Build Size & Strength With Isometric Co-Contractions: 4% Increase in Arm Circumference and ~20% More Strength With Less Than 10 Minutes of "Flexing" Per Week

Big guns without weights? True - the question yet remains: "How big?"

I am psyched and the reason is the advanced access publication of the results of the latest study from the Department of Sports and Life Science at the National Institute of Fitness and Sports in Kanoya, Japan (Maeo. 2013b).

Why? Well, it claims to solve two of the most urgent issues that keep our sedentary fellow men (and women ;-) from working out: The lack of equipment and the lack of time, exactly those two factors the average American and European slacker pleads as an excuse for not making the necessary, since potentially life-saving physical investments into "metabolic currency" (this is a term my good friend Carl Lanore uses to refer functional muscle mass).

"Big guns without weights? You're kiddin', bro!"

Actually the idea of using simultaneous voluntary contractions of antagonistic muscle pairs (aka co-contraction) to improve muscle strength in the absence of external apparatuses is not new. The voluntary co-con traction of elbow flexors and extensors you can see in the photo in the red "This is how it's done" box, for example, may look ludacris (imagine doing that at the gym), its efficacy is however backed by previous research and its working principle is as simple as ingenious: Biceps and triceps, i.e. elbow flexor and extensor, produce resistive forces that act against each other (Tyler. 1986), so that one muscle actually "trains" the other.

You can learn more about training biceps & triceps at the SuppVersity

Training the Individual Parts of the Triceps

Find the Best Triceps Exercises (EMG Data)

Explore the Best Biceps Exercises (EMG Data)

Train Bis + Tris on a Single Day & Grow!

Add 0.5 Inch To Your Arms in 5 Minutes

Disproportionate Triceps Growth? Is It Real?

In their initial investigation into the effects of muscular co-contraction, the results of which have been published in the International Journal of Sports Medicine in July 2013 (Maeo. 2013b), the researchers have been able to confirm that the muscular activity that occurs during the voluntary co-contractions is a sufficient training stimulus for improving the strength capability of both muscles (Maeo et al. 2013a).

"In fact, previous studies that adopted co-contraction training for elbow flexors and extensors (Driss et al. 2013; MacKenzie et al. 2010; Maeo et al. 2013) found significant increases in the strength capability, as well as agonist electromyographic (EMG) activity during isometric maximal voluntary contraction (MVV) (MacKenzie et al. 2010; Maeo et al. 2013), of the two muscle groups. the previous findings cited above support the idea that co-contraction can be an effective training modality, which does not require any external apparatus, for increasing muscle strength." (Maeo. 2013b)

So, while we are pretty certain that "standing there and contracting your bis and tris" can increase muscle strength (learn how to build strength), there is a scarcity of evidence that would allow us to make reliable statements about the effects of voluntary muscular cocontractions on muscle size (learn how to build muscle). It is thus only logical that the intention of Sumiaki Maeo's, Yasuhide Yoshitake's, Yohei Takai's, Tetsuo Fukunaga's and Hiroaki Kanehisa's follow up study was "to clarify neuromuscular adaptations following 12-week maximal voluntary co-contraction training" (Maeo. 2013b). In that, the researchers hypothesized that

• 

  If you feel like a shadow of yourself, betaine may help | learn more

  the training modality with maximal voluntary co-contraction would increase both size and strength capability of the exercised muscles, and
• training unsing co-contractions does not change involuntary coactivation level during MVC of the agonist alone

In other words: The researchers wanted to make sure that (a) this form of training builds strength and muscle and (b) that it does not have lasting potentially performance decreasing effects on the co-activation of the triceps / biceps, when you actually want to use only one of them (imagine you want to curl the weight up and your triceps works against you).

The study protocol

To satisfy their research interest, the researchers from the Department of Sports and Life Science at the Japanese National Institute of Fitness and Sports in Kanoya recruited 16 healthy young men.

Don't neglect the proven benefits of periodization: "Six Weeks On + Three Weeks Off" Macrocycle Yields Identical Gains Strength and Size Gains as Continuous Training | more

The guys, who were in their early twenties, lean, healthy and habitually active, but not involved in regular exercise programs with a duration and frequency of more than two 30 minute exercise sessions per week, were then randomly assigned to two groups: A training group (T) with 9 participants and an inactive control group (C) with 7 participants. It goes without saying that all participants had to abstain from additional physical activity over the course of the whole study period during.

In those 12 weeks the subjects in the the subjects in T group participated in a 12-week training program with maximal voluntary co-contraction of the elbow flexors and extensors of the right arm 3 times per week.

Usually this would be the paragraph of this SuppVersity article, where I would give you a concise summary of the exercise protocol. In view of the fact that I doubt that many of you are actually familiar with muscular co-contractions, I decided to use a somewhat abridged quote of  the scientists' lengthy, but comprehensive explanation of the procedure (see red box).

This is how it's done: In a standing position with the feet shoulder width apart, upper arm vertical to the ground, the elbow joint at 90° (full extension = 180°), forearm in a neutral (middle of supinated and pronated) position you will perform a 4-s muscle isometric co-contraction followed by 4-s muscle relaxation (total volume: 10 times per set, 5 sets per session; rest: 2 min between sets). Make sure to perform each voluntary co-contraction as rapidly as possible and sustain maximal effort for full 4s!

Basically what the subjects were doing could be summarize as 10x4s maximal isometric muscle contractions with 4s break between each contraction for one set and 5 of these sets with an interim of 2 minutes between each of them three times per week.

Now for those surprisingly impressive results

If you do the math and add up the actual time under tension for this 12-week experimental intervention, you will get 10 × 4s isometric contractions × 5 sets × 3 / week × 12 weeks = 7200s or 2h. That's not really much considering the fact that it lead to strength and size increases of +15% / +27% and 4% / 4% in the elbow flexors (biceps) and extensors (triceps) of the previously more or less untrained, but no necessarily sedentary subjects.

Figure 1: Pre vs. post measures of muscle thickness, MVC torque and coactivation level (Maeo. 2013b)

As you can read in the small box in Figure 1 the increases in size and strength did not occur rapidly after two or three weeks and were then followed by a plateau.In fact, the researchers recorded statistically significant strength and measurable, but statistically not yet significant size gains after 4 weeks.

Probably effective for increases in dynamic performance, as well

Now, brute strength and a huge muscle mass are by no means what all athletes are striving for. For many athletes improving their dynamic performance and strength, which would have required the measurement of changes in isokinetic torques for elbow flexors and extensors in both eccentric and concentric conditions, is at least as important. It is thus more than noteworthy that data from Maoe et al.'s previous 4-week study (Maeo. 2013a),

"[...]in which untrained individuals conducted 4-week co-contraction training, showed that the co-contraction training significantly increased isokinetic torques for elbow flexors and extensors in both eccentric and concentric conditions." (Maeo. 2013b)

As the researchers rightly point out, we do thus have reason to believe that "contraction training is also effective for improving dynamic performance, at least for untrained individuals" (Maeo. 2013b). With respect to trained athletes, the reaserchers do yet argue that they'd require higher exercise intensities to achieve additional improvement in muscle strength than non-athletes (Alway. 1992; Cormie. 2011). This, as well as the emphasis sports specific training puts on ballistic, plyometric, and weightlifting exercises involving sports-specific and/or multi-joint movements (Cormie. 2011), make it difficult to believe that similar training results could be achieved by performing maximal voluntary co-contraction.

Suggested read: "Advanced Trainees Benefit from Increased Training Volume!" | more

Great! But nothing a trained individual can benefit from? It's obvious that someone with a 50cm biceps is not going to add another 2cm in 12 weeks in the course of which he lies around on the sofy and performs 5 sets of voluntary maximal co-contructions thrice a week.

