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STRENGTH TRAINING ADAPTATIONS

lecture
A basic introduction of muscle growth

Note: most of the references for the physiology sections of this document are in the recommended
reading documents.

Muscle cell anatomy

Before diving into the topic of muscle growth, it is useful to understand the basics of the structure
of muscle cells. A muscle cell is different from any other human cell. Most human cells are round
and contain one nucleus that is located inside the cell, as illustrated below.

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In contrast, a muscle cell is a long, cylindrical cell 50 – 100 µm in diameter, which is about the
diameter of a human hair. One muscle cell can span the entire length of the muscle. Muscle cells
are grouped in bundles that may contain up to 150 muscle cells. Each muscle cell possesses not
just one but multiple nuclei, which are located at the outer boarders of the cell. Each nucleus
controls a region of the muscle protein. Because of their unique structure, muscle cells are often
referred to as muscle fibers.

Source: Baechle TR, Earle RW. Essentials of Strength Training and Conditioning. 2008.

Each muscle fiber is surrounded by the muscle fiber membrane. A muscle fiber contains many
components, among them mitochondria, which are responsible for energy (ATP) generation,
stored glycogen, fat particles and, most importantly for us, contractile components: the pieces
that make your muscles flex.

Contractile components consist of protein filaments, called myofibrils. Each muscle cell contains
hundreds of myofibrils. Each myofibril is about 1 µm in diameter. The components of myofibrils
– myofilaments myosin and actin – are responsible for the contraction of the muscle cell. Myosin
and actin filaments are organized to form the smallest contractile unit of the muscle, the
sarcomere. Sarcomeres occur over the entire length of the muscle fiber and are connected

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through actin filaments. At each connection between two sarcomeres, aligned actin filaments are
anchored at the so called Z-line.

Figure adapted from Baechle TR, Earle RW. Essentials of Strength Training and Conditioning. 2008.

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Muscle growth physiology

Muscle hypertrophy vs. hyperplasia

Muscle growth can occur via muscle hypertrophy and hyperplasia.

 Hypertrophy is an enlargement of contractile elements (the myofibrils composed of

myosin and actin that are inside the muscle cell).
 Hyperplasia is an increase in the number of muscle fibers (= muscle cells).

Hypertrophy vs. hyperplasia

Hyperplasia likely does not occur in humans. Older research in animals suggested that it did,
particularly the infamous weighted stretching research in birds, but newer muscle fiber counting
methods have falsified this research. As you can imagine, counting muscle fibers is tricky business.
It’s like counting the number of hairs on someone’s head. Even if hyperplasia occurs in humans,

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its extent appears to be trivial and it’s highly doubtful we can meaningfully target it with our
training. So in practice, you may as well think of muscle growth as being equal to muscle
hypertrophy.

Muscle hypertrophy in series vs. in parallel

Muscle hypertrophy may occur via the addition of sarcomeres in series, resulting in a lengthening
of the muscle fibers, or in parallel, resulting in an increase in the muscle’s thickness as more
muscle fibers are packed together next to each other (larger cross-sectional area). Since there is
an obvious limit on how long a muscle can become while remaining functional, most muscle
growth occurs by an increase in sarcomeres in parallel.

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Myofibrillar vs. sarcoplasmic hypertrophy

There are 2 types of muscle hypertrophy, depending on which components in the muscle fibers
increase in size: myofbrillar and sarcoplasmic.

 Myofibrillar hypertrophy is the growth of the myofibrils (myosin and actin), the
contractile components of the muscle tissue.

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 Sarcoplasmic hypertrophy is the growth of any other component of the muscle fibers,
the sarcoplasm.

Sarcoplasm is the cytoplasm of the muscle fiber. It’s the fluid the myofibrils are located in. It
contains many components, among them contractile components, other proteins,
mitochondria, stored glycogen and fat particles.

There is controversy over whether sarcoplasmic hypertrophy occurs in humans, but this is in
part a semantic discussion. There is no doubt in science that sarcoplasmic hypertrophy occurs.
The only controversy in scientific circles is whether sarcoplasmic hypertrophy can outpace
myofibrillar hypertrophy in the long term, leading to an increase in the ratio of sarcoplasm to
myofibrils, as illustrated above.

