ACTN3 Deficiency: Domestication of The Modern Human - Part 1 - Dispelling The Myths

Author's Note:

I am writing this because:

1. It has been the main focus of my physiology research for the past three years. 

2. I finally feel competent and confident enough to draw scientific hypotheses from that research.

3. Everyone else is wrong (what a surprise), and it bothers me something terrible. 

Introduction

Assuming you are an otherwise healthy adult human of ordinary size and proportion, your athletic potential is almost entirely determined by a single gene. Though many publications have referred to ACTN3 as ["the speed gene", "the sports gene", "the athlete gene", etc.], it is actually much more than that. In this article I will demonstrate that the deletion of this protein from the human genome is not a chance modification spurred on by externalities, but a hard-coded response to specific stimuli. 

In part 1 of this article I will provide a background on the gene and its function. I will also cover current scientific theories on the same and dismantle them with ruthless aplomb. 

In part 2 of this article I will explore gene-based training methodologies and nutritional planning for humans, both wild and domestic.

Disclaimer: Because I wish to finish this article in this lifetime and have very little time to write, non-controversial background information will be dramatically oversimplified. As always, I urge you to take nothing for granted, and to independently verify anything you question. 

Let us begin

In the microscopic world of Chromosome 11 sits a gene to encode the protein Alpha-Actinin-3. On the 577th position of this gene sits either an Arginine (R) or a premature stop codon (X). If there is an Arginine, you can properly encode the protein, if there is a stop codon, you cannot. Because we receive a copy from each parent, it is possible to have 2 copies of arginine (RR), one copy or arginine and a stop codon (RX), or two stop codons (XX). 

In fitness we often talk about fast/slow twitch fibers, or even of type I/IIa/IIb/IIx fibers, but there is rarely a dive into what defines a particular type of fiber. Yes, aerobic to the left and anaerobic to the right, but where is the line?

A "fast twitch" muscle fiber usually contains several isoforms of Myosin Heavy-Chain (MHC), Alpha-Actinin-2 (ACTN2), and Alpha-Actinin-3 (ACTN3). 

A "slow twitch" muscle fiber contains Myosin Light-Chain, as well as the slower isoform of MHC, ACTN2, and certain structural remodeling proteins not present in fast twitch fibers.

Given this definition, you might think that ACTN3 deficient people have no fast twitch muscle fibers, and you would be correct. 

Because ACTN3 deficient people still produce MHC, and all isoforms of MHC can bind to ACTN2, muscular development is severely impaired, but still possible. The resulting musculature (MHC dominant with no ACTN3) has no common name, but I will refer to it as "medium twitch".

ACTN3 deficiency results in smaller, slower, weaker humans with slower recovery and greater susceptibility to injury. This may be why 100% of non-human animals still have two copies of ACTN3. Among humans, ~84% have at least one working copy. I count myself among the 16% who do not. Why has mother nature so forsaken us? First, let us establish why she has not. 

The Fury 

When I developed my theory of hypertrophy, there was an abundance of research on the topic, the answers to the pertinent questions were just scattered. There were already solid papers on hypoxia, transporter proteins, and sarcoplasmic function, it just so happened that no one else bothered to put it all together. 

On ACTN3 there is next to nothing. It was discovered in 1993. A genetic panel was done on two brothers in Sri Lanka who suffered from an uncommon form of muscular dystrophy. Doctors noticed they both lacked ACTN3, and hypothesized that such deficiency was causal (makes me feel great, every time). After testing the seemingly healthy parents (also ACTN3 deficient), that hypothesis was dropped and the world was left to ponder the function of this mysterious protein.

28 years later and the scientific community somehow managed to distance itself even further from the answer. I do not blame the community at large; I owe the diligent scholars of muscle function a great deal in allowing me to develop my own theories. Conversely, I have never seen such lazy, misguided, and contradictory research as I have in searching for an answer to the ACTN3 question. Bad data begets bad data, and the obsession with sarcoplasmic reticulum calcium leak has generated a slew of papers which insist that this single facet of ACTN3 deficiency is not only its defining feature, but its evolutionary prerogative. They are wrong on both counts.

The Acknowledged Facts

1. ACTN3 deficiency causes greater rates of leakage of Ca2+ ions from the sarcoplasmic reticulum. The affects of this are attenuated by similar increases in Ca2+ binding proteins. 

2. ACTN3 deficiency causes huge increases in calcineurin during muscle contraction. Calsarcin-2, which would normally bind calcineurin in the presence of ACTN3, is instead bound by ACTN2. The excess calcineurin signals the muscle to adapt aerobically (transition towards slow twitch). 

Both of these processes result in more mitochondrial activity, resulting in more ATP being shuttled through the Krebs cycle. 

3. ACTN3 deficiency exists primarily in non-African populations.

4. The ACTN3 XX polymorphism appears to exhibit positive selection. 

The Worst Theory

Increased leakage of Ca2+ creates a transient state of energy inefficiency, causing an increased rate of muscular contraction, and thus creating a thermogenic effect. Increased mitochondrial activity means more processing of ATP, which also creates a thermogenic effect. Africa is hot. From these facts they theorize that ACTN3 deficiency is an adaptation to cold.