This does yet not mean that this relatively unknown training stimulus cannot make a valuable addition to his training regimen... and let's be honest, haven't we all had a pro-bodybuilder give us a bro-scientific lecture on how flexing, in and out of itself nothing, but a voluntary maximal contraction (albeit not necessarily with antagonistic co-contractions for every muscle part) is a vital part of any hypertrophy oriented strength training routine?

References:

• Alway, S. E., Grumbt, W. H., Stray-Gundersen, J. & Gonyea, W. J. (1992). Effects of resistance training on elbow flexors of highly competitive bodybuilders. Journal of Applied Physiology, 72(4), 1512-1521.
• Cormie, P., McGuigan, M. R., & Newton, R. U. (2011). Developing maximal neuromuscular power. Sports medicine, 41(1), 17-38.
• Maeo, S., Yoshitake, Y., Takai, Y., Fukunaga, T., & Kanehisa, H. (2013). Neuromuscular adaptations following 12-week maximal voluntary co-contraction training. European Journal of Applied Physiology, 1-11.
• Maeo, S., Yoshitake, Y., Takai, Y., Fukunaga, T., & Kanehisa, H. (2013). Effect of short-term maximal voluntary co-contraction training on neuromuscular function. International journal of sports medicine, (EFirst). 
• Tyler, A. E., & Hutton, R. S. (1986). Was Sherrington right about co-contractions?. Brain research, 370(1), 171-175.

Intermittent Thoughts on Building Muscle: The Skeletal Muscle Hypertrophy 101 - Part 2: Getting Big Means Growing Beyond Temporary Physiological Limits.

Image 1: This is another type of "dysfunctional muscle"; distinct from the one we are talking about, here

Although I assume that you all have read the last installment of the Intermittent Thoughts, I took FatFree's comment that he (or she?) was missing the "too comlicated check box" from the old design to the heart (I do so with every comment, btw, so keep them coming) and kick off today's installment of "The Thoughts" with a brief and even more "dumbed down" summary of what we have learned about the (possibly) ascertained and, even if human skeletal muscle hyperplasia existed, dominant factors in the trinity of skeletal muscle growth: Protein synthestic increases in myonuclear domain sizes and the satellite cell driven incorporation of new myonuclei.

Getting big goes beyond ballooning up

You probably will remember the balloon-metaphor, I introduced in the red infobox toward the end of the last installment. Let's briefly get back to that and use it to reavaluate the results from the Quaisar study (Qaisar. 2011, see also "What is Hypertrophy"). Rizwan Qaisar and his colleagues from the Uppsala University in Sweden had analyzed the differential effect of insulin-like growth factor 1 (IGF1) over- and myostatin-underexpression on muscular size and function (the latter is important, since we know that a complete lack of the "muscle growth blocker" myostatin leads to huge, but disfunctional / weak muscles). 

Figure 1: Domain sizes of EDL and soleus muscle fibers in wild-type control, myostatin negative and IGF1 overexpressing mice (data based on Qaisar. 2011)

Now to really understand the meaning of what may be the main message of the study, it is imperative to understand the basic architecture of muscle fibers. If you think about a complete muscle fiber as a bundle of ballons that is wrapped into a strechable net, then each balloon would represent one myonuclear domain. The owe their name to the fact that they actually are the "domains" which surrounding a single myonucleus (lat. plural "myonuclei") within a given skeletal myocyte, which - contrary to other cells in your body - has the ability to hold multiple nuclei. Now, the most obvious determinant of the myonuclear domain size is the ratio of protein in- to protein efflux. And it is this connection on which researchers base their belief that by simply measuring the protein synthetic response to exercise and/or supplementation would suffice to predict long-term increases in muscle size (and subsequently strength / performance).

Growth is limited and myostatin is not just a pain in the ass of anyone who wants to "get big"

Image 2: Sketch of a mammalian skeletal muscle fiber - myonucleus (turqouis), mitochondria (blue),  sarcoplasmic rectilium (buff), tubules (orange), myofibrils (pinkish)  - Artist: Lesley Skeates. Originally from Gray's Anatomy 29th ed. Elsevier. 2008

If you take another look at the data from the Qaisar study (cf. figure 1), you will notice that uncontrolled growth in "one dimension", i.e. exclusive increases in domain size, generates larger muscles, but at the same time renders them dysfunctional, a process of which Qaisar and his colleagues believe that it is caused by a decrease in the number of strongly attached cross-bridges, which are the primary source of the small specific force in muscle fibers with very large MNDs. This hypothesis is by the way supported by a lowered myosin (contractive motor-protein) content per muscle volume in the myostatin negative mice.

In order to really understand why this is the case, it may help if you take a look at the (awesome) sketch of a mammalian skeletal muscle fiber on the right (image 2). The myonuclei are colored in turquois-green, they are connected to the mitochondrion (blue) and the sarcoplasmic rectilium (buff), which is traversed by transverse tubules (orange, and not easy to distinguish). The major part of the muscle fiber is yet made up by myofibrils, which are protein chains containing actin, myosin, and titin...

Ah... wtf. Before someone wants to click the "too complicated"-button again, let's just say the myofibrils are the ones who do the actual work. Now, with the increased domain size (obviously the domain is the "zone" comprising all the aforementioned components that a single nucleus is "responsible" for) and the consequent decrease in myosin content (per volume), as well as the reduced number / density of cross-bridges, i.e. links between the myofibrils to coordinate their action, the muscle loses its functionality. Just like a labor brigade with 5 smaller, smart guys who listen precicely to what their foreman says and work hand in hand can get the job done more efficiently than 5 big, but dump guys, who do not even listen to what their foreman tells them, this type of one-dimensional growth, i.e. an exclusive increase in domain sizes, goes at the expense of muscle function.

From satellite cells to broadcasting towers and back again

Image 3: Myonuclei have a domain, similar to the broadcasting area of a transmitter mast.

So, the myonuclear domain, has nothing to do with some sort of "fenced off" area that is protected by a cell membrane. In physics, we would probably talk about a field, a field of influence, just like an electromagnetic field, with the exception that the signalling from the nucleus does not work via EM radiation, but via gene-signalling... mTOR & Co says hello ;-) Satellite cell recruitment and the "installation" of new myonuclei would thusly be equal to the installation of new broadcasting towers, which make the existing system more effective and allow for further expansion. If you are a mobile communications veteran, who knows the "good" (or rather bad) old days of poor reception you'll know what I mean.

In this context it may be interesting that a very recent study by Antonios Matsakas et al. was able to show that the voluntary wheel running or swimming was able to restore the function of the "over-blown" muscle of myostatin-null (MSTN-) mice (Matsakas. 2011). Another clear cut evidence that exercise induces structural changes which go well beyond the accrual of protein that is not adequately controlled in the MSTN- mice.

Do you take my point now? Ok, then let's get on...

The expression of myostatin, which prevents the myonuclear domains from further expansion is thusly a means by which your body maintains muscular function. Contrary to my friend Adelfo, your body has no interest in looking like Phil Heath... the only reason it has to grow is to be able to survive and survival requires functional strength, not size. There is yet some leeway as far as increase in domain sizes are concerned and it is this leeway that explains the "exorbitant" gains you have been making when you first hit the gym. The lazy bastard (sorry ;-) you have been before, your myonuclear domains were probably far beyond their "functional" limit and, consequent to the acute protein synthetic response to your 1001 biceps curls, "ballooned up" until, just as Darryn S. Willoughby observed it in his 2004 study (Willoughby. 2004), the contemporary increase in skeletal muscle myostatin content brought the expansion of the "bloated" myonuclear domains to an "abrupt halt" (at least that was probably your perception).

