Sarcoplasmic Hypertrophy: The Bros

Were Probably Right

December 17, 2015 by Greg Nuckols 13 Comments

What youre getting yourself into

1.

Sarcoplasmic hypertrophy growth of the sarcoplasm that outpaces the

growth of the myofibrils does seem to happen to a significant degree.

2.

Simple increases in glycogen storage dont seem to be the primary driver of

sarcoplasmic hypertrophy. It seems to be driven by an increase in sarcoplasmic
protein content.

3.

The degree to which sarcoplasmic hypertrophy takes place may be influenced

by training, but whether you can specifically train for sarcoplasmic vs.
myofibrillar hypertrophy is unclear. More than anything, it seems to be a
natural consequence of muscle growth itself.

4.

Looking at strength differences between bodybuilders and powerlifters or

weightlifters is not a valid way to assess degree of sarcoplasmic hypertrophy.

However, dismissing sarcoplasmic hypertrophy simply because there are better

explanations for the observed differences in relative strength is foolhardy.
5.

Its unclear whether steroids increase the amount of sarcoplasmic hypertrophy

that takes place.

You may have heard the old piece of bodybuilding forum wisdom:
Bodybuilders are bigger than powerlifters/weightlifters but still lift less
because they have more sarcoplasmic hypertrophy, bro.
You may have seen pictures like this before as well, from very credible sources:

From The Science and Practice of Strength Training by Zatsiorsky and Kraemer one
of the top books I recommend to all lifters and coaches. Both authors are absolute

giants in the field.

Click to expand.

If youre not sure what were even talking about here, let me catch you up:
Its been proposed that there are two ways your muscle fibers can grow:
1.

Myofibrillar hypertrophy, which is accomplished via the growth and

multiplication of the myofibrils inside each muscle fiber. The myofibrils are the
actual motors of the muscle fiber, made up of contractile proteins that make the

muscle fiber contract. This is illustrated by the picture on the far right in the
image above.
2.

Sarcoplasmic hypertrophy, which is, in theory, accomplished by the expansion of

the sarcoplasm (the cytoplasm of the muscle) inside the muscle fiber. This is
illustrated by the middle picture in the image above.

Now, just to define these terms as accurately as possible, no one is suggesting

that the sarcoplasm cant expand at all. Rather, myofibrillar hypertrophy
implies that the sarcoplasm expands at roughly the same rate as the myofibrils
grow and expand (so if myofibrils took up 80% of the room within the muscle
fiber before, and the sarcoplasm took up 20% of the room within the muscle
fiber, with a doubling in fiber size, that proportion would still hold), and
sarcoplasmic hypertrophy implies that the sarcoplasm expands at a
significantly faster rate than the myofibrils grow and divide (so if there was an
80/20 ratio initially, it may be 70/30 or 60/40 after sarcoplasmic
hypertrophy).
So, does sarcoplasmic hypertrophy happen, and does it meaningfully
contribute to overall muscle growth? Thats the million dollar question.
Ive been skeptical of sarcoplasmic hypertrophy for a long time, mainly
because it wasnt an adequate explanation for the problem it sought to
address.
The situation where sarcoplasmic hypertrophy is most often invoked is when
comparing bodybuilders to powerlifters or weightlifters. How can some 280
lb. bodybuilder get out-squatted by a 180 lb. strength athlete? Sarcoplasmic
hypertrophy explains this difference, the thinking goes. The bodybuilders
must just have non-functional sarcoplasmic hypertrophy, making their
muscles bigger without making them stronger since its the myofibrils that
contain the contractile proteins.

However, as Im sure any consistent reader of this site is aware, strength also
has a massive skill component. The strength athletes are consistently
squatting really heavy loads in training, so theyll generally be more skillful
squatters. If the bodybuilders changed their training style for a few months,
their squat numbers would skyrocket. You can see this both in the real world
(it didnt take too long for Stan Efferding to squat 900+ after switching from
bodybuilding to powerlifting, for example), and in scientific research (its a
consistent enough finding that strength is pattern-specific and load-specific
that its not even worth citing specific studies).
On second reflection, though, I realized that I may have been in the wrong for
dismissing sarcoplasmic hypertrophy just because its a poor explanation for
the phenomenon its invoked to explain. Expressed more formally, if someone
claims A causes C, but B is actually a more likely cause for C than A, you
cant then conclude that A doesnt exist. You just conclude that B is a better
explanation for C than A is.
Heres a ridiculous example to make this point clear: If someone claimed that
cats caused that building to explode, but it was later discovered that there
was a leak in the gas main that ignited, you could only conclude that the gas
catching fire was a better explanation for the explosion. You could not
conclude that cats dont exist.
So, the main argument for sarcoplasmic hypertrophy falls flat (because theres
a better explanation for the strength difference), and the main argument
against it is based on somewhat sneaky logical fallacy.
With all of that out of the way, we can start to really dig into this topic with a
clean slate.
So, first of all, when people talk about sarcoplasmic hypertrophy, theyre
talking about something thats long-lasting, directly influenced by training,
and that makes a meaningful difference in muscle size. In other words, you