Why They Are Wrong

1. They acknowledge that leakage and reuptake of Ca2+ is mediated by Sarcoplasmic Reticulum Calcium ATPase 1 (SERCA1), but conveniently forget that SERCA1 is a transporter protein expressed preferentially in fast-twitch fibers. They focus on increased SERCA1 expression in ACTN3 deficiency within individual muscle cells without considering alterations in overall thermogenesis by fiber type distribution. A "medium twitch" fiber might express more SERCA1 than an ordinary fast-twitch fiber, but there are fewer of those fibers in ACTN3 deficient individuals. If total thermogenesis between XX/RR individuals is comparable, increased SERCA1 expression would be a compensatory mechanism to ACTN3 deficiency, rather than the reason for it. If total thermogenesis is greater in RR individuals (which I posit to be the case), it would be an incomplete compensatory mechanism. 

Translation: A man named XX makes 10 boilers a day in each of his three factories, for a total of 30 boilers. A man named RR makes only 7 boilers a day in each factory, but he owns six factories, for a total of 42 boilers. The man named XX generates more heat per factory, but the man named RR generates more total heat. 

2. Increased mitochondrial activity is, by definition, increased efficiency. Researchers will sometimes suggest that ACTN3 was lost due to concurrent "food scarcity" and "cold climate". The argument is preposterous because they ascribe the same functionality of mitochondria to have opposite effects. We are to believe that the additional ATP processing generates excess heat while simultaneously sparing calories. 

3. Every study that cites a latitudinal argument is simply bad science. There is NO latitudinal correlation to the presence or absence of ACTN3. Yes, the African Savannah, where nearly every individual has 2 working copies of ACTN3, is close to the equator. So is Sri Lanka, where ACTN3 deficiency was discovered. So is Mexico, where about a quarter of the population is ACTN3 deficient. Every adaptation that occurs outside of the African continent is not a response to cold weather. Large universities and otherwise intelligent researchers proffering the "Africa is hot" hypothesis as an answer to every question is infuriating. 

Theory #2

ACTN3 deficiency is correlated with distance from Africa and was positively selected in such populations due to improved endurance and caloric efficiency. This is evidenced by the highest rates of deficiency being observed in indigenous American populations, and the second highest rates being observed in South Asian populations. 

My Analysis

It provides a plausible explanation for why the null (XX) variant was positively selected in certain populations, but it says nothing of why it exists to begin with. Accomplishing more work while burning fewer calories is especially advantageous for nomadic peoples, so it is logical that those most suited to travel would travel most. I do not disagree that many high deficiency populations are distant from Africa, but there are also quite a few very close to Africa, such as my own. Thus, it is not "correlated" with distance from Africa, because the rate of deficiency is very high in nearby Italy (~22%), but much lower moving north to Lithuania (~10%) or east to Iran (~11%). Populations far from Africa have higher rates of deficiency, but distance from Africa is not determinative of rate. 

Theory #3

ACTN3 deficiency developed as an adaptive mechanism to support novel hunting strategies that coincided with migration away from the wildlife-rich savannah. Chief among these is "persistence hunting", whereby a heat and energy efficient human can pursue a less efficient animal until the animal relents from exhaustion. There are several variations of this theory, but they are all built upon the same foundation, namely the 2004 Bramble & Lieberman article available here: https://scholar.harvard.edu/dlieberman/publications/endurance-running-and-evolution-homo

The premise is that modern humans have undergone a broad series of adaptations which make them uniquely suited to endurance running. The only other mammals with comparable abilities to sustain speed over long distances are wild dogs and hyenas (scavengers). Early ACTN3-deficient man would be better suited to either run other animals to death, or to run efficiently towards already dead animals and compete with other scavengers. 

My Analysis

I greatly enjoyed that the above article was focused on biomechanics. From that perspective, it was brilliant and I have no complaints. I cannot, however, agree with its reasoning. There is no evidence that persistence hunting (or scavenging) was widely practiced by early man, and no circumstance to suggest that it should be practiced with greater frequency outside of Africa. 

There are several other issues with this theory:

1. Persistence hunting relies on the hunter's comparative advantage in heat dissipation. This advantage is only significant when the environment is hot. Such a strategy would be less effective as humans migrated to colder climates, meaning the adaptation would have occurred only in the populations which have no use for it. 

2. The only people (ancient or contemporary) known to regularly practice persistence hunting are the San of Southern Africa. Their ancestors diverged from other African populations about 200,000 years ago, which is about 140,000 years prior to the migration north which would populate the rest of the world. They have been doing it for 200,000 years with two copies of ACTN3. There is no reason to believe that the group which migrated north about 60,000 years ago would biologically adapt to the San lifestyle, when they themselves have found no reason to make such adaptations. 

