt anybody cares if the size increases are sarcoplasmic or myofibrillar.  Nobody cares how strong a bodybuilder is (well except for the bench): it’s just about being big.  Then again, there is that visual muscle density issue to consider.

If heavier training is needed to increase the myofibril concentration to improve muscular density then it’s not sufficient to just get big through sarcoplasmic expansion.  There is also that whole “Losing the size gains quickly” thing which the one study actually seems to support as being for real.  If you train high-volume for 3 months and all the size gains go away in 10 days off, well….you best get to lifting some heavy weights.

And here I think there are some interesting implications to this data.  Again, I am working from the basic belief that you do get preferential types of adaptations to specific types of training.  Good old SAID: Specific Adaptations to Imposed Demands.  Stress the myofibrils (with tension) and they grow primarily.  Stress the energetic components and they grow primarily.  Stress both and maybe you get the best of all worlds.

Training Implications

As I mentioned above, for performance athletes the training implications are fairly clear cut: if the goal is to increase performance, then the goal is to increase myofibrillar concentrations and that means training in such a way as to accomplish that (this is on top of maximizing other factors such as technique, neural factors, etc.).  Size for the sake of size makes no sense if it doesn’t make you stronger or perform better.

But what about for bodybuilders.  As above, size is size on stage and nobody really cares whether it’s myofibrillar or sarcoplasmic.    But presumably to generate maximum size, training both myofibrillar and sarcoplasmic components makes the most sense.  And the logical implication of that is that both high-tension and high-volume training should be done at one point or another to generate the specific adaptations.

And there are fairly endless ways you could do this so long as each of the different components is being stimulated to adapt.

Do them Sequentially

One would be to sequence training in a fairly linear fashion.  So you’d first do a higher volume block to preferentially increase sarcoplasmic fractions and energy production component.  This might be combined with aerobic work to increase mitochondrial fucntion.

That would be followed with heavier tension work to increase myofibrillar density (and then perhaps a short block of neural training to maximize strength so you can use heavier weights on the next go around).  Then go back to volume then back to density then to neural (basically as I laid out in my Periodization for Bodybuilders series because frankly none of this is new).

As Haun et. al mention

Indeed, as posited by Stone et al. [41] decades ago, it is possible, if not likely, that higher- volume/lower-load training resulting in sarcoplasmic expansion and metabolic conditioning preceding lower-volume/higher-load training can produce more favorable strength outcomes.

So this isn’t even a new idea.   But very little is these days (and most of the new ideas such as “Volume is the primary driver on hypertrophy” and “Metabolites drive muscle growth” are wrong anyway but those are other articles for other days).

In this type of sequential approach, a question we might ask is how long each phase should be and I don’t know that there are any good answers at this point.  The big question would be how long it takes to maximize one or the other adaptations and we don’t know at this point.  Perhaps 4-6 weeks of high volume (12-15 reps or higher) into 4-6 weeks of heavier tension training (5-8 reps) to 2-3 weeks of pure strength training (5’s and lower), take an easy week and then repeat?

The problem here, and eventually I will write an article on the whole to do about linear periodization is the potential to lose on adaptation while you focus on another.  You don’t want to lose myofibrillar proteins doing nothing but high-volume pump training which you then have to rebuild.  But some maintenance work for whatever you’re not focusing on can prevent that.

Do them Simultaneously on the Same Day

A solution to that would be to do them simultaneously.   My generic bulking routine, and generally every hypertrophy approach I’ve ever written always contains a tension element and a fatigue element.  The GBR is multiple sets of 6-8 (RIR = 2 so 2 reps from failure) followed by multiple sets of 12-15 on a short rest (and if you thought it mattered you could finish with some super high rep set or whatever) for each muscle group.

The old powerbuilding routines were no different.  You did your 5 sets of 5 followed by a pile of higher rep short rest stuff.  McCallum’s Get Big program was like this.  5X5 heavy and then something like 8 sets of 8 or 8 sets of 10 on 30 seconds. Tension and fatigue.

