Phosphocreatine: Your body's primary energy currency
Adenosine triphosphate is often called the universal energy donor, but a better label would be the body's 'primary energy currency'
When your muscles need energy, your body knows three different ways to supply the goods
If you happened to step inadvertently in front of a bus, your continued existence would suddenly hinge on your muscles’ supply of high-energy phosphates. True, your visual system would also play a role in your survival, but it is the job of your muscles to get you out of harm’s way by jumping clear of the bus just in time. And activity of this kind is determined to a large extent by the phosphates floating around in your muscular protoplasm.
Your muscles need energy to clear the bus bumper, but they can’t wait for your heart to get revved up, for a cascade of oxygen-rich blood to hurry through your arteries or for the incoming oxygen to assist with the breakdown carbohydrate or fat, in order to release the required amount of energy. That looming double-decker is indifferent to the niceties of aerobic metabolism, and depending on this rather laborious process would be, quite literally, fatal.
In this situation, your muscles need energy to be delivered in a very small fraction of a second, and that energy is derived from a unique high-energy phosphate compound called adenosine triphosphate, aka ATP. ATP is always present in your muscle cells – and indeed in all the living cells in your body; without it, your cells would quickly stop working and die. Because it supplies energy to all cells, adenosine triphosphate (ATP) is often called the universal energy donor, but a better label would be the body’s ‘primary energy currency’.
The energy contained in any food you eat – carbohydrate, protein or fat – must be stored as energy within adenosine triphosphate (ATP) molecules before it can be used by any cell in your body. To put it another way, although we often talk about muscles ‘burning’ carbohydrate for energy, the carbohydrate is as directly useful to your muscle cells as foreign currency in your local supermarket. Change that currency into sterling and you are ready to go; change the carbohydrate energy into adenosine triphosphate (ATP) energy and your muscles are fit for work.
Adenosine triphosphate (ATP) provides all of the energy needed for muscular contractions, for the secretion of gastric juice after a meal, for the cognitive processes which take place in your brain as you read this article and, indeed, for every single activity you undertake. Carbohydrate, fat and protein are not directly usable by cells, but adenosine triphosphate (ATP) is: in fact, it is the only energy molecule that is directly serviceable.
Since adenosine triphosphate (ATP) is so important, you might think that your cells would stockpile the stuff big-time, but that is not the way it works. Stubbornly, your cells, including your muscle cells, refuse to store large quantities of the precious high-energy phosphate, being much more interested in hoarding carbohydrate and fat. Because of this, and since muscular exercise depends on a steady, often expansive, supply of adenosine triphosphate (ATP) to provide the energy needed for muscular contractions, muscles need dependable ‘metabolic pathways’, which can provide adenosine triphosphate (ATP) at a rapid, reliable rate. If there is not going to be much adenosine triphosphate (ATP) ‘at the ready’, there has to be some way to make it quickly.
Phosphocreatine: the best source of rapidly available energy
As it happens, humans have three such ATP-creating pathways (ie three unique and distinct series of chemical reactions which have the sole purpose of creating ATP). The simplest and most rapid pathway (and thus the one most useful for a confrontation with a careening bus) involves a rather generous little fellow found inside muscle cells, called phosphocreatine. Phosphocreatine cannot provide energy for muscle contractions directly (only ATP can do that). It is very willing, however, to donate a high-energy phosphate group to a chemical called ADP to form that energy kingpin, adenosine triphosphate (ATP). This critically important reaction (in which phosphate and ADP combine to make ATP) is catalysed by an enzyme called creatine kinase, which is consequently found in significant concentrations inside muscle cells. The ubiquity of creatine kinase in muscle tissue explains why high levels of creatine kinase in the blood are associated with muscle breakdowns, including the kinds of catastrophes which can occur in cardiac muscle tissue after a heart attack.
One nice feature of phosphocreatine is that its intramuscular levels are not as tightly capped as adenosine triphosphate (ATP) concentrations. Basically, while your muscles strive to keep adenosine triphosphate (ATP) levels fairly modest, they allow phosphocreatine concentrations to soar quite dramatically. This, of course, helps to explain why creatine supplementation has been so successful in high-power athletics; creatine added to the diet is absorbed readily and makes its way to the muscles, where it combines with the phosphates which are always lying around to make phosphocreatine. If you have a substantial amount of phosphocreatine in your muscle cells, you should be able to generate a lot of ATP in a very short period of time. You will be a great bus jumper – and if you are an athlete you will have the potential to improve your high-jumping and short-sprint abilities, too.
