|Image 1: This is another type of "dysfunctional muscle"; distinct from the one we are talking about, here|
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)|
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|
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.|
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)|
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:
- 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.
|Image 4: Our bodies respond to different training routines by distinct changes in the muscular structure.|
"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.