Showing posts with label lactate. Show all posts
Showing posts with label lactate. Show all posts

Tuesday, April 1, 2008

Lactate & Thresholds for Training

Lactate & Thresholds for Training
From www.lactate.com

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What is the "anaerobic threshold"?

Before we define the "anaerobic threshold" (AT) it should be pointed out that there is no clear consensus on what this term means. This was and still is a controversial area. So when we define it, the reader should know that others may use a different definition. Many sports scientists would prefer to eliminate the term altogether. However, it is still commonly used by coaches, training books, the popular press and many sports scientists.

Originally some sports scientists thought that there was a point of exertion where the body started to use anaerobic energy heavily. This point corresponded to a sudden change in the patterns of oxygen consumption compared to carbon dioxide output as well as a rapid accumulation of lactate in the blood. Because it was a sudden change, like the passing from one physiological state to another, it was called a threshold. Because it was thought that the changes in metabolism at this point were 1) due to limited oxygen and 2) the start of using anaerobic energy, it was called anaerobic. Hence the term "anaerobic threshold" was used. It was an unfortunate choice of terms since it probably has led a lot of sports scientists, researchers and coaches down the wrong path.

"Anaerobic" is not appropriate since anaerobic energy is produced even at resting levels. As exercise gets more intense but still very much below the point that is designated as the "anaerobic threshold" anaerobic energy increases even though very little additional lactate may show up in the blood. If the athlete is well conditioned, most of the pyruvate* produced by the anaerobic system is utilized immediately for aerobic energy. In these athletes there will be little indication of increased lactate production even though the anaerobic system is being actively utilized. Also above the point that is designated as the "anaerobic threshold" there is still a steady increase in the use of aerobic energy till VO2 max. Thus, the use of the term "anaerobic threshold" is a misnomer because there is no sudden switch to anaerobic metabolism and there is a continued increase in the use of aerobic energy. Something completely different is happening at this point.

*Pyruvate is the end product of the anaerobic system called glycolysis. Glycolysis is what one is referring to nearly all the time they use the term anaerobic. Pyruvate is either immediately used for aerobic energy in the cell or converted into lactate. Very little pyruvate remains as itself which is why lactate is always the term used.

A quick history of thresholds.

In 1959 Wildor Hollman of the German Sports University in Cologne presented a paper on what he called "point of optimal ventilatory efficiency" at the Third Pan American Congress of Sports Medicine. The presentation was based on the author's hypothesis that the ventilatory and lactic acid threshold exists and how to determine each. In 1964 Wasserman and McIlroy used the term "anaerobic threshold" to describe similar phenomena and the term "threshold" became popular internationally. In the early 1970's, Alois Mader, was working with runners in East Germany and discovered that when these runners used a pace faster than the one that generated 4 mmol/l in a progressive exercise test that they quickly became exhausted. When the runners ran at a slightly slower pace they were able to continue running for an extended period of time. Mader escaped from East Germany and went to work with Hollman at the German Sports University in Cologne and popularized the 4 mmol/l lactate measurement. At the same time some researchers were using the term "maximum steady state" but had not yet connected it with lactate levels. In the late 1970 two German researchers, Kinderman and Keul started using the term maximal lactate steady state to describe the point where an athlete could not go any faster or harder without proceeding to exhaustion. Since that time the term "threshold" and "maximal lactate steady state" have become part of the training and testing lexicon. In 1981, Bertil Slodin, a researcher at the Karolinska Institute in Stockholm and a Canadian Ph.D. student there named Ira Jacobs, used the term "onset of blood lactate accumulation" or "OBLA" to refer to effort level in runners that corresponded to the point at which blood lactate begins to increase exponentially. A blood lactate level of 4 mmol/l was associated with this point and in most instances today "OBLA" means a 4 mmol/l blood lactate concentration. All these researchers quickly realized that the lactate level at which this threshold took place varied substantially between athletes while the myth has persisted that they said the 4 mmol/l level was the actual threshold level.

What is the currently accepted use of the term "anaerobic threshold"?

The most common use of the term "anaerobic threshold" is to describe a phenomenon that takes place in all athletes - namely the maximal speed or effort that an athlete can maintain and still have no increase in lactate. At this speed or effort, lactate levels in the blood remain constant. Any increase in effort or speed above this level will cause lactate and its associated high acid levels to increase steadily. This will eventually force the athlete to slow down or stop. The time to cessation or slowing down will depend upon how far the athlete is above the maximum steady state effort, the event the athlete is competing in, the type of athlete (strength or endurance) and conditioning.

It is possible for the athlete to exceed the anaerobic threshold level by small amounts and still exercise or compete for a substantial period of time, sometimes up to 25-30 minutes. The lactate levels will gradually increase in the blood but will not stop exercise for this time. However, substantial increases above the anaerobic threshold will usually shut down the athlete very quickly, often in as little as 20-40 seconds.

Because the anaerobic threshold represents a point where the lactate in the blood reaches a maximum steady state and is an equilibrium between lactate production and lactate clearance, we like two other terms better. The first is maximum lactate steady state (MLSS or MaxLass). This emphasizes the steady state and equilibrium concepts. The second is "lactate threshold" (LT). This retains the threshold concept but puts the emphasis on "lactate" and not "anaerobic". Both of these terms describe the same point of exertion.

The following chart illustrates the concept of a maximum lactate steady state. The swimmer below is able to maintain 1.33 m/s with a constant lactate level of about 3.8 mmol/l. At 1.34 m/s the swimmer is able to continue for an extended time as lactate slowly builds up and finally stops between 20 and 25 minutes. At 1.36 m/s the swimmer stops after 15 minutes. The maximum lactate steady state lies somewhere between 1.33 m/s and 1.34 m/s. For practical purposes it is assumed that the lactate threshold or maximum lactate steady state is 1.33 m/s.

What other terms are used to express this concept?

Many have used other terms such as the individual anaerobic threshold (IAT) and the "onset of blood lactate accumulation" (OBLA). The term IAT (Individual Anaerobic Threshold) has become popular in contrast to the original assumption of many that the anaerobic threshold nearly always took place at blood lactate levels of 4 mmol/l. Several sports scientists wanted to emphasize that the anaerobic threshold or MLSS takes place at different lactate levels for different athletes and that using a fixed level of 4 mmol/l for everyone was very misleading. In fact IAT's or MLSS's range normally from 2 mmol/l to 6 mmol/ with some people outside this range. Also MLSS's vary between sports for the same individual. So triathletes cannot use a fixed lactate level to determine their MLSS for each of the sports in which they compete.

Despite all the problems with the term "anaerobic threshold" the abbreviation AT has become an accepted part of training terminology. It will probably not go away for a long while because it remains a favourite with coaches, athletes, the press and even a lot of sports scientists. However, the term "lactate threshold" or LT is now becoming more popular. This has happened in the last 5 years.