3. East Africans, particularly Nilotic peoples, have evolved to possess most of the known "endurance" genes, as well as mechanically advantageous proportions (long legs, narrow hips, proximal weight distribution). They are inarguably "built" for distance running; no amount of training by athletes from other backgrounds has been able to overcome this genetic advantage. Despite an inordinate number of modifications which favor endurance running, East African populations almost universally possess two functional copies of ACTN3. 

Theory #4

ACTN3 deficiency predates migration out of Africa by about 20,000 years, but only underwent positive selection in populations outside Africa. Long runs of homozygosity surrounding the relevant gene indicate that widespread deficiency is the result of population bottlenecks. Basically, ACTN3 deficiency was washed out in Africa because of a large base population, but flourished in migrating populations due to small numbers and inbreeding. 

My Analysis

This theory is based on a different calculation than most. We cannot determine the actual age of a single polymorphism, so we derive estimates from algorithms and statistical models. Most estimates place the appearance of the first ACTN3 null gene at about 60,000 years ago. This model places it at more than 80,000 years ago. I disagree with both models, but I will address that later. I see two major issues with this theory:

1. Though there was undoubtedly a population bottleneck (and inbreeding) during the African exodus, successive bottlenecks should exhibit a linear increase in rates of deficiency. The initial Middle Eastern bottleneck should have resulted in less homogeneity than later bottlenecks in the far east. Under this model, it should be impossible that Israel has a higher rate of deficiency (~18%) than Russia (~14%).

2. The importance of the Middle Eastern bottleneck is overstated. While it is true that a proportionately small group of humans migrated out of Africa, the humans that remained did not form a unified social unit. Humans tended to form loose confederacies of no more than 500 members, regardless of their geographical location. More population diversity in greater Africa does not mean more genetic variability within individual societies. If ACTN3 deficiency existed for 20,000 years prior to migration out of Africa, it would still be there. 

Discussion: Poor Quality Muscle For Everyone

People misunderstand the function and significance of this gene because they misrepresent it as redundant. If we begin our analysis by assuming the gene is superfluous, or easily discarded for negligible benefits, we are handicapped by bias. It is a very important gene. No other animal on our planet has seen fit to discard it. Without it, we do not have true fast-twitch muscle fibers. We have turned ourselves into softer, slower, weaker versions of our ancestors; easy prey for any predator with a bit of resolve. 

Throughout our evolutionary history, we have compromised all of our physical and sensory attributes for the benefit of the brain, and this is no different. Our brains, particularly our prefrontal cortexes, have coevolved with our skeletal muscles. As the two largest consumers of resources, they are engaged in a sort of cold war over the finite (at the time of mutation, anyway) resources. The loss of ACTN3 means smaller, more aerobic muscles, as well as a 50% reduction in glycogenolysis. Efficient muscles that process glucose through the mitochondria, instead of through the wasteful Cori cycle, extract a lot more energy per molecule. A strong shift towards oxidative metabolism saves energy by using fatty acids (even more efficient). Conversely, the brain is now at liberty to engage in more non-oxidative metabolism, capitalizing on the available glucose to create the very same lactate which was denied to the muscles. It even uses the very same monocarboxylate transporters I discussed in my theory of hypertrophy. 

Earlier I mentioned that I did not agree with other estimates for the age of the ACTN3 null variant. As tempting as it is to believe that all 16% of us are direct descendants of one guy who had sex with every fertile woman in Egypt some 60,000 years ago, I do not believe it to be true. I think it is of much more recent origin, and that it has arisen in different populations concurrently (though assisted by inbreeding). I had previously sought to tie it to agriculture, as areas of early agriculture have populations disproportionately lacking ACTN3. I cannot definitively state that there is a correlation, however, as the Clovis burial site houses the 12,000 year old remains of a man without ACTN3.

Despite it predating modern agriculture, it is highly likely to have been influenced by diet. Readily available sources of glucose, such as fruits and cereal grains would have proliferated in temperate areas. Positive selection may have been a result of survivability in a low protein, high carbohydrate environment, which has been the environment of most humans for most of history. Unless increased lactate production in astrocytes and decreased lactate production in skeletal muscle confers an evolutionary benefit in the modern world, I do not anticipate that positive selection will continue.   

I do, however, believe it to be hard-coded into existing human DNA, regardless of whether the protein is currently being expressed. Even in populations such as the Maasai and Yoruba, where having two functional copies of ACTN3 is near universal, individual proteins (which do not cause loss of function, unlike R577X) are disappearing. Multiple generations of well-fed and under-exercised people will cause more spontaneous deletion. If our ancestors’ DNA thought it a worthwhile tradeoff while animal attack was a leading cause of death, modern DNA will eventually come around.

We are fast evolving away from our current physical form. Future humans will look somewhat like aliens (grays, if you will) as stereotypically portrayed, with large brains and frail bodies. One can only imagine how boring our sports will become.      