The phosphagen system works best for short bursts of high-intensity action
All physiological systems have their limits, however, and the system we have just described, which also goes by the monikers ‘ATP-PC system’ or ‘phosphagen system’, has definite limitations. For one thing, the system can probably provide energy for no more than about 8-10 seconds of intense muscular exertion, even in an individual who has ‘creatine-loaded’ his or her muscles. This is, of course, enough to help you survive your bus dilemma (unless the bus perversely decides to follow you down the street), and the system works wonderfully well for high-jumpers, power weightlifters, 50m sprinters, pole-vaulters, cricket bowlers, footballers and other athletes whose sports call for short bursts of high-intensity exertion.
Unfortunately, however, the phosphagen system is of little help in activities lasting longer than 10 seconds. If you wanted to run as fast as possible for 200m, for example, your phosphagen system would ordinarily get you less than halfway towards your goal. Without another ATP-generating pathway to bank on, you would fall into an exhausted heap, well short of your target. Incidentally, this limitation of the phosphagen system explains why creatine supplementation has often been linked with better performances in high-power, short-duration sports, but not in endurance events(1).
The fact that the phosphagen system ‘works’ for only about 8-10 seconds might seem a bit puzzling to you. After all, if creatine is still hanging around inside muscle fibres after it donates its phosphate to ADP, why can’t it simply pick up some of the phosphate (which is a natural constituent of cells) and thus form phosphocreatine again, rejuvenating the ATP-creation process? That’s pretty good thinking, but the adenosine triphosphate (ATP)from exercise, when the ATP present is not being used to help muscles contract.
Fortunately, you, and the rest of the animal kingdom, possess an important second ATP-producing pathway which allows intense activity to be sustained for a longer period of time. This second system, known as glycolysis, takes a little longer to get started, but it can be rolling after about 8-10 seconds, making it a nice complement to the phosphagen system. Glycolysis involves the breakdown of carbohydrate (glucose or glycogen) within muscle cells to form two molecules of pyruvic acid or lactic acid. As with the phosphagen system, not even a droplet of oxygen is required for this to happen. However, glycolysis does not hinge on phosphocreatine; rather, the energy locked up in a glucose molecule is utilised in a way which allows a phosphate group to link up with ADP, forming our old friend ATP once again. For every molecule of glucose which is split during glycolysis, two robust molecules of usable ATP are formed.
Glycolysis is the dominant adenosine triphosphate (ATP) production system for strenuous activities which require more than 10 seconds, but less than about two minutes, to complete. Your ability to generate energy via glycolysis is sometimes referred to as your ‘anaerobic capacity’, since no oxygen is required to make it happen.
For activities lasting longer than two minutes, the well-known ‘aerobic’ pathway for adenosine triphosphate (ATP) production holds sway. During aerobic adenosine triphosphate (ATP) production, which occurs inside special cellular structures called mitochondria, energy-containing hydrogens are stripped away from segments of carbohydrates, proteins and fats and used to combine phosphate with ADP to make – you guessed it – ATP!
Without oxygen, aerobic energy release would grind to a halt
The pathway is termed aerobic because oxygen is the final hydrogen-acceptor in the overall process, and without it the entire series of energy-releasing reactions would grind to a halt; similarly, the rate at which ATP is generated aerobically can be increased only in line with an increased rate of oxygen supply to muscle cells. If you can grasp these principles, you will also understand why increases in VO2max (‘maximal aerobic capacity’) often lead to improvements in endurance performance. To put it simply, if your muscles can use oxygen at a higher rate (to accept hydrogens), you can generate adenosine triphosphate (ATP) at a higher rate too, and you thus have the potential to exercise more intensely during endurance events.
It is important to understand that the three adenosine triphosphate (ATP) pathways are generally associated with three different speeds of movement, and that the phosphagen system has become wedded in our minds to maximal speeds, the glycolytic (‘anaerobic’) system to fast speeds and the aerobic process to more modest paces.