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Emphasis on the long term, as short term sarcoplasmic hypertrophy is easily realized. A high
carbohydrate diet will increase the amount of intramuscular glyocogen, for example. Voila,
sarcoplasmic hypertrophy. Same for muscle damage, as discussed below.

But can the sarcoplasm’s portion of the muscle fiber increase over the long run, more
permanently?

Yes. Exercise, mostly aerobic endurance training but to a lesser extent also strength training,
increases glycogen storage capacity. It’s not a major difference, but it’s systematic. Strength
trained individuals store more glycogen in their muscles than sedentary individuals and each
gram of glycogen attracts ~3 grams of water into the muscle. So this technically constitutes
sarcoplasmic hypertrophy. Other osmotic (water attracting) components in the muscle fibers,
such as proteins, probably increase in concentration as well, since untrained individuals who
start strength training have been found to experience an increase in intramuscular water
concentration and a decrease in myofibrillary density.

Cross-sectional comparison of untrained individuals, novices and elite lifters showed that the
elite lifters had an even lower myofibrillary density and there was no difference between
bodybuilders and powerlifters, suggesting that sarcoplasmic hypertrophy simply occurs as a
result of strength training regardless of how exactly you train. The sample sizes of this study
were very low, so these data do not rule out that you may be able to target sarcoplasmic
hypertrophy with your training.

However, it’s clear if you run the numbers that the amount of total muscle growth will
normally be only a few percent, far outweighed by focusing on myofibrillary hypertrophy, as this
is the dominant form of muscle growth in the literature.

Moreover, as you’ve seen in the course topic on nutrient timing in relation to the anabolic
window, sarcoplasmic protein synthesis is normally considerably lower than myofibrillary
protein synthesis.

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Last but not least, there is no research whatsoever showing how you can target sarcoplasmic
hypertrophy (presumably with more endurance like training, but that may reduce myofibrillary
muscle growth).

In sum, much like hyperplasia, sarcoplasmic hypertrophy is something you can largely forget
about in practice. Sarcoplasmic hypertrophy probably occurs, but its contribution of muscle
growth is small compared to myofibrillary hypertrophy and it’s unclear if and how you could
target it in your training.

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Mechanisms of muscle growth

Muscle hypertrophy occurs when enough biomechanical tension is applied to the muscle fibers
that their structural integrity is compromised. As an adaptive response to this stress, the
muscle fibers undergo changes in their structure. This remodeling process can include an
increase in the size of the muscle.

Here’s a the ultra CliffsNotes on how muscle grows.

1. When you put tension on a muscle, its muscle fibers deform and trigger chemical activity
(mechanotransduction).
2. The muscle fibers release growth factors like insulin-like growth factor 1 (IGF-1) and
myokines like IL-6 to signal the need for repair (myogenic signaling).
3. The mTOR master enzyme integrates all the signals for muscle growth, such as amino acid
availability and the presence of growth factors, and then translates this information for your
genes (translation initiation).
4. Your genes are located within muscle cell nuclei that function as command centers in their
region of a muscle fiber. They contain the blueprint to create new proteins (protein synthesis).
5. Nearby satellite cells are activated, they divide and their formed daughter cells fuse to the
disrupted muscle fibers to donate their nuclei to the muscle cells and enlarge them (myonuclear
addition) and aid in the creation of more new muscle proteins.

Metabolic stress

In addition to mechanical tension, metabolic stress has been proposed as a possible mechanism
of muscle growth. While the term metabolic stress has become common in the evidence-based
fitness community since Brad Schoenfeld popularized it, it lacks a clear scientification definition.
Metabolic stress refers to the accumulation of metabolic byproducts in the muscle, like lactate,
phosphate (Pi) and hydrogen ion (H+) along with hypoxia, i.e. the oxygen shortage, during
exercise. As you’ve learned, lactate is a byproduct of glucose production and glucose
production increases along with exercise intensity. Lactate, often incorrectly referred to as
lactic acid, is an acid and thus causes acidosis in your muscles, which is largely responsible for

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what you feel as ‘the burn’ during high rep strength training. As such, that feeling and metabolic
stress correlate. Fatty acid oxidation is too slow a production pathway and too reliant on
oxygen to fuel high intensity exericse. So metabolic stress is particularly high during exercise
with a large demand for glucose. Metabolic stress also increases when the clearance of
metabolic byproducts is hindered, such as by constant tension exercise or blood flow
restriction.