Figure 2: Relative myofibrillar protein content and myostatin mRNA expression in the thigh muscles of 11 previously untrained subjects in response to a 12-week (3x per week) resistance training regimen with 3 sets of leg presses and knee extensions à 6-8 reps @85-95% of the 1RM (data calculated based on Willoughby. 2004)

As the relative amount of myofibrillar protein content and myostatin mRNA expression in skeletal muscle from the previously 22 untrained male subjects of the Willoughby study shows (cf. figure 2), the myofibrillar protein accretion is accompanied by profound increases in the expression of muscular myostatin. Or, put simply, the bodies of the subjects, whose thigh volume increase by roughly 16% in the course of the 12-week study period, were sensing that without structural changes, this type of muscle growth would eventually lead to huge, yet dysfunctional muscle fibers - something that obviously would not promote survival and is thusly not part of our genetic program.

Structural changes facilitate new growth

On the other hand, the constant overload to which (I hope) you are exposing yourself in the gym signals your body that without increasing strength (again, your body does not care about size), it will not last much longer is the "adverse environment" of the gym. So, the only way to "survive" is to rebuild / restructure the muscles, a process of which we have seen in the last installment of this series that it goes hand in hand with decreases in the number of purported hypertrophy prone "ultra-fast" twitch type IIb muscle fibers (or rather the content of respective myosin heavy chains within your muscles). Whether the resulting phenotype is that of a bodybuilder, characterized by increases in both the number and size of slow-twitch type I and fast-twitch (intermediate) type II-x fibers, or that of a powerlifter, characterized mainly by increases in the number and size of (intermediate) type II-x fibers, depends on the training stimulus, alone:

Image 4: Our bodies respond to different training routines by distinct changes in the muscular structure.

• Wanna get strong like a German Olympic gold medalist Matthias Steiner? Then goto the gym, 10x a day and do a 1-rep max plus minimal auxiliary work like people the Bulgarian O-lifters are supposed to do. 
• Wanna get big like Arnold? Then follow his example and break into your local gym on Sunday (Arnold's was not open 24/7 back in the day, but that did not stop him from training) and pump out rep after rep, after rep to make sure your body understands that you want to maximize both type-I as well as type-II fiber size.

This does not mean that you cannot get big and strong, it does yet mean that a competitive bodybuilder will - per pound of lean body mass - always be weaker than a powerlifter.

"I need YOU!" ... to pick my brain and steer this series in the right direction

The sixty-four-thousand-dollar question now is: What is the "best" way to let your body know what you (not even your brain, but rather your mind) wants? And even at the risk that I am losing my "guru status" now, I want to be honest with you: I don't know the answer... at least not yet ;-) I thusly depend on your help, on people like Steven Acerra, who is constantly picking my brain with interesting questions and studies on facebook, Mike T Nelson, who lately jumped in on an interesting discussion on training stimuli, "Fat Free", Aaron, Matt, Erik Istre, Lerner (whose comments I have been missing lately) and all the rest of you who chime in with questions, suggestions or the simple assessment that the "good Dr. Andro" is once again making things only more complicated ;-)

And as a food for thought, I give you a sneak peak at what should come next in this series: It is the intricate relation of protein and endocrine signaling by which your muscles and no central governor or transient elevations in isolated systemic testosterone, growth hormone or insulin levels regulate the concomitant increases in muscle protein synthesis and satellite cell recruitement and changes in the myosin heavy chain composition. So, assuming that this installment of the Intermittent Thoughts did not raise further questions as far as the basics are concerned, the next installment will revolve around the role of IGF1 and its local (=intra-muscular) cousins MGF and IGF-IEa, which appear to play a key role in the the coordination of the restructuring process that will keep your muscles functional, even when you are approaching a Olympia stage ready bodybuilding physique.

Intermittent Thoughts on Building Muscle: The Skeletal Muscle Hypertrophy 101 - Part 1: What is Hypertrophy?

Image 1: Governator, Arnold Schwarzenegger, as a teen and in his early twenties. What - puberty aside - were the underlying mechanisms of the obvious increase in sleeve-size? I mean on a strictly myocellular level, of course ;-)

Those of you, who have been following the Intermittent Thoughts series over the last weeks will probably already have realized that I finally dropped the "Intermittent Fasting" from the title... this is something I have been thinking about for quite some time now. After all, the series has evolved way beyond its initial focus on a specific dietary protocol and has become more of an educational "how do you find your way to success"-series. With the format, intermittent thoughts, being still the same, the upcoming posts in this series, which will certainly touch on the topic of intermittent fasting, again, will be titled "Intermittent Thoughts on..." whatever the topic of the week may be... and for this week's installment the latter is going to be "Building Muscle: The Skeletal Muscle Hypertrophy 101".

I can already foresee that this is only the first in yet another series of posts. An introduction into the myocellular mechanisms that turn a normal teen like into a symbol of physical culture, or, to put it simply:  

What actually is skeletal muscle hypertrophy? 

Before I even try to answer this question let me remind you of something you have learned about "growth" in one of the previous installments of this series. In "Building Muscle Starts With Losing Weight" you have learned that one of the greatest fallacies of "classical" bulking, as in "eating everything that cannot escape your ravenous hunger for mass", is adipocyte hyperplasia. You may also remember that this increase in the number of fat cells occurs, when your existing fat stores are ready to burst and your body is in need of new storage capacities. Analogously, you would expect your muscle fibers to "hypertrophy" (from mechanical overload and constant nutrient abundance) until they are "ready to burst" and then divide and form new muscle fibers. (Un?)fortunately, myocytes are not adipocytes and thusly things are working somewhat different, here.

Figure 1: Overview over the three (?) pathways by which your skeletal muscles "grow".

If you take a look at the graphical overview I have come up with in figure 1, you will see that there are two, maybe three distinct pathways which contribute to what the average trainee subsumes under "hypertrophy".

1. Pathway A - hypertrophy via satellite cell recruitment and increases in the number of myonuclei per muscle fiber,
2. Pathway B - hypertrophy via increases in myonuclear domain size within an existing muscle fiber, and
3. Pathway C - hyperplasia, which would be the increase in muscle size by cell division and thusly an increase in the number of muscle fibers

The existence of different fiber types, or to be precise, the co-existence of different fiber types (fast twitch, slow twitch and various sub-types) at varying ratios within a single muscle group complicate things even further. Instead of giving you the usual theoretical lowdown on type I and type II fibers and how the former are supposedly used for endurance and the latter for strength training, I want to discuss the matter from a more practical perspective and first pose the question: What is that we actually want? 

I mean, you do not want "hypertrophy", but you want to get big and buffed, right?

Assuming that this is the case we should initially define "big and buffed" on a myofibrillar level by taking a look at how the muscles of the forerunners of physical culture actually look like - and I promise, what you will be learning today will, once again(!), go against conventional wisdom. Or would you have expected that bodybuilding is a sport that is characterized by a loss in highly glycolytic type IIb fibers and increases in both the intermediate type IIa, as well as the "endurance type" slow-twitch muscles? No? Well, then you should have a look at the data in figure 2:

Figure 2: Fiber composition of bodybuilders, recreational lifters, endurance rowers and sedentary control; determined via myosin heavy chain (MHC) isoform content of the triceps brachii muscle (data adapted from Jurimäe. 1997)

The results of the 1997 muscle biopsies by Jurimäe et al.  (cf. figure 2) clearly show that "getting big and jacked" is by no means about maximizing the "hypertrophy-prone type II fibers", as you may have read it numerous times on one of the thousand bulletin boards, or the numerous blogs of self-proclaimed fitness experts (Jurimäe. 1997). A bodybuilder is rather a person who has maximized the expression of myosin heavy chain I and IIa. Specifically with reference to the latter, the authors write:

It is interesting to note that Kraemer et al. (1995) have reported a lack of change in the area of fibres consisting predominantly of MHC type IIb proteins (i.e. FTb fibres) as a consequence of a 12-week resistance training programme. This suggests that a shift from MHC type IIb proteins to type IIa MHC isoforms may be a necessary prerequisite for FT fibre hypertrophy to occur. Consistent with this was the significant negative correlation (r = -0.67) between the percentage of MHC type IIb isoforms and arm circumference. Similarly, the smaller arm girth of the C group may have been partially due to the greater content of MHC type IIb isoforms in this group.