can get some increases in sarcoplasmic volume by taking creatine, carb

loading, by doing blood flow restriction training, or by causing muscle
damage, but none of these things cause the type of sarcoplasmic hypertrophy
people are interested in. None of them cause a very large increase in muscle
volume in the first place, and theyre all transient. Stop taking creatine or carb
loading, and the water goes away. The fluid retention in the muscles after a
session of blood flow restriction training or a training session that causes a lot
muscle damage dissipates within 72 hours, and the effect gets progressively
smaller over time.
We first have to ask ourselves: Where could this sarcoplasmic hypertrophy be
coming from in the first place?
There are two primary places:
1.

An increase in osmotic non-protein solutes in the muscle fiber, which will then
attract more water.

2.

An increase of sarcoplasmic proteins (including all organelles except for nuclei

and myofibrils) relative to contractile proteins.

Solutes in the Muscle

Increasing solutes inside the muscle is the first way that you could potentially
induce sarcoplasmic hypertrophy.
Im sure you remember pictures like this from high school biology:

If you could cause sarcoplasmic hypertrophy by increasing the amount of

solutes inside the muscle fibers, it would be a scenario like the picture on the
right. Since water follows solutes, and since muscle fibers are permeable to
water, if you added more stuff (other than contractile proteins) inside the
muscle fiber, water would follow, and voila, sarcoplasmic hypertrophy.
Unfortunately, thats really not feasible for non-protein solutes.
Ion concentrations (sodium, potassium, bicarbonate, calcium, hydrogen, etc.)
wont change too much long-term as long as you have healthy kidneys.
You have some fatty acids stored in muscle fibers as well, and those lipid
droplets can grow and divide with training (specifically aerobic training), but
they dont attract much water, and they make up such a small fraction of the
space inside a muscle fiber that theres really no way they could make much of
a difference.
Finally, you have glycogen. And yes, glycogen storage capacity can increase
with training. However, maximal glycogen concentrations can increase with
just about any type of training; they may just increase a bit more with aerobic
training or the type of lifting people think will cause sarcoplasmic hypertrophy
(lighter, high volume, bodybuilder-style training). Ultimately, glycogen

concentrations simply cant make a huge difference either, though. Even

when you infuse glucose and insulin directly into a muscle for 8 hours,
glycogen concentrations peak at about 4 grams of glycogen per 100 grams of
muscle. One gram of glycogen is stored with 3 grams of water, so, at most,
muscle glycogen plus the water associated with it makes up 12% of the total
mass of a muscle.
Average skeletal muscle glycogen concentrations are closer to 1.5-2 grams of
glycogen per 100 grams of muscle. In other words, going from average
glycogen concentrations to 100% maxed-out glycogen concentrations would
increase total muscle mass by about 6-7%, and that increase would be
sarcoplasmic hypertrophy. However, a) a 6-7% increase isnt a huge
increase (certainly not as large of an increase as most people expect), and b)
since regular strength training increases glycogen storage capacity in the first
place, the difference in maximum glycogen concentrations would make a
difference of maybe 2-3%, not 6-7%. Ultimately, glycogen concentrations are
more influenced by diet than by training, and, again, any increase would be
transient, so this doesnt fit the bill.*
*Note that glycogen doesnt fit the bill because its effects are transient. If you
go from fully depleted to fully repleted, that can make a noticeable difference
(compare pictures of bodybuilders in their last few weeks of dieting versus
how they look on stage for a dramatic illustration), but its not a permanent
change, and training style doesnt affect how much of a glycogen pump you
can get to a tremendous degree.

Non-Contractile Proteins
Could an increase in non-contractile proteins relative to contractile proteins
cause sarcoplasmic hypertrophy?
Maybe.