So now what? If you are a soft and doughy man of the future, I will provide guidance on how to retain a respectable human form. If you are a hard and lean relic of the past, I will provide guidance on how to make the most of what you have.

Locked Out

 I was locked out of creatorofchampions.blogspot.com. It says author is "unknown" because they can't handle the truth. It was me. I was the author!

Originally written on December 24, 2014

Muscular Hypertrophy as a Histological Defense Mechanism

Abstract

Prevailing theories of hypertrophy assert that it is a form of overcompensation in response to microtrauma induced by mechanical loading. There is undoubtedly some degree of soft tissue remodeling in accordance with Davis’ law, but no degree of physiological cross-sectional area augmentation can adequately explain the extreme degree of hypertrophy observed in many strength and physique athletes. Increases in muscle mass without correlating increases in contractile force are attributed to sarcoplasmic hypertrophy; a proliferation of sarcoplasm in response to chronic deficiencies in localized glycogen stores induced by anaerobic training. The functionally superfluous muscle mass exhibited by the aforementioned athletes can indeed be attributed to a glycogen-mediated increase in cell volume, but the process by which this occurs has been misinterpreted as a relative function of soft tissue restructuring. The widely accepted hypotheses of cellular alteration as a response to mechanical stress and/or imposed energy demands implies the existence of a uniquely maladaptive and redundant evolutionary trait suited more to modern aesthetics than Pleistocene survival. It is far more likely that structural adaptations of individual myocytes serve to facilitate acid-base homeostasis, which is threatened by intracellular hydrogen ions liberated via glycolysis. Intracellular alkalization via lactate dehydrogenase is subject to feedback inhibition, which consigns the rate of glycolysis to the efficiency of monocarboxylate transporters. All measures of anaerobic efficiency, to include glycogen storage and utilization, are manifestly dependent on the modulation of transporter proteins. This research aims to demonstrate that muscular hypertrophy is the collateral result of survival-based structural modifications, and therefore only tangentially related to conventional loading-based training protocols.    

Addendum - The Devil's Playthings

We've established that knowing where you stand is essential for Deadlifting, but what is to be done with those wandering hands?

Because I'm writing this guide for my class, in preparation for The Segugio's practicum of merciless scrutiny, I will restrict it to a collection of key points, rather than a comprehensive tome on the art of grasping.

• The purpose of an alternate grip is to provide bar stability and prevent rolling.
• The dominant hand should be supinated, to allow the non-dominant side to work at a comparative mechanical advantage.
• The goal of dominant hand supination is equilibrium in the distribution of applied forces, or, as some may phrase it: "making sure one side doesn't rise faster than the other".
• An alternate grip can be used on ANY Deadlift.   
• The only condition for using an alternate grip is that your hand spacing be shoulder-width. 
• In an alternate grip, one shoulder is medially rotated, while the other is laterally rotated. Horizontal abduction/adduction causes a progressive disparity in the distance from each hand to the center-line of the body, and thereby inhibits a streamlined transfer of force.
• ^This may also be phrased as "one arm gets shorter than the other".
• In almost all cases, a narrower grip offers better leverage. Never grip wider than absolutely necessary.
• An alternate grip is often used as default in the Conventional Deadlift, because the narrowest grip which can be achieved [without disrupting the line of pull] is approximately shoulder-width. One should keep in mind, however, that...
• An alternate grip can be used on ANY Deadlift.  
• A Sumo Deadlift with an alternate grip is sometimes referred to as a Mixed-Grip Deadlift, but it's still a Sumo, and the execution, aside from hand spacing, is identical. 
• Hand spacing on a double-pronated Sumo should be as close as possible while still allowing a proper set-up (too close inhibits retraction of scapula).

If you're reading this, it's very likely that you'll be assigned one of the Deadlifts. You're welcome.

End Transmission. 

Handbook For The Recently Deceased

The last article ended somewhat abruptly, due to the nature of my priorities, or perhaps the priorities of my nature. In either case, I regret nothing. Though I sought to make the tables as simple as possible, I'm sure I failed. The only thing more certain than the accuracy of my writing is its incomprehensibility. That being said, any ambiguities which may exist are explained in the notes below. I know it reads like stereo instructions, but give it a try, anyway. 

• "Wide" stance means as wide as can be maintained with hips below knees and neutral foot position. This is not very wide for most people.
• "Jump" stance is slightly inside the hips with quadriceps loaded. The same stance that would be taken with a hang clean. 
• Hip Angle is a measure of the position of the hip in relation to the knee, where 0 degrees is vertical alignment with hip above knee, and 180 degrees is vertical alignment with knee above hip.
• Leverage is an approximation of the lifter's mechanical advantage given their position in relation to the bar. A more advantageous lever requires less applied force to break inertia. 
• As mechanical advantage increases, a successful lift is increasingly determined by [external] force distribution.
• As mechanical advantage decreases, a successful lift is increasingly determined by [intramuscular] force generation. 
• Rep range is my suggestion based on the applicability of each exercise towards certain ends.
• A properly executed Sumo Deadlift requires torque from lateral rotation and abduction, which means stance must be reset after every rep. 
• Intensity is expressed as a percentage of Conventional 1RM. You can't lift 105% of your 1RM, and you shouldn't attempt a 1RM with a Stiff-Legged Deadlift. 