Or put simply,  the "strong" type IIb fibers have a very limited (if any) propensity for hypertrophy. So that, in order to maximize growth, it is necessary to trigger a shift towards the more "intermediate" type IIa fibers. If you take into consideration, how almost all bodybuilders got, where they are now, i.e. by a volume training approach, this is actually something you should have been able to infer simply from what has been and is still working for 99% of the trainees.

Figure 3: Intercorrelations between myosin heavy chain (MHC) isoforms and isoinertial (1-RM max), isometric (extension) and isokinetic (extension peak torque) strength indices (data adapted from Jurimäe. 1997)

Moreover, the data in figure 3 shows that this does not necessarily mean that they have to sacrifice their strength, as the percentage of type IIa fibers does not only correlate with increased muscle size, but also with increased isoinertial (1-RM max, r=0.66), isometric (workload, r=0.51) and isokinetic (peak torque, 0.61). strength. Getting big and buffed and getting strong thusly both require a profound shift in the "God given" fiber composition, but why?

Skeletal muscle hyperplasia - yes or  no? While there are a handful of studies which speak of hyperplastic responses to stretch or other form artificial overload, many (if not all) of them have been done on avian myofibers (Kelly. 1996), which, due to their special make-up, make it a) very difficult to distinguish between increasing overlap due to the longitudinal growth of intrafascicularly terminating skeletal muscle fibers and "real" hyperplasia and b) may not even translate to human beings. That's the reason, why I will disregard the issue of hyperplasia in the following discussion.

A very recent study by an international group of scientists from Sweden and the USA, may provide some insights, into why these fiber-transformations are necessary if you want to grow tree-trunk legs and sleeve-bursting arms. In this study, which was published on November 28, 2011, in the FASEB Journal (Qaisar. 2011), Rizwan Qaisar and his colleagues provide a detailed analysis of the the muscle fiber composition of mice who are either myostatin-negative or over-express the muscle building growth hormone IGF1 (we are talking about intra-muscular IGF1, here! More on that in future installments of the series).

Figure 4: Cross sectional area (CSA), number of mynuclei and myonuclear domain size of myostatin negative mice and mice overexpressing IGF1 relative to wild-type control (data calculated based on Qaisar. 2011)

As you would expect, both the myostatin-negative, as well as the IGF1 mice were more muscular than their wild-type cousins. There were, as you can see in figure 4, yet significant differences in fiber sizes (CSA), the number of myonuclei per fiber, and the domain sizes of the individual myonuclei in the exclusively fast-twitch extensor digitorum longus (EDL) and the predominantly slow-twitch soleus muscle.

Image 2: The balloon metaphor of skeletal muscle hypertrophy.

Note: If you picture a muscle fiber as a number of balloons which are held together by an elastic net, then the myonuclei would be within the individual balloons, which, in turn, would represent the myonuclear domains. You could thusly increase the muscle size, i.e. stretch the net, by either inflating the balloons, i.e. increasing the domain size, or simply adding more balloons to the net. The latter would then be equivalent to the recruitement of new myonuclei from the satellite cell pool in the sarcoplasma of the muscle fibers.

If you take a closer look at the data you will notice that in the IGF1 mice the predominantly fast-twitch EDL muscle growths mainly by increases in myonuclei number, a feature that is absent in the predominantly slow-twitch soleus fibers. The profound increases in myonuclear domain size that occur in the myostatin-negative mice, on the other hand, result in profound reductions in muscle function.

Figure 5: Specific force, stiffness and myosin content (secondary axes) of EDL and soleus muscle in wild-type control, myostatin negative and IGF1 overexpressing mice (data based on Qaisar. 2011)

Both specific force, as well as as muscle stiffness, are profoundly reduced in the EDL muscle of the myostatin negative mice (cf. figure 5), because they have surpassed the maximally sustainable domain size and have thusly become dysfunctional.

Figure 6: Domain sizes of EDL and soleus muscle fibers in wild-type control, myostatin negative and IGF1 overexpressing mice (data based on Qaisar. 2011)

This becomes even more obvious if we take a look at the domain sizes in isolation (cf. figure 6). It is the "uncontrolled" growth that is partly a result of a lack of satellite cell recruitment and consequent increases in myonuclei number, which cripples most of the animals with mutations in the myostatin gene.

Muscle hypertrophy = increases in myonuclear number & domain size

Healthy muscle growth, that is the intermittent take-away of this installment of the Intermittent Thoughts on building muscle, is thusly a direct result of "hypertrophy", as it is commonly associated with increased protein synthesis (and decreased or constant protein breakdown) and the subsequent expansions of individual myonuclear domains and the recruitement of satellite cells, which will then form new myonuclei.

As you may have noticed from the increasing amount of typos, of which I have probably overlooked 50% (sorry for that), my Sunday time-budget is already exhausted, so that I will have to postpone the discussion of what triggers these processes to the next installment. I do yet hope that the stuff you learned today provides enough food for thought to get you through the week ;-)

Intermittent Thoughts on Intermittent Fasting - Programing Success: Accept Your Weaknesses, Learn From Your Mistakes, Identify Your Strengths and Build a Better Body!

Image 1: You may call it "toning" or "shaping", but in the end it's bodybuilding in the literal sense.

Assuming that you are all "lean and mean" by now and thus ready to build some serious muscle (for those who missed it, read last week's installment on "Why you better lean out before bulking"), we can finally delve into your first steps on your way to ... wait. I hope you did not forget your "motivational elevator pitch" from the first part of this part of the Intermittent Thoughts, where I asked you to come to terms with what it actually is that you want to achieve. Now, the good news is that regardless of whether you are just sick of that lose skin on your upper arms or want to compete against Phil Heath at the 2012 Mr. Olympia, there are a few fundamental principles that apply regardless of whether you are striving for "toned" 11 inch arms or Coleman-esque 22 inch guns.

Gaining weight? Yes! Getting fat? No!

With that we have actually arrived at the very first of three key points, I promised to address in this issue (cf. end of last installment): effective ways to measure your progress. In the "weight loss installment" of this series you have already learned that other than the morbidly obese "King Size Homer", physical culturists and athletes who do not compete in weight-classes are ill-advised to step onto the scale too often.

Figure 1: Lee Priest's transformation is certainly amazing, but let's be honest, do you really want to run around like Michelin man in the off-season and then have to resort to extreme measures to get back in shape for a few days, only? (comparison posted by "Tibo" at the SRTrading Forum)

While dieters (here indicating people who want to lose fat), may get discouraged, because their weight-loss stalls, when they are actually just beginning to finally add some muscle to their increasingly lean physique, many self-proclaimed (hobby-)bodybuilders think that "gaining muscle" is all about increasing their off-season weight (interestingly, many of those people do not even compete and define their off-season as the time when they do not go to the beach to impress the ladies). What could make sense for a professional bodybuilder like Lee Priest (cf. figure 1) certainly is not an appropriate approach for the average gym-rat, whose "weight loss arsenal" is less well-stocked than the ones of a high level pro-bodybuilder ;-) Or put more simply, when former chubby, like Peter Griffin (cf. "Healthy Weight Loss") bulks up the way, Lee did, he will not (and I guarantee that) be able to drop that fat again and achieve the grainy look from figure 1 (right) within a few weeks time before a contest, by diet and exercise (and OTC fatburners), alone...