Protein and glycogen draw similar amounts of water into muscle fibers (1
gram of each is stored with about 3 grams of water). So, if the concentration
of sarcoplasmic proteins is higher than the concentration of glycogen (so that
they could make a more meaningful difference in overall muscle size), and the
concentration of sarcoplasmic proteins can be altered with training,
maybe that would be a reasonable avenue by which sarcoplasmic hypertrophy
could take place.
It was surprisingly difficult to find a source that compared the total amount of
sarcoplasmic and myofibrillar proteins in skeletal muscle. Im guessing that
most of that work is really old, and really buried in the PubMed and Google
Scholar search results. An introductory textbook about meat science (i.e. for
people who want to work in the meat processing industry) said that
concentrations of myofibrillar proteins were about 3x higher than
concentrations of sarcoplasmic proteins in mammals. That roughly matches
a study on guinea pigs and rabbits that was published way back in the 60s.

Stroma proteins are

mainly connective tissue, so we can disregard them for the sake of this article.

Now were getting somewhere. If a 3:1 ratio is typical, then maybe that spread
could change.
Most studies that measure rates of myofibrillar and sarcoplasmic protein
synthesis separately find that they dont always follow the exact same pattern

in response to the same stimulus. However, most of this data actually

weakens the case for sarcoplasmic hypertrophy. Although lifting increases
protein synthesis rates for both myofibrillar and sarcoplasmic proteins, the
increase is generally larger and more sustained for myofibrillar proteins. The
only two major instances where sarcoplasmic protein balance consistently has
the advantage are inactivityand aging; sarcoplasmic protein breakdown
proceeds at a slower rate with complete unloading, and sarcoplasmic protein
synthesis doesnt decrease with age, whereas myofibrillar protein synthesis
does. Also, we need to keep in mind that measuring rates of protein
synthesis doesnt necessarily tell us much about long-term hypertrophy.
However, these studies do show that sarcoplasmic protein concentrations in
the muscle arent pegged to myofibrillar protein concentrations in any
major way. In fact, in the rabbit study referenced earlier, the researchers saw
a pretty big spread in the ratio of myofibrillar and sarcoplasmic proteins. In
young, active rabbits, the ratio was a bit under the standard 3:1 about 2.4:1.
However, in rabbits that were forced to be inactive, that ratio shifted to about
1.6:1, and by middle age, the rabbits actually had slightly higher
concentrations of sarcoplasmic proteins than myofibrillar proteins.

Groups 1 and 2 were young and active. Group 3 was young and inactive. Group 4 was
middle aged.

So at this point, the savvier readers are asking themselves: If they could do
this type of biochemical analysis back in the 60s, how the heck dont we have
a clear answer about sarcoplasmic hypertrophy in humans yet in 2015?
Thats a good question.

There are two main reasons, both of which are discussed in this paper.
1.

To do this type of biochemical analysis, you need a pretty hefty tissue sample.
The smaller the sample, the more room there is for error. Improved lab
techniques may have solved this problem in the past 50 years, but at least at the
time this paper was published, they needed to take an entire gram of muscle tissue
to run the analysis. One gram of muscle tissue is roughly one cubic centimeter. I
dont think youll find many human subjects willing to let a researcher rip that
large of a tissue sample out of their muscles.

2.

Histological techniques (basically analyzing muscle under a microscope) wont be

able to accurately detect changes in sarcoplasmic versus myofibrillar protein
densities. To quote the authors: It would be feasible to carry out such an
investigation with the aid of histological methods, but they have two major
disadvantages. First, fixation and staining are accompanied by shrinkage of
sections, rendering impossible sufficiently precise determinations of the
proportions of sarcoplasm and of myofilaments in the total cell volume. Secondly,
the myofilaments are forming myofibrils which are not clearly separated from the
sarcoplasm in sections studied by histological methods. Electron microscopical
examination has disclosed that myofibrils have no envelope; moreover, it is known
that various chemical constituents of sarcoplasm, such as creatine phosphate,
adenosine triphosphate and mitochondrial products, are capable of freely passing
into and out of the myofibrils. Also, large molecules, for example inulin with a
molecular weight of 6,000, can penetrate into the myofibril. It is difficult to tell
whether the larger sarcoplasm-protein molecules actually pass into the myofibrils;
but, at least theoretically, there is room for them between the myofilaments, which
in the I bands are separated by wide spaces as judged by the lack of staining with
osmium. Hence, methods other than histological seem to be preferable for
studying the relationship between sarcoplasmic volume and myofilamental
volume.