Metabolic stress may contribute to muscle growth in various ways, as shown below. However,
the evidence for the importance of metabolic stress is almost entirely based on in vitro research
on isolated muscle cells in the lab. With the exception of extreme cases like blood flow
restriction training (discussed in the course topic on advanced training techniques), there is no
evidence that metabolic stress plays an important role in muscle growth independent of
mechanical tension. In fact, in many cases where metabolic stress was proposed to be beneficial
for muscle growth, it even turned out to be detrimental, as you’ll see in the coming topics.

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Muscle damage

In addition to mechanical tension and metabolic stress, muscle damage has been suggested to
be the third mechanism for exercise-induced muscle hypertrophy. This pathway of muscle
growth is again popularized chiefly by Brad Schoenfeld. The extent of muscle damage can vary
from minor tissue injuries on a macromolecular level and ‘micro tears’ to large tears in muscle
and connective tissue, which is generally associated with injuries, depending on the type of
exercise performed.

To quote Schoenfeld: “Damage can be specific to just a few macromolecules of tissue or result
in large tears in the sarcolemma, basal lamina, and supportive connective tissue, and induces
injury to contractile elements and the cytoskeleton. Because the weakest sarcomeres are
located at different regions of each myofibril, the nonuniform lengthening causes a shearing of
myofibrils. This deforms membranes, particularly T-tubules, leading to a disruption of calcium
homeostasis and consequently damage because of tearing of membranes and/or opening
of stretch-activated channels.
The response to myotrauma has been likened to the acute inflammatory response to infection.
Once damage is perceived by the body, neutrophils migrate to the area of microtrauma
and agents are then released by damaged fibers that attract macrophages and lymphocytes.
Macrophages remove cellular debris to help maintain the fiber’s ultrastructure and produce
cytokines that activate myoblasts, macrophages and lymphocytes. This is believed to lead to the
release of various growth factors that regulate satellite cell proliferation and differentiation.”

Muscle damage generates inflammation. Damaged muscle cells release pro-inflammatory

molecules that attract neutrophils, a type of white blood cells. Neutrophils destroy dead muscle
cells and produce molecules that attract other inflammatory cells. Macrophages, another type of
white blood cells, infiltrate the damaged muscle to remove cell debris. Additionally,
macrophages secrete growth factors and other molecules which play an important role in
muscle repair. The neutrophils can attack healthy cells, worsening the muscle damage, so
excessive inflammation may delay muscle recovery. However, inflammation is a normal part of
the muscular repair process and inhibiting this inflammation can therefore reduce muscle

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recovery and growth, as you’ve learned in the course section on the signal-to-noise theory of
inflammation and muscle growth (see course document on dietary fat).

After muscle damage, fluid and plasma proteins move into the injured tissue. This can create
muscle swelling and is one of the reasons your muscles may appear larger after just a single
workout even though minimal actual muscle growth has yet occurred.

Satellite cells are important helpers of the muscle repair process. Muscle damage leads to the
activation of dormant satellite cells. After multiplication daughter cells diffuse to damaged
muscle sides and help regenerating the muscle by fusing with damaged muscle fibers.

Muscle damage is related to the muscle soreness you feel in the days after certain types of
exercise, particularly novel stresses and eccentric (lengthening) muscle contractions. The pain
normally starts around 6 hours post-workout and peaks 48 hours after the exercise before
gradually subsiding. Researchers call this delayed onset muscle soreness (DOMS).