Figure 2: Other than for the "pros" with their versatile arsenal of "weight loss tools", the journey of the dirtily bulking average self-proclaimed hardgainer is a one-way street.

And even for the self-proclaimed "ectomorph" there is nothing worse than a dirty bulk, where the number on the scale serves as his / her yardstick of success. This is especially true, because many self-proclaimed "hard gainers" are lean mostly because they are still eating like a bird (or missing even the most fundamental basics like a sufficient protein intake of at least 1g/kg per day), even when they claim that would eat until they puke. If those people start forcing down tons of calories in form of sugary weight gainers, most of their weight gain will come from fat. Their initially low fat cell count will soon have to increase to provide enough storage capacity for the "valuable" energy, so that, rather sooner than later, the former "ekto" finds himself in a similar situation as Peter Griffin, who, no matter what he will do, will always have a harder time leaning out than his friends who have never gotten chubby in the first place.

Bottom line: Do not rely on the scale too much. Yes, you want it to go up steadily, but faster weight gain does not automatically equate greater muscle gain. Keep a close eye on your waist circumference and decide a priori when (no matter how close you may be to your superordinate goal, e.g. "achieving 20" arms") you need to cut back on calories to avoid "adipolateral damage" ;-)

Taking stock also implies coming to terms with yourself

Image 2: Just as when you are "dieting", the scale is not the best meter for your progress. A measuring tape, a notebook and a digital camera should be your tools of choice.

Assuming that you have decided that you could use some additional muscle on your scrawny frame, another often overlooked thing you will have to do even before you start "bulking" is to take stock of how "scrawny" you actually are - not by stepping on the scale, but by taking, or rather have someone take measures of your waist, your arms, your chest, your shoulder and thigh cicircumferences. Just like any good custom tailor would do. You will then take a camera and shoot photos, from the front, from the side and (don't neglect that!) from the back. Depending on how much progress you have already made, this may seem ridiculous or even embarrassing at first. After all, you probably do not look any of the cover models you are looking up to... but remember: You take these photos as a yardstick - your yardstick. It won't help you if you keep admiring the girls and guys from the magazine-covers and shy away from your own mirror image.

In order to make a change you must initially objectively assess and accept where exactly you are standing in order to decide what you want to change and by which means you can achieve that. As long as you keep thinking of you and your body as disconnected units, you will never achieve whatever physique it may be that you are dreaming of. So, this kind of  initial stock taking is way more than just setting the baseline reference. It is (at least for many trainees) also a matter of coming to terms with theirselves.

Bottom Line: You are your own yardstick. The figures on your measuring tape and your weekly progress pics are objective measures of your progress, which is defined against where you are coming from. 10" arms are an awesome achievement, if 8" where you are coming from!

Build on your strengths while working on your weaknesses

Start out with your strengths! What is that you like about your physique? What is your most developed muscle part? And if you are already training... ask yourself what it may have been that you have done right, here. I remember that I have always been pissed off that my legs appeared to grow like crazy, while my arms and "most importantly" (my perception at that time) my chest "just wouldn't grow". I looked at the figures and pictures and then peeked at my routine. "How on earth can my legs grow like that if I only train them once a week and do nothing like some warm ups on the leg extensions and some squats?" It was back then, when I eventually realized two things:

Image 3: Do you really think anyone would know Tom Platz, today, if he had decided to neglect his strength (obviously his legs)?

1. Everybody has certain strong and certain weak body parts. Part of this is genetics. Especially if you have not reached your "full genetic potential", an even more important factor is however what you do in the gym, at work or in your free time. If you are carrying beverage crates all day, chances are that your "strong" body parts are your neck and your back, no matter if those are the muscle groups with the greatest genetic potential. If, on the other hand, you are like I once was and have a reasonable training plan for your legs (because people say that you have to train legs ;-), but are so eager to grow your chest and arms that you totally overtrain them, you must not wonder if you grow tree-trunk legs, whie your arms and chest shrivel away.


2. Success comes from building on your strengths, and working on your weaknesses. It does not make sense to stop training legs, to "save the energy" for whatever other bodypart you feel is lagging behind. Not only will you run the risk that your former strength becomes your future weakness. You could also end up with two not one weaknesses by overtraining your weak and detraining your strong body parts.

For me that meant that I had to maintain my leg regimen and adapt my chest and arms routine by cutting out a lot of high volume auxiliary movements and focusing on improving my strength and technique on those movements of which I felt that they worked - and YES! This meant that the classic bench press was no longer a part of my routine!

Bottom line: Cherish your strengths and stop lamenting about your weaknesses. Analyze and build on what worked for you and acknowledge and learn from your own mistakes.

Hearing and listening to what your body is telling you

Image 4: Cable crosses certainly cannot replace the bench or dips, but they allow you to practice to flex your chest against resistance.

I see, that was a shocker. Dr. Andro does not do bench presses!? Well, not exactly, I have reincorporated them into my routine months later only to rotate them out again with the next change in my regimen. While the bench may have built massive chests like the ones of Arnold Schwarzenegger or Franco Culambo, but it just did not build mine.  

Sticking to what does not work, because people keep telling you that it does work is probably the most stupid and yet most common mistake I see in the gym.

If you read all the information in the "SuppVersity EMG Series", then you will be aware which exercises work best for the average trainee in the Boeckh-Behrens and Buskies study. You do not even know if these are also those exercises that work best for "the average trainee in general", but you can easily find out if these are the exercises that work best for you - and more importantly, if they are not, you should give a damn about how they rank in anyone's "Top List" (mine included!).

Bottom line: Never, I repeat, never(!) assume that what worked for someone else, or even the majority of the participants in a scientific study must also work for you. Listen to advice, build new routines based on scientific studies, experiment, but do not stick to a routine / exercise if, after 2 weeks, your body still keeps telling your that it ain't right for you.

Weight is important in weight lifting, posing is key in body+building

Image 5: If you want to maximize muscle gains, posing - or rather learning to flex your muscles against resistance is obligatory (img Johnny Jackson)

In case you are now wondering how on earth you can find out if the bench press or the dip (which is my favorite for chest) is right for you, when you do not have access to the complex measuring apparatus Boeckh-Behrens & Buskies used in their studies, I assume that you have never been posing or deliberately practiced the so-called "mind-muscle-connection" - have you? What? "Posing is ridiculous?" Well, that was what I thought as well, when I began training. I mean, I never even remotely thought about competing, so why on earth would I practice posing? The reason is simple and has little to do with the ability to showcase your muscles, but all with your brains ability to address the motor neurons on your muscle fibers.

If there is one thing I want you take away about goal setting for muscle building from this installment of the Intermittent Thoughts then it is that your primary goal in the gym must always be to work the muscle against resistance and not to break personal records. Here lies a fundamental difference between weight lifting (as in O-lifting or powerlifting) and bodybuilding. As someone whose primary goal is to improve his physique, the lifting weights is only a means to a completely different ends.

If all you want  is to build a bigger bench, fine! But don't expect to make similar gains as someone who understands that he is at the gym to work his muscles, not his ego. By practicing posing and doing what I like to call 1-2 "acclimatization sets" with ~50% of the weight you would use for 6-8 reps before every exercise, not as a warm-up but to memorize the movement pattern, to feel and flex the target muscle and to be able to transfer this pattern to your working sets, you will soon be able to decide which exercises are working for you, and which aren't.

Bottom line: You are not in the gym to move maximal amounts of weight, but to induce maximal muscular stimulation. This requires that you train your mind-muscle-connection and accept that the weights you are using are just a means to another end - the physique of your dreams. Remember: You increase your weights to keep challenging your muscle, and thusly to be able to record a new personal best in the notebook with your body measures, not the one where you keep track of your weights.