So, keeping in mind that we probably arent going to get a tidy answer based
on direct evidence, we need to turn to indirect evidence, which comes from

two different sources: measuring intramuscular water concentrations, and

examining functional characteristics of individual muscle fibers.
There are, to my knowledge, only two studies examining changes in
intramuscular water after strength training.
The first one, published in 2014, did find an increase in intramuscular water
concentrations, which may lead one to believe that sarcoplasmic hypertrophy
had happened. However, Im not sure that we can put a ton of stock in it.
The biggest issue with the study was simply that the participants didnt gain
very much muscle in the first place. The men gained about 1.3 kg. of muscle,
and the women gained about 0.8 kg. of muscle. This was a 12-week study
on untrained participants. In other words, the amount of muscle they gained
was so small, especially considering the circumstances, that I just dont think
we can take much away from this study. Any amount of sarcoplasmic
hypertrophy would necessarily be trivial because, well, the total amount of
muscle they gained was trivial.
The second one is a classic from 1982. The researchers trained participants
for six months and examined their muscle pre-training and post-training, and
compared their muscles to those of elite powerlifters and bodybuilders. The
powerlifters and bodybuilders were lumped together, so its impossible to
draw a distinction between them, but that does give us a reference point for
people who are very highly trained.
After six months of training, the participants gained a ton of muscle. In fact,
the size of their individual muscle fibers had nearly caught up with the elite
lifters, so lack of growth isnt a problem in this study.
The participants myofibrillar density slightly decreased and their
sarcoplasmic volume relative to fiber size slightly increased over the course of
the study. The changes were small, but reached statistical significance. When

comparing the participants to the group of elite lifters, those trends were even
more stark. The elite lifters myofibrillar density was way lower (almost 10%
lower), and their sarcoplasmic volume relative to fiber size was way higher
(about 10% higher). In other words, a tiny bit of sarcoplasmic hypertrophy
occurred in the participants, and while you cant infer a causal relationship
since the elite lifters didnt undergo an intervention as well, it certainly seems
like quite a bit more sarcoplasmic hypertrophy separated the participants and
the elite lifters.
Also, note that mitochondrial density decreased over the six months of
training, and was even lower in the elite lifters. 6 of the 7 elite lifters also used
or had used steroids. More on both of those things a bit later.

From
MacDougall (1982)

(You may be asking yourself, How did they determine myofibrillar and
sarcoplasmic volume if doing so requires such a large tissue sample? Im
honestly not sure; it wasnt clear in the methods section. They cite two other
papers that apparently describe the method in more detail, but I dont have
access to them. Apparently they used electron microscopy, which doesnt

require as large of a tissue sample, so this may be more easily study-able these
days.)
Now, lets turn our attention to functional data.
You can estimate myofibrillar density by measuring the amount of force a
single muscle fiber can produce, and dividing that force by the cross sectional
area of the muscle fiber. This is called the specific tension of the fiber. A
higher specific tension means higher myofibrillar density at face value, and a
lower specific tension means lower myofibrillar density (and thus a higher
proportion of sarcoplasm), in most circumstances. Typically, the only major
factor that can throw off this relationship in non-fatigued muscle is posttranslational modifications of contractile proteins. In other words, if the actin
and myosin that cause muscle contraction are modified in some way that
causes them to not function properly, that can cause a drop in specific tension
independent of myofibrillar density. But, in most circumstances (because
post-translational modification is pretty rare), specific tension gives you a
pretty good estimate of myofibrillar density.
Now, you may balk at the idea of trying to draw any conclusions from studies
of single muscle fibers, but bear in mind that using single fibers is one of the
only ways to mitigate the effects of a whole host of confounding factors,
including (to quote a study on this very topic), differences in intramuscular
fibre orientation or pennation, the presence of intramuscular connective
tissue, differences in mechanical leverage related to joint position, the possible
coactivation of antagonist muscles during strength testing, and variation in
motor unit recruitment patterns, central drive and subject motivation.
A recent study compared individual muscle fibers from bodybuilders, power
athletes (American football players, track and field athletes, and weightlifters),
and control subjects.

