Welcome to the second part of this series of articles, and in case you missed the first one you can read it here.
Sarcomere Hypertrophy
This type of hypertrophy refers to increasing the volume of contractile machinery. Up to 80% of a muscle cell’s density is made up of contractile machinery, so this leaves a lot of potential for increasing muscle size. Muscles that have undergone training (weight/strength training) respond to exercise by increasing the number of actin/myosin filaments. This leads to increased muscle size and strength.
As you should know by now, in order for a muscle to increase in size and strength, it must be ‘broken down’ first. ‘Broken down’ and ‘building up’ are subjects in their own rights and it is pertinent that we look at these in a bit more detail.
Exercise Induced Muscular Cell Damage
When a muscle fiber undergoes enough tension for a period of time, it begins to show signs of fatigue. This process impairs the actin/myosin activity within the body by hindering the ‘cross bridge’ cycling that is necessary for the contractile filaments to maintain force production.
Furthermore, this impairment leads to post-workout breaches within the plasma membrane. This causes calcium to leak into the muscle cells. It is important to remember that there is a lot of calcium in the blood, and once muscle cells give-way by tearing, this calcium seeps into the cells.
This process increases the calcium levels and activates enzymes known as ‘calpains’, which remove pieces of damaged contractile filaments. Then a protein known as ‘ubiquitin’, which exists in all muscle cells, begins to bind pieces of filaments. After this, white blood cells known as ‘neutrophils’ become chemically attracted to the area concerned and begin to increase in numbers.
Toxins are now released which include oxygen radicals, and they increase membrane permeability and phagocytize (ingest and destroy) any tissue debris that was released as a result of the calcium-induced pathways. Neutrophils do not remain present for longer than a couple of days and they are complimented by the appearance of monocytes which are attracted by the damaged area.
Monocytes are a type of phagocytic cells and they enter the damaged muscle and form into macrophages that also release toxins that phagocytize the damaged tissue. Once this stage commences, any damaged fibers are broken down by lysosomal proteases, free O2 radicals and various other substances that are produced by macrophages.
The muscle at this stage is in a weaker state than it was before it underwent training. Macrophages play an essential role in repairing muscular tissue. If the damaged muscle is not invaded by macrophages, the activation of satellite cells and muscle rehabilitation will not occur. Furthermore, increased intracellular Ca++ concentrations are associated with the activation of an enzyme know as ‘Phospholipase A2’.
This enzyme releases arachidonic acids from the plasma membrane which is then formed into prostaglandins as well as other eicosanoids that play a contributory function to the degradative processes.
The Muscle Growth Process
Muscle cells contain many nuclei and other intracellular matter, and nuclei are associated with the protein synthesis processes. A single nuclei is only capable of supporting the manufacturing of a limited amount of protein. If muscle cells did not consist of multiple nuclei then they would be very small cells. So for muscles to grow beyond their current size, they have to increase the number of the nuclei present in the area, also known as the ‘myonuclei number’.
The muscle cells are surrounded by myogenic stem cells called ‘satellite cells’ or sometimes known as ‘myoblasts’. Under the correct conditions these cells morph into a type of muscle-cells and donate their nuclei to the muscular fibers, helping to increase the myonuclei number.
In order for this to take place:
1. The number of satellite cells has to increase and this is known as ‘proliferation’.
2. They have to become more like muscle cells. This is known as ‘differentiation’.
3. They have to fuse with any needy muscle cells.
When the muscle cell wall, which is known as ‘sarcolemma’ is damaged by tension from the workout, growth factors are produced and released within the cells. There are a number of types of growth factors and these include:
• Insulin-like Growth Factor 1 (IGF-1)
• Fibroblast Growth Factor (FGF)
• Transforming Growth Factor - Beta Superfamily (TGF-beta)
These growth factors then leave the cell and make their way out to the surrounding area because sarcolemma permeability has increased as a result of the damage that occurred during contraction.
Once outside the muscle cells, FGF and IFG-1 cause the satellite cells to proliferate and differentiate, while the role of the TGF-beta is of mediation – in this particular case, it inhibits growth. The satellite cells then fuse with the muscle cells and donate their nuclei which gives the muscles the ability to grow. Now the factors that promote protein synthesis such as IGF-1, the growth hormone (GH), testosterone and some prostaglandins help to commence the growth process.
The protein synthesis takes place because of the existence of a genetically coded substance known as ‘messenger RNA’ (mRNA) that 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 holds the instructions for the ribosomes to synthesize proteins, and the process of constructing contractile and structural proteins from amino acids taken into the cells from the bloodstream is set off.
In Part 3 we will further discuss about the substances that influence this process: IGF-1, GH, testosterone and prostaglandins.
About The Author
James McDuffy works for The Muscle Growth Expert. You can visit his website for more info on different aspects of bodybuilding and the science behind muscle growth.
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