Preliminary conclusion(s)

Although, I did not get totally side-tracked this time, I still have to postpone the scientifically based considerations of the implications of the biological underpinnings of skeletal muscle "hypertrophy" (and maybe hyperplasia), at which I have been hinting in yesterday's blogpost, to another installment of the Intermittent Thoughts.

Note, in view of the pictures I have been using in this part of the series, I may have evoked the false impression that these rules apply exclusively to "bodybuilders". This is however not the case. There is no fundamental difference between training "to look good naked" and training for the "Mr. Olympia", as far as the take-home messages from this installment of the Intermittent Thoughts are concerned. Flexing your muscles, "posing" and practicing the mind-muscle-connection for example could be even more important for the ladies who want to "tone" their physiques than for the skinny ectomorph whose primary goal is to "get big".

For the time being, you would be well-advised to get yourself a measuring tape and a camera to take stock of where you are, physique-wise, to (re-)evaluate your strengths and weaknesses, to identify what worked for you and to get to know and learn to flex all the muscles in your body - and yes, there are more than biceps and chest, or chest and biceps ;-)

"Just One More Set" (1/2): Metabolic Response to 10,000kg vs. 20,000kg Regimen. EPOC: Do Reps and Loads Both Figure? And What About Elite Athletes Do They Need More?

"Ah come on, just another set!" ... "I don't know man, we've already pumped away 100,000kg today... do you really believe that's going to be productive, I mean, yeah, we are cuttin', but still... I mean I don't dig this epic!", "EPOC man, it's called EPOC!" *shakes his head* "Call it whatever you want, bro, I am out!"

If you want, you can think of today's SuppVersity post as an extension to yesterday's "Bigger, Stronger, Faster" special of the On Short Notice series; to be more precise: As a practically more relevant version of the rodent study on hypertrophy vs. strength training that was part of the aforementioned post. Yep, we are "talking volume" today. How much is too much?  And though this is never-ending debate, it appears that at least as far as research goes, a little more debating certainly would not hurt. Therefore I am happy to have not one, but two studies for you which don't just address this issue, but have also been conducted with human subjects!

In view of the fact that these are no "short notices", I will discuss one today and the other tomorrow - yep, that means that you can already make a mental note to come back tomorrow ;-)

"Just one more set, ..." - how productive can that be?

Today's study comes from the Human Performance Laboratory at the Florida State University and deals with the energetic side of things - specifically the often-cited EPOC (excess post-exercise oxygen consumption), which is often touted as one of the most important aspects why strength training in general and higher volume / intensity strength training, in particularly, would have the edge over cardio training. The reasoning is easy: You don't burn so much energy while you work out, but in the time after, your body will (a) still expend more energy per minute / hour and (b) has the advantage of emptied glycogen stores, which will force it to tap into its body fat stores the source for the required energy.

All of you who have read the complete Athletes' Triad series, will by now already know that at least argument (b) is pretty idiotic, because it wouldn't allow you to replenish your muscle and liver glycogen after workouts and thus pave the way into the dreaded vicious circle of the athlete's triad. The former argument, on the other hand has - on a way more general level - only been confirmed a couple of days ago (see "Scientists resolve the paradox of stable muscle metabolism but greater mitochondrial respiration in muscle of inactive vs. active subjects", read more), the question still remains: How much weight do you have to lift to set the 'afterburner' into full gear? 

10 metric tonne or 20 metric tonnes? What do you say?

I see, you are laughing, but basically the above question is what the George J. Abboud and his colleagues tried to find out, when they recruited 8 healthy men aged19-29 yrs who had 

"at least 12 months of RT experience with no more than 2 wks rest at a time, less than a total of 4 wks off within the last 6 months, or 9 wks off within the last 12 months [and] reported no prior or current use of illegal performance enhancing substances." (Abboud. 2012)

Suggested read "Three is More Than One: Higher Volume Increases Strength Gains in Legs, and Satellite Cell Recruitment and Fiber Size in Legs & Traps."

As usual the subjects had to fill food logs for the three days before the testing and were instructed to replicate the same eating pattern on the second occasion in which they were randomly assigned to perform a standardized resistance training (RT) regimen consisting of 4 exercises performed on a non-counterbalanced smith machine so that the range of motion during

• bench press, 
• squat, 
• bent-over row and 
• Romanian deadlift 

could be controlled for easily. Other than the equipment and the exercises, which were identical on both occasions, the volume of the training sessions varied and if you express this volme in kg or metric tons, it was a competition of 10,000 kg (10 metric tonnes) vs. 20,000 kg (20 metric tonnes) of weight. 

"The loads were divided between the 4 exercises as follows: 35% to squats, 30% to bench press, 20% to bent-over rows and 15% to Romanian deadlift. For each set, subjects lifted approximately 85% of their 1RM for 6-8 repetitions. If 6 repetitions could not be completed at any point, the load was reduced by 10% for the subsequent set." (Abboud. 2012)

Both sessions were supervised by three testers : One monitored the metabolic cart, one made sure the proper range of motion was used and one monitored the proper lifting form. The subjects had to perform the concentric portion of each lift with maximal speed and ensure a controlled eccentric descent. A specific time interval was not dictated. Sets were stopped if "subjects broke form" (Abboud. 2012) and 2 minutes of rest were given between sets. In this fashion the subjects simply kept lifting set after set until the volume prescription for the respective trial was reached.

Figure 1: Resting metabolic rate (RMR) per kg body weight, 30min energy expenditure and respiratory exchange ratio (RER; lower values = higher fat, lower glucose  oxidation)  after low and high volume trial (based on Abboud. 2012)

As you can see in figure 1 there were differences as far as the effects of the high (20,000) vs. low (10,000kg) regimen on the resting metabolic rate, 30 min energy expenditure, and the respiratory quotient (lower values = higher fat, lower glucose oxidation), but in view of the fact that the high volume group moved 2x more weight and should thus (at least theoretically) have expended twice the energy (assuming they performed all reps with perfect form and identical speed), those differences are more than disappointing. 

The minuscle effect size is yet not the most "disappointing" (or "surprising" ?) result

In fact, contrary to the low volume workout the 20,000kg workout did not produce any increases in resting metabolic rate and 30min energy expenditure, at all - put simply: There was no EPOC after the high volume training. And this did not change over the whole 48h period (and I know you guys, you won't rest longer anyway ;-).

Now you may say that this was a crazy protocol, but let's do the math, let's assume the guys did squat 100kg, benched and rowed their own body weight of ~80kg and deadlifted 125kg. With 10 reps per set thats 1,000kg + 2x800kg + 1,250kg per set respectively. If they did three sets per exercise they would thus already be up to 9,950kg! If you still think that's crazy, let's hear what the scientists have to say:

"As subjects in the present study were well adapted to RT, the training stimulus needed to elicit increases in EPOC arguably needed to be much higher compared to that used in previous research  Two studies using intensities of 70% 1RM report significant increases in RMR. Melby et al. had subjects perform 6 setsof 10 different exercises for a total of 60 sets. The repetition range for this protocol was 8-12 repetitions per set. This amounts to approximately 600 repetitions performed during the course of the exercise bout. The range of load-volume lifted by these subjects was 15,000-38,000 kg. [...]" (Abboud. 2012)

The list goes on and you just have to go to your gym and I guarantee you, no matter how few people are on the floor you will see a guy who (often without noticing is) will be pounding away much more word within a single workout. Moreover, the the subjects in the present study completed their trials
with a drastically lower number of repetitions -  a mean of 199. Had they performed the crazy rep-volume of the Melby study, they would probably have come close to 50,000 kg. This raises an interesting question is "volume" correctly defined by giving the total amount of weight you lift? Or is the number of reps maybe more important as far as the after-burner EPOC is concerned?

Too much of a good thing? But what if you are a highly trained athlete?