What is the mechanism behind the lactate threshold?
Below the lactate threshold most of the lactate produced is being used as fuel for aerobic energy some place in the body. It could be used very close to the muscle generating the lactate or carried by the blood stream to other muscles and be used for aerobic energy. It is also used by the heart and some is converted back to glycogen. Physiologically the body as a whole is in equilibrium between lactate production and lactate elimination. The rise in blood lactate levels above resting levels as exercise intensity increases is an indication that some muscle fibers are not able to handle all the exercise load aerobically. The excess lactate produced from these muscle fibers moves to areas of lower concentration such as the blood stream, neighboring muscle fibers and the space between the muscles. Other muscle fibers have plenty of excess capacity for aerobic energy and these fibers can use the lactate produced by the fibers with limited aerobic capacity.

When we measure the lactate in the blood stream we are observing the movement of the lactate from muscle fibers that produce the lactate to those parts of the body that can utilize it. As exercise intensity increases the body reaches a point where it cannot utilize all the lactate produced. Above this point, which we call the maximum lactate steady state (MLSS), anaerobic threshold (AT) or lactate threshold (LT), the athlete is not able to eliminate lactate at the same rate as it is produced. As a result lactate starts to accumulate rapidly. It should be noted that the rate at which lactate accumulates above the threshold varies. Generally, the slower the rate of lactate accumulation above the threshold the better the performance in long distance events. For shorter competitions such as those found in swimming, rowing, track cycling and running (events 5000 meters or under), the ability to utilize the anaerobic energy system to a high level (produce lactate quickly) is important.

How can one change the lactate threshold?

With training the lactate threshold will change primarily for three reasons; lactate utilization increases, lactate production declines or lactate clearance increases. Here's how it works:

Lactate Utilization Increases - Training can affect the utilization of lactate primarily in two different ways. However, to better understand the following discussion you should remember that lactate is produced from pyruvate and pyruvate is the end product of the anaerobic process. See the diagram below.

First, better oxygen utilization. With certain types of training there are adaptations within the muscle fiber that let it utilize more of the available oxygen. These changes within the muscle are physical as well as chemical. This higher utilization of oxygen means more of the pyruvate will be used for aerobic energy. When this happens less of the pyruvate will be converted to lactate. Often there is plenty of oxygen available in the muscle fiber but the fiber does not have the capacity to process the pyruvate aerobically. Changing this condition is one of the fundamental objectives of training. (#1 on Chart below)

Better oxygen delivery - Other types of training can bring about adaptations in the cardiovascular system, making it stronger and more efficient. This enables delivery of more oxygen to the muscles and at a faster rate. There is considerable evidence that as more oxygen is delivered to the muscles, less lactate is produced. This doesn't mean the anaerobically supplied energy decreases with improved oxygen uptake (the same amount of pyruvate is produced). It means more of the pyruvate will be used in the aerobic process and thus less will be converted to lactate. So for the same amount of anaerobically delivered energy less lactate will be found in the blood stream if the oxygen to the muscle increases. (#2 on Chart below)

One of the main adaptations that facilitates oxygen delivery is more capillaries. Another change that increases oxygen delivery is an increase in the proportion of red blood cells to plasma in the blood. The higher the percentage of red blood cells the more oxygen that can be delivered to the muscles. Some types of altitude training have an effect on the oxygen carrying ability of the blood.

Despite the better oxygen delivery, some lactate will be produced in muscles that receive plenty of oxygen because of other reasons.

Second - Pyruvate Production decreases. This happens either because adaptations cause more fat to be used or because anaerobic capacity decreases.

More use of fats, less production of pyruvate. There will be less production of pyruvate as the muscles adapt to use more fats as fuel for aerobic energy. The higher utilization of fat means there is less need for glycolysis and consequently less pyruvate is produced. Certain types of endurance training enable the body to process fats easier. (#3 on Chart below) It should be noted that this adaptation does not imply that the anaerobic process is not as strong, just that the signals that activate it are not as frequent. This is in contrast to the next situation where anaerobic capacity is actually lower.

Lower anaerobic capacity, less production of pyruvate, Some types of training actually change the anaerobic capacity. In fact some coaches and sports scientists believe this is the main reason for short term changes in the lactate threshold. When this happens the lactate threshold will automatically change because pyruvate production is changed. When the anaerobic capacity is lowered less pyruvate is produced for a given effort level. Thus, the lactate threshold will increase without any change in the ability of the body to process aerobic energy or to shuttle lactate. When the body is faced with less pyruvate being produced, less will be converted to lactate at any given effort level. Similarly, an increase in the anaerobic capacity will lower the lactate threshold without any change in the in the ability of the body to process aerobic energy or to shuttle lactate. In this case the body has to deal with more lactate. The lactate threshold is always an equilibrium between lactate production and lactate elimination. (#4 on Chart below)

It is thought that the anaerobic capacity of an athlete is innately capped. There is a maximum rate of anaerobic energy production which the athlete seems unable to exceed. However, certain types of training affect the rate at which the anaerobic system can produce energy. Are these contradictory statements? No. It seems that the anaerobic capacity can be lowered from its innate maximum by specific types of training, usually associated with endurance training. High volume low level workouts will suppress the anaerobic capacity as well as long hard workouts near the lactate threshold.

The anaerobic capacity can be brought back to its innate levels by high intensity training well above VO2 max. This will cause the lactate threshold to be lowered. This is not something an endurance athlete would want to do before an important race but swimmers, rowers, runners, speed skaters, track cyclists etc are very interested in having a high anaerobic capacity for important competitions. There have been studies of swimmers which have shown that there is no improvement in the lactate threshold late in the season as important competitions get near. Several prominent sports physiologists have then said that this shows that the lactate testing has little relevance for swimming. Nothing could be further from the truth. What is happening to swimmers is that late in the season training intensity increases substantially and this raises anaerobic capacity back to innate levels. This has the effect of lowering the lactate threshold or keeping it at about the same level. If coaches are not aware what is happening to the anaerobic system then they could prescribe the wrong training for the athletes. By the way this may be a controversial area. I say "may be" because there is not much written on it and so it hasn't been discussed much. It is definitely not considered a factor in why the lactate threshold changes by many sports scientists. However, it is consistent with what a lot of coaches observe in their training programs. Some sports scientists are starting to write more about it.

Lactate Clearance - Training helps the body becomes more efficient at removing lactate from the producing muscles and shuttling it to other parts of the body where it can be used. This eases the acid levels in the producing muscles and thus lets them operate at a higher energy level before producing the acidosis levels that slow down energy production. (#5 on Chart below)

Also training for better oxygen delivery can help the lactate shuttle as the increased capillary system will help clear the lactate out of producing muscles and into the blood stream. The same adaptation facilitates the transfer of lactate from the blood to other muscles for elimination.

Buffering - The muscles can be trained to buffer some of the acid accumulating in the producing muscles. The hydrogen ions causing the problems with contraction are neutralized and this allows even more lactate to be produced before there are problems with contraction. However, it probably does not affect the threshold since it does not slow down lactate production. Buffering enables the athlete to compete for a longer time at effort levels above the threshold. Little is written about how to train this buffering capacity though it is thought to take intense workouts to increase the buffering capacity of the muscles. Coaches often prescribe intense workouts called "lactate tolerance" sets to do two things; 1) get the athletes accustomed to the pain that accompanies high acidosis and 2) increase the buffering ability of the producing muscles. (#6 on Chart below)

Detraining - Lower training levels or stopping training altogether can reverse a lot of these processes and this will also affect the lactate threshold.