The bodybuilders had the largest muscle fibers by a mile (88% larger than the
controls, and 67% larger than the power athletes). The bodybuilders muscle
fibers produced more force than the control subjects, but they actually
produced slightly less force than the power athletes muscle fibers (the
difference in total force between bodybuilders and power athletes fibers was
not statistically significant, however).
Here was the really interesting part: Per unit of cross-sectional area,
bodybuilders muscle fibers produced way less force than either the power
athletes or the controls (66% less than the power athletes, and 41% less than
the controls).
After obtaining this result, the researchers performed another analysis to see
whether post-translational modifications explained the difference, and
concluded any possible post-translational modifications played, at most, a
minor difference.
In other words, the bros were right all along. Training like a bodybuilder
causes nonfunctional sarcoplasmic hypertrophy.
Right?
Not so fast. There are three problems with jumping to that conclusion from
this study:
1.

There wasnt actually an intervention. It could just be that people with a

particular type of abnormal muscle fibers are more likely to become bodybuilders.

2.

The sample sizes for this study were pretty small.

3.

This little line is telling: A negative trend between fiber cross-sectional area and
specific tension has been reported before in single muscle fibre segments of
untrained people and frogs. In the present study, this negative trend is

apparent across all groups (emphasis mine). It has been suggested that this
may be related to accumulation of inorganic phosphate, due to longer diffusion
times from the interior of the fibre to the surrounding incubation medium.

The third point is probably the most important point.

While total muscle cross-sectional area generally correlates quite strongly with
capacity for torque production, single fiber studies tell a different story.
This one in particular illustrates the difference. In the largest study on single
fibers that Im aware of, the researchers actually found that capacity for force
production was more strongly related to muscle fiber diameter than crosssectional area. They plotted peak force against diameter on a log/log scale,
and found that the slope for both type 1 and type 2 fibers was very close to 1.
As youll remember from a previous article, the slope of a log/log graph tells
you the exponential relationship between two variables. In the previous
article on allometric scaling, the slope of the line comparing mass versus
strength was 2/3 and the slope of the line comparing mass versus metabolic
rate was 3/4. If the slope is 1, that means the relationship is linear, not
exponential (since raising something to the first power doesnt do anything).
Most importantly, they concluded that the slope of the line of best fit for that
log/log plot was almost certainly not 2, even when accounting for variability
and potential error. If the slope was 2, that would mean that peak force
scaled with the square of the diameter, which, in turn, would mean that peak
force scaled linearly with cross-sectional area. In other words, since theres
almost no way that the slope of the log/log plot was 2 (p<.0001 for both type 1
and type 2 fibers), that means you should expect the peak force of a single
fiber to be more closely related to fiber diameter than cross-sectional area.
Through that lens, lets look at the data from the study comparing
bodybuilders, power athletes, and controls again.

Since absolute values werent reported for all measures, I made both crosssectional area and peak force relative to the controls, and just used arbitrary
units. I maintained the relationships (percentage differences) reported in the
study.
Power
Controls

Bodybuilders
Athletes

Cross-sectional area

10

11.26

18.8

3.57

3.79

4.89

1.5

1.33

1.06

1.37

Diameter
(calculated)

Peak Force

Predicted Peak
Force

Using the more appropriate relationship (force relative to fiber diameter,

instead of cross-sectional area), we see a different picture from the one
painted above. The bodybuilders muscle fibers produced almost the exact
same amount of force per unit of diameter as the controls fibers (bottom row
the bodybuilders fibers only produced about 3% less force per unit of
diameter than the controls). This is in contrast to the 41% difference when
using specific tension (force relative to CSA). The power athletes fibers still
had way higher peak forces relative to diameter than either of the other
groups.

In other words, the issue wasnt that the bodybuilders were doing something
wrong that decreased force relative to CSA; based on how much larger their
muscle fibers were than controls, their muscles produced about as much force
as youd expect based on fiber diameter. Its more likely that either the power
athletes were doing something right to increase force relative to fiber
dimension above what would be expected, or that people whose fibers are
naturally capable of producing more force than they should are more drawn
to being power athletes in the first place likely a combination of both factors.
But keep in mind, even for power athletes, specific tension decreased as fiber
size increased.
However, this leads us to another quandary. Since myofibrillar density should
still scale linearly with cross-sectional area, but muscle force scales linearly
with diameter instead does sarcoplasmic hypertrophy simply go hand in
hand with hypertrophy itself? Is an increase in or maintenance of myofibrillar
density actually the weird thing to happen?
Maybe.
But since I doubt well have many more single-fiber studies in the near future,
because of how time and labor-intensive they are, and how low a priority this
type of research is for serious athletes. It would be directly relevant to
geriatrics though (so if there are any exercise physiologists reading this who
work with elderly people, consider this a subtle hint). For the time being,
though, the best we can do is look at whole muscle studies, and muse about
mechanisms.
The first study that comes to mind is this one on elite level powerlifters that
found very strong correlations between muscle thickness (rather than crosssectional area) and strength.
Most studies show that strength trained peoples whole muscles have higher
specific tensions than those of untrained people. However, this study (to the