A previous study, by Hackney et al. would support the notion that heavy lifting is an obligatory part of the EPOC equation. In the latter study, EPOC trained individuals who used a lower load-volume than the trainees in the study at hand  had increased resting metabolic rates for up to 72h (Hackney. 2008). Since the Hackney study also put an emphasis on eccentric contractions and will thus probably have lead to even greater muscle damage than the protocol of the study at hand (CK(10,000kg) = 729U/L vs.CK(20,000kg)  = 1,159IU/L), Abboud et al. speculate that ...

"[a]s protein synthesis required for repair is energetically expensive, it is logical that untrained subjects will show greater and longer alterations in EPOC post-RT. Judging by training history, strength levels and CK responses, subjects in the present study had most likely reached a higher level of adaptation than ones in previous studies, and therefore were less sensitive to the metabolic effects of recovery from RT." (Abboud. 2012)

In other words, for you, probably a seasoned strength trainee, the 'more is more' principle is not going to yield better results - even if your goal is to shed body fat. And ...

"Although RT is an important component in any weight loss program to attenuate the loss of fat free mass and therefore better preserve RMR, it is unlikely that the total energetic cost (during and post-exercise) of a typical duration workout will be adequate for significant weight reduction in highly trained recreational lifters without caloric restriction and/or additional aerobic or high intensity interval training." (Abboud. 2012)

And since I rarely encounter a conclusion that's so to the point, I'll leave you with that for today and remind you to come back tomorrow to learn, when and for which body parts doing somewhat more may still be beneficial - read me tomorrow ;-)

References:

• Abboud GJ, Greer BK, Campbell SC, Panton LB. Effects of Load-Volume on EPOC after Acute Bouts of Resistance Training in Resistance Trained Males. J Strength Cond Res. 2012 Oct 18.
• Hackney KJ, Engels HJ, and Gretebeck RJ. Resting energy expenditure and delayed-onset muscle soreness after full-body resistance trainingwith an eccentric concentration. J Strength Cond Res. 2008; 22: 1602-1609.
• Melby C, Scholl C, Edwards G, and Bullough R. Effect of acute resistance exercise on postexercise energy expenditure and resting metabolic rate. J Appl Physiol. 1993; 75: 1847-1853.

Intermittent Thoughts on Intermittent Fasting - Programing Success: Building Muscle Begins With Losing Body Fat.

Image 1: Arnold does the "double bicep" + vacuums. If you want to look like a bodybuilder, muscle alone is not enough.

First, I want to thank Jahed, Pablo, RF, Angimal, Garrett and Rudolf for their patience. After all, it has been two weeks now since you have submitted your (meta-)goals, which were all more related to building muscle and increasing performance, then to losing body fat, which was the topic the last installment of the Intermittent Thoughts dealt with. Yet although, at first sight, both topics have little (to nothing) to do with each other, there are are at least three important factors by which a reduction in body fat is very well related to increased muscularity and skeletal muscle hypertrophy. Let's get back to the "Peter Griffin" type of chubby person from the last installment, for a few seconds. Imagine "Peter" has packed on, say 10lbs of lean muscle and now stands in front of you, does the "double bicep" and vacuums, just like Arnold does in image 1... what? Why are you laughing?

Do you want muscles? Or do you want to look muscular?

Now, obviously the first intersection of bodyfat and muscularity (in a broader sense) relates to the question whether or not your body fat level is low enough for any increases in skeletal muscle mass to be visible. I mean +10lbs on the ripped frame of a 202lbs (now 212lbs) bodybuilder look absolutely freekish. On our Peter Griffin, a gain of 10lbs of lean muscle tissue will probably go completely unrecognized - this also puts "chubby" beginners at risk of neglecting the strength training component of their exercise regimen, because, from a mere "cosmetic" stand point, each gram of body fat they drop will make a significant difference in terms of the way they look. Building muscle beneath the thick layers of adipose tissue, on the other hand, initially appears to have little value... but remember: looks are deceptive, and I hope that my elaborations in the last installment made it quite clear "building a bigger metabolic engine" and not starving the latter away on a low-calorie diet, is the cornerstone of maintainable reductions in body fat levels.

Figure 1: Where are you on the fat/muscle mass (FFMI = weight/height[in m]²) continuum? *indicates age-group 20-29 in the NHANES dataset (data based on data from Hattori. 1999; Picket. 2005; CDC, NHANES data from 2010)

Interestingly enough, being lean, or, I should say, the metabolic and endocrine consequences of being lean actually have way more profound implications on "building muscle", than the mere advantage of the immediate visibility of the newly acquired lean body tissue. On "the boards" (meaning bulletin boards like bodybuilding.com, anabolicminds, etc.) it is a recurrent topic whether you should "bulk" (people there interpret that mainly as "eat to gain" and often as "overeat to gain") or "cut" (meaning lose fat) first. And while the answer obviously depends on where you are starting from, it stands out of question that the average American male (aged 27-62) who gets fatter and fatter every year and currently has a body fat percentage of 24.9% (Rohrmann. 2011) would be ill-advised to even think about the word "bulking".

Image 2: Just to put the 24.9% body fat of the average American male into perspective. The average bodyfat percentage of a sekitori sumo wrestler is 28.6%
(Hattori. 1999)!

Please note, that the "no bulk with high body fat percentage" rule does also apply to the female physical culturists out there. The reason that I am mainly addressing the male faction of my readership here, is that women are not so stupid to think, they would have to down 2-3 portions of "weight gainers" (these products are exactly what they are called, they will make you gain weight, not muscle) and 4-5 protein shakes in addition to a hypo-caloric (junkfood-)diet in order to build a muscular physique, anyways. Things would be different, though if the physique of a sekitori sumo wrestler (one of the higher ranked sumos, cf. image 2), is what you are aspiring. In that case you can start "bulking" with weight gainers and all the other "high class" products the industry has to offer... I mean the average sekitori sumo has 109kg of lean muscle tissue hidden somwhere beyond the 45.4kg of fat he is carrying around the dohyo.

If you want to "program success" and your "motivational elevator pitch" from part one of this part of the Intermittent Thoughts Series contains sentences like "look like a cover model." (Garrett; November 14, 2011 3:05 AM) or "[building] a stronger body, bodyfat below 8%" (RF, November 7, 2011 12:22 PM) or my favorite one which obviously nobody was dared to say, yet 90% of the Men's Health readers probably have on their minds "build muscle just to look good at the beach / impress the ladies", it is imperative that you lose your love handles first! Not to (just) to be able to see the gains you are making, but to set yourself up for optimal lean muscle gains (in essence, this is also related to the assumption Jahed Momand's assumption made in his "motivational elevator pitch" that leaning out prior to building his maximal clean and jerk and snatch to compete at 85kg probably is the smartest way to go, after all a low body fat percentage is obligatory if you want to be competitive in the lower weight classes).

The endocrine advantage of low(er) body fat percentages

The first and often overlooked advantage of a decent degree of leanness (cf. "active American", figure 1) is a hormonal one. According to the findings of the latest (published) NHANES data (National Health and Nutrition Examination Survey III; Rohrmann. 2011) there is a direct correlation between body-fatness as measured by BMI, waist circumference and body fat levels, on the one hand, and total and free testosterone and estrogen levels and their binding globulin SHBG:

Total and free testosterone and sex hormone binding globulin concentrations decreased, whereas total and free estradiol increased with increasing BMI, waist circumference, and percent body fat (all p trend < 0.05). 

Further statistical analysis of the data reveals that a body fat increase of one-quartile (e.g. from the lower 1/4 of the study population to the next fatter quartile) goes hand in hand with a decreases in sex hormones into the next lower quartile (e.g. from the highest into the next lower quartile). A sample calculation for a 50 year old white non-smoker revealed that for each 5.2cm increase in body waist circumference or +2.7% increase in body fat, the free testosterone level decreased by 2%. With an increase of "only" +3.7cm or +1.8% in waist circumference or body-fatness, respectively you can however bump up your estrogen levels by 2%.