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Inflammation and activation of the immune system, particularly the myokine IL-6, are involved in
the process of satellite cell activation and muscle growth. However, just like with metabolic
stress, the actual empirical data in humans that muscle damage has an independent positive
relation with mechanical tension is lacking. Muscle damage is not required for muscle growth
and muscle damage does not correlate with muscle growth at all. In terms of protein balance,
muscle damage only increases protein breakdown and turn-over, so while absolute protein
synthesis levels increase as a result of muscle damage, net protein synthesis isn’t any higher
because most protein synthesis is merely the result of repairing damaged muscle fibers, not the
construction of new muscle tissue.

Similarly, there appears to be no relation between delayed onset muscle soreness (DOMS) and
muscle growth. DOMS is mostly experienced after performing exercise you’re not accustomed
to, such as by performing a high volume of an exercise you’ve never done before. After this
initial training session, adaptations that are called the repeated bout effect greatly reduce
DOMS if you perform said exercise again, even if it’s months later. There is also great
interindividual variability in DOMS. Some people are almost always sore after training, whereas
other people rarely are. Moreover, muscle groups within the same individual have the same
variance and this does not appear to be related to muscle growth. An an example, Menno has
virtually never experienced DOMS in his delts, though those are arguably his best body part.

It should be noted that although DOMS is a consequence of muscle damage, it is not an

accurate measure of muscle damage. The correlation between soreness and indices of
recovery, such as maximal isometric strength or plasma creatinine kinase level, is low.
Interestingly, the exact mechanism of DOMS is still unclear. Presumably, inflamed microscopic
tears in the connective tissue trigger nearby nerve cells, which cause the feeling of pain.

As such, DOMS is not a sign your program is effective and is more of a nuisance that you can’t
do much about. Fortunately, it is generally harmless and can be trained through. Within reason
of course: if after a thorough warm-up you still can’t perform a certain exercise with full range
of motion because you’re too store, you probably want to skip that exercise that session to
avoid excessive muscle damage and injury.

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Systemic factors (incl. hormones)

Mechanical tension, metabolic stress and muscle damage are all local factors. They occur within
the muscle and the resulting muscle growth happens within that same muscle. In contrast,
systemic factors have also been hypothesized to play a role in muscle growth. The most
common example of systemic factors are hormones.

For example, strength training newbies are often told to train their legs. When they protest
that they don’t really care about leg muscle growth, they’re told that training their legs will
make their upper body larger too. The argument is that heavy compound leg work like squats
increases the production of anabolic hormones. The increases in circulating testosterone,
growth hormone and IGF-1 then amplify the training effect in other body parts.

It sounds plausible and there is no doubt that testosterone in particular is a strongly anabolic
hormone in muscle tissue. But are the short lived peaks in anabolic hormone concentrations
enough to meaningfully affect muscle growth?

Hansen et al. (2001) found that performing leg presses directly after biceps curls resulted in
greater elevations in growth hormone and testosterone and greater isometric strength
development than just performing biceps curls. However, while the subjects were untrained,
the leg press + curls group had significantly lower isometric strength at baseline, so this
confounder could explain the greater strength development in this group, as opposed to
hormonal mechanisms. This confounder would also explain why isokinetic strength (we’ll get to
the exact definitions in the course topic on exercise selection) and standing biceps curl 1RM
increased similarly between the groups. Overall, this study is highly inconclusive.

Rønnestad et al. (2011) conducted a very similar study and found that performing leg presses
before performing biceps curls increased biceps CSA at the largest point along with a greater
improvement in biceps curl 1RM. However, total muscle volume increased similarly between
groups, suggesting the greater CSA change at that one particular point was measurement error

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due to misaligning the CSA slices during the MRI. And the greater 1RM biceps curl strength gain
did not correspond with the similar increases in peak power and biceps training loads between
the groups. It is unclear how their 1RM could have improved more while their actual training
loads throughout the study did not. So while this study suggests a benefit of performing heavy
lower body compound work before upper body isolation work to reap the benefits of
increased anabolic hormone levels, skepticism towards these results is justified.

Thirdly, Mangine et al. (2017) found that exercise induced testosterone spikes are related to
muscle growth across individuals. This was cross-sectional research, however, so it cannot
demonstrate causality.