best of my knowledge) is the only one that compared whole muscle specific
tension (force/CSA) to single fiber specific tension pre- and post-training.
They found that specific tension for single fibers was unchanged, but specific
tension for the whole muscle increased. They posited that lateral force
transmission (muscle fibers side-by-side linking up with each other to aid in
force transmission) was the most likely cause for the increase in whole-muscle
specific tension, and that myofibrillar density within the individual fibers
themselves was unchanged since single fiber specific tension didnt change.
This study and this study had similar results for single fibers (unchanged
specific tension) pre- and post-training, but the researchers didnt compare
those results to changes in whole-muscle specific tension. This study and
this study on the other hand, observed an increase in whole-muscle specific
tension and single fiber specific tension without any overall muscle
hypertrophy, although the second study was confounded by the fact that it was
performed on elderly subjects, who naturally experience a decrease in specific
tension with age (so the increase in specific tension just got them back to
normal).
There are also a host of other factors, such as increased muscle activation,
decreased activation of antagonist muscles, and even changes in muscle
architecture that favorably alter the muscle moment arm that could increase
force production relative to CSA as well.
With those confounding factors in mind, high-intensity training does seem to
produce larger increases in specific tension than lighter training does, and
bodybuilders regularly produceless force per unit of muscle CSA than strength
athletes do, and sometimes even less than untrained controls. In this study as
well, there was a negative correlation between CSA and specific tension.
In this study, on the other hand, bodybuilders actually produced more knee
extension torque per unit of CSA than powerlifters did.

On the whole, it seems that strength training increases force/CSA for the
whole muscle, but likely doesnt affect force/CSA (and myofibrillar density, by
extension) at the level of individual fibers unless no actual muscle growth
takes place. On the other hand, in most studies, bodybuilders force/CSA is
lower than strength athletes, and is often similar to untrained controls. This
is in line with the broader observation that force relative to size is most
strongly related to fiber diameter, and that it generally decreases as fiber size
increases. Strength training bucks that trend and maintains the relationship
between force and CSA, but bodybuilding-style training simply seems to
maintain the trend of specific tension decreasing with increasing fiber size, as
seen in larger studies.
So, does this mean that sarcoplasmic hypertrophy (an increased percentage of
sarcoplasmic proteins relative to myofibrillar proteins) typically goes hand in
hand with muscle hypertrophy?
Possibly.
Remember, there are still a few other potential confounding factors. Most
notably, the fact that larger fibers may accumulate inorganic phosphate.
Inorganic phosphate directly decreases the force of muscle contraction by
screwing with how well myosin can bind to actin, so that would account for a
decrease in force/CSA without a change in myofibrillar density. However,
keep in mind that this is just a proposed mechanism, not a proven one in this
particular context. Usually inorganic phosphate only accumulates as the
muscles fatigue (when youre splitting phosphates off ATPs faster than your
energy systems can replenish ATP levels); however, its known that inorganic
phosphate accumulation is one of the main reasons force/CSA decreases after
limb immobilization, so its possible for it to accumulate in non-fatigued fibers
under some circumstances.
There is a potential rationale for levels of inorganic phosphate rising in the
muscles of bodybuilders inorganic phosphate can act as a buffer when

muscular pH drops during training. Maybe bodybuilders muscles accumulate

inorganic phosphate as a response to high rep training that causes local
muscular acidosis. However, its one of the less important cellular buffers,
and even if that would explain how inorganic phosphate accumulated in
bodybuilders muscles, that still wouldnt help explain the more general trend
of decreased force/CSA with increasing fiber size, especially in type I muscle
fibers (which rely more on aerobic metabolism, and dont reach as low of
pHs).
Lets just assume for the moment that accumulation of inorganic phosphate
plays, at most, a minor role. Lets also assume that post-translational
modifications dont play a major role (and they generally dont, outside of
elderly populations and animals that dont produce myostatin). The only
other option (that Im aware of) to explain the declining force/CSA with
increasing fiber size is a decrease in myofibrillar density. In other words:
sarcoplasmic hypertrophy.
So now we need to ask ourselves: Why would this happen in the first place?
And why might it happen more with bodybuilders than strength or power
athletes?
The simplest explanation I can think of: energy.
A hefty portion of the sarcoplasmic proteins are involved in the various steps
of anaerobic metabolism. As a muscle fiber gets larger, it naturally relies less
and less on aerobic metabolism for two major reasons:
1.