How does one train to change the threshold in all these different ways?

This is an interesting question since we haven't seen anyone address it completely. There is a lot of advice on how to change the threshold but none approaches it on the basis of changing six different processes. Also one type of exercise may work on more than one of the six processes. For example, whatever causes capillaries to increase will reduce the production of lactate but will also help the lactate shuttle. Also different types of training may be necessary to effectively change a process. To lower the anaerobic capacity may require a combination of intense workouts near the lactate threshold plus long slow training. Obviously what will work for the regional level athlete may not work for the athlete preparing for Olympic trials since highly trained athletes may have maxed out on several different adaptations. Also what may work for enhancing one of these factors may hinder another since often training exercises are not surgically precise.

The closest we have seen anyone answer this question is the book by Jan Olbrecht which looks at training exercises based on how they will change specific aspects of conditioning. It is a book on swimming but provides a template or schema for developing training exercises that are appropriate for any endurance sport. Also Olbrecht's book emphasizes that these adaptations have to be timed in a precise sequence. Some take several months and even years while others can be done in a few weeks once some of the other adaptations have taken place. Olbrecht works with swimmers, triathletes, runners, rowers and soccer teams. His athletes won 28 medals at the Athen's Olympics.

Are there other thresholds?

There is the point at which the baseline lactate rate starts to rise. (A baseline level is the amount of lactate generated at a slow pace used for recovery or warm-up. See the chart below.) Some have called this the "aerobic threshold." This particular point has some meaning because it represents an effort level at which the lactate in the blood starts to rise. Some have suggested that this point is the effort level at which the body starts to recruit fast twitch fibers. Fast twitch fibers generally produce more lactate than slow twitch fibers. However, this point responds to training just as the lactate threshold does so what is going on in the body at this point is probably a combination of things, one of which may be a recruitment of new fiber types. But it is too simplistic to describe this point as the point where fast twitch fibers are first recruited.

If you want to get really confused, some sports scientists have identified a third threshold which they identify as the effort level that generates 1.0 mmol/l of lactate above the baseline. Some have called this pace or effort the "lactate threshold". However, we use "lactate threshold" to mean the maximum lactate steady state and we will just refer to this third threshold as 1.0 mmol/l above baseline. This lactate level is approximately the lactate level that a marathoner maintains during a race and is definitely below the MLSS for most athletes.


You will notice on the chart above that we did not indicate the lactate threshold. That is because there is no clear point on the curve that can be identified with this effort level. The other two effort levels are more easily identified which is one of the reasons they are popular. However, they require that several lactate readings be taken in order to clearly identify the baseline and where it starts to rise.

Different training programs use these different levels. Coaches and athletes should know what each means in case they hear them used. However, the biological processes at the lactate threshold, the point 1.0 mmol/l above baseline and the point at which lactate starts to rise may be quite different metabolically from athlete to athlete. We identified 6 processes that affect the lactate threshold. It is unlikely that two athletes with the same lactate threshold have identical physiological profiles. In other words if you compared two athletes at each of these thresholds you may find very different processes going on within the athletes even if the effort levels at the threshold are similar. For example, two athletes at the lactate threshold may be using the aerobic and anaerobic systems quite differently.

The coach is trying to maximize the energy produced for these two athletes during a competition and not necessarily manipulate a particular threshold. Thus, the coach tries to find the optimal balance between aerobic capacity and anaerobic capacity depending upon how the competition will unfold and the current conditioning level of the athletes.

Are these thresholds important?

This is an interesting question. Since there is a lot written about them it must be for a reason. Also we spent a lot of time above discussing how to train to change the lactate threshold. We have just mentioned that the pace that is 1.0 mmol above the baseline lactate readings corresponds roughly to the pace that a marathon is run at. Hence it is very useful for distance runners to know this point and judge their progress by how much this point is changing with training. A well trained athlete can run, bike, swim or row for several hours at this pace and not slow down. Ironman triathletes and road cyclists also compete at a pace close to this level or just below it.

While knowing the lactate threshold is important for competition, knowing the threshold exactly may have less relevance for training despite our long discussion above. Above the lactate threshold there will be an accumulation of acid in many of the working muscles because production is outstripping clearance and this is extremely relevant during many types of competition. However, during training it is not as important to know or act on the lactate threshold pace or effort even though much of training has the objective to change it. First, there is nothing special, biological or metabolic, happening at the lactate threshold or at any other threshold. There is no new fiber group being recruited or transition to something different (even though the term "threshold' is used the processes are all continuous). The important thing that happens above the threshold is that the increasing acidosis will shut down the muscles in a short time. Thus the total volume of possible exercise will be less. Also, frequent efforts at levels above threshold may damage the muscle cell structure and end up lowering aerobic capacity instead of increasing it.

For the "more is better" school the lactate threshold represents the highest effort level that the athlete can maintain for a long time. Thus, prescribing workouts at this level will provide the most difficult stimulus the body can handle for an extended period of time. This approach has some problems. Namely,
- working out at the lactate threshold will not recruit all the fibers in the muscles used for a sport and thus not train every muscle that will be needed in competition. The percentage of fibers recruited at the lactate threshold will vary a lot between athletes. One athlete who has a LT at 70% of VO2 max will not use as many fibers at LT as the athlete who has an LT at 93% of VO2 max. As we mentioned above what happens at LT may not be the same for each athlete. Thus, coaches have to design workouts for each athlete based on each conditioning profile. Even two marathoners who have the same LT pace may have very different conditioning profiles. The two may have very different anaerobic capacities and should train differently because of this.

One way to train all the fibers is to do interval training at high intensities near VO2 max. This way the athlete whose LT is 70% of VO2 max can train all the fibers.

- Too frequent extended workouts at the LT is a formula for over-training if used too frequently. What is too frequently? This is a murky area. But a runner who completes a marathon will usually do so at a pace that is lower than the lactate threshold. This runner often needs several weeks to recover fully because of muscle damage. Very few would prescribe a marathon as a workout. However, some coaches/training advisers recommend frequent LT workouts and intervals above threshold. These workouts accumulate substantial mileage during a week and often come close to subjecting the body to the same volume and intensity as a marathon. Even if spaced out every 2-3 days such workouts and competitions done too frequently will break down rather than build up aerobic endurance. If the purpose or training is to break down cellular processes and then give them time to rebuild to a higher level, it is hard to see how continual high intensity workouts will allow the rebuilding process.

Is measuring these thresholds necessary?

The answer is NO! Some very successful coaches have questioned the value of finding the lactate threshold. They don't claim it doesn't exist or that it isn't a good predictor of endurance. They say it is not necessary to measure it to prescribe good training. Their positions have been stated above but to summarize them:

The lactate threshold is difficult to measure and takes too much training time to find it. There is a much a simpler approach, also using lactate testing, that works just as well.

There is no proven benefit to train at the threshold versus training at several different levels. In fact given that there are a multitude of adaptations an athlete desires it is important not to be pre-occupied with training at the threshold.