Figure 2: Relative free testosterone and free estradiol levels in men from the NHANES study; data expressed relative to serum levels of "lean" men with <84.9cm ~ 33.4" waist circumference; values above the bars are the differences between relative testosterone vs. estradiol levels compared to "lean" men (calculated based on Rohrmann. 2011)

In view of the differential response of androgenic and estrogenic free (i.e. "active") hormones to changes in body-fatness (cf. figure 2), it is no wonder that we see a characteristic and in terms of lean muscle gains highly unfavorable pattern in the "fatter" quartiles of the study population, with maximal  free estradiol levels (1.08pg/ml; +30% vs. min) and minimal free testosterone levels (0.097ng/ml; -13% vs. max) in the "fattest" quartile of the study population (I deliberately selected waist circumference over "body fat levels" which were measured by bio-impedence, as my body fat marker of choice). Even if you as a SuppVersity reader should by now be aware that testosterone alone does not "build muscle", its highly facilitative effect on exercise induced increases in lean body tissue is significantly blunted by the fat-induced reduction in free testosterone and the (by the way fat promoting) increase in free estradiol in "chubby" men.

The endocrine factor: By leaning out first you set the hormonal scene (a higher testosterone to estrogen ratio) for optimal lean muscle gains.

The metabolic advantage of lower body fat levels

While testosterone and estrogen levels obviously figure large in the orchestrate that determines whether the nutrients you ingest (remember no one of you eats "calories") end up being stored as body fat, used as "fuel" or building block for lean muscle tissue, insulin, the "most anabolic agent in the world" (a quote from steroids.com; obviously a very questionable statement), may play an even greater role, when it comes to building muscle, not fat. Those of you have have listened to Dr. Layne Norton's and Dr. Connelly's dissertations on the largely misunderstood role of insulin in relation to the protein synthetic response to exercise, as well as its highly undesirable effects on fat storage during the last episodes of BodyRX Radio, will be aware that the often touted idea that "insulin is the most anabolic agent in the world" applies, above all else, to adipose tissue.

Image 3: "Insulin the most anabolic agent in the world"!? Correct, if we are talking about fat,  not muscle tissue ;-)

While "broscience" and the producers of sugary "weight gainers" and "post-workout recovery formulas" still maintain the myth of the "muscle building insulin spike" the (post-workout) ingestion of large amounts of fast-acting carbohydrates would provide, a recent study from Stuart Phillips lab at McMasters University into the purported benefits of the "insulin spike" produced by the co-ingesting 50g of carbohydrates with your 25g of whey protein post-workout found neither an increase in muscle protein synthesis, nor decreases in muscle protein breakdown, which are often cited as another benefit of increased insulin levels (Staples. 2011). More specifically, the additional +1,250% (!) increase in insulin (over +400% with whey alone) did not have any additional effect on protein synthesis, or, in other words: With insulin some (here 5x above fasted baseline) appears to be good, more, on the other hand is not only not better, it is in fact worse.

That being said, the improvements in insulin sensitivity which go hand in hand with reductions in body fat levels (increases in leptin sensitivity, reductions in inflammation, etc.) will decrease your basal, as well as your postprandial insulin levels, because your body will simply need less of the storage hormone to get the job done. This, in turn, will allow you to fuel your workouts with appropriate (not exorbitant) amounts of carbohydrates without running the risk of storing additional body fat. This is particularly true, in view of the fact that the "type of insulin sensitivity" you acquire when you selectively lose body fat (not muscle) favors the storage of blood sugar as muscle glycogen over its conversion to triglycerides and subsequent storage in adipose tissue (note that the latter happens both in obese and insulin resistant, as well as in "reduced obese" individuals, who have lost a lot of body mass, not fat, on prolonged calorie restricted diets).

The metabolic factor: By reducing your body fat levels first (leaning out vs. just losing weight) you decrease the risk that (superfluous) carbohydrates (and other nutrients) get stored as body fat.

The anti-livelong-obesity advantage of lower body fat levels

Image 4: There are two ways to get fat, adipose tissue hypertrophy and adipose tissue hyperplasia. While you obviously want to avoid both, only the latter is potentially irreversible (Otto. 2005).

The third and maybe most far-reaching  advantage of lowering your body fat level before bulking up is actually related to the leeway you have in terms of the unavoidable fat gain that is part of every "bulk" no matter how "clean" it may be (see also red box below). It should be obvious that just as the myonuclei in your skeletal muscle have a limited capacity to "grow" (also to hypertrophy, i.e. to simply increase their size /we will discuss the three pathways of muscle growth in one of the upcoming installments in more detail), your fat cells can only store a finite amount of lipids before they begin to "burst from the seams" (some scientists even believe that this is part of what triggers the detrimental inflammatory cascade in obese individuals). When that is about to happen, the only way your body can protect itself from suffocating in glucose and triglycerides that can neither be burned as fuel nor stored in the bristling adipocytes is to generate new fat cells (adipocyte hyperplasia).

My definition of a clean bulk: You may now be shocked to hear that even a "clean bulk" will necessarily also increase the amount of body fat you are carrying. That, and this is a very important point, does yet not mean that your body fat % must necessarily increase. A "clean bulk" by (my) definition is a bulk where you add more muscle than fat tissue to your frame. Now, even if you you were an absolute zero in math, you should recognize that this implies that your body fat percentage would actually drop, although your overall body fat levels may increase. Keep that in mind, whenever you are trying to gain muscle. Your goal should never be to cut fat (reduce overall fat mass) and build muscle (increase lean muscle tissue) at the same time - if you try that you program stagnancy, not progress!
Now, the unfortunate truth is that it is pretty easy to "empty" those cells again (you can do this in weeks), yet uncertain on which time-scales (if at all) and by which means (other than surgery) you can get rid of newly acquired adipocytes ever again.

An infant usually has about 5 to 6 billion fat cells, the number of which naturally increases during early childhood and puberty, so that the average healthy adult ends up with 25 to 30 billion fat cells. If those 30 billion adipocytes are already filled up when you start bulking, chances are that your body feels compelled to increase its storage capacity, so that - in the worse case - you end up with the roughly 75 billion fat cells, the typical overweight adult is carrying around on his "chubby" frame. If you still insist that you are not "big" enough and continue to eat whatever you can grab, the number of fat cells can increase up to 250, even 300 billion... it stands to reason that even when you emptied all of those, you would still be "fat".

The anti-obesity factor: By leaning out first, you reduce the risk of a (potentially irreversible) increase in adipocyte number that may set you up for lifelong weight problems.

An intermittent conclusion on the first step of programming skeletal muscle hypertophy

Image 5: After a handful of unsuccesful bulking efforts, SuppVersity Student Duong Nguyen eventually made it right - he leaned out first. If you are interested in his subsequent bulk, check out his blog!

As you may notice, I (once again) went off on a tangent. I hope you don't mind that you have not yet learned about effective ways measure your progress, about how to improve your gains by setting realistic, but challenging goals and about the often-overlooked impact the mind-muscle will (not could!) have on the real world outcomes of your efforts in the gym, in this installment of the Intermittent Thoughts.

But hey! For (hopefully) a minority of you the "time to bulk" may not have come anyways ;-) So, if you have not achieved a degree of leanness comparable to that of the "average active American" (cf. figure 1), I suggest you re-read last week's installment on setting yourself up for body-fat loss and thusly take appropriate measures to increase the effectiveness of your first or next "bulk" and decrease the propensity of doing permanent "aesthetic" or even metabolic damage.

As for the rest of you, I would hope that you could at least gain a few new insights into the challenges your not so lean friends are facing when they are trying to gain muscle without adding another inch to their waistlines.