• The Primary Joint Actions are the mechanical processes by which the majority of work is done.
• The Secondary Joint Actions are the mechanical processes by which a comparatively smaller, but uniquely relevant amount of work is done.
• Initiation reflects the muscle group which exerts the greatest amount of force on the bar from the starting position. 
• Sticking Point is, for various reasons, the most likely place where the war against gravity will be lost.
• Limiting Variable is the most common impediment to proper execution. 

The Physics of Necromancy

There's a bar on the ground loaded with 225. It's collared and chalked and there's no one nearby. You want to ignore it. You hope that someone will appear to lift it, but it doesn't happen. You are relieved to see a gym employee walking the floor, as they will surely dismantle equipment not in use. You watch in horror as they calmly walk by it, completely oblivious to the siren's call. You can't resist the urge any longer. You know that the only way to get relief is to pick it up and put it back exactly where you found it. But how? How does one properly manipulate weighted belles against gravity to accomplish this "dead-lift"?

Training to Strengths

There is no universal formula to gauge perfect leverage on a Deadlift. If such a thing could exist, I would have invented it by now. We vary both in absolute and proportional dimensions; that is, even if two people had the same height, weight, mobility, and training experience, their ideal starting positions may be entirely different. One person may have excessively long arms and legs, and narrow shoulders. Another may have a long torso, short arms, and broad shoulders. Finding the position of greatest mechanical advantage is a perpetual game of trial and error.

In a perfect world, that would be the end of my article.

Finding this elusive angle should be done under the guidance of a professional, as we very often confuse what feels right for what is actually right. Deadlifts are uncomfortable, particularly those variants which require a prolonged state of tetanus for the proper distribution of forces. Most people you will meet have anterior tilt to some degree, usually severe. There are muscle imbalances which may be pronounced in athletes training in anterior dominant (boxing) or posterior dominant (sprinting) sports. Finding an ideal position should not be a product of deficiencies. No one has an ideal angle of 20 degrees; they simply lack the ability to hinge. With proper mobility and flexibility, we can employ all (or none, do what you like) styles of Deadlift in our training.  

Addressing Weaknesses

Other than those who learned from Segugio, I've never seen a Sumo Deadlift executed correctly. Poor hip mobility is a fact of life for most people, and seems "normal", but in fact it's a debilitating problem which is denying an already depressed population the sublime pleasures of hinging and thrusting. The Deadlift consists of five sequential preparatory cues followed by one execution cue:

1. Placement of feet as close to bar as possible without interfering with the line of pull against gravity.
2. Placement of hands in a mechanically advantageous position.
3. Retract and depress scapula by locking the lats (creates initial pull)
4. Extend the elbow by locking the triceps (prevents interference in line of pull by smaller muscles)

Your knees should still be fully extended! Start over!

5. Drop the hips while keeping your upper body entirely rigid, creating a lever and ensuring that the downward force of your body exerts upward force on the bar.

If it's not extremely uncomfortable, you're wrong! Start over!

6. Drive through the heels, extending the knees, hips, and trunk simultaneously.

*My skilled hands are busy. I'll get back to this article later. Maybe. Tables below.

Hypertrophy Hyperbole

There has never been a greater schism between what I believe, and what I'd like to believe. We were wrong. All of us, myself included.

How did this happen?

Bodybuilding, our beloved sport, is an American obsession. Had it enough appeal somewhere else, I would have left long ago. This isn't a tirade about what I think is right or wrong about our fair nation, but a context in which to interpret the decades of deception. 

Bodybuilding was able to grow as an industry not due to its appeal as a spectator sport, but its appeal as a means for personal physical improvement. Of course, this was (still is) exploited to its maximum potential. The "secret" to success is whatever ridiculous idea can be sold at the highest profit margin. This is not to say that the industry is evil; it preys on the vanity and stupidity of the masses no more or less than any other. As often happens, however, profit began to define reality, and mainstream science was manipulated to support the whims of supplement manufacturers and magazine publishers.

Each and every month, there is at least one "pro bodybuilder" routine posted in every major bodybuilding publication. That they've been some variation of the same 3-4 sets of 8-12 reps for the last half century seems to go unnoticed. Of course, the bodybuilder uses X Product with X Protocol, which is why he looks the way he does. Only by combining a sugary tub of dust with an obviously ineffective routine can one achieve such excellence.

This is all old news to anyone even casually involved in the sport. We often cite ridiculous claims made by manufacturers, but never stop to think of the overarching structure which allows this nonsense to thrive. All of the accredited personal training organizations have bought into the lies, using selective "science" to back the preposterous claims of the bodybuilding world. Check your NASM book, or even your CSCS book. The key to hypertrophy is doing a few sets of 8-12. Science which counters this is very strongly suppressed, as it would be ruinous to the fitness world.