Unless youre doing dedicated aerobic training, mitochondrial density

(mitochondria are the sites of aerobic metabolism) generally decreases. This was
seen in MacDougalls study; mitochondrial density dropped over six months as the
participants muscle grew, and it was lower yet for the elite lifters.

2.

The ratio of capillaries per unit of muscle fiber CSA generally decreases with
increasing fiber size, unless youre doing dedicated aerobic training. This means
you cant get as much oxygen to the mitochondria closest to the myofibrils further
inside the muscle fiber since theres a longer diffusion distance from the muscle
cell membrane (the sarcolemma) to the mitochondria deep inside the cell. This, in
turn, favors a shift toward anaerobic metabolism.

This idea makes sense in light of the single fiber study from earlier comparing
bodybuilders, power athletes, and controls; not only were the bodybuilders
fibers much larger, but they were also the only group not doing dedicated
cardiovascular training.
However, it doesnt fully explain why specific tension (and thus myofibrillar
density) wouldnt drop off with heavy strength training, but may with lighter,
higher volume bodybuilding-style training. Increased training volume in
general, and particularly increased training close to failure with lighter
loads imposes greater energetic demands on the muscle, which should help
spur on some of those aerobic adaptations (increased capillary density and
increased mitochondrial density) that would decrease the need for increased
levels of proteins associated with anaerobic metabolism.
I think (though I realize that this explanation is flimsy) that since
bodybuilding-style training is both more aerobically and anaerobically taxing,
the hugely increased anaerobic demands may lead to larger anaerobic
adaptations that outweigh the increased aerobic adaptations. With heavy
triples, youre barely going to burn through your stored ATP and
phosphocreatine, so you dont need to get a ton of your energy of anaerobic
glycolytic metabolism; thats entirely different when youre hitting multiple
challenging sets of 8-15 reps.
Looking at changes in sarcoplasmic protein metabolism after different
workouts and specifically separating mitochondrial proteins from other
sarcoplasmic proteins may help shed some light on this idea, but some studies

include mitochondrial proteins in the sarcoplasmic protein fraction (like this

one, which showed that sarcoplasmic muscle protein synthesis was elevated
24 hours post-workout after training to failure with 30% 1rm loads, but not
90% 1rm loads, or this one, which showed that a slower lifting cadence caused
larger increases in sarcoplasmic protein synthesis than faster lifting cadences),
and others separate mitochondrial proteins out and only analyze the nonmitochondrial sarcoplasmic proteins (like his one, or this one, which showed
that a slower lifting cadence caused larger increases in sarcoplasmic protein
synthesis than faster lifting cadences).
One last thing before wrapping up: I know Im going to get a question or 30
about steroids. Do they contribute to sarcoplasmic hypertrophy?
Bro wisdom says yes. A lot of people report gaining a lot of weight very
quickly when they go on steroids (much more than could be explained by plain
old myofibrillar hypertrophy) and losing it very quickly when they come off,
likely indicating shifts in the amount of water theyre storing. However, its
not always apparent that the water is being stored in muscles themselves
(some people report feeling like their muscles are full, while other perceive it
to be more like bloating), and thus far, the two studies that have actually
looked into this issue reported no increases in intra-muscular water (one on
testosterone, and one on nandrolone).
However, dosing may be an issue: The dosages people run in the real world
rarely get studied, for ethical reasons. Also, in MacDougalls study,
sarcoplasmic volume relative to fiber volume was much higher for the elite
lifters (most of whom used steroids) relative to the normal participants in the
study. On the other hand, in the single fiber study comparing bodybuilders to
power athletes and untrained controls, they didnt find any significant
differences between the fibers of the bodybuilders who reported steroid use
and those who didnt report steroid use. However, in this study, drug-free
strength athletes could produce almost 50% more force per unit of quad mass

than bodybuilders on steroids could (though training differences likely factor

in as well).
In other words, its hard to say for sure what role, if any, steroids play.
So, just to wrap this sucker up:
1.

