Sport, movement and molecules

This essay was written by Mike Ferenczi and was first published in the 1995 Mill Hill Essays.

Athletic records are broken every year, but have you ever wondered what determines the limits of sporting achievements? The answer lies in the human struggle against the laws of physics. In the end, most sports are constrained by the energy required to accelerate a mass to reach a maximum speed, by the energy required to lift against the forces of gravity, or by the power required to maintain one’s speed in spite of the drag resistance of air or water. In the one hundred metre sprint, an athlete accelerates a hefty one hundred kilograms to reach a speed of more than forty kilometres per hour in about fifty strides. Although the sprinter may not need to breathe for most of the ten seconds of the race, his heart, a muscle which only stops once a lifetime, will be pumping two hundred millilitres of blood in every heart beat, or about four buckets-full per minute. In untrained, maximally exercising normal young males, the heart output is about half this because their heart capacity per beat is so much lower.

And yet, records keep on improving. Part of the answer is that athletes are getting bigger. The average height of decathlon athletes in the 1930 Olympics was one metre seventy six centimetres. By 1960, their height was one metre and eighty four centimetres. In track and field events, the winners in running, jumping or throwing events are usually bigger than their less successful competitors, except in the ten kilometre race and the marathon. The bigger the body, the greater the capacity to pump oxygen (O2) round it. Every litre of O2 taken in through the lungs, about one fifth of the air breathed in, allows the body to burn up twenty kilojoules of energy from its energy sources. This corresponds to a one kilowatt electric heater being turned on for twenty seconds. Measuring the O2 intake is a convenient way to measure fitness or athletic ability. It is a routine procedure in physiological laboratories where, for example, athletes run on a treadmill to simulate a slight uphill run, whilst breathing through a measuring apparatus, and it provides revealing insights. For example there is a strong correlation between the maximum O2 uptake during maximal exercise and competition results in sports such as rowing.

So where is the energy used up in exercise coming from? The body stores the energy in a number of compartments. A good analogy is the way an individual or a company may hold its money. There is cash such as coins in the pocket or bank notes in the wallet for immediate needs, there is money deposited in a current or cheque account, then there is money tied up in a variety of accounts which is more or less easily turned into cash, such as savings accounts, company shares or government bonds. In the body, cash, or the immediate energy source is in two forms. The coins can be represented by ATP (adenosine triphosphate), the immediate fuel or chemical used up in the muscle cells by the proteins responsible for muscle contraction. As it is being used up, ATP turns into ADP (adenosine diphosphate). The useful energy of ATP resides in the chemical bond attaching the third phosphate to the rest of the molecule. This is called a “high-energy” bond.

The banknotes can be represented by phosphocreatine, another small molecule which, through the action of enzymes, rapidly changes ADP back to ATP. In all, there is about three times as much phosphocreatine as ATP in muscle. The energy from both is immediately available to the muscles. It does not require O2, breathing or blood flow. But of course, it runs out quickly. An athlete may have six to eight seconds worth of this cash, and this is the energy predominantly used up during a sprint. There isn’t quite enough of it for the whole ten seconds of the race, and this may be why sprinters slow down in the very last seconds.

The quick access bank accounts are represented by sugar stores, in particular a form of complex sugar called glycogen stored in the muscle and liver. This is the energy used up towards the end of a sprinter’s race, and in exertions lasting up to ninety seconds. These sugars provide a most useful source of energy, but they are used at a cost, namely the accumulation of lactic acid, a by-product of sugar breakdown, which results in acidification of the body. As the acidity of the blood increases the enzymes responsible for muscle contraction become less effective and fatigue sets in.

To replenish the readily available energy stores, and to sustain longer lasting effort, the savings and investment accounts need to be used. Their use in what are called aerobic mechanisms involves breathing O2. By these, the first products of sugar breakdown are converted in specialised cellular compartments called mitochondria, all the way down to carbon dioxide (CO2) and water (H2O) in a process called respiration. CO2 is then eliminated from the blood through the lungs. This overall process is very efficient, but it is not instantaneous. It is limited by how fast O2 can be delivered to the cells’ power stations, the mitochondria, and how quickly CO2 can be removed.

When further demands are made on the body, the investment accounts, the fat reserves, are brought into action and they are also broken down aerobically to provide ATP. When these are exhausted, usually as a result of starvation, the proteins of the muscles themselves may be broken down; mercifully not a bankrupt situation athletes find themselves in.

The body is very adaptable, and when put under pressure, the heart rate and respiration rate will adapt as much as possible to provide adequate O2 supply to the muscles. In long distance running and all exercises lasting more than a few minutes, it is the ability of the body to deliver O2 to the relevant organs which seems to be the determinant of performance. Here, it is not only the ability of the muscle machinery to produce ATP which counts, but also the pumping ability of the heart and the capacity of the lungs which play a vital role.