All of the studies which support the "hypertrophy rep range" idea were done on groups of untrained individuals. What they don't tell you is that while any sort of muscoskeletal stimulus will cause hypertrophy in an untrained person, this is no longer the case after 18-24 months of consistent training. They're safe in pushing the idea, because less than 1% of the people who spend money in bodybuilding will ever meet that threshold.

I've often said that the truth doesn't sell. I had no idea how right I was.  

The Science of Strength

Strength protocols are extremely popular recommendations to novice trainees these days. Replete with junk science, bad advice, and self-aggrandizing horse shit, works of Grade-A toilet paper such as "Starting Strength" have flooded the internet. It's particularly offensive because of its viral replication strategy, outlined below:

1. Novice idiot is convinced to read "starting strength", trains for a few months, experiences gains
2. Novice idiot considers himself an expert, pitches the gospel to unsuspecting and desperate minds

Warning: RAEL SYINTS BEGINS HERE

First, let us understand:

Strength is the amount of force a muscle can exert at a constant speed. If you can move 500lbs across the space of one meter in three seconds (bench press), you are strong.

Power is the amount of total force output measured in work/time. If you can move 200lbs across the space of three meters in one second (snatch), you are powerful.

Adaptations are specific to the stimulus provided. This is agreed upon many times over and is not a point of contention. Adaptations, however, are also versatile, which makes similar adaptations redundant. Though we would all be fine with redundancy of superpowers, our bodies (playa haters) find such things to be a pointless waste of resources. Your body will only adapt if it absolutely has to. If one adaptation is sufficient to cover multiple stresses, you do not "need" another. Hence, we have biofeedback mechanisms which prevent anything from altering homeostasis. When homeostasis is altered, it is ALWAYS by the most cost-efficient means.

Power is mostly a measure of neural efficiency. If you train "explosively", your body adapts by increasing the surface area of the axon terminal at the neuromuscular junction, thereby increasing acetylcholine output, which leads to a more rapid and complete depolarization of the muscle cell. The calcium pump fires according to the strength of this action potential, which determines how hard the muscle contracts. Existing motor neurons adapt to efficiently innervate more and more existing myocytes. Tendon strength increases (so that your trigger-happy calcium pump doesn't tear the muscle off the bone), Golgi Tendon Organ desensitizes, phosphocreatine stores may increase, and dormant (but already existing!) Type IIB muscle fibers may become active.

Strength is basically a measure of neural efficiency, but the increased time under tension causes significant muscle damage and inflammation, which necessitates further adaptations. Existing muscle cells repair the damage, and sometimes (especially during the first 18 months of training) we're fortunate enough to have them use building materials of ever-increasing quality. A strength training stimulus will also elicit a limited degree of hypertrophy in an untrained person, as a base amount of musculature is necessary for any athletic performance. Once said degree of muscularity is achieved (still very very far removed from bodybuilder status), existing muscles continue to strengthen themselves, assuming consistent stimulus. There will be a volume-dependent (though still very limited) increase in glycogen storage, glycolytic enzymes, and intracellular fluid.

Hypertrophy was (until I wrote this article) believed to occur via magic when training with repetitions above the strength threshold (~8), but below the "endurance" threshold (~16). The idea of  "endurance" is founded on the laughable belief that high rep ranges primarily stimulate Type 1 (oxidative) muscle fibers. Get it? Because oxygen is being used before the lactate threshold is surpassed! How/Why this differs from every other physical activity ever is never explained.

Back to hypertrophy. In order to push the pseudo-scientific idea that something special occurs between reps 8 and 16 (or 6 and 20, if you prefer), the bodybuilding media has cherry-picked and improperly applied certain biological theories. Because these theories are laden with actual facts, and applicable in other contexts, it's very hard to see why what they're selling is bullshit. I'll do my best to explain:

What they say: Muscle fiber size runs from small to large Type I -> Type IIA -> Type IIB -> Type IIX
The larger (anaerobic) cells also have the most potential for growth, therefore the most size is to be gained from training heavy.

Why it's bullshit: Muscle fiber type distribution varies among muscle groups. The greatest size increases will come from hypertrophy of the existing fibers, not hypertrophy of the fibers you wish were there.

What they say: Heavy training causes the conversion of smaller fibers to larger fibers Type I -> Type II, etc. Therefore, we should convert as many fibers as possible to the most anaerobic type.

Why it's bullshit: Sedentary people have the greatest proportion of Type IIX fibers. Anaerobic cells cost less to maintain, and are seldom activated. Fiber type conversion only happens in extremely specialized athletes (ultramarathoners and olympic lifters), as someone probably mentioned in the greatest cardio article ever written.

What they say: Muscles are activated according to the size principle (smallest muscle fibers required to exert the necessary force). Since our concern is stimulating anaerobic fibers, we should use the heaviest possible weight (with good form).

