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Muscular Growth: How Does A Muscle Grow?
Let's get right into this and start with a segment from the Neuromuscular System series:
Muscle biopsies of serious weight trainers have shown that it was the size of the individual fibers within their muscles that was responsible for the abnormal muscle size and not the actual number of muscle fibers present.
...although extreme conditions may result in modest hyperplasia. This tells us that the formation of new muscle cells (hyperplasia) is, at most, likely to be only a minor factor in increasing muscle size. The mechanism responsible for supercompensation is hypertrophy - the increase in size of existing muscle fibers.
Taking another segment from the Neuromuscular System series:
It is also worthy of note that contractile machinery comprises about 80% of muscle fiber volume. The rest of the volume is accounted for by tissue that supplies energy to the muscle or is involved with the neural drive.
This tells us that there are a couple of ways to increase muscle size.
Increase the volume of the tissue that supplies energy to the muscle or is involved with the neural drive - called sarcoplasmic hypertrophy.
Increase the volume of contractile machinery - called sarcomere hypertrophy.
Let's take a look at both routes.
Sarcoplasmic Hypertrophy
Increasing the volume of the tissue that supplies energy to the muscle or is involved with the neural drive: Intimately involved in the production of ATP are intracellular bodies called "mitochondria". Muscle fibers will adapt to high volume (and higher rep) training sessions by increasing the number of mitochondria in the cells. They will also increase the concentrations of the enzymes involved in the oxidative phosphorylation and anaerobic glycolysis mechanisms of energy production and increase the volume of sarcoplasmic fluid inside the cell (including glycogen) and also the fluid between the actual cells. This type of hypertrophy produces very little in the way of added strength but has profound effects on increasing strength-endurance (the ability to do reps with a certain weight) because it dramatically increases the muscles' ability to produce ATP. Adaptations of this sort are characteristic of Bodybuilders' muscles.
It should also be obvious that as the volume of the tissue that supplies energy to the muscle represents only around 20% of the total muscle cell volume in untrained individuals, this isn't where the real size potential lies.
Sarcoplasmic hypertrophy of muscle cells does directly produce moderate increases in size . But also, as you'll know from the Neuromuscular System series, ATP is the source of energy for all muscular contraction - type II fibers included. Wouldn't having more of this in the muscle, and having the ability to produce greater intramuscular quantities at any one time, be an asset? The answer is, cleary, "yes". That's where a major portion of the importance of sarcoplasmic hypertrophy comes into Bodybuilding. (We'll deal with training to produce this type of adaptation in an article on the 'Training Related Articles' page.)
As for increasing the tissue that is involved with the neural drive, this would theoretically occur in response to the need for contracting cells with hypertrophied contractile machinery. Directly, it would produce very little in the way of added size.
In addition, there are other intracellular bodies who's growth and/or proliferation would fall under the category of sarcoplasmic hypertrophy. These would be organelles such as the "ribosomes", which are involved in protein synthesis. As in the case of neural drive machinery, in most cases they would increase in size or number only to support sarcomere hypertrophy. They would have little direct impact on overall muscle size.
Sarcomere Hypertrophy
Increasing the volume of contractile machinery: The vast majority of the volume of each muscle cell (~80%) is made up of contractile machinery. Therefore, there lies the greatest potential for increasing muscle cell size. Trained muscle responds by increasing the number of actin/myosin filaments (sarcomeres) that it contains - this is what is responsible for increased strength and size. But before a muscle will grow like this it has to be "broken down". Let's take a look at both the "breaking down" and "building up" processes:
The Process Of Exercise-Induced Muscle Cell Damage
Actin/myosin filaments sustain "damage" during high-tension contractions. In addition, breaches in plasma membrane integrity allow calcium to leak into the muscle cells after training (there is much more calcium in the blood than in the muscle cells). This intracellular increase in calcium levels activates enzymes called "calpains" which "break off" pieces of the damaged contractile filaments (called "easily releasable myofilaments"). Following this, a protein called "ubiquitin" (which is present in all muscle cells) binds to the removed pieces of filaments thus "identifying" them for destructive purposes. At this time, neutrophils (a type of granular white blood cell that is highly destructive) are chemically attracted to the area and rapidly increase in number. They release toxins, including oxygen radicals, which increase membrane permeability and phagocytize (ingest and "destroy") the tissue debris that the calcium-mediated pathways released. Neutrophils don't remain around more than a day or two, but are complimented by the appearance of monocytes also attracted to the damaged area. Monocytes (a type of phagocytic cell) enter the damaged muscle and form into macrophages (another phagocytic cell) that also release toxins and phagocytize damaged tissue. Once the phagocytic stage commences, the damaged fibers are rapidly broken down by lysosomal proteases, free O2 radicals, and other substances produced by macrophages. As you can tell, the muscle is now in a weaker state than before it was trained. Incidently, macrophages have an essential role in initiating tissue repair. Unless damaged muscle is invaded by macrophages, activation of satellite cells and muscle repair does not occur.
Also, increased intracellular Ca++ concentrations are known to activate an enzyme called phospholipase A2. This enzyme releases arachidonic acid from the plasma membrane which is then formed into prostaglandins (primarily PGE2) and other eicosanoids that contribute to the degradative processes.
So, now that we've seen how the muscle gets damaged, how does it grow?
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 so much 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 has (called the "myonuclei number"). How does it do this? Well, 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 (very nice of them). For this to happen, to any degree, 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 actually inhibits growth - but everything can't be perfect. After this process the satellite cells then fuse with the muscle cells and donate their nuclei. The muscle cell can now grow.
So now factors that promote protein synthesis such as IGF-1, growth hormone (GH), testosterone and some prostaglandins can go to work. How does that all happen? Read on...
Protein synthesis occurs because a genetically-coded subtsance called "messenger RNA" (mRNA) is sent out from the nucleus and goes to organelles called "ribosomes". 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:
Muscular Growth: How Does A Muscle Grow?
Let's get right into this and start with a segment from the Neuromuscular System series:
Muscle biopsies of serious weight trainers have shown that it was the size of the individual fibers within their muscles that was responsible for the abnormal muscle size and not the actual number of muscle fibers present.
...although extreme conditions may result in modest hyperplasia. This tells us that the formation of new muscle cells (hyperplasia) is, at most, likely to be only a minor factor in increasing muscle size. The mechanism responsible for supercompensation is hypertrophy - the increase in size of existing muscle fibers.
Taking another segment from the Neuromuscular System series:
It is also worthy of note that contractile machinery comprises about 80% of muscle fiber volume. The rest of the volume is accounted for by tissue that supplies energy to the muscle or is involved with the neural drive.
This tells us that there are a couple of ways to increase muscle size.
Increase the volume of the tissue that supplies energy to the muscle or is involved with the neural drive - called sarcoplasmic hypertrophy.
Increase the volume of contractile machinery - called sarcomere hypertrophy.
Let's take a look at both routes.
Sarcoplasmic Hypertrophy
Increasing the volume of the tissue that supplies energy to the muscle or is involved with the neural drive: Intimately involved in the production of ATP are intracellular bodies called "mitochondria". Muscle fibers will adapt to high volume (and higher rep) training sessions by increasing the number of mitochondria in the cells. They will also increase the concentrations of the enzymes involved in the oxidative phosphorylation and anaerobic glycolysis mechanisms of energy production and increase the volume of sarcoplasmic fluid inside the cell (including glycogen) and also the fluid between the actual cells. This type of hypertrophy produces very little in the way of added strength but has profound effects on increasing strength-endurance (the ability to do reps with a certain weight) because it dramatically increases the muscles' ability to produce ATP. Adaptations of this sort are characteristic of Bodybuilders' muscles.
It should also be obvious that as the volume of the tissue that supplies energy to the muscle represents only around 20% of the total muscle cell volume in untrained individuals, this isn't where the real size potential lies.