Several other lines of research have not supported ‘the hormone hypothesis’.

 Significant muscle growth can occur without acute post-workout elevations in anabolic
hormones.
 Several studies find no correlation within strength trainees between acute post-workout
anabolic hormone levels and muscle growth or strength development [2, 3], though in
other research there are positive, albeit mixed and inconsistent, relations between
muscle growth and testosterone, growth hormone, MGF and even cortisol. Given the
mixed and inconsistent nature of these relations, it is very possible that they are a case
of mistaking correlation for causation.
 While a good case can be made for testosterone’s anabolic effects, which can tell your
genes to start synthesizing muscle protein, reduce protein breakdown and activate
satellite cells, growth hormone, in contrast to popular belief, is not anabolic in
myofibrillar tissue, only in the surrounding connective tissue like your tendons and
bones. Most of the increase in lean body mass following growth hormone usage is
merely water retention. During your workouts, growth hormone seems to be primarily
active to mobilize fuel stores, such as by increasing fat burning (lipolysis), and its
production is related mostly to metabolic stress, particularly blood lactate levels and
hypoxia. IGF-1, in turn, seems to be more strongly related to muscle anabolism in
effects, particularly its splice variant mechano growth factor (MGF). However, IGF-1 is

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produced and used largely within the muscle, so its relevance for other muscle groups is
highly dubious.
 West et al. (2009) found that while performing high volume leg curls and extensions
directly after biceps curls increased growth hormone, IGF-1 and testosterone levels, it
did not affect cellular anabolic signaling or muscle protein synthesis in the biceps. West
et al. (2010) found that this same protocol also did not result in superior muscle growth
or strength development of the biceps.
 Spiering et al. (2008) similarly found that performing a high volume of bench presses,
shoulder presses and rows before performing leg extensions did not affect anabolic
signaling in the quadriceps.

It is possible that the key to systemic hormonal support lies in performing the heavy compound
work first, like Rønnestad et al. Since the greater increases in testosterone and growth
hormone levels only last approximately 30 minutes, it is conceivable their benefits only appear
during this period.

In conclusion, while it would be premature to dismiss the role of anabolic hormone levels
during the post-workout period as broscience altogether, if systemic factors like acute post-
workout anabolic hormone elevations play a direct role in muscle growth, it is small compared
to the local effects like mechanical tension. A small benefit may be derived though by
performing heavy compound exercises directly before other exercises. Since it is generally
prudent to perform heavy lower body compound exercises before upper body isolation work
anyway, for reasons we’ll get into in the course topic on exercise ordering, this is an advisable
programming practice.

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Strength training adaptations

lectures
 General Adaptation Syndrome (GAS)
 Strength vs. size

Recommended reading
 Human exercise-mediated skeletal muscle hypertrophy is an intrinsic process
 The acute physiological response to exercise

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Functional training and strength vs size.

Bodybuilding has a reputation for being the least functional sport there is. The sole aim of
bodybuilding is improving your body composition without regard for actual performance.
However, depending on your definition of ‘functional training’, bodybuilding may in fact be the
most functional form of training there is.

Let’s define our terms here. Regardless of how you specifically define it, ‘functional training’
according to many people refers to some measure of transferability of performance across
activities (‘carry-over’). An activity is functional if it improves performance, defined below, in
many other activities. So a leg extension is generally regarded as less functional than a squat,
because leg extension strength doesn’t transfer as well to many other activities, whereas a
strong squat makes you better at jumping, sprinting, etc.

Now let’s define performance.

In the broad sense, as the term is used in fitness, performance generally refers to the ability to
produce force during a given movement (= F in physics). This is straightforward for Olympic
Weightlifting, Powerlifting and CrossFit, where someone’s score and force production are
almost perfectly correlated. You move more weight, you get a better score.

However, it also applies in most sports: more force equals a faster sprint, a stronger punch, a
higher jump, etc. Even an elderly person that has trouble standing up straight without shaking is
often a matter of force. Where we informally talk about ‘losing balance’, physically the problem
is a lack of force production to produce the desired movement and direction and increasing
force production capacity is what solves the problem.