Sarcoplasmic hypertrophy has never been directly, convincingly measured in

humans at least not up to the standards it would take to convince me personally.
One study showed increases in intracellular water post-training, but the overall
hypertrophy was very small in the study, so Im not ready to put too much faith in
it. Another study did show a very small degree of sarcoplasmic hypertrophy along
with very robust overall hypertrophy after six months of training, but due to the
very tiny degree of sarcoplasmic hypertrophy measured, its also probably not
worth putting a whole ton of faith in. The elite lifters in that study did have way
more sarcoplasmic volume relative to muscle volume, but since they werent
involved in an intervention, its impossible to know whether that difference was
due to training, or due to pre-existing differences.

2.

Though non-protein solutes in the muscle (like glycogen) could potentially

contribute slightly, any effect they could have would be small and transient. An
increase in the proportion of sarcoplasmic protein relative to myofibrillar protein
would be the much more likely cause, if sarcoplasmic hypertrophy did occur.

3.

We know that sarcoplasmic protein synthesis and breakdown arent directly

hitched to myofibrillar protein synthesis and breakdown, and that in mammalian
muscle, while a 3:1 myofibrillar:sarcoplasmic protein ratio is typical, a 1:1 ratio has
been observed (albeit, in middle aged rabbits) without any obvious ill effects.

4.

Peak force of single muscle fibers is more closely related to muscle fiber diameter
than muscle fiber cross-sectional area. In general, as CSA increases, force relative
to CSA decreases. Without alternative explanations (all of which are unlikely
under most circumstances in healthy, young people things like inorganic
phosphate accumulation and post-translational modifications of contractile

proteins), the most obvious reason for this decrease is a decrease in myofibrillar
density sarcoplasmic hypertrophy.
5.

Though the picture painted by the current scientific literature is still hazy, it
seems that strength training preserves the relationship between force and CSA as
the fibers grow, but bodybuilding-style training may not. However, some of the
studies that showed increased force/CSA used lighter loads (60%1rm), and one
study even showed bodybuilders quad torque/CSA was higher than powerlifters.

6.

It could just be that the odds of sarcoplasmic hypertrophy increase as muscle

fibers get increasingly larger. As fibers grow, capillary density relative to fiber area
decreases, and mitochondrial density decreases, increasing the reliance on
anaerobic metabolism, which is carried out by sarcoplasmic proteins. Even in elite
powerlifters, it was muscle thicknesses that correlated very tightly with strength
(although that study didnt measure CSA as well it could have revealed just as
strong of correlations).

7.

Based on the current evidence on highly trained subjects, there are too many
confounding factors to tell whether different training styles increase the odds of
sarcoplasmic hypertrophy. In vivomeasurements are influenced by muscle
attachment points, muscle activation, co-contraction of antagonist muscles,
motivation, muscle moment arms, pennation angles, etc. Thus far, most of the
direct comparisons we have are in vivo comparisons; so far there arent many
single-fiber studies to tease out whats going on at the cellular level (which is
where youd need to look if you wanted to study sarcoplasmic hypertrophy). The
only study we have comparing the muscle fibers of bodybuilders and power
athletes seems to indicate sarcoplasmic hypertrophy in the bodybuilders, but that
could be due to innate differences independent of training, or simply be related to
how much larger the bodybuilders muscle fibers were.

Ill admit Im finishing this article with an opinion much different from the
one I started with. As of about 5 days ago, I was confident that sarcoplasmic
hypertrophy was either a myth or, at most, played only a trivial role in overall
muscle hypertrophy. Now Im confident that it happens and, while Im not

totally convinced, Im much more open to the idea of it having a notable effect
on overall muscle growth. Im still skeptical that training in a specific manner
will either minimize the risk of sarcoplasmic hypertrophy (from the
perspective of a powerlifter) or increase your chances of sarcoplasmic
hypertrophy (from the perspective of a bodybuilder), but Im open to the idea
that it could.
Ultimately, this is a question that wont be settled until we have a lot more
high-quality single fiber studies (or unless some brave souls want to donate a
cubic centimeter of their muscles to science). People with strong backgrounds
in muscle physiology come down on both sides of this debate. Dr. Stuart
Phillips and Dr. Anders Nedergaard think its hogwash, Dr. Brad
Schoenfeld thinks it happens, but that it plays only a small role in overall
muscle growth, andLyle McDonald seems convinced that it happens and that
it can play a meaningful role in muscle growth.