The Science of Iron

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.

Advertisement

Drunken Science

In my last post, I talked about the societal impact of alcohol and its place in our everyday culture; today, however, my inner nerd has taken it upon himself to get stuck into the real meat of the question of alcohol, the chemistry and biology of it all, and how all the science fits together.

To a scientist, the word ‘alcohol’ does not refer to a specific substance at all, but rather to a family of chemical compounds containing an oxygen and hydrogen atom bonded to one another (known as an OH group) on the end of a chain of carbon atoms. Different members of the family (or ‘homologous series’, to give it its proper name) have different numbers of carbon atoms and have slightly different physical properties (such as melting point), and they also react chemically to form slightly different compounds. The stuff we drink is that with two carbon atoms in its chain, and is technically known as ethanol.

There are a few things about ethanol that make it special stuff to us humans, and all of them refer to chemical reactions and biological interactions. The first is the formation of it; there are many different types of sugar found in nature (fructose & sucrose are two common examples; the ‘-ose’ ending is what denotes them as sugars), but one of the most common is glucose, with six carbon atoms. This is the substance our body converts starch and other sugars into in order to use for energy or store as glycogen. As such, many biological systems are so primed to convert other sugars into glucose, and it just so happens that when glucose breaks down in the presence of the right enzymes, it forms carbon dioxide and an alcohol; ethanol, to be precise, in a process known as either glycolosis (to a scientist) or fermentation (to everyone else).

Yeast performs this process in order to respire (ie produce energy) anaerobically (in the absence of oxygen), so leading to the two most common cases where this reaction occurs. The first we know as brewing, in which an anaerobic atmosphere is deliberately produced to make alcohol; the other occurs when baking bread. The yeast we put in the bread causes the sugar (ie glucose) in it to produce carbon dioxide, which is what causes the bread to rise since it has been filled with gas, whilst the ethanol tends to boil off in the heat of the baking process. For industrial purposes, ethanol is made by hydrating (reacting with water) an oil by-product called ethene, but the product isn’t generally something you’d want to drink.

But anyway, back to the booze itself, and this time what happens upon its entry into the body. Exactly why alcohol acts as a depressant and intoxicant (if that’s a proper word) is down to a very complex interaction with various parts and receptors of the brain that I am not nearly intelligent enough to understand, let alone explain. However, what I can explain is what happens when the body gets round to breaking the alcohol down and getting rid of the stuff. This takes place in the liver, an amazing organ that performs hundreds of jobs within the body and contains a vast repetoir of enzymes. One of these is known as alcohol dehydrogenase, which has the task of oxidising the alcohol (not a simple task, and one impossible without enzymes) into something the body can get rid of. However, most ethanol we drink is what is known as a primary alcohol (meaning the OH group is on the end of the carbon chain), and this causes it to oxidise in two stages, only the first of which can be done using alcohol dehydrogenase. This process converts the alcohol into an aldehyde (with an oxygen chemically double-bonded to the carbon where the OH group was), which in the case of ethanol is called acetaldehyde (or ethanal). This molecule cannot be broken down straight away, and instead gets itself lodged in the body’s tissues in such a way (thanks to its shape) to produce mild toxins, activate our immune system and make us feel generally lousy. This is also known as having a hangover, and only ends when the body is able to complete the second stage of the oxidation process and convert the acetaldehyde into acetic acid, which the body can get rid of relatively easily. Acetic acid is commonly known as the active ingredient in vinegar, which is why alcoholics smell so bad and are often said to be ‘pickled’.

This process occurs in the same way when other alcohols enter the body, but ethanol is unique in how harmless (relatively speaking) its aldehyde is. Methanol, for example, can also be oxidised by alcohol dehydrogenase, but the aldehyde it produces (officially called methanal) is commonly known as formaldehyde; a highly toxic substance used in preservation work and as a disinfectant that will quickly poison the body. It is for this reason that methanol is present in the fuel commonly known as ‘meths’- ethanol actually produces more energy per gram and makes up 90% of the fuel by volume, but since it is cheaper than most alcoholic drinks the toxic methanol is put in to prevent it being drunk by severely desperate alcoholics. Not that it stops many of them; methanol poisoning is a leading cause of death among many homeless people.

Homeless people were also responsible for a major discovery in the field of alcohol research, concerning the causes of alcoholism. For many years it was thought that alcoholics were purely addicts mentally rather than biologically, and had just ‘let it get to them’, but some years ago a young student (I believe she was Canadian, but certainty of that fact and her name both escape me) was looking for some fresh cadavers for her PhD research. She went to the police and asked if she could use the bodies of the various dead homeless people who they found on their morning beats, and when she started dissecting them she noticed signs of a compound in them that was known to be linked to heroin addiction. She mentioned to a friend that all these people appeared to be on heroin, but her friend said that these people barely had enough to buy drink, let alone something as expensive as heroin. This young doctor-to-be realised she might be onto something here, and changed the focus of her research onto studying how alcohol was broken down by different bodies, and discovered something quite astonishing. Inside serious alcoholics, ethanol was being broken down into this substance previously only linked to heroin addiction, leading her to believe that for some unlucky people, the behaviour of their bodies made alcohol as addictive to them as heroin was to others. Whilst this research has by no means settled the issue, it did demonstrate two important facts; firstly, that whilst alcoholism certainly has some links to mental issues, it is also fundamentally biological and genetic by nature and cannot be solely put down as the fault of the victim’s brain. Secondly, it ‘sciencified’ (my apologies to grammar nazis everywhere for making that word up) a fact already known by many reformed drinkers; that when a former alcoholic stops drinking, they can never go back. Not even one drink. There can be no ‘just having one’, or drinking socially with friends, because if one more drink hits their body, deprived for so long, there’s a very good chance it could kill them.

Still, that’s not a reason to get totally down about alcohol, for two very good reasons. The first of these comes from some (admittely rather spurious) research suggesting that ‘addictive personalities’, including alcoholics, are far more likely to do well in life, have good jobs and overall succeed; alcoholics are, by nature, present at the top as well as the bottom of our society. The other concerns the one bit of science I haven’t tried to explain here- your body is remarkably good at dealing with alcohol, and we all know it can make us feel better, so if only for your mental health a little drink now and then isn’t an all bad thing after all. And anyway, it makes for some killer YouTube videos…