In PART I we discussed about sarcoplasmic hypertrophy and the increase of non-contractile muscle tissue. In part II we’ll take a look at myofibrilar growth.
Myofibrillar Hypertrophy
Myofibrillar hypertrophy is the increase in the volume of the contractile parts inside the muscle fibers. Almost 80% of the muscle fiber’s density is comprised of these contractile parts, which leaves a great potential for muscle size growth. Muscles that have been trained either in a bodybuilding or strength training fashion, respond to the training stimulus by increasing the number of the contractile parts, which are actually actin and myosin filaments.
This ultimately leads to increased muscle strength and size. As it was mentioned numerous times before, if you want the muscle to become bigger and stronger, you need to “break it down” first. Breaking a muscle down and building muscle are two subjects which overlap but are different enough so that they can be examined separately.
Muscle cell damage induced by exercise
Once a muscle fiber has spent a certain period of time under tension, it starts to show signs of fatigue. This then starts to impair the activity of actin and myosin inside the body by inhibiting the ‘cross bridge’ cycling which is essential for the contractile parts to be able to produce force. Additionally, this inhibition causes post-workout breaches inside the plasma membrane, which causes calcium leakage inside the muscle cells. It’s worth noting that calcium is present in the blood, and once the muscle fibers start to tear away, the calcium starts seeping inside the cells.
This leaking process increases the levels of calcium and activates specific enzymes called ‘calpains’, whose role is to remove the damaged parts of the contractile filaments. Afterward, a protein called ‘ubiquitin’, which is found in every muscle fiber starts binding filament pieces. Next, white blood cells called ‘neutrophils’ start to gather around the area and slowly increase in numbers.
The Breakdown Process
Now, toxins are being released including oxygen radicals, which increase the permeability of the membrane and start devouring and destroying any tissue left-overs that were produced by the pathways induced by the calcium leakage. Neutrophils don’t stay in the area for more than two or three days and are complemented by the arrival of monocytes that are attracted by the area that is damaged.
Monocytes are a specific type of phagocytic cells which enter the damaged muscle fiber and transform into macrophages which also produce toxins which further destroy the damaged area. When this process starts, the damaged muscle fibers are broken down by lysosomal proteases, free radicals and many other compounds released by the macrophages.
At this stage, the muscle is in a considerably weaker state than before training. The macrophages have a key role in repairing the damaged muscle tissue. If macrophages do not come to the damaged area, the satellite cells activation and muscle rehabilitation won’t happen. Plus, the increased Ca++ levels between the cells are related to the activation of the enzyme called ‘Phospholipase A2’. This particular enzyme produces arachidonic acids from the membrane, which is then transformed into prostaglandins, plus other compounds known as eicosanoids which have a contributing role in the degradative processes.
Continues on next page…