Sarcoplasmic hypertrophy of muscle cells does directly produce moderate increases in size . But also, as you'll know from the Neuromuscular System series, ATP is the source of energy for all muscular contraction - type II fibers included. Wouldn't having more of this in the muscle, and having the ability to produce greater intramuscular quantities at any one time, be an asset? The answer is, cleary, "yes". That's where a major portion of the importance of sarcoplasmic hypertrophy comes into Bodybuilding. (We'll deal with training to produce this type of adaptation in an article on the 'Training Related Articles' page.)
As for increasing the tissue that is involved with the neural drive, this would theoretically occur in response to the need for contracting cells with hypertrophied contractile machinery. Directly, it would produce very little in the way of added size.
In addition, there are other intracellular bodies who's growth and/or proliferation would fall under the category of sarcoplasmic hypertrophy. These would be organelles such as the "ribosomes", which are involved in protein synthesis. As in the case of neural drive machinery, in most cases they would increase in size or number only to support sarcomere hypertrophy. They would have little direct impact on overall muscle size.
Sarcomere Hypertrophy
Increasing the volume of contractile machinery: The vast majority of the volume of each muscle cell (~80%) is made up of contractile machinery. Therefore, there lies the greatest potential for increasing muscle cell size. Trained muscle responds by increasing the number of actin/myosin filaments (sarcomeres) that it contains - this is what is responsible for increased strength and size. But before a muscle will grow like this it has to be "broken down". Let's take a look at both the "breaking down" and "building up" processes:
The Process Of Exercise-Induced Muscle Cell Damage
Actin/myosin filaments sustain "damage" during high-tension contractions. In addition, breaches in plasma membrane integrity allow calcium to leak into the muscle cells after training (there is much more calcium in the blood than in the muscle cells). This intracellular increase in calcium levels activates enzymes called "calpains" which "break off" pieces of the damaged contractile filaments (called "easily releasable myofilaments"). Following this, a protein called "ubiquitin" (which is present in all muscle cells) binds to the removed pieces of filaments thus "identifying" them for destructive purposes. At this time, neutrophils (a type of granular white blood cell that is highly destructive) are chemically attracted to the area and rapidly increase in number. They release toxins, including oxygen radicals, which increase membrane permeability and phagocytize (ingest and "destroy") the tissue debris that the calcium-mediated pathways released. Neutrophils don't remain around more than a day or two, but are complimented by the appearance of monocytes also attracted to the damaged area. Monocytes (a type of phagocytic cell) enter the damaged muscle and form into macrophages (another phagocytic cell) that also release toxins and phagocytize damaged tissue. Once the phagocytic stage commences, the damaged fibers are rapidly broken down by lysosomal proteases, free O2 radicals, and other substances produced by macrophages. As you can tell, the muscle is now in a weaker state than before it was trained. Incidently, macrophages have an essential role in initiating tissue repair. Unless damaged muscle is invaded by macrophages, activation of satellite cells and muscle repair does not occur.
Also, increased intracellular Ca++ concentrations are known to activate an enzyme called phospholipase A2. This enzyme releases arachidonic acid from the plasma membrane which is then formed into prostaglandins (primarily PGE2) and other eicosanoids that contribute to the degradative processes.
So, now that we've seen how the muscle gets damaged, how does it grow?
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 so much 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 has (called the "myonuclei number"). How does it do this? Well, 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 (very nice of them). For this to happen, to any degree, 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 actually inhibits growth - but everything can't be perfect. After this process the satellite cells then fuse with the muscle cells and donate their nuclei. The muscle cell can now grow.
So now factors that promote protein synthesis such as IGF-1, growth hormone (GH), testosterone and some prostaglandins can go to work. How does that all happen? Read on...
Protein synthesis occurs because a genetically-coded subtsance called "messenger RNA" (mRNA) is sent out from the nucleus and goes to organelles called "ribosomes". 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:
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