I have mentioned before that I am something of a casual gymgoer- it’s only a relatively recent hobby, and only in the last couple of months have I given any serious thought and research to my regime (in which time I have also come to realise that some my advice in previous posts was either lacking in detail or partially wrong- sorry, it’s still basically useful). However, whilst the internet is, as could be reasonably expected, inundated with advice about training programs, tips on technique & exercises to work different muscle groups (often wildly disagreeing with one another), there is very little available information concerning the basic science behind building muscle- it’s just not something the average gymgoer knows. Since I am fond of a little research now and then, I thought I might attempt an explanation of some of the basic biology involved.
DISCLAIMER: I am not a biologist, and am getting this information via the internet and a bit of ad libbing, so don’t take this as anything more than a basic guideline
Everything in your body is made up of tiny, individual cells, each a small sac consisting of a complex (and surprisingly ‘intelligent’) membrane, a nucleus to act as its ‘brain’ (although no-one is entirely sure exactly how they work) and a lot of watery, chemical-y stuff called cytoplasm squelching about and reacting with things. It follows from this that to increase the size of an organ or tissue requires these cells to do one of two things; increase in number (hyperplasia) or in size (hypertrophy). The former case is mainly associated with growths such as neoplasia (tumours), and has only been shown to have an impact on muscles in response to the injection of growth hormones, so when we’re talking about strength, fitness and muscle building we’re really interested in going for hypertrophy.
Hypertrophy itself is still a fairly broad term biologically, and only two aspects of it are interesting from an exercise point of view; muscular and ventricular hypertrophy. As the respective names suggest, the former case relates to the size of cells in skeletal muscle increasing, whilst the latter is concerned with the increase in size & strength of the muscles making up the walls of the heart (the largest chambers of which are called the ventricles). Both are part of the body’s long-term response to exercise, and for both the basic principle is the same- but before I get onto that, a quick overview of exactly how muscles work may be in order.
A muscle cell (or muscle fibre) is on of the largest in the body, vaguely tubular in shape and consisting in part of many smaller structures known as myofibrils (or muscle fibrils). Muscle cells are also unusual in that they contain multiple cell nuclei, as a response to their size & complex function, and instead of cytoplasm contain another liquid called sarcoplasm (more densely packed with glycogen fuel and proteins to bind oxygen, and thus enabling the muscles to respire more quickly & efficiently in response to sudden & severe demand). These myofibrils consist of multiple sections called myofilaments, (themselves made of a family of proteins called myosins) joined end-to-end as repeating units known as sarcomeres. This structure is only present in skeletal, rather than smooth muscle cells (giving the latter a more regular, smoothly connected structure when viewed under the microscope, hence the name) and are responsible for the increased strength available to skeletal muscles. When a muscle fibril receives an electrical impulse from the brain or spinal cord, certain areas or ‘bands’ making up the sarcomeres shrink in size, causing the muscle as a whole to contract. When the impulse is removed, the muscle relaxes; but it cannot extend itself, so another muscle working with it in what is known as an antagonistic pair will have to pull back on it to return it to its original position.
Now, when that process is repeated a lot in a small time frame, or when a large load is placed on the muscle fibre, the fibrils can become damaged. If they are actually torn then a pulled muscle results, but if the damage is (relatively) minor then the body can repair it by shipping in more amino acids (the building blocks of the proteins that make up our bodies) and fuel (glycogen and, most importantly, oxygen). However, to try and safeguard against any future such event causing damage the body does its bit to overcompensate on its repairs, rebuilding the protein structures a little more strongly and overcompensating for the lost fuel in the sarcoplasm. This is the basic principle of muscular hypertrophy; the body’s repair systems overcompensating for minor damage.
There are yet more subdivisions to consider, for there are two main types of muscular hypertrophy. The first is myofibrillated hypertrophy, concerning the rebuilding of the myofibrils with more proteins so they are stronger and able to pull against larger loads. This enables the muscle to lift larger weights & makes one stronger, and is the prominent result of doing few repetitions of a high load, since this causes the most damage to the myofibrils themselves. The other type is sarcoplasmic hypertrophy, concerning the packing of more sarcoplasm into the muscle cell to better supply the muscle with fuel & oxygen. This helps the muscle deal better with exercise and builds a greater degree of muscular endurance, and also increases the size of the muscle, as the increased liquid in it causes it to swell in volume. It is best achieved by doing more repetitions on a lower load, since this longer-term exercise puts more strain on the ability of the sarcoplasm to supply oxygen. It is also advisable to do fewer sets (but do them properly) of this type of training since it is more tiring; muscles get tired and hurt due to the buildup of lactic acid in them caused by an insufficient supply of oxygen requiring them to respire anaerobically. This is why more training on a lower weight feels like harder work, but is actually going to be less beneficial if you are aiming to build muscular strength.
Ventricular (or cardiac) hypertrophy combines both of these effects in a response to the increased load placed on the muscles in the heart from regular exercise. It causes the walls of the ventricles to thicken as a result of sarcoplasmic hypertrophy, and also makes them stronger so that the heart has to beat less often (but more powerfully) to supply blood to the body. In elite athletes, this has another effect; in response to exercise the heart’s response is not so much to beat more frequently, but to do so more strongly, swelling more in size as it pumps to send more blood around the body with each beat. Athletic heart syndrome, where the slowing of the pulse and swelling of heart size are especially magnified, can even be mistaken for severe heart disease by an ill-informed doctor.
So… yeah, that’s how muscle builds (I apologise, by the way, for my heinous overuse of the word ‘since’ in the above explanation). I should point out quickly that this is not a fast process; each successive rebuilding of the muscle only increases the strength of that muscle by a small amount, even for serious weight training, and the body’s natural tendency to let a muscle degrade over time if it is not well-used means that hard work must constantly be put in to maintain the effect of increased muscular size, strength and endurance. But then again, I suppose that’s partly what we like about the gym; the knowledge that we have earned our strength, and that our willingness to put in the hard work is what is setting us apart from those sitting on the sofa watching TV. If that doesn’t sound too massively arrogant.