Modes of training have also tended to fall into three general ‘baskets’. Athletes whose events last no more than 10 seconds tend to train by engaging in short intervals of work lasting less than 10 seconds. If they have some physiological awareness, they might say that they are working on their phosphagen systems.
How training modes reflect the different energy production systems
Meanwhile, athletes who compete for 10-120 seconds run a bit slower during training, and their work intervals generally reflect their competing times, as you might expect. Such athletes may talk about building anaerobic capacity or – less commonly – maximising their glycolytic potential.
Finally, athletes who compete for longer than 120 seconds tend to work at slower speeds over intervals lasting from 2-10 minutes and during continuous efforts which may last for considerably longer. These endurance athletes are intent on maximising their aerobic capacities and may talk about improved heart function, enhanced breathing capacity, vine-like growths of capillaries around their muscle fibres and the increased ability of their muscles to use oxygen.
Is this thinking correct? Should the 100m ‘phosphagen-based’ sprinter, for example, completely eschew longer glycolytic or aerobic running? Should the 90-second, glycolysis-loving athlete avoid phosphagen-enhancing efforts or exertions lasting more than two minutes, since such activities would tax the ‘wrong’ energy-production systems? And should the aerobic, endurance athlete be quarantined from phosphagenic and glycolytic efforts?
We can start with the easiest answer: the ‘phosphagen athlete’ does not need to worry about conducting training efforts which use the glycolytic or aerobic systems. Stretch though we might, it is not possible to construct a compelling argument for such training, especially since scientific evidence suggests that longer-duration work intervals might convert fast-twitch muscle cells into their slow-twitch brethren. Of course, stoking the phosphagen system is not the whole story for such athletes. Simple manipulations of phosphocreatine and creatine kinase may well help an athlete sprint faster, but by themselves they will not produce an athlete’s best-possible performances, which are about more than chemicals. Short-distance sprinters will also want to boost leg-muscle size, in order to produce more propulsive force and improve nervous system control of their muscles, so that force can be produced more quickly and efficiently.
How about the endurance athlete? Should he/she engage in the type of training which is ordinarily the province of the phosphagen or glycolysis athlete? To answer that question completely, let’s picture a real life situation. We could use any endurance sport as an example, but let’s assume that you are a well-trained competitive cyclist participating in a 100k road race – a true endurance event. You are doing very well, but there is an athlete about 25m ahead of you whom you would like to ‘pick off’. You know it’s going to be tough, but you shift into a higher gear and pick up your rpms. In 10 seconds or so, you’re right up against him, but you’re a little fatigued from your sprint and scared he’ll pass you back; so you keep up your sudden surging for a full 60 seconds before falling back to your normal pace, and when you look back over your shoulder you are satisfied that you have left your competitor in the dust, or at least a bit behind you on the tarmac.
What ATP systems did you rely on for your sudden sprint – your incredible burst of speed? Did you use your phosphagen system to catch up with your rival in 10 seconds, then your glycolytic system to power past him over the next 50 seconds?
If you answered these questions affirmatively, you certainly deserve an ‘A’ for following this article so far. Unfortunately, however, your very logical assumptions would be wrong: the truth is that most of the energy for the sprint, both the high-speed 10-second component and the follow-up 50-second surge, would be produced via the aerobic pathway.
Why the energy production rules change after just two minutes
To understand the error of your ways, you simply need to remember that the rules we have established so far (in which the phosphagen system controls exercise lasting 10 seconds or less, glycolysis controls exercise lasting 10-120 seconds and the aerobic pathway dominates anything longer) apply when the exercise begins from a relatively quiescent physiological state. When you start from physiological ‘ground zero’, the phosphagen system is ready to go, but it takes about 10 seconds for glycolysis to get kicking and two minutes for oxygen to really penetrate your cells in significant amounts, allowing aerobic metabolism to take hold.
However, everything changes when you have been exercising for a while. In fact, everything changes when you have been exerting yourself for as little as two minutes. Let’s turn to our biking example again: while you were cruising along during your 100k race, you were probably working at about 85% of your maximal aerobic capacity (VO2max). During your sudden one-minute sprint, you probably soared to around 95% of VO2max; in other words, your aerobic ATP-generating system had enough ‘room’ to handle the increase in cycling intensity; you simply stepped up the rate at which you were using oxygen to ‘catch’ hydrogen inside your muscle cells. You were going fast, but your aerobic system was good enough to handle your speed. True, glycolysis probably perked up as you pedalled furiously along. However, for each molecule of glucose broken down, the aerobic pathway generates about 19 times as much usable energy as glycolysis. Thus, it is hard to argue that glycolysis (or your anaerobic capacity) got you through your sprint; the glycolytic system’s contribution was, in fact, pretty puny. You can also forget about the phosphagen system, which gave up the ghost after just 10 seconds of your ride.
That makes it seem as though the endurance athlete does not need to worry about glycolysis, the phosphagen system or even the fast training speeds associated with improving those systems. But hold on: if we change the event slightly our picture comes into a different focus. Think, for example, of the 1,500m runner competing to the best of his ability; by definition, this individual is an endurance athlete whose performance depends primarily on the aerobic pathway for ATP generation (since the event takes at least 3:26 – the current world record – to complete). Two minutes into the event, however, our athlete has already reached VO2max, and thus the ‘kick’ which occurs during the last lap can not be propelled by advanced use of the aerobic pathway; glycolysis must plug the gap. Thus, it’s clear that endurance athletes who reach VO2max during their competitions must train like glycolytic competitors as well as carrying out their aerobic training. In general, athletes who compete in events lasting 12-13 minutes or less will ‘hit’ VO2max as they compete, and thus their fate in competition might depend strongly on glycolytic capacity.
What about those taking part in longer events? Perhaps surprisingly, they also need to train like the glycolytic gladiators. Even a marathon runner or 100k biker, each of whom might obtain less than 1% of total ATP during competition from glycolysis, should spend significant amounts of time training fast, using work intervals as short as 30 seconds. From an ATP-generation standpoint this would not seem logical, but it is important not to get too trapped by our ATP-creating paradigm. Other factors besides ATP-pathway development are also important for athletic success. One such factor is maximal speed: as an athlete’s maximum rate of movement increases, usual race paces will feel easier and more sustainable; one way to enhance max velocity is to carry out short-interval, high-intensity efforts from the realm of glycolytic training.
Economy of movement is also critically important to endurance athletes. Economy is simply the oxygen cost of moving at a specific speed (that is, the rate of oxygen consumption associated with that speed). As economy improves, specific speeds are sustained at a lower percentage of VO2max and feel appreciably easier, allowing the athlete to ‘graduate’ to higher speeds in competitions. As it turns out, scientific research indicates that high-speed training, using work intervals lasting 10-120 seconds, is one of the most potent ways of upgrading economy.
A workout designed to enhance glycolysis may be highly aerobic
And don’t forget about our continuity rule. When an endurance athlete begins a workout by blasting along very quickly for 30 seconds, a significant amount of the energy will come from the phosphagen system and an even greater amount from glycolysis, with the aerobic pathway chipping in almost nothing. However, as the workout continues (assuming that the athlete utilises typical recovery intervals of 30 seconds), the rate of oxygen consumption will rise dramatically. In fact, after the seventh or eighth interval the athlete may be exercising right at VO2max and will probably stay there for the remainder of the workout. Exercise scientists believe that training at VO2max is one of the very best ways to enhance the aerobic adenosine triphosphate (ATP) pathway; so we have a workout seemingly designed to enhance glycolysis which is actually incredibly good for aerobic ATP production.
What about athletes who compete in events lasting 10-120 seconds? How should they train? Fast starts are essential in such competitions, so they will have to do some training which bears a resemblance to the sub-10-second phosphagenic athlete’s work. Ten-second max efforts from a standing start, with very long recovery intervals to allow the phosphagen system to restore itself, should do the trick. The 10-120-second athlete will also have to do some traditional aerobic work, using intervals lasting longer than two minutes. This is because even if the competition lasts only 30 seconds, the aerobic pathway will be chipping in 20% of the needed energy; if the event lasts 60 seconds, aerobics will add 30% of the juice, and so on. Thus, the 10-120-second athlete, who may never hit VO2max during competitions, will still need to develop the aerobic system, to a certain extent, to make sure it is ready to chip in its little piece of the energy pie during races.
- Journal of the American College of Nutrition, vol 17, pp 216-234, 1998
adenosine triphosphate, phosphocreatine
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