In a one hundred metre sprint, the energy expenditure is thirty three kilojoules, or three and one third kilowatts during each second of the run. Eighty-five percent of this energy comes from breaking down ATP and phosphocreatine. This is only the equivalent of the aerobic sugar breakdown brought about by one and a half litres of oxygen, but it is released more quickly than the aerobic processes would allow. The remaining fifteen percent of the energy comes from the aerobic breakdown of the sugar stores. The heart rate will have increased to more than one hundred beats per minute even before the race, in anticipation of the body’s demands, but it is only after the race that the aerobic processes will come into play to replenish the cellular energy stores.

Training has a dramatic and very specific effect on the body’s musculature and circulation. Muscles and the muscle cells within each muscle specialise in the performance of specific types of contractions. Some muscles, for example those involved in the maintenance of posture, are designed to perform long lasting contractions, with the minimum of energy consumption. Other muscles on the other hand may only occasionally be called into action, but the action requires very fast movements, such as those required to escape from an attack. These muscles may be extremely effective at providing lightning-fast movement, but will be unable to sustain these movements for very long.

Each muscle is made up of a variety of muscle fibres which fall into two main categories. Type I fibres are slow acting. The time taken by them to reach maximal contraction when called into action by a nerve signal is about one tenth of a second. They are rich in mitochondria and in a protein called myoglobin which is designed to retain O2. These are the fibres that are highly developed in long distance runners, cyclists, skaters and cross-country skiers, clearly designed for aerobic exercise. They are usually found in the core of the muscles and are richly supplied with capillary blood vessels to deliver O2 and to remove CO2. By contrast, type II fibres are fast acting. Their time to reach peak force is only four hundredths of a second after the nerve signal, and they are able to shorten more quickly than type I fibres. They are rich in glycogen and in the enzyme responsible for its breakdown, but are less well supplied with blood capillaries. These fibres, designed for anaerobic exercise, are most abundant on the surface of the long muscles, and are highly developed in sprinters, jumpers and throwers.

Training affects the type of muscle fibres in the muscles, their biochemical composition, and also the size and shape of the muscles. Each muscle cell contains thin bundles of muscle proteins called myofibril. These are about one thousandth of a millimetre in diameter and are several centimetres long. The number of myofibril in each muscle cell will increase upon training, making the trained muscle larger, and therefore better able to cope with the demands made on it. The capillary blood flow will also adapt to provide adequate oxygenation, and the length of the muscle cells will also change slightly, depending on the type of exercise.

So what are the processes which allow the energy found in ATP to be converted into physical performance? Considerable progress has been made in this area over the past one hundred years, but before this, muscle contraction was quite a mystery. The ancient Greeks knew that muscles were responsible for movement, but they thought that contraction came about as muscles were inflated by the air we breathe. Arteries were believed to carry air to the muscles and to cause the muscles to increase in breadth, but to diminish in length. In the second century however, Galen of Pergamon observed that arteries carried blood, not air. He also recognised that although not under voluntary control, other organs such as the heart, the uterus and the oesophagus had contractile properties. Still, the idea that muscles contracted by being blown up, by blood or other body liquid, persisted until the eighteenth century. The principle was demonstrated by the lifting of a weight which, when attached to an empty pig’s bladder, was seen to rise as the bladder was filled with water and became more rounded in shape. There were tests in which a strong man was to plunge his arm into a water-filled barrel and was asked to contract his muscles. The idea was that inflation of the muscle would result in a rise in water level in the barrel. In the best experiments however the opposite was found, a small drop in the water level is caused by reduction in the volume of blood in the arm caused by the muscle-induced compression of the blood vessels. Real progress came with the development of microscopes in the nineteenth century and the study of the fibres dissected from muscles. Very quickly it became apparent that muscle cells from muscles such as those of the thigh had a banded appearance, an indication of a complex underlying structure. It was observed that the distance between the bands decreased as the muscle shortened, and that the overall volume of the cells did not change. Further progress came with the isolation of the muscle proteins, and their characterisation.

We now know that there are two main proteins, actin and myosin, which form the bulk of all skelWe now know that there are two main proteins, actin and myosin, which form the bulk of all skeletal muscles, and that they are precisely arranged into arrays of filaments. Thin filaments are made up of actin molecules, and thick filaments are made up of myosin molecules. The filaments are about two thousandths of a millimetre long and form bundles about one thousandth of a millimetre in diameter within the muscle cells. Bundles of actin filaments alternate with bundles of myosin filaments, all along the length of the muscle cell, which can be tens of centimetres long. This alternation of bundles is what gives muscles their banded appearance in the microscope. The bundles of actin and myosin filaments are not completely separated from each other, they overlap by a variable amount, depending on the degree of stretch of the muscles. And now, we are getting down to the nitty gritty of the muscle machinery.