So functional training requires an activity to have a high degree of transferability of force

production across various movements. What defines force production capacity? The body’s
ability to produce force during a given movement is controlled by 2 primary categories of
components.

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1. Morphological components. This in practice largely comes down to muscle size, since
this correlates with many of the other components, like internal leverage arm and
pennation angle. Other morphological components, like myofilament density, aren’t
nearly as important.
2. Neurological components. This basically refers to the ability of your central nervous
system, specifically your brain’s motor cortex, to control your muscles.

Menno likes to use the following metaphor: “Muscle size is the body’s engine of strength and
your nervous system is the driver.” Together, they determine your performance.

Now here’s the kicker: the second component, neural adaptation, is highly specific. Your
nervous system becomes better at performing the specific movement you’re doing with little
transfer to other activities. Here are some examples.

 Partial range of motion strength training makes you stronger specifically in the part of
motion you’re training with only ~15% transfer to the rest of the movement.
That’s why you see many guys in the gym that can quarter squat a ton, yet when they
have to go ass-to-grass, they have to strip off literally the majority of the weight.
 The optimal training methods for 1 to 10 meter sprints are significantly different from
30 meter sprints, though both are already extremely short distances.
 There is very little relation between different measures of core strength, even though
it’s the same set of muscle groups (abs, back, etc.) performing a similar task (stabilizing
the torso).
Unpublished research from Osaka University of Health and Sport Sciences found that there
is no significant relation between trunk stability (i.e. planks) and trunk flexion (i.e.
crunches).
Other unpublished research from Saeterbakken et al. in Norway found that the
relations between core strength, core stability and core endurance were “non-existing
to medium” (data below).

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Unsurprisingly then, the typical ‘functional training’ activities like core training and the
Functional Movement Screen are “not strong predictors of performance… Despite the
emphasis fitness professionals have placed on functional movement and core training for
increased performance, our results suggest otherwise.” [2]

The lack of carry-over of many forms of exercise to other exercises may be hard to grasp for
some people. Part of the reason for this is that our language is fundamentally flawed to
understand biomechanics. We talk about strength and power as traits, when they are in fact
skills. Strictly speaking, a person cannot be strong or be powerful. A Powerlifter isn’t strong: a
Powerlifter has a strong bench press, deadlift and squat. Nor is an Olympic Weightlifter
powerful: a weightliftes has a powerful Clean & Jerk and Snatch.

Since the nervous system is highly movement specific in its function, that leaves muscle size as
the main component of functional capacity. Muscle size is the only true trait that increases force
production capacity without any limitation of movement specificity. If you make a muscle bigger,
it will increase your ability to generate force during every movement that that muscle is
involved in.
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Secondly, the other thing bodybuilders excel at, which is achieving a low body fat percentage, is
also strongly linked to performance during many movements. Given the same muscle mass, the
lower your fat mass and thereby your total bodyweight, the higher your relative strength. This is
particularly important during weightbearing activities, which basically includes all ground sports.

And this isn’t just theory and logic. There is actually a ton of data showing that muscle size and
a low body fat percentage (= bodybuilding) determine performance in a wide range of activities
(= functionality). These include:

 Elite volleyball
 Swimming
 Competitive sprinting (just look at top level sprinters)
 Elite surfing
 Major League Baseball. Along with American Football, these are one of the few sports
that caught on to the performance benefits of being highly muscular early on. Between
1970 and 2010, the average BMI of baseball players grew by about 3 points. Linemen
have increased in weight by over 50% between 1950 and 2010. Moreover, there is a
clear upward hierarchy in size from the lower to the higher divisions of the sports.
More muscular players perform better.
 Basketball
 Judo
 Soccer
 Firefighting
 Track and field throwing
 Australian football
 Rugby

Best of all, we have Powerlifting and Olympic weightlifting, the sports that supposedly stand in
stark contrast to bodybuilding because they train for performance instead of body composition.

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Yet the reality is that more muscular Powerlifters and Olympic Weightlifters consisently
outperform their less muscular competition.

In Olympic weightlifters, there is an extremely tight relation between body mass and
performance.

In powerlifters, the relation is even stronger with a 0.86 to 0.95 correlation between fat-free
mass and performance in the powerlifts. The correlation is strongest for the squat, followed by
the deadlift and lastly the bench press.

Other studies have researched what distinguishes stronger and weaker powerlifters.
Anthropometric variance – differences in individual body structures – actually doesn’t explain a
lot of the variance in performance, especially at the elite level. The greatest difference between
stronger and weaker lifters is simply that the stronger ones have more lean body mass [2]. As
Keogh et al. (2009) noted, “relatively few significant anthropometric differences were observed.
However, stronger lifters had significantly greater muscle mass and larger muscular girths in
absolute terms as well as greater Brugsch Index (chest girth/height) and "Phantom"-normalized
muscle mass, upper arm, chest, and forearm girths. In terms of the segment lengths and bone
breadths, the only significant difference was that stronger lifters had a significantly shorter
lower leg than weaker lifters. Because the majority of the significant differences were for
muscle mass and muscular girths, it would appear likely that these differences contributed to
the stronger lifters' superior performance. Powerlifters may therefore need to devote some of
their training to the development of greater levels of muscular hypertrophy if they wish to
continue to improve their performance.”

In general, as competitive pressure, the celebrity status of athletes and the financial rewards
increase, athletes in many sports are becoming ever more muscular.

Interestingly, there is good reason to believe the current research underestimates the
correlation between muscle size and strength due to a methodological problem. A good

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measure of muscle size is its cross-sectional area (CSA) at its largest point: the literal thickness
of a muscle, illustrated below.

Anatomical/morphological cross-sectional area. An even better measure is physiological CSA (PCSA),

because this takes into account the directionality of the muscle fibers (pennation angle) and measures
the cross-section perpendicular to their longitudinal axis rather than assuming all muscle fibers run
straight from top to bottom.

Most research measures CSA at rest and then correlates this with a measure of strength, often
maximal voluntary isometric contraction (MVIC: contracting a muscle as hard as you can
without moving it) to make sure the muscle size and strength measurements are performed
with the muscle in the same position. However, testing this correlation at rest underestimates
the relation between strength and size, because the correlation between CSA and MVIC is
stronger during intense contractions than at rest. In short, methodological limitations mean that
the relation between muscle size and strength we see in the lab is probably an underestimation
of the actual relation during strength training.

As a final example of the non-specific benefits of bodybuilding for performance, consider

training for jumping performance. Many ‘functional trainers’ have argued that you should train
quarter squats to improve your jump, because this is a movement that resembles actual
jumping. However, full squats build more muscle and lead to greater increases in jumping
performance than quarter squats.

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So where most athletes are specialized in specific movements and have certain skills,
bodybuilders are the most functional in a sense because their size makes them good jacks-of-all-
trades.

Recommended reading
The adaptations to strength training: morphological and neurological contributions to
increased strength

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Key take-home messages

 Muscle growth is part of the adaptation process your body goes through after muscle
tissue has undergone significant stress, starting with recovery (repairing damaged
muscle tissue) and ending with supercompensation (building new muscle tissue). As
such, adaptation is not something to avoid. It is the very goal of training.
 Muscle growth is primarily a local/regional/intrinsic process. Muscles grow
independently of each other based on factors occurring within that very muscle.
 The primary type of stress inducing muscle growth is mechanical tension on the muscle
fibers. Muscle damage, metabolic stress and exercise induced anabolic hormone
elevations have been postulated to play a role as well, but their supporting evidence is
much less compelling.
 Strength is influenced by muscle size but also by several other factors, chiefly:
o biomechanical factors, such as the muscle’s pennation angle and the positions of
its tendons that influence the muscle’s leverage;
o neural factors, such as inter- and intramuscular coordination of muscle (fibers)
and the speed of motor unit contractions (rate coding) that optimize how the
tension produced by your muscle fibers is translated into movement;
o metabolic factors, such as calcium metabolism.
In practice, however, within an individual, total muscle mass and strength
training performance are highly correlated.

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