Why it's bullshit: The size principle applies just as well in a fatigued state. You can work anaerobically with a heavy weight, but a light weight becomes equally anaerobic after a few reps. 

Now that we've covered what doesn't cause hypertrophy, we can get to the depressing truth about what does.

End Game

Hypertrophy is not a measure of strength, nor of power, nor of ability. Hypertrophy is only incidentally related to any other form of training. It's a very costly response to a stress that cannot be handled via less expensive means.

The primary factors influencing hypertrophy are: Hypoxia and Acidity

Hypertrophy is a measure of metabolic waste. Fast glycolysis creates H+ ions, which accumulate due to occlusion, and decrease the pH of the muscle. The H+ must be neutralized with Pyruvate (formed internally, from glycogen) to create Lactate, which is then shuttled to the liver to create glucose, which returns to the muscle to repeat the process. Vascularization occurs because the [toxic] blood is trapped in the working muscle, and needs to be cleared before the pH of your blood drops and you die of acidosis.

During a "pump", interstitial fluid increases, and myocyte size decreases (beacuse osmosis). During this bout of hypoxia, intramuscular IGF-1 stimulates cell proliferation. Regulatory Volume Increase (no, seriously, that's what it's called) occurs on site via charged ions moving through the proton gradient in spite of osmotic pressure. When normal oxygen levels are restored, the myocytes are expanded, and the proliferated cells become differentiated. These small cells are repeatedly exposed to high osmotic pressure, and their proton gradients adapt to become aggressively resistant, increasing cell volume with each bout.

What does it all mean?

An effective hypertrophy protocol requires little complexity and much less weight than we'd all like to believe. Training with moderate volume and light weight, and taking all sets to failure with 15-30 second intervals is pretty much all that's needed.

I attempted to train for hypertrophy in accordance with the aforementioned theory this morning. I concluded that I'm happy just the way I am. 

 

Fact Check: Metabolic Damage

I strongly prefer to present the affirmative truth, rather than challenge the claims of other fitness personae, but this rebuttal was specifically requested, and I'm not one to deny pleasures.

I've always had mixed opinions towards the ideas of Layne Norton, but it's safe to say he's not my least favorite person in the world. I recently watched his Metabolic Damage series (biolayne 9, 15, 16, 20). My assessment is provided below.

Opening disposition: 0 (neutral)
Bonus: +10 for hating Lyle McDonald
Penalty: -10 for exceptionally boring videos

biolayne 9

4:33  "...they essentially get no caloric value from that type of cardio"
In reference to people on very low calorie diets. It's one thing to argue about a reduced metabolic rate, it's quite another to claim that hungry people are able to create ATP without substrates.

8:28 "...it's also there to maximize your metabolic capacity"
In reference to ideal utilization of an offseason period. We are in absolute agreement.

10:33 "...really focus on slowly and deliberately adding calories over time"
In reference to intake progression during the offseason. Agree. There should be regular minute transition phases between the peak of a precontest diet and the peak of an offseason diet.  

11:03 "...you should eat the maximum amount of calories that you possibly can while still losing bodyfat at the appropriate rate"
In reference to not drastically cutting calories during contest prep. This guy seems legit, I'm starting to wonder why someone would consider us so different.

12:19 "...low intensity cardio has been shown to reduce metabolic rate over time"
Ah. Curiosity sated. It's technically not an inaccurate statement, it's just an irrelevant one. Aerobic fitness reduces your resting metabolic rate (2-5%). I sure hope so. If you get winded during the walk from your parking spot to your destination, you'll burn more calories on the trip than a fit person. I think I'll accept the trade-off and just park a little farther from the door.

12:46 "... you actually get to the point where you need that amount of cardio just to maintain your weight"
No. You don't get 100% energy efficiency from becoming aerobically fit. Over time, you'll require less energy expenditure to do the same task, but the decline in expenditure does not cover the increase in ability.

Running at 6mph for 1 hour may initially burn 1,200 calories
When you've become fit, it may only burn 900 calories
At that level of fitness, you can maintain an 8mph pace at the same PER (perceived exertion rate) for the hour, and burn 1,400 calories

Even if you choose not to progress, and even at maximal efficiency, that hour of running will still incur the energy costs of work. You still moved an object from point A to point B using ATP as fuel, even if you used 1/4 of the fuel an obese person would require. Energy efficiency is not energy independence!

13:16 "...I would even say one hour of low intensity cardio a day is complete overkill"
Sure sounds like it. If it's a 20 minute walk to the train station, and the elevator is broken at work, you need to be sure to bring a wheelchair, lest you destroy your mitochondria from such reckless expenditure. We are aerobic creatures! It takes about 90 minutes to even achieve maximum substrate efficiency (where your body is maximally reliant on beta-oxidation for energy production). Looks like someone needs to read The Seugio Unified Theory of Cardio.