Where the myosin and actin filaments overlap is where muscle contraction takes place. Part of the myosin molecule extends out of the thick filaments and makes contact in the overlap zone with the actin molecules on the thin filament. These parts, called myosin heads, are also the sites where the molecules of ATP are broken down and where the energy is used to increase the overlap between the thick and the thin filaments, thereby causing the muscle to shorten, even against an appreciable load. The force that a muscle produces is high, of the order of about thirty tons weight per square metre of muscle cross-section or forty three pounds per square inch. This force is such that if an unexpected sharp shock is applied to the limb, a bone is as likely to break as the muscle or the tendon are to tear. It is what we call isometric force, the force that muscles can hold or sustain, but too high for muscles to shorten against. In an isometric contraction, such as in arm wrestling, there is no movement of the limb, no weight is lifted and no external work is carried out. This means that the efficiency of the contraction is zero, but plenty of energy is consumed and released as heat carried to the skin by the flow of blood from the muscles. However considerably more energy is consumed when the muscles do shorten against a load, with some of the energy being transformed into useful mechanical work, such as lifting a weight or gaining energy of movement. If one measures the work optimally produced by a muscle, and the chemical energy used up by the muscle, the maximum efficiency under optimal conditions is about fifty percent. For every movement, there is one most efficient contraction speed, or one most efficient force which can be exerted. The most efficient movement will also occur over a rather narrow range of movement. Bicycles are sold in a wide range of sizes, and saddle height is always adjusted to provide the most comfortable riding position. However the movement range depends on the length of the pedal cranks, the metal shafts linking the pedals to the bike. Cranks should be about one fifth of the leg length, but unfortunately usual commercial cranks are best suited for leg lengths of eighty-five or eighty-seven and a half centimetres. If that’s not you, bad luck, your cycling will be less enjoyable than it could be. The overall efficiency of exercise, such as in running or riding a bike, is of the order of twenty to thirty percent, somewhat less than the muscle efficiency, since energy is needed for breathing, pumping blood and moving other muscles, such as may be necessary for balance.

When I started research as a graduate student about twenty years ago, the understanding of the biochemical reactions that take place in the myosin heads was being elucidated, and already much was known about the mechanical characteristics of the bonds between the myosin heads and the thin filament. However little was known about the shape of the myosin head, or the manner with which it interacts with the thin filament. How does the myosin head move, how does it generate the force, and how is the breakdown of ATP linked to these processes? Some of these questions still need answering, but enormous progress has been made. By preparing extremely pure myosin heads in the laboratory, it has been possible to crystallise them, and using the technique of x-ray diffraction, it has been possible to measure the distance between all the atoms which form the heads, with a resolution of a few ten millionths of a millimetre. Unfortunately the technique does not allow us to see how the atoms move, or to determine how the protein attaches to the thin filaments. Other techniques have evolved which do allow measurement of the force and of the speed of movement developed by a few molecules of myosin. In current theories, myosin molecules repeatedly attach to a specialised site on the actin filament and exert a tug on the filament to encourage it to slide. When shortening as fast as possible, the thin and thick filaments can be seen in a microscope to slide past each other with a speed of about four thousandths of a millimetre per second. This is quite a crawl, about fourteen metres per hour, but the arrangement of the myosin heads in a muscle means that in each millimetre length of muscle, about eight hundred myosin heads contribute to the overall shortening speed of the muscle, so that in a muscle one hundred millimetres long, the shortening speed is one thousand one hundred and fifty two metres per hour, and the speed of movement is further increased by the leverage of the limbs. To achieve this performance, each myosin head undergoes a complicated series of operations about twenty to forty times every second: the head attaches to the thin filament, the proteins move (or generate force), the head detaches and is then ready to attach further along on the thin filament, ready to start the cycle again. At the same time, a molecule of ATP breaks down transferring energy to the protein. The waste products are then removed, making the head available to the next molecule of ATP.

The mechanical and the chemical cycles interact closely. For example, when the muscle is producing a lot of work, such as lifting a weight rapidly, ATP molecules are broken down rapidly. When the muscle is just holding a force, without shortening, ATP molecules are broken down about one third as quickly, and this is also true when the muscle is shortening so rapidly that it cannot exert much force. However when the muscle is resting, ATP is broken down four hundred times more slowly. At the level of the whole body, the difference between maximal and gentle exercise is also marked. A cyclist pedalling at full speed is burning six times the energy that he is when ironing his shirt. This adaptation of the body’s muscles to the variable demands made upon them is wide ranging. There is the short term adaptation which guarantees that the muscle activity is as economical as possible. There is the use of various pools of energy to allow strenuous exercise for long periods of time. There is the adaptation of the body to various types of exercise where the muscle cells accumulate the sugars and enzymes required for their breakdown. Also, through exercise, muscles are able to develop the most appropriate type of cell, and to change their shape and size. In the end however there are areas which are not influenced directly by exercise. Every person’s body has biochemical and anatomical characteristics determined by our genes and by our diet and environment in early life which may make us better at running, playing football or swimming. Ultimately, the mental preparation and the state of mind during the competition is what may decide between coming first or second.

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