The Process Of Exercise-Induced Muscle Growth
It was mentioned in the The Neuromuscular System Part I: What A Weight Trainer Needs To Know About Muscle article that muscle cells have many nuclei and other intracellular organelles. This is because nuclei are intimately involved in the protein synthesis process (don't forget, actin and myosin are proteins), and a single nuclei can only support the manufacturing of a limited amount of protein. If muscle cells didn't have multiple nuclei they would be very small muscle cells indeed. So if a muscle is to grow beyond its current size (i.e. synthesize contractile proteins - actin and myosin) it has to increase the number of nuclei that it contains (called the 'myonuclei number'). How does it do this?
Around the muscle cells are myogenic stem cells called 'satellite cells' (or 'myoblasts'). Under the right conditions these cells become more 'like' muscle cells and actually donate their nuclei to the muscle fibers, thereby increasing myonuclei number. For this to happen, several things need to take place. One, the number of satellite cells has to increase (called 'proliferation'). Two, they have to become more 'like' muscle cells (called 'differentiation'). And three, they have to fuse with the needy muscle cells.
When the sarcolemma (the muscle cell wall) is 'damaged' by tension (as in weight training or even stretching) growth factors are produced and released in the cell. There are several different types of growth factors. The most significant are:
Insulin-like Growth Factor 1 (IGF-1)
Fibroblast Growth Factor (FGF)
Transforming Growth Factor -Beta Superfamily (TGF-beta)
These growth factors can then leave the cell and go out into the surrounding area because sarcolemma permeabilty has been increased due to the 'damage' done during contraction. Once outside the muscle cell these growth factors cause the satellite cells to proliferate (mainly FGF does this) and differentiate (mainly IGF-1 does this). TGF-beta's role is one of mediation - in this case it inhibits growth. After this process the satellite cells then fuse with the muscle cells and donate their nuclei, giving the muscle cells the 'ability' to grow.
Now factors that promote protein synthesis such as IGF-1, growth hormone (GH), testosterone and some prostaglandins can commence the growth process. Protein synthesis occurs because a genetically-coded subtsance called 'messenger RNA' (mRNA) is sent out from the nucleus to the ribosomes. The nucleus is believed to release increased mRNA in response to tension and/or myofibrillar damage done as a result of insufficient cycling of actin-myosin cross-bridges during intense muscular contractions, though this mechanism is not fully understood. The mRNA contains the 'instructions' for the ribosomes to synthesize proteins, and so the process of constructing contractile (actin and myosin) and structural proteins (for the other components of the cell) from the amino acids taken into the cell from the bloodstream is set off. Several substances can influence this process. A short overview of the major ones are found below:
IGF-1: IGF-1 comes in two varieties - paracrine IGF-1 is made primarily in the liver and autocrine IGF-1 is made locally in other cells. Paracrine IGF-1 travels through the bloodstream to the various tissues of the body, but autocrine IGF-1 is local in that in affects only tissues in the area in which it is released. Receptors on the surface of the cells are necessary for paracrine IGF-1 to enter the cells and exert its anabolic effects. But autocrine IGF-1, which is manufactured and released in the muscle cell as a response to high tension contractions, operates independently of receptors on the surface because it's already inside. Once inside the cell, IGF-1 interacts with calcium-activated enzymes and sets off a process that results in protein synthesis (and the calcium ions that were released during muscle contraction and also the ones that leak into the muscle after the sarcolemma is damaged ensure that the necessary enzymes are calcium-activated). A large part of this increase in protein synthesis rate is due to the fact that the IGF-1/calcium/enzyme complexes make protein synthesis at the ribosomes more efficient.
By the way, insulin works at the ribosome in a similar manner, hence the name insulin-like growth factor-1 (IGF-1). So get some quick digesting carbs in after your workout to raise insulin levels.
GH: GH is thought to work, primarily, by causing the cells (both liver and muscle cells) to release IGF-1. Effective training causes a rise in GH levels in the bloodstream; this GH prompts the liver to release paracrine IGF-1 several hours afterward, and also the muscle cells to release autocrine IGF-1, thus leading to another potential growth induction.
Prostaglandins: Certain prostaglandins are released during contraction (and stretch); two of the most significant to growth being PGE2 and PGF2-alpha. PGE2 increases protein degradation, whereas PGF2-alpha increases protein synthesis. But PGE2 isn't all bad because it also powerfully induces satellite cell proliferation and infusion. The mechanism of PGF2-alpha's action is much less clear but is suspected to be connected to increasing protein synthesis 'efficiency' at the ribosomes.
Testosterone: 'Free' testosterone (the kind that isn't bound to a binding protein) travels freely across the muscle cell membrane and, once inside, activates what's called the 'androgen receptor'. 'Bound' testosterone (the kind that is bound to a binding protein) must first activate receptors on the cell surface before it can enter (the number of receptors on the surface is what controls this pathway). Once the androgen receptor is activated by testosterone it travels to the nucleus and sets off the protein synthesis process. In this way, testosterone directly causes protein synthesis and is, by far, the most powerful anabolic agent found naturally in the human body. Testosterone also increases the satellite cells' sensitivity to IGF-1 and FGF, thereby promoting satellite cell proliferation and differentiation. It also increases the body's systemic output of GH and IGF-1. Resistance training causes a spike in testosterone level.
After a workout, to facilitate the growth process, muscle cells are more 'receptive' to testosterone, systemic IGF-1 and GH.
The whole process of cellular damage and subsequent overcompensation (the cells grow back a little bigger than they were before) can take anywhere in the neighbourhood of several hours to several days, depending on the severity and type of training. Trained individuals, however, have been shown, in several studies, to complete the protein synthesis cycle within 36-48 hours after intense 'conventional' Bodybuilding-type weight training. This is strong evidence to support the idea that muscles should be trained every 48 hours. But there are more things to consider, and that's what we'll do in articles on the 'Training Related Articles' page.
Clearly, increasing the volume of muscular contractile elements is the key to increasing muscle size and strength. Since the type II fibers contain the most actin/myosin filaments, and generate the highest tensions, they have the greatest potential for strengthening/growth. The prerequisite, of course, is that you have to lift weights heavy enough to recruit the type II fibers - and for them to twitch fast enough to develop significant tension. You also have to subject them to that tension long enough for significant damage to occur to the muscle fibers.
In Part II of this series I'll present the reasons why you want to increase intracellular mitochondria number and discuss further why Weightlifters are, as a group, stronger than Bodybuilders but usually smaller. I'll also wrap up with some very 'innocent', yet profound, recommendations regarding muscle growth and strengthening.
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