13:33 "...but think about a marathon runner, or a swimmer, or somebody who does a ton of low intensity cardio. If you look at somebody training for a marathon, there is no way they should be able to eat enough calories to maintain their bodyweight, but they do (maintain their weight)"
You mean like Michael Phelps? Or triaheletes who eat 6-7,000 calories on a training day? The above quote is absolutely baseless. Layne might believe that endurance athletes simply exist at the same weight regardless of diet, but they're often just as dedicated to their nutrition as people in the strength world.

14:27 "...Anybody who's been through a long contest prep doing a lot of low intensity cardio probably knows exactly what I'm talking about."
I sure don't, but maybe I'm stupid. Maybe if you explained it to Jay Cutler or Kai Greene. Low intensity steady-state cardio seems to work for every Mr. Olympia ever, and Ronnie Coleman won eight straight. According to Layne, low intensity cardio stops working after an initial metabolic adjustment, but somehow, Coleman was able to get lean every year using the same stairmaster. Someone should go tell those guys that they're wasting their time.

14:39 "...Low intensity steady state cardio is a mindless easy form of cardio"
I think someone is confusing an old lady falling asleep on a treadmill for a trained athlete maintaining a steady pace for 90 minutes.

15:06 "...An hour of steady state cardio at 3mph on a treadmill, either that, or doing six 30-second sprints"
In reference to a study demonstrating that the aforementioned sprint intervals proved more successful at targeting bodyfat. Somehow I feel it fair to infer that the people involved in this experiment were not exactly stellar athletes. Untrained people responding to severe adaptive stress vs. using artificially low intensity to ensure no aerobic adaptations occur. Perhaps this dumb shit can convince people with no background in science, but it's utter garbage to the trained eye.

15:50 "...I don't wanna hear about 'you burn a greater percentage of fat while burning low intensity cardio' "
I wonder why. Is it because it's true? Yeah, better to not hear it then; people hate the truth.

21:48 "...That dieting and binging cycle is about the worst thing you can go through"
Advocating slow diet transitions. Now he's making sense again.

23:32 "...They end up spinning their wheels over time"
In reference to people who plan unreasonably restrictive diets and compensate with a weekly cheat meal. I've warned time and time again about not underestimating the power of insulin. His rationale may be different, but we agree on planning diets with no cheat meals.

25:19 "...Or maybe even some low intensity cardio"
In reference to people finding ways to continue progressing without drastic cuts in calories. I agree with his statement. I don't think he agrees with his statement.

biolayne 15

7:10 "...I'm talking about anybody who wants long term fat loss"
In reference to the importance of metabolic capacity for the achievement of goals. Absolutely. There will be a Segugio article on this very topic in the near future.

9:20 "...Eating as many calories as you possibly can, doing as little cardio as you possibly can, while still losing weight"
In reference to weight loss at the beginning of a cut. It's valid to an extent, but the benefits of cardio generally far exceed the benefits of inefficient metabolism.

10:22 "...You add calories extremely slowly"
In reference to using very slow caloric progression rather than transition phases when starting a bulk. Again, I agree that his argument is valid, but he seems to have convinced himself that expenditure doesn't exist. He's advocating that calories be raised in very small (~30) weekly increments. It's not wrong, it's just almost impossible to do. Let's hope his athletes are mindful of the extra oat flake that fell out of the scoop. Don't eat it... he's watching.

biolayne 16

10:47 "...The bodyfat set point theory"
I don't care to discuss this at length at the moment, suffice to say we agree.

17:06 "...Exercise induced thermogenesis goes down"
In reference to steady state cardio (of course). Not incorrect, just entirely misleading.

19:04 "...The adaptations your body makes while you're doing that is trying to get you back to homeostasis"
In reference to the body's propensity to set conditions for fat storage during very low calorie diets. This is proven. I addressed it as a consideration when planning fasted cardio. Yes, my article really was that good.

29:07 "...If we go very low calorie with excessive exercise"
This accounts for two entirely separate conditions. Just because they're often done in tandem doesn't mean their effects are interchangeable.

31:36 "...And now you're doing that two hours of cardio a day"
False premise. This is again presenting cardio as an intrinsic by-product of a starvation diet.

33:00 "...Fat loss resumes"
In reference to slowly cutting intake to maintain rate of fat loss after creating an "energy cushion" (amirite) via increase of metabolic capacity. I agree. I'm just curious as to why someone who has championed maintaining the highest possible level of caloric intake doesn't first increase expenditure. The Segugio would. Ooooooh.

35:22 "...If you don't plan for this stuff, you're going to fail"
In reference to understanding your body's defense mechanisms deployed during periods of caloric restriction. Correct. This is why crash diets don't work. The reference used here was rather excellent.

biolayne 20

5:59 "...What I'm not okay with is suffering for the sake of suffering"
It doesn't have to be related to fitness. I addressed this concern in a piece I wrote while in service.

Closing disposition: -1 (slightly unfavorable)
(11 positive, 12 negative, 3 neutral) I started with a mixed opinion of his work, and I'm ending with about the same opinion. Alright then, cardio time.