You got big and strong at the same time.  The old 20 rep squat used to be a backdown after heavy sets of 5’s.  I had this silly book years ago that described the 6/20 method for growth: a heavy set of 6 followed immediately by a set of 20.  I guess the bros were onto something.

Tension plus fatigue for the win.  It always has been and always will be.  In the model being described the high tension work is developing the actual myofibrils and the fatigue work the other components (sarcoplasmic, glycogen storage, etc.).

Do them Simultaneously in the Same Week

The tension and fatigue workouts wouldn’t have to be on the same day and you might do them across a week.   Have one heavy day of training (heavy sets of 5-8) and one pump day of training (lighter sets of 12-15 or higher).  Just to ensure that all components of the muscle are being stressed.  Or go nuts with daily undulation periodization, one days of 5’s, one day of 12’s and one day of 30’s or whatever.

Hatfield wrote about that decades ago with his ABC training although he was trying to target specific fiber types with the different repetition ranges.  That might or might not be going on in the first place but he might have been right for the wrong reasons all along with the heavy work stimulating myofibrillar components and the higher rep work stimulating sarcoplasmic.

My own Ultimate Diet 2.0 is structured like this in a weekly fashion. Monday and Tuesday you do high volume short rest pump training, Thursday you do intermediate (8RM) tension training and Saturday 5RM strength training.  It’s specific to that diet but various types of undulating periodization are at least conceptually similar.

Let me note that the high rep training in UD2 is NOT aimed at sarcoplasmic expansion but glycogen depletion as part of the diet cycle.  And I doubt highly that 2 workouts have any real acute impact here.  Then again, over 6-8 weeks, stressing all the different components progressively might accomplish exactly that.

Train What’s Limiting

We might even go further. Here I am working from the idea described above that:

  • The adaptations to training are specific in the sense I’ve been describing
  • One or the other adaptations can become limiting to further growth

Basically, the idea that these different explanations for sarcoplasmic growth are not mutually exlusive.  So consider a situation where someone has reached the point where there is no longer sufficient “space” or “energy support” to make more myofibrils.

Presumptively they’ve been working on primarily tension based heavy training for a while and have hit a plateau or whatever.  In that case, switching to a high volume/fatigue based approach to specifically increase sarcoplasmic volume might be the best approach to allow for further myofibrillar growth.

In contrast, someone with lower myofibril density might benefit from a higher intensity block to increase myofibrillar density.  Sadly, I know of no way to determine this outside of looking at past training practices (I suppose one might find a way to examine maximal strength relative to bodyweight or LBM as a proxy for this).

Perhaps this also explains why some people “do better” with one type of training or the other at any given time in their career: a different type of training is addressing a different limiting factor for them.  It might even lend some idea to “switching” it up from time to time or moving from volume to intensity and back again.  If nothing else, higher volume lighter training gives the joints a break and even that can be beneficial for long-term training progress.

Mind you this is predicated on the idea that different types of training do generate preferential adaptations and a systematic study of this will be nice to see.  But it all fits with what we know about physiology, how the body adapts, etc. I’ll happily accept it research shows this not to be the case but I wouldn’t lay odds that it will.

Low intensity endurance work, glycolytic HIIT and sprint work all generate different neurological, muscular, central and training adaptations, right?  So we might ask how could different types of strength training NOT do the same.

The End?

And that’s kind of that.  The flow on this article sucked, it’s too long and it kind of petered out at the end but that’s my take on this data. It was something to get done while I try to finish my analysis of the Barbalho study (HI MIKE!) and another looking at the metabolite theory of growth (another newish idea that is wrong).

So yeah, there ya’ go: sarcoplasmic growth would appear to be a real thing.  Just like I and other have been saying for a while now.  And the folks who have been denying it kind of have to suck it because that’s 5 papers saying it’s a thing with other indirect studies supporting it too.

It’s not just one paper, Tad.  Hell, it’s more literature in support of it existing than there is to support stupid high volumes of training as being superior for growth….just sayin’. And those anecdotes that the evidence based crew has suddenly decided are valid (for them but not for stuff they don’t like) don’t mean shit in this regard.

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