The VO2 max increases, suggesting an increased capacity for muscles to work and so to increase the oxygen consumption of the mitochondria. There is an increased ability to store muscle and liver glycogen. The rate of fat use increases while the rate of glycogen utilisation decreases during exercise at all work rates, and there is a shift in the lactate turnpoint to a higher work rate or percentage VO2 max.

Before we look at the anatomical and biochemical changes in trained muscle which explain these changes, we must deal with the last point, and the myths and facts surrounding lactate.

Lactate: myths and facts

In most of the sections covered so far, we have dealt with endurance training, that is exercise at intensities less than 100 percent of VO2 max. At these intensities nearly all energy comes from oxygen-dependent mitochondrial metabolism.

However, supramaximal exercise, for example sprinting over 100m and 200m, requires speeds which need a huge rate of energy production. This cannot be achieved purely by oxygen-dependent (or oxidative) metabolism. But people run these distances at speeds of around 36km per hour, which would require oxygen to be used at a rate of 140 ml per kg, a level of oxygen consumption which has never been measured in a human. So, there are obviously ways of producing energy from oxygen-independent pathways in the cells.

ATP and phosphocreatine (Pcr) are stored in the muscles and can provide energy for about 7 seconds of maximum exercise.

When intensive exercise, such as sprinting, begins, then the metabolic pathway called glycolysis is activated. This supplements the energy produced from the ATP and Pcr stores. Glycogen is broken down to its products pyruvate and lactate. As this happens ATP is produced which will replenish the muscle's ATP stores.

The pathways for carbohydrate and fat metabolism by liver, muscle and brain. (click picture to enlarge)

In theory the amount of glycogen in the muscles could maintain a sprint for at least 80 seconds. But, even the world's best sprinters can only maintain peak speed for about 20 seconds. So obviously something is limiting them. What happens is that by products of glycolysis and of the breakdown of ATP and Pcr accumulate within the muscle fibres, so reducing the sprinters muscle's ability to continue to contract at high intensity. So the runner slows down. This prevents normal human muscle from completely exhausting its energy content to a level where cell death will occur.

So, what is lactate? We've seen above that lactate is one of the by products of the breakdown of glycogen called glycolysis. In high intensity exercise lasting more than 30 seconds, glycolysis is the most important energy producing pathway. This causes large increases in muscle and blood lactate levels.

There are many misconceptions about lactate, one of the most common being that it is build up lactate which causes muscle pain and fatigue. This is not true! Lactate is both produced and used by muscles. As the exercise rate increases and as more carbohydrate is used to fuel exercise, so the rate of lactate production increases. Lactate does not exist as lactic acid in the body, but is usually in combination with sodium, as sodium lactate.

It was originally believed that muscles only produced lactate when their oxygen supply was inadequate for contraction. However, we now know that muscles can release lactate even when they have more than enough oxygen available, so lactate production does not equal lack of oxygen. In fact there is little evidence that muscles ever actually become anaerobic during exercise. Lactate is a product of contraction, not its cause.

Lactate is actually one of the most important energy fuels in the body. Through something called the "lactate shuttle" carbohydrate can be transferred from one muscle group to another while muscles are resting or exercising. For example, during and after leg exercise, glycogen reserves in the inactive arms are metabolised to lactate which is transported to the legs in the blood giving an additional energy source and helping replenish leg muscle glycogen after exercise.

What is the "lactate turnpoint"? For many years there was a belief that blood lactate concentrations suddenly increase at a threshold exercise intensity called either the "anaerobic threshold", the "lactate turnpoint" or the "ventilation threshold".

We now know that blood lactate levels in fact start to increase, although at levels almost too low to measure, as soon as exercise starts. Only when exercise becomes more intense do levels rise to an easily measurable figure. This explains the early idea that there was a sudden increase in lactate levels at a particular level of exercise; the so-called lactate threshold or turnpoint.

With the mathematical techniques now available, we know that blood lactate levels rise as a continuous function of exercise intensity without showing an abrupt threshold effect. Lactate is a natural by product of carbohydrate metabolism, so increasing blood levels of lactate simply indicate that more carbohydrate is being used, not that the muscle is becoming more anaerobic.

However, the term "lactate turnpoint" is still used, particularly as one of the measures which defines increasing fitness with endurance training. When this is used it refers to the exercise intensity at which blood lactate levels begin to rise visibly.

What is the importance of lactate in training? Lactate seems to be produced as the by product of a process which prevents the muscles from becoming acidic too rapidly. Endurance training shifts the lactate turnpoint to a higher percentage of VO2 max, and appears as an early response to training, usually within the first two to three weeks. The visually determined lactate turnpoint is apparently an accurate predictor of marathon performance. The addition of high intensity training improves performance still further since it improves on the changes in lactate metabolism produced by base training.

To summarise, lactate is not the cause of fatigue in any form of exercise. It is rapidly removed from the muscles and blood after exercise, and is not the cause of muscle stiffness after a hard training session.

Changes in skeletal muscle metabolism with training

The number of blood capillaries (small vessels) surrounding muscle fibres increases with training, and the blood flow to the muscles is increased with training. This may allow a faster rate of fat delivery to the muscles, so increasing their ability to produce energy from fats.

Sprint training increases the activity of the glycolytic pathways and also the ability of the muscles to continue exercising in the face of high levels of acidity.

Endurance training, on the other hand, produces changes in the mitochondria. These increase in number and in size, and alter their composition. The mitochindrial enzymes which are involved in the Krebs cycle and respiratory chain increase, so increasing their energy producing capacity. There is also an increase in the concentration of the enzymes associated with fatty acid metabolism. This all leads to an increase in the capacity for muscle glycogen, triglyceride and myoglobin storage. The increase in glycogen storage capacity can be seen as early as the fourth day of training.

So, with training fat can provide more energy at higher exercise intensities than it can before training, sparing carbohydrate metabolism. The rate of carbohydrate metabolism is slowed, and lactate is a by product of carbohydrate metabolism. So less lactate is produced by trained muscles, at least partly explaining the shift in the lactate turnpoint with training.

Endurance training increases the ability of tissues such as the heart, liver, kidneys and inactive and active skeletal muscles to extract and metabolise any lactate produced by the active muscles. This adaptation may be the best explanation for the reduced rate of blood lactate accumulation during exercise seen in trained muscles.

Muscle acidity is also lower at any work rate after training.

It now seems that muscle contractility, and not oxygen, is the most important determinant of performance. Training may effect these changes through increased skeletal muscle myosin ATPase activity and an improvement in calcium handling by the sarcoplasmic reticulum.

It is possible to show an increase in VO2 max within a week of starting intensive training. Changes in heart rate, blood pressure, the lactate turnpoint and glycogen storage can be seen even earlier. However, unless intensity is increased very slowly, VO2 max will reach its maximum within three weeks. De-training will result in a rapid fall in VO2 max in the first two to three weeks, with a more gradual decline thereafter.

How does this happen? It seems that muscle enzyme levels show a gradual and progressive increase with training. The rate and size of these changes seems to be a function of the total amount of muscle contractile activity. The rate can be increased either by increasing exercise intensity, or increasing exercise duration. Increasing exercise intensity seems to produce more rapid and greater results than increasing duration.

But muscle enzymes will not continue to increase forever. Work on rats showed that 60 minutes of training 5 days a week at any exercise intensity produced the maximum adaptation in mitochindrial enzyme content. Further training produced no further changes.

So, there is a limit to the amount by which mitochondrial enzymes can adapt to training, and that this limit is reached faster, and with less total training time, by high intensity exercise for short periods, than by lower intensity exercise for longer periods.

What happens when you stop training? It seems that the elevated levels of mitochondrial enzymes are lost within about four to eight weeks in people who have trained for less than six months. There is a much more gradual decline in those who have been training for years. Even after 12 weeks of inactivity these people have mitochondrial enzyme contents at least 40 to 50 percent above those who have never trained. This may mean that they had higher mitochondrial enzyme contents before they started training, or that training over many years produces specific changes which have not yet been measured. It is commonly known that people who have trained for many years do not become completely unfit if they stop for a while.

Another interesting finding is that if training volume is reduced, fitness is not affected, as long as the intensity of the exercise remains high.

How does all this knowledge affect training? We know that mitochondrial adaptations to training occur only in trained muscles, and then only in the muscle fibres which are active during a specific exercise. So training for a specific event or sport must concentrate on using the correct muscle groups, so training a specific group of fibres and their appropriate metabolic pathways. For example, a runner who trains exclusively on the flat, will be untrained for uphill running since different muscle groups are involved in flat and uphill running.

Studies of de-training suggest that it probably isn't necessary to maintain high intensity training all year round. As long as the intensity of training is maintained, then the amount of training can be decreased by as much as two-thirds. In addition, before competition, tapering by maintaining intensity, but reducing volume, may enhance performance more than simply by resting.

Different training intensities produce different training effect, so it is possible to tailor individual training programmes and goals. For example, sprinters must aim to increase muscle contractility and so the rates of ATP resynthesis and of glycolysis. Middle distance runners need to adapt their muscles to resist the increasing acidity which develops during high intensity exercise. Endurance athletes must shift their lactate turnpoint to a higher work rate, increase their capacity to use fat, so sparing carbohydrate stores during exercise, and increase their ability to store liver and muscle glycogen before exercise. They must also increase their capacity for carbohydrate use during endurance exercise.

A good working knowledge of biochemical changes during training can definitely help to increase performance. However, for those of us who are recreational athletes, it is worth remembering that it is your genes which ultimately determine how well you will perform. If you are doing everything right and still not making the times you want in the Two Oceans or the Argus, don't push yourself until you are overtrained. Accept your limitations and enjoy your sport.

(Source: The Lore of Running. Third Edition, Oxford University Press. 1992. Tim Noakes.)