What causes hypertrophy
Introduction
Hypertrophy is specified as an increase or growth in muscle cells, usually leading to a more toned and aesthetic physique. In this, I talk about the structure of the muscle and how hypertrophy occurs in many forms.
To understand hypertrophy optimally you first need a solid foundation of knowledge about the basic structure of the muscle and how it contracts, if you feel you already have a solid foundation of knowledge about this please skip ahead. This is not necessary to know but it will help you understand the following information on hypertrophy.
The structure of the muscle
(sorry about the poor artwork and handwriting)
Whole muscle- connective tissue, contains everything in the muscle
Fascicle- connective tissue that holds discrete parts of the muscle, which contain the muscle fibres the amount of these varies in different muscles depending on their size
Perimysium- connective tissue that surrounds the fascicle
Nucleus- important for building proteins, the muscle has many nuclei
Organelles- in between the myofibrils, which contain mitochondria (for ATP) and the sarcoplasmic reticulum (to store calcium)
Myofibril- contains contractile proteins and the sarcoplasm which is the cytoplasm for skeletal muscle, there are about 50-2000 of these per muscle fibre.
Muscle fibre- connective tissue that contains the myofibrils and is striated, there are about 20-60 muscle fibres per fascicle
Endomysium-connective tissue surrounding the muscle fibre, underneath there is the cell membrane known as the sarcolemma
Satellite cells- aids muscle growth (talked about later), situated between the sarcolemma and the basal lamina
Fascia-connective tissue that surrounds the whole muscle
How muscles contract
For a muscle to contract first a signal must be sent down through the motor neuron to the muscle. For this to happen sodium channels on the motor neuron open and sodium diffuses into the neuron which makes the inside of the membrane slightly positive, this stimulates the next channel to open, this is known as a voltage-gated sodium channel. This process causes a positive charge to run all the way along a neurone until it opens calcium channels at the terminal of the neurone so calcium can flow into the neurone. The calcium stimulates vesicles in the terminal to fuse with the cell membrane and release the neurotransmitter acetylcholine which crosses the synapse and binds to acetylcholine receptors on the myofibril, which causes them to open chemically gated channels so sodium outside the cell can enter the myofibril. If acetylcholine doesn’t cross the synapse in 1-millisecond acetylcholine esterase recycles the acetylcholine back into the pre-synaptic terminal so it can be reused. T-tubules have acetylcholine receptors which run deep into the muscle, this helps sodium reach the sarcoplasmic reticulum and causes it to release calcium.
One motor neuron will innervate multiple muscle fibres, so if the motor neuron sends a signal it will cause the contraction of multiple muscle fibres, which is known as the all-or-none principle.
Sarcomeres (inside myofibril) are lined up in series and in parallel in the muscle, they are the part of the muscle which causes a muscular contraction. The striated appearance of a muscle is due to the stacking of sarcomeres.
Sarcomere structure:
Calcium binds with troponin on the actin (a contractile protein, also known as the thin filament) and the troponin wrapped around the actin falls away, this only happens if ATP (an important energy molecule) is present. This means the myosin heads can now bind with the binding pockets of the actin.
ATP binds to the myosin heads, ATP disassociates to ADP and a phosphate which stays attached to the myosin, this allows for the myosin heads to cock and bind to the actin. ADP and the phosphate are then released and the head moves to force the z discs closer together, this is known as a power stroke and the titin’s spring-like structure shortens. The myosin head remains stuck to the actin molecule until another ATP molecule comes along and binds to the myosin and releases the head, this process can repeat to cause a muscular contraction as the ATP turns to ADP and a phosphate. 98% of the muscle fibres run all the way along a muscle so this causes shortening of the entire muscle, this will pull on bones and cause movement of certain body parts.
When a muscle is in the stretched position the sarcomeres will stretch and their is therefore less cross bridging between the actin and myosin filaments, however, the actin and myosin heads are closer and force potential is therefore high. When a muscle is shortened the sarcomeres will shorten and the actin filaments will overlap and their is therefore less opportunity for actin and myosin to begin cross bridging.
Different types and stimuli of hypertrophy
There are 3 different types of hypertrophy, each of these can occur, intensify, induce and co-vary another, myofibrillar hypertrophy is an increase in contractile proteins and in sarcomeres in series or in parallel. Connective tissue hypertrophy is an increase in connective tissue, which takes up up to 20% of the muscle. Sarcoplasmic hypertrophy is an increase in the size or amount of organelles such as mitochondria (for energy), sarcoplasmic reticulum, titin, nebulin (stabilises actin), T-tubules or metabolic products. Up to 3% of the muscle is glycogen and 5% triglycerides and you can increase the quantity of these by training in the larger rep range (8-12 reps) in particular. Bodybuilders tend to have more connective tissue and sarcoplasmic hypertrophy because they usually have more stores of glycogen and more connective tissue products as compared to powerlifters.
There are 3 stimuli of hypertrophy, mechanical tension is the most important, followed by metabolic stress and muscle damage. It is unsure if muscle damage causes muscle growth or if they both occur due to the same or similar things.
70% of proteins in the muscle are myofibrillar proteins, 20% sarcoplasmic proteins and 10% mitochondrial proteins.
Mechanical tension
Mechanical tension is the force generated by the muscle fibres, components within the muscle fibre known as mechanoreceptors detect the forces produced by the muscle fibre and transduce these forces into a signalling cascade which results in muscle protein synthesis. The more tension detected the more muscle growth stimulated. The duration of the signal output is proportional to how much muscular growth it occurs, to stimulate this you can use a larger ROM (range of motion) or do more reps, sets or both, but this doesn't necessarily promote going to failure (when you no longer can perform another rep of an exercise with good form) because at failure there is no extra motor unit recruitment as compared to 2 or 3 RIR (reps in reserve) so it will likely not cause any noticeable extra muscle gain, as backed by studies. But you must go close to failure as this is where the larger, faster twitch fibres grow the most, this is because the motor neurons that innervate these muscles are stimulated the best here.
If there is stress on connective tissue it can grow, due to collagen synthesis increasing 24 hours after the stress occurs, which over time causes an increase in connective tissue.
Metabolic stress
Not as great of a stimulus for muscle growth as mechanical tension is metabolic stress, when working anaerobically byproducts particularly lactate quickly accumulate which stimulates muscle growth. This is directly proportional to how many and for how long metabolites are present in the muscle. Since the most metabolites accumulate closer to failure, it is promoted that you train close to but not to failure, for the reasons discussed earlier.
Cell swelling particularly for faster twitch muscle fibres triggers muscle growth, not to say you need a ‘crazy pump’ to promote muscle growth, but it will probably help. The swelling occurs as the contractions cause an increase in blood flow to the muscle, muscular contractions not allowing blood out of the muscle and metabolite accumulation which also triggers swelling as this causes water to be pulled into the cell, this is because when we need more ATP than we have oxygen available we get energy from the phosphoketolase pathway (not important to know for the purpose of hypertrophy), which produces lactate as a byproduct, this has a strong osmotic gradient and it pulls water into the muscle cell causing it to swell. The swelling puts pressure on the cell membrane which stimulates amino acid transport, anabolism (protein synthesis), growth hormone and testosterone. This is why high reps (8-12 reps) tend to be better for hypertrophy.
Hypoxia is the state of oxygen not being sufficiently available to tissue, in this case, we‘re talking about muscle, this state can be induced by partaking in blood flow restriction training, which makes the muscle work more anaerobically (without oxygen) for energy, increasing lactate accumulation. In a low oxygen environment, relative oxygen species accumulate, such as nitric oxide which tells blood vessels to dilate, so when you are out of the hypoxic state you get hyperemia (more blood flow to that area) carrying with them all the metabolites necessary for growth, therefore increasing hypertrophy.
Muscle damage
As the muscle lengthens damage occurs to the myofibrillar units, this creates an inflammatory response in order to promote repair of the muscle, it also stimulates satellite cells to fuse with the muscle cell and donate their nuclei so more amino acids and therefore proteins can be produced. The nuclei can also transcribe more growth pathways for muscle growth such as MTOR (an enzyme that can be signalled to increase protein synthesis), MAPKs (an enzyme that regulates cell proliferation, differentiation, motility and survival) and calcium signalling pathway (helps cell growth and proliferation). When damage is done to the muscle in the eccentric portion of an exercise (when the muscle is contracting and lengthening), by controlling the part of the exercise when the muscle is getting stretched, there will be an increase in the number of sarcomeres in series. Whilst, when damage is done to the muscle in the concentric portion of an exercise (when the muscle is contracting and shortening) sarcomeres will increase in parallel.
Conclusion
Using the information given, we now know that to optimally stimulate hypertrophy it is best to exercise within a high rep range (8-12reps) with about 2 RIR (reps in reserve) by the end of the set if you are looking to increase the rate of hypertrophy, it appears it will be best to add sets, reps or ROM (range of motion) as opposed to intensity each set, providing you were already training at a high enough intensity (of about 2 RIR), as to stimulate mechanoreceptors the best and therefore muscle protein synthesis. Each rep should be slow and controlled with special attention to the eccentric portion where it is challenging to keep the reps slow due to the ease of just dropping the weights, this will cause the most muscle growth. However, don’t make the reps too slow as you want to try and activate the fast-twitch muscle fibres which are the largest and most prone to growth, do this by keeping each rep at about an approximate 3-second eccentric portion and a 1.5-second concentric portion, this may get difficult to perform as the exercise continues and fatigue sets in, training in this way will cause large limitations for an increase in muscular strength, especially for more advanced lifters and for very advanced lifters they may even experience a decrease in strength as this training style fails to cause major adaptions to the neuromuscular system or maintain adaptions already created through specialised strength training, as the neuromuscular system is very important in the case of strength gains.
Hopefully, this gave you a decent understanding of how hypertrophy occurs, however, by only using information from this you will not have all the necessary knowledge to train optimally, as this wasn’t the goal of the previous information given, as the goal was purely to give you information on what is going on inside the muscle to cause hypertrophy.
Disclaimer: use the information provided in this article at your own risk, as I will not be liable for any harm that may be caused by it.
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