The threshold will mean different things to different athletes and they are not always obvious. For example, a well conditioned top endurance athlete will have a lactate threshold at an extremely high effort level. This effort at threshold will be very stressful on the aerobic system since the athlete may be close to VO2 max at this point. Because the aerobic system is highly developed for this athlete, it will be using most of the pyruvate produced by the anaerobic system. There will be little lactate in the blood till the anaerobic system is highly engaged. Thus, at threshold the elite athlete is utilizing not only the aerobic system at a high percentage of max but also the anaerobic system at very high levels. Both systems are under high stress.

For regional athletes who compete in local endurance events and have a much lower aerobic capacity there may not be too much demand on their aerobic system at the lactate threshold. They will not be very close to VO2 max at LT and it is highly unlikely that they will stress their aerobic system at threshold as much as the elite athlete will. Also it doesn't take much activation of the anaerobic system to produce the lactate that will be in the blood at threshold. Hence the regional level athlete is not nearly under the same stress as the elite level athlete at threshold. This sounds counterintuitive to most people but is easily understood once you realize what causes the threshold.

This point of view has evolved from the experiences of many sports scientists from the University of Cologne.

How long can an athlete exercise at these thresholds?

This will obviously vary by athlete depending on training level, types of recent workouts, muscle composition, diets, tolerance for discomfort, the environment and other factors. The pace just below 1.0 mmol above baseline can be sustained for hours. The athlete is burning a high percentage of fat at this pace and there is enough fat in us for hours of exercise (even those athletes with low body fat). A lot of training for long distance endurance athletes is aimed at training the muscles to burn more fat.

Most athletes can usually train at the lactate threshold (LT or MLSS) for about 60 minutes continuously. Some can train up to 90 minutes. The limiting factor is fuel for energy (glycogen) and this will depend mainly on recent workouts and diet. When the athlete runs very low on glycogen the muscles cannot sustain the LT pace or effort and will slow down. It will be 36-72 hours before glycogen stores are fully replenished. Let us illustrate the importance of glycogen with two ice hockey games. A couple of years ago, four teams were competing for the NCAA hockey Championship. The semifinals were on Friday and the finals were just a day later on Saturday for financial reasons. Hockey doesn't attract much of a television audience so most money generated by a championship is through attendance. People will not wait around a few extra days for a championship game. Well, one of the semi-final games finished in regulation with a winner while the other went to three sudden death overtimes of 20 minutes each. If you've ever watched a good hockey game you know it is the most intense sport on the planet. During a sudden death playoff game there is only one gear and it is all out. The teams that played the three overtime game were using as much anaerobic energy and glycogen as possible. During the finals, one day later, the team that won in regulation walked over the team that played three overtimes. One commentator said they must have had a let down psychologically after the dramatic overtime win. Nonsense! They didn't have any glycogen to fuel the high intensity efforts needed for hockey.

Similarly, an athlete that does an extended workout at LT or higher will be unable to complete a similar workout until the body's glycogen is replaced, often several days. Not every athlete is the same on this. But just because an athlete can do a long LT workout it may not necessarily be a good thing to do. Some coaches caution that training sessions at the lactate threshold for a prolonged time can be very counter productive.

Should an athlete train at levels higher than LT?

Certainly. The real question is how much training above the LT should an athlete do and at what level. This is a very controversial area. There are studies that show high intensity training provides excellent results and there are studies that show that lower levels produce the best results. There is research that shows that the best aerobic training is workouts near VO2 max but that you can not do too many of them. A lot of what gets published is based on research studies done by academics and is based on 8-12 weeks of training because that is when academics have students to use as subjects. Basing long term training objectives on this type of information is risky.

One coach said that if you are in a hurry, then you will have to include a lot of high intensity workouts. There is no other way to train muscle fibers that don't get recruited till high intensity efforts.

Another coach who took a different tack said that you are "training to train". Early season workouts are mostly below threshold so that the athlete will develop the base to do more intense workouts later in the season or in later years. He described training like a ladder. You have to train at the first rung before you can attempt the second step. As you move up the ladder your body is better able to handle the highly intense training that will eventually come. This obviously will depend on the sport, the amount of time available for training and the timing of important competitions.

Before leaving this question we refer the reader back to the diagram above which illustrates the various factors affecting the anaerobic threshold. There are so many different factors which affect performance (and the diagram doesn't cover them all) it is irresponsible for someone to say this is his or her "favorite workout" in the sense that this is what will condition the athlete better. These may make good magazine articles but they don't make good sense in training.

No workout, no matter what the intensity or the distance, can hope to train more than one or two of the factors affecting performance. Successful training is the culmination of a variety of different types of training. There are so many adaptations that training must provoke and each of these adaptations needs a different intensity and duration. Giving the training a different intensity is like putting an address on a letter. If you only put one or two addresses on the letter it will only go to one or two places. By using only a couple of different intensities in training only a couple of different adaptations will happen.

The purpose of testing and other assessment procedures (competition results and success in training) is to tell the coach and athlete what adaptations are necessary for further improvement. Then the athlete's "favorite workout" will be the one that provokes the adaptation to realize this improvement and not what is a popular workout.

What type of tests are done to find the lactate threshold?

There are several types of tests to measure the lactate an athlete produces. These tests are often referred to as protocols. The most common type of test is what is called a graded exercise test. It has several other names such as a step test or a progressive exercise test. An example of such a test is the chart above of a runner on a treadmill. Essentially this test is a series of exercises at progressively higher intensities.

The athlete will ride a bike on a track or an ergometer, swim several laps in a pool, run on a tread mill or a track, row on an ergometer or complete some other form of steady state exercise. They will start at a low level of effort. After completing the first stage, the coach or sports scientist will take a blood lactate reading as well as other measures such as heart rate, perceived effort, or measures of oxygen consumption if they have the specialized equipment. (These tests are best done in the field because transferring results from a laboratory setting to the practice environment sometimes introduces unpredictable differences.)

After the first step or stage is completed, the athlete completes a second step at a higher effort level. The athlete then completes additional steps as determined by the coach or person supervising the tests. This procedure is described in more detail in the Lactate Tutorial. The athletes usually complete the test by attempting a level of exercise that will cause them to reach exhaustion but this is not necessary and may actually be counter productive. At every step and at exhaustion, a lactate reading and other measures are taken.

The measurements taken are lactate readings which can be easily done with a portable lactate analyzer; heart rates which many athletes and coaches measure with a heart rate monitor; and perceived exertion which the athlete estimates. Usually, a coach or a trained assistant with a little practice takes the measurements while the athlete is performing the exercise. We know of experienced athletes who have conducted these tests by themselves on a track or an ergometer. However, most athletes have trouble taking their own lactate readings when they are substantially above threshold.

From this testing a coach can estimate the lactate threshold. We emphasize the word "estimate". This type of testing will narrow down the LT range and experienced coaches will be able to come very close to it by knowing the athlete and seeing the shape of the curve. Coaches should do a confirmation test of the LT to be sure. This is just a steady state workout at the estimated LT and is best done in a field setting. The coach will take a couple of lactate readings during the workout to confirm that the athlete is really at threshold.

Friday, February 22, 2008

Lactic Acid, Blood Lactate and the “Lactic Acid Myth"

Lactic Acid, Blood Lactate and the “Lactic Acid Myth"
From Sport Fitness Advisor
http://www.sport-fitness-advisor.com/
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Many coaches and athletes routinely perceive lactic acid, or more specifically lactate, as a dead end waste product that is completely unfavourable to all athletic performance. This assumption however, may longer be considered accurate - so much so that it has been labelled ‘the mythology of lactic acid’ (1).

While Sports Scientists are largely in agreement that lactate behaves more like an athlete’s friend than foe, recent research has now begun to question one of the basic tenets of muscular fatigue – increased acidity or lactic acidosis.

This article explores some of the current understanding about how lactate and lactic acid functions in the human body, particularly during exercise. It examines the compounds’ roles in fatigue and energy metabolism and as a limiting factor in performance.
A basic understanding of energy metabolism during exercise is helpful to appreciate some of the current issues surrounding lactic acid.

Lactic Acid and Oxygen
Recall that the end product of glycolysis is pyruvic acid. Traditionally, it was believed that oxygen availability, or lack thereof, lead to the conversion of pyruvic acid into lactic acid and accompanying increases in muscle and blood lactate.

Over the past 35 years, evidence has mounted against this idea (3,4,25). The best evidence seems to suggest that oxygen availability is only one of several factors that cause an increase in muscle and blood lactate during submaximal exercise. In fact, lactic acid can be formed anytime glycolysis takes place regardless of the presence or absence of oxygen and is even produced at rest (2).

Historically, the lactate threshold has often been referred to as the point at which energy is generated through predominantly anaerobic metabolism. Yet the onset of blood lactate accumulation (OBLA) only represents the balance between lactate production and removal and suggests nothing about the aerobic or anaerobic metabolism per se (8).

Researchers have been unable to show a lack of oxygen in the muscles at an exercise intensity above the lactate threshold (8). Instead OBLA may be caused by many different factors other than those associated with anoxia or dysoxia.

For a more detailed discussion of other factors leading to the increased production of lactic acid and blood lactate, see Gladden’s 2003 paper Lactate metabolism during exercise (5).

Lactate is Not a Waste Product
Before the 1970’s lactic acid was considered a waste by-product resulting from a lack of available oxygen to the working muscles. It was blamed for the ‘burning’ sensation during vigorous exercise, delayed onset muscle soreness and central to the process of fatigue. The general consensus was, and still is amongst many coaches and athletes, that lactic acid is responsible for fatigue and exhaustion in all types of exercise.

On the contrary, lactic acid only accumulates within muscle during relatively short, highly intense exercise such as sprint swimming or running. Endurance athletes, such as marathon runners for example can have near-resting lactic acid levels following a race despite being exhausted (2).

In 1984, George Brooks (6) proposed the lactate shuttle hypothesis and at present, the cell-to-cell lactate shuttle has almost unanimous experimental support. This hypothesis questioned many of the widely held beliefs about lactate.

Far from being a waste product, the formation of lactate allows the metabolism of carbohydrates to continue through glycolysis (2). Keep in mind from the energy systems that glycolysis allows rapid production of energy required to sustain intense exercise.

The heart, brain and most slow twitch fibres are very apt at clearing lactate from the blood – to the extent that they prefer lactate as a source of fuel (27,28,29). Note however, that lactate must first be converted into pyruvate before it can be used as a source of energy.

Clearance of lactate from the blood can occur either through oxidation within the muscle fibre in which it was produced or it can be transported to other muscles fibres for oxidation (31,30). Lactate that is not oxidized in this way diffuses from the exercising muscle into the capillaries and it is transported via the blood to the liver (31). Through a process known as the Cori cycle, lactate can be converted to pyruvate in the presence of oxygen, which can then be converted into glucose (2). This glucose can either be metabolized by working muscles or stored in the muscles as glycogen for later use (2).

So lactate should be viewed as a useful form of potential energy that is oxidized during moderate-low intensity exercise, during recovery and at rest (28,30). Unlike lactic acid, lactate is not thought to be fatigue-producing (31).

Based on this more sympathetic view of lactate, sports nutrition companies have introduced sodium lactate into sports drinks and there is some tentative support that these may have an ergogenic effect (9,18).

What the lactate shuttle model essentially shows is that lactate is a crucial intermediary in numerous cellular, localized and whole body metabolic processes, and may help to prolong submaximal activity, rather than hinder it.

Lactate Accumulation
During intense exercise, muscle and blood lactate can rise to very high levels (10). This accumulation above resting levels represents the balance of production and removal. It says nothing about whether accumulation is due to an increased rate of production or decreased rate of removal, or both. Similarly, if lactate concentrations in the blood do not rise above resting levels during or immediately following exercise, it also infers nothing about lactate or lactic acid production during that activity. It may be that lactic acid production is several times higher than at rest but that it is matched by its removal showing no net increase (26).

A common misinterpretation is that blood lactate or even lactic acid, has a direct detrimental effect on muscle performance. However, most researchers agree that any negative effect on performance associated with blood lactate accumulation is due to an increase in hydrogen ions. When lactic acid dissociates it forms lactate and hydrogen ions - which leads to an increase in acidity. So it is not accurate to blame either lactate or lactic acid for having a direct negative impact on muscular performance.

The increase in hydrogen ions and subsequent acidity of the internal environment is called acidosis. It is thought to have an unfavorable effect on muscle contraction (10) and there has been considerable research to demonstrate that this is the case (11,12,13,14,15,16,17).

Lactic Acidosis
So this unfavourable acidosis is the result of an increased concentration or accumulation of hydrogen ions. It may seem logical to conclude then, that any increase in production of lactic acid and hence lactate is detrimental as it will increase the production of hydrogen ions.

However, accumulation is the key term here as an increased production of hydrogen ions (due to an increase production of lactic acid) will have no detrimental effect if clearance is just as fast. In fact Robergs et al. (19) takes it a step further…

They suggest that lactate production (especially if accompanied by a high capacity for lactate removal) may be more likely to delay the onset of acidosis (19, 25). The reasons for this, amongst others, are that lactate serves to consume hydrogen ions and allows the transport of hydrogen ions from the cell. Similarly, they maintain, there is a wealth of research evidence to show that acidosis is caused by reactions other than lactate production (19).

Rogers et al. do conclude however, that increased lactate concentration, although not causative, coincides with cellular acidosis and remains a good indirect marker for the onset of fatigue.

Acidosis and Fatigue
As mentioned earlier, there has been substantial research to show that an increase concentration of hydrogen ions and a decrease in pH (increase in acidity) within muscle or plasma, causes fatigue. Additionally, induced acidosis can impair muscle contractility even in non-fatigued humans and several mechanisms to explain such effects have been provided.

Yet in the last 10 years a number of high profile papers have challenged even this most basic assumption of fatigue. A 2006 review of these by Cairns (18) suggests that experiments on isolated muscle show that acidosis has little detrimental effect or may even improve muscle performance during high-intensity exercise.

In place of acidosis it may be inorganic phosphate that is major cause of muscle fatigue (20). Recall that an inorganic phosphate is produced during the breakdown of ATP to ADP. However, there are several limitations regarding this phosphate hypothesis (21). Another proposal for a major contributor to fatigue, rather than acidosis, is the accumulation of potassium ions in muscle interstitium (22,23,24).

Contrary to this new research (which is by no means definitive) is the argument that if acidosis plays no role in fatigue then it is surprising that alkalosis (through sodium bicarbonate consumption for example) can improve exercise performance in events lasting 1-10 minutes. To reconcile this, Cairns (18) hypothesizes that while acidosis has little detrimental effect or may even improve muscle performance in isolated muscle, severe blood plasma acidosis may impair performance by causing a reduced central nervous system drive to muscle.

Lactate Accumulation and Exercise
At rest the normal range for blood lactate is 0.5 – 2.2 mmol per litre (32,33). It is thought that complete exhaustion occurs somewhere in the range of 20 – 25 mmol/L for most individuals (34) although values greater than 30 mmol/L have been recorded (35).

Blood lactate concentrations peak about 5 minutes after the cessation of intense exercise (assuming cessation is due to exhaustion from acidosis) (32). The delay is attributed to the time required to buffer and transport lactic acid from the tissue to the blood (36). A return to pre-exercise levels of blood lactate usually occurs within an hour and light activity during the post-exercise period has been shown to accelerate this clearance (32,35,37). Training can also increase the rate of lactate clearance in both aerobically and anaerobically trained athletes compared to untrained individuals (32,38,39).

Interestingly, Stone et al (40) noted that trained individuals generated higher levels of blood lactate at the point of failure compared to untrained subjects when exercising intensely (squats). The time and amount of work they completed, unsurprisingly, was greater in the trained group. This seems to suggest that training may induce greater tolerance to lactate accumulation and it may also add weight to the argument that lactate serves to delay acidosis and fatigue. At any absolute workload (i.e. when both groups were lifting the same weight) the trained group had lower levels of blood lactate.

This indicates that training-induced adaptations include a lower blood lactate concentration at any given workload and higher blood lactate concentration during maximal exercise (32,41,42).
The ‘anaerobic’ or lactate threshold is based on the point at which blood lactate abruptly accumulates. It can be used as a prediction for race performance and to prescribe training intensity.

To Summerize...
 Lack of oxygen is not necessarily responsible for an increase in lactate production or even lactate accumulation. Other causative factors may play a more significant role.
 Blood lactate accumulation represents only the balance of production and removal. It says nothing about the absolute values of either of these.
 Only relatively short, very intense activity causes lactc acid to accumulate. Lactic acid is not thought to be a contributor to fatigue in low-moderate intensity activity of any duration.
 Lactate is an important substrate that can be used during submaximal exercise, recovery and at rest. It is the preferred source of fuel for the heart and brain.
 Lactic acid or lactate ‘pooling’ is not the cause of delayed muscle soreness.
 Lactate accumulation and not necessarily an increase in production, causes an increase concentration of hydrogen ions and corresponding acidosis. Lactate production may actually help to curb the development of acidosis.
 Acidosis is thought to be a primary factor in muscular fatigue and is based on a good deal of research. Recent research is contesting this claim but it is still too early to dismiss acidity as a cause of fatigue.
 Training accelerates lactate clearance, reduces lactate accumulation at any given workload and results in a greater level of lactate accumulation during maximal effort.
This is clearly an area that is far from resolved but what seems clear is that lactate can no longer be labelled definitively as the athlete’s enemy. On the contrary, gathering evidence suggests that many aspects of lactate production are beneficial to athletic performance.

References
1) Brooks GA, Fahey TD and White TP. (1996) Exercise Physiology Human Bioenergetics and Its Applications: 2nd Edition. Mountain View, CA: Mayfield Pub
2) Wilmore JH and Costill DL. (2005) Physiology of Sport and Exercise: 3rd Edition. Champaign, IL: Human Kinetics
3) Connett RJ, Gayeski TEJ & Honig CR. Lactate efflux is unrelated to intracellular PO2 in a working red muscle in situ. J Appl Physiol. 1986, 61, 402–408
4) Gladden LB (1996). Lactate transport and exchange during exercise. In Handbook of Physiology, section 12, Exercise: Regulation and Integration of Multiple Systems, ed. Rowell LB & Shepherd JT, pp. 614–648. Oxford University Press, New York
5) Gladden LB (2003). Lactate metabolism during exercise. In Principles of Exercise Biochemistry, 3rd edn, ed. Poortmans JR, pp. 152–196. Karger, Basel
6) Brooks GA (1985a). Lactate: glycolytic product and oxidative substrate during sustained exercise in mammals – the ‘lactate shuttle.’ In Comparative Physiology and Biochemistry: Current Topics and Trends, vol. A, Respiration-Metabolism-Circulation, ed. Gilles R, pp. 208–218. Springer, Berlin
7) Donovan CM, Brooks GA. Endurance training affects lactate clearance, not lactate production. Am J Physiol. 1983, Jan;244(1):E83-92
8) Stager JM and Tanner DA. (2005) Swimming: 2nd Edition; An International Olympic Committee Publication. Oxford UK: Blackwell Science Ltd
9) Van Montfoort MC, Van Dieren L, Hopkins WG, Shearman JP. Effects of ingestion of bicarbonate, citrate, lactate, and chloride on sprint running. Med Sci Sports Exerc. 2004 Jul;36(7):1239-43
10) Fitts RH (2003). Mechanisms of muscular fatigue. In Principles of Exercise Biochemistry, 3rd edn, ed. Poortmans JR, pp. 279–300. Karger, Basel
11) Barany M and Arus C. (1990) Lactic acid production in intact muscle, as followed by 13C and 1H nuclear magnetic resonance. In Human Muscle Power, NL Jones, N McCartney and AJ McComas, eds. Champaign, IL: Human Kinetics
12) Fabiato A and Fabiato F. Effects of pH on the myofilaments and the sarcoplasmic reticulum of skinned cells of cardiac and skeletal muscle. J Physiol. 1978, 276:233-255
13) Fuchs F, Reddy Y, Briggs FN. The interaction of cations with the calcium-binding site of troponin. Biochim Biophys Acta.1970, Nov 17;221(2):407-9
14) Hakkinen K. Effects of fatiguing heavy resistance loading on voluntary neural activation and force production in males and females. In: Proceedings of the second North American Congress on Biomechanics. Chicago: The Organizing Committe. 1992. pp.567-568
15) Hermansen L. Effect of metabolic changes on force generation in skeletal muscle during maximal exercise. In Human Muscle Fatigue, R Porter and J Whelan eds. London: Pitman Medical. 1981
16) Nakamaru Y, Schwartz A. The influence of hydrogen ion concentration on calcium binding and release by skeletal muscle sarcoplasmic reticulum. J Gen Physiol. 1972 Jan;59(1):22-32
17) Tesch P. Muscle fatigue in man. With special reference to lactate accumulation during short term intense exercise. Acta Physiol Scand Suppl. 1980;480:1-40
18) Cairns SP. Lactic acid and exercise performance : culprit or friend? Sports Med. 2006;36(4):279-91
19) Robergs RA, Ghiasvand F, Parker D. Biochemistry of exercise-induced metabolic acidosis. Am J Physiol Regul Integr Comp Physiol. 2004 Sep;287(3):R502-16
20) Westerblad H, Allen DG & LƤnnergren J. Muscle fatigue: Lactic acid or inorganic phosphate the major cause? News Physiol Sci. 2002, 17, 17–21
21) L. B. Gladden. Lactate metabolism: a new paradigm for the third millennium. 2003, J Physiol. 558.1 pp 5-30
22) J Bangsbo, K Madsen, B Kiens and EA Richter Effect of muscle acidity on muscle metabolism and fatigue during intense exercise in man. The Journal of Physiology. Vol 495, Issue 2 587-596
23) C. Juel, H. Pilegaard, J. J. Nielsen, and J. Bangsbo Interstitial K+ in human skeletal muscle during and after dynamic graded exercise determined by microdialysis. Am J Physiol Regul Integr Comp Physiol. 2000, 278: R400-R406
24) Ole M. Sejersted and Gisela SjĆøgaard Dynamics and Consequences of Potassium Shifts in Skeletal Muscle and Heart During Exercise Physiol. 2000, Rev. 80: 1411-1481
25) Brooks GA. Lactate doesn't necessarily cause fatigue: why are we surprised? J Physiol. 2001 Oct 1;536(Pt 1):1
26) Donovan CM & Brooks GA. Endurance training effects lactate clearance, not lactate production. American Journal of Physiology, Endocrinology and Metabolism. 1983. 7: E83-E92
27) York JW, Oscai LB, Penney DG. Alterations in skeletal muscle lactate dehydrogenase isozymes following exercise training. Biochem Biophys Res Commun. 1974 Dec 23;61(4):1387-93
28) Mazzeo RS, Brooks GA, Schoeller DA, Budinger TF. Disposal of blood [1-13C]lactate in humans during rest and exercise. J Appl Physiol. 1986 Jan;60(1):232-41
29) Barnard RJ, Edgerton VR, Furukawa T, Peter JB. Histochemical, biochemical, and contractile properties of red, white, and intermediate fibers. Am J Physiol. 1971 Feb;220(2):410-4
30) Brooks GA. The lactate shuttle during exercise and recovery. Med Sci Sports Exerc. 1986 Jun;18(3):360-8
31) Brooks GA and Fahey TD. (1984) Exercise Physiology Human Bioenergetics and Its Applications: 2nd Edition. Mountain View, CA: Mayfield Pub
32) Gollnick PD, Bayly WM, Hodgson DR. Exercise intensity, training, diet, and lactate concentration in muscle and blood. Med Sci Sports Exerc. 1986 Jun;18(3):334-40
33) McGee DS, Jesse TC, Stone MG and Blessing D. Leg and hip endurance adaptations to three different weight-training programs. J Appl Sport Sci Res 1992, 6(2):92-95
34) Mainwood GW, Renaud JM. The effect of acid-base balance on fatigue of skeletal muscle. Can J Physiol Pharmacol. 1985 May;63(5):403-16
35) Hermansen L, Stensvold I.Production and removal of lactate during exercise in man. Acta Physiol Scand. 1972, Oct;86(2):191-201
36) Juel C. Intracellular pH recovery and lactate efflux in mouse soleus muscles stimulated in vitro: the involvement of sodium/proton exchange and a lactate carrier. Acta Physiol Scand. 1988 Mar;132(3):363-71
37) Freund H, Gendry P. Lactate kinetics after short strenuous exercise in man. Eur J Appl Physiol Occup Physiol. 1978 Aug 15;39(2):123-35
38) McMillan JL, Ston MH, Sartin J, Kieth R, Marple D, Brown C and Lweis RD. 20-hour physiological responses to a single weight-training session. J Strength Cond Res. 1993, 7(1):9-21
39) Pierce K, Rozenek R, Stone M and Blessing D. The effects of weight training on plasma cortisol, lactate, heart, anxiety and perceived exertion. J Appl Sports Sci Res. 1987, 1(3):58
40) Stone MH, Pierce K, Godsen R, Wilson D and Blessing R. Heart rate and lactate levels during weight-training in trained and untrained men. Phys Sportsmed. 1987, 15(5):97-105
41) Sutton JR. Hormonal and metabolic responses to exercise in subject of high and low work capacities. Med Sci Sports. 1978 Spring;10(1):1-6
42) Jacobs I. Blood lactate. Implications for training and sports performance. Sports Med. 1986 Jan-Feb;3(1):10-25

Monday, January 28, 2008

The Lactate Threshold

Physiology – The Lactate Threshold
By Stephen Sieler
From MAPP http://home.hia.no/~stephens/
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In exercise physiology, there have been few topics more frequently investigated, or more vigorously debated than the lactate threshold. It is the details, not the basics that create the big research problems. However, it is the basics that have great application to training and performance. So, we'll stick to those.

What is Lactic Acid and Where Does it Come From?
When you consume carbohydrate, it consists of several different sugar molecules; sucrose, fructose, glucose to name a few. However, by the time the liver does it's job, all of this sugar is converted to glucose which can be taken up by all cells. Muscle fibers take up glucose and either use it immediately, or store it in the form of long glucose chains called glycogen. During exercise, glycogen is broken down to glucose which then goes through a sequence of enzymatic reactions that do not require oxygen to proceed. All of these reactions occur out in the cell fluid, or cytosol. They can occur very rapidly and yield some ATP in the process. This pathway is called the anaerobic (no oxygen) glycolysis (glucose breakdown) pathway. Every single glucose molecule must go through this sequence of reactions for useful energy to be withdrawn and converted to ATP, the energy molecule, that fuels muscle contraction, and all other cellular energy dependant functions.

The Metabolic Fork in the Road
There is a critical metabolic fork in the road at the end of this chemical pathway. At this fork, glucose has been converted from one 6 carbon molecule to two, 3 carbon molecules called pyruvic acid, or pyruvate. This pyruvate can either be shuttled into the mitochondria via the enzyme pyruvate dehydrogenase, or be converted to lactic acid via the enzyme lactate dehydrogenase. Entry into the mitochondria exposes the pyruvate to further enzymatic breakdown, oxidation, and a high ATP yield per glucose. Conversion to lactate means a temporary dead end in the energy yielding process, and the potential for contractile fatigue due to decreasing cellular pH if lactic acid accumulation proceeds unchecked. Like a leaf floating in a river, the pyruvate molecule has no "say" in which metabolic direction is taken.

Which Way will MY pyruvate go during exercise?
I am sure you have surmised that that is a critical question with big implications for performance. I will try to answer the question at three levels: a single muscle fiber, an entire muscle that is active during exercise, and the entire exercising body.

The Muscle Cell at Work
In a single contracting muscle fiber. The frequency and duration of contractions will determine ATP demand. ATP demand will be met by metabolizing a combination of two energy sources: fatty acids and glucose molecules(ignoring the small contribution of protein for now). As ATP demand increases, the rate of glucose flux through glycolytic pathway increases. Therefore at high workloads within the single fiber, the rate of pyruvic acid production will be very high. If the muscle fiber has a lot of mitochondria (and therefore more Pyruvate Dehydrogenase), pyruvate will tend to be converted to Acetyl CoA and move into the mitochondria, with relatively little lactate production. Additionally, fatty acid metabolism will account for a higher percentage of the ATP need. Fat metabolism does not produce lactate, ever! If lactate is produced from glucose breakdown, it will tend to diffuse from the area of high concentration inside the muscle cell to lower concentration out of the muscle fiber and into extracellular fluid, then into the capillaries.

The Whole Muscle at Work
Now let's look at an entire muscle, say the vastus lateralis of the quadriceps group during cycling. At a low workload, glycolytic flux is low and the pyruvate produced is primarily shuttled into the mitochondria for oxidative breakdown. Since the workload is low, primarily slow twitch fibers are active. These fibers have high mitochondrial volume. As workload increases, more fibers are recruited and recruited fibers have higher duty cycles. Now ATP demand has increased in the previously active fibers, resulting in higher rates of pyruvic acid production. A greater proportion of this now is converted to lactic acid rather than entering the mitochondria, due to competition between LDH and PDH. Meanwhile, some Fast twitch motor units are starting to be recruited. This will add to the lactate efflux from the muscle due to the lower mitochondrial volume of these fibers. The rate of lactate appearance in the blood stream increases.

The Body at Work
The vastus is just one of several muscles that are very active in cycling. With increasing intensity, increased muscle mass is called on to meet the force production requirements. All of these muscles are contributing more or less lactic acid to the extracellular space and blood volume, depending on their fiber type composition, training status and activity level. However, the body is not just producing lactate, but also consuming it. The heart, the liver, the kidneys and inactive muscles are all locations where lactic acid can be taken up from the blood and either converted back to pyruvic acid and metabolized in the mitochondria or used as a building block to resynthesize glucose (the liver). These sites have low intracellular lactate concentration, so lactic acid diffuses INTO these cells from the circulatory system. If the rate of uptake or dissappearance of lactate equals the rate of production or appearance in the blood, then blood lactate concentration stays constant (or nearly so). When the rate of lactate production exceeds the rate of disappearance, lactic acid accumulates in the blood volume, then we see the ONSET of BLOOD LACTATE ACCUMULATION (OBLA). This is the "Lactate Threshold" (LT).

Performance Implications
Lactic Acid production is not all bad. If we could not produce lactate, our ability to perform brief high intensity exercise would be almost eliminated. However, As I am sure you are aware, lactic acid is the demon of the endurance athlete. Cellular accumulation of the protons (increased acidity) that dissociate from lactate results in inhibition of muscle contraction. Blame those heavy legs on the protons! The bottom line is that exercise intensities above the OBLA point can only be sustained for a few minutes to perhaps one hour depending on how high the workload is above the intensity at OBLA. Exercise at or below this intensity may be sustainable for hours. The causes of fatigue at these sub-LT intensities include carbohydrate depletion and dehydration.


Factors that Influence the Rate of Lactate Accumulation in the body
Absolute Exercise Intensity- for reasons mentioned above.
Training Status of Active Muscles- Higher mitochondrial volume improves capacity for oxidative metabolism at high glyolytic flux rates. Additionally, improved fatty acid oxidation capacity results in decreased glucose utilization at submaximal exercise intensities. Fat metabolism proceeds via a different pathway than glucose, and lactic acid is not produced. High capillary density improves both oxygen delivery to the mitochondria and washout of waste products from the active muscles.


Fiber Type Composition- Slow twitch fibers produce less lactate at a given workload than fast twitch fibers, independent of training status.
Distribution of Workload - A large muscle mass working at a moderate intensity will develop less lactate than a small muscle mass working at a high intensity. For example, the rower must learn to effectively distribute force development among the muscles of the legs back and arms, rather than focusing all of the load on the legs, or the upper body.


Rate of Blood Lactate Clearance- With training, blood flow to organs such as the liver and kidneys decreases less at any given exercise workload, due to decreased sympathetic stimulation. This results in increaed lactate removal from the circulatory sytem by these organs.


Measuring the Lactate Threshold
We have previously discussed the value of a high maximal oxygen consumption for the endurance athlete. A big VO2 max sets the ceiling for our sustainable work rate. It is a measure of the size of our performance engine. However, the Lactate Threshold greatly influences the actual percentage of that engine power that can be used continuously.


Most of you will never have this measured in a laboratory, but a brief description of a lactate threshold test is still useful, because it will lead us into some specific applications for your racing and training. The test consists of sucessive stages of exercise on a treadmill, bicycle ergometer, swimming flume, rowing machine etc. Initially the exercise intensity is about 50- 60% of the VO2 max. Each stage generally lasts about 5 minutes. Near the end of each stage, heart rate is recorded, oxygen consumption is measured, and a sample of blood is withdrawn, using a needle prick of the finger or earlobe. Using special instrumentation, blood lactate concentration can be determined during the test. After these measurements, the workload is increased and the steps repeated. Through a 6 stage test, we would expect to achieve a distribution of intensities that are below, at , and above the intensity of OBLA or the lactate threshold. The data from a test would generally look simililar to the example below.


Interpreting the Data
For purposes of interpretation, let's say that the athlete above had a maximal heart rate of 182, and a VO2 max or 61 ml/min/kg. These were also determined using a bicycle test. So they are good values for comparison. Looking at the green dots, we see that blood lactate concentration does not begins to increase until during the 4th workload,from a concentration of abouu 1 mM to 2.5 mM. This is the break point. The subjects VO2 was 45 ml/min/kg at this point. So we determine that his LT occurs at 45/61 or about 74% of VO2 max. If we look at the heart rate at this point, it is 158. Now we have a heart rate at lactate threshold. 158 = about 85% of his max heart rate. This is useful for the athlete. When he is cycling, he can judge his training intensities based on this important value. If he is a time trialist, this would approximate his racing heart rate for the hour long event.


So, Do I race at My LT Intensity?
This depends on your race duration. If your are rowing 2000 meters, running a 5k race etc., your exercise intensity will be well above the AT. Consequently, the blood lactate measured after these events is extremely high in elite athletes, on the order of 15mM (resting levels are below 1 mM). In races lasting from 30 minutes to 1 hour, well trained athletes also perform at an intensity above LT, but by a smaller margin. It appears that in these events, top performers achieve what might be termed a "maximal lactate steady state". Blood lactate may increase to 8 to 10 mM within minutes, and then stabilize for the race duration. A high but stable lactate concentration may seem to contradict the idea of the LT. But, remember that blood lactate concentration is the consequence of both production and clearance. It seems likely that at these higher lactate concentrations, uptake by non-working muscles is optimized. At any rate, measurements in cyclists, runners and skiers demonstrate the fact that elite performers can sustain work levels substantially above the LT for up to one hour.


Specificity of the Lactate Threshold
It is important to know that the lactate threshold is highly specific to the exercise task. So if this cyclist tries to get on his brand new, previously unused, rowing machine and row at a heart rate of 158, he will quickly become fatigued. Rowing employs different muscles and neuromuscular patterns. Since these muscles are less trained, the cyclist's rowing LT will be considerably lower. This specificity is an important concept to understand when using heart rate as a guide in "cross training activities", as well as for the multi-event athlete.


Effect of Training
For reasons mentioned above, training results in a decrease in lactate production at any given exercise intensity. Untrained individuals usually reