How do muscles get bigger?

How do muscles get bigger?

Mitchell Casey

So you want to get gainz/ hyooge/ jacked/ shredded?

Well knowing how muscle growth occurs is a good start! 💪💪

I'm still surprised that most health professionals aren't taught this before graduating.😣😣 So if you're someone who prescribes strength exercises to clients for a living then this article is for you! 🤓🤓

Let's start with the basic anatomy of a muscle group as seen in image 1 (8). Muscles are divided by connective tissue (perimysium) into groups of fibres called fascicles. These fascicles can contain hundreds of muscle fibres and as you can see in image 2 (8), each muscle fibre contains hundreds of rod-like myofibrils. Each myofibril then contains hundreds of thousands of sarcomeres which are the building blocks of muscles and contain the actin and mysoin molecules that form crossbridges and overlap to produce a contraction and generate force. Another thing to note is that muscle fibres have their own source of stems cells called satellite cells which play an important role in cell repair and growth.

For muscle growth to occur, sarcomeres need to be produced by the muscle cell and can be added in parallel to other myofibrils which would increase the diameter of the fibre, or in series, increasing muscle length. And it is typically eccentric contractions and training at longer muscle lengths that promotes longitudinal hypertrophy (1).

There are thought to be three primary mechanisms for this exercise-induced muscle hypertrophy to occur. These are mechanical tension, metabolic stress and muscle damage (5).

 

 

MECHANICAL TENSION

Schoenfeld (2010) has identified that this is the primary mechanism of muscle hypertrophy and it occurs through a process called mechanotransduction. When a muscle fibre contracts, the sarcomeres within it shorten in length and bulge out from the sides. This physically stretches the wall of the muscle cell which is detected by stretch receptors as a threat to it's structure. This tension then leads to the activation of several myogenic (muscle building) pathways such as mTOR, MAPK and calcium dependant pathways (3). The downstream effects of this is an increased production of sarcomeric proteins. And when the mechanical tension is great enough, the satellite cells we mentioned earlier become active and bind themselves to myofibrils to donate their nucleus, giving the muscle more machinery to produce more protein! 🏗🏗

 

METABOLIC STRESS

Metabolic stress is another well known mechanism and occurs when lactate and other metabolites accumulate in the cell as a result of anaerobic glycolysis (using glycogen faster than oxygen can be delivered). In a resistance training context, this is training with higher reps and shorter rest periods to get that glorious pump.🔥🔥 This is also how occlusion training works.

It was long thought that this type of training caused growth through an acute increase in growth hormone production however Morton et al. 2016 showed no correlation between the these events. What most likely happens from this form of training is several things.

1. Metabolites such as lactate and hydrogen ions will accumulate and draw water into the cell through osmosis causing swelling. This swelling then stretches the wall of the muscle fibre and the same process as above occurs.💧💧

2. The accumulation of metabolites also causes fatigue in the muscle by reducing the release of calcium from the sarcoplasmic reticulum and also by reduced the sensitivity of actin and myosin to calcium (2). This increases the activation of higher threshold motor units and their associated larger muscle fibres which are capable of generating more tension and therefore more stretch on the cell walls.

3. Muscle fatigue also slows contraction velocity which allows more time for cross bridges to form and therefore more tension and again, more stretch.

So metabolic stress does work, but most likely through an increase in mechanical tension (6). 🤯🤯

 

MUSCLE DAMAGE

Trauma to muscle cells was long thought to be a major contributor to muscle hypertrophy. However, the research presented above has shown that the primary mechanism of muscle hypertrophy is in fact mechanical tension 🤥🤥. Now whether or not muscle damage augments this hypertrophy is still yet to be determined. On one hand, there is theoretical rationale linking exercise induced muscle damage to hypertrophy via the activation of satellite cells, up-regulation of the IGF-1 system and the activation of myogenic pathways. But on the other hand, the muscle has to use valuable energy producing proteins to repair the damage before any of the proteins can contribute to increasing fibre size (7).

So there you have it! But what does this mean for your training if muscle hypertrophy is a goal? Well it's probably best to use a combination of increasing mechanical tension as well as inducing metabolic stress. To increase mechanical tension you need to do something very simple but very overlooked by many health practitioners.... progressively overload your volume load (sets x reps x load). This means increasing the weight and/or volume you are lifting... and note that muscle growth doesn't just happen between 8-12 reps (more on this in my next blog).

And to utilise metabolic stress, complete your final set with a finisher. These can be

Drop sets- dropping the weight of consecutive sets with no rest

Cluster sets- using a heavy weight and resting mid set until you complete all reps

Pyramids- increasing and decreasing the weight

50's- doing 50 reps in a row

There are lots more options!

 

 

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References:

(1) Brynnel, A., Hernandez, Y., Kiss, B., Lindqvist, J., Adler, M., Kolb, J., ... & Ottenheijm, C. (2018). Downsizing the molecular spring of the giant protein titin reveals that skeletal muscle titin determines passive stiffness and drives longitudinal hypertrophy. eLife, 7, e40532.

(2) Cheng, A. J., Place, N., & Westerblad, H. (2018). Molecular basis for exercise-induced fatigue: the importance of strictly controlled cellular Ca2+ handling. Cold Spring Harbor perspectives in medicine, 8(2), a029710. (3) Glass, D. J. (2003). Signalling pathways that mediate skeletal muscle hypertrophy and atrophy. Nature cell biology, 5(2), 87. (4) Morton, R. W., Oikawa, S. Y., Wavell, C. G., Mazara, N., McGlory, C., Quadrilatero, J., ... & Phillips, S. M. (2016). Neither load nor systemic hormones determine resistance training-mediated hypertrophy or strength gains in resistance-trained young men. American Journal of Physiology-Heart and Circulatory Physiology. (5) Schoenfeld, B. J. (2010). The mechanisms of muscle hypertrophy and their application to resistance training. The Journal of Strength & Conditioning Research, 24(10), 2857-2872.

(6) Schoenfeld, B. J. (2013). Potential mechanisms for a role of metabolic stress in hypertrophic adaptations to resistance training. Sports medicine, 43(3), 179-194.

(7) Schoenfeld, B. J., & Contreras, B. (2018). Exercise-Induced Muscle Damage and Hypertrophy: A Closer Look Reveals the Jury is Still Out. SportRxiv. March, 19.

(8) Structure of skeletal muscle. (2016, Mat 16). Retrieved from https://www.teachpe.com/anatomy/structure_skeletal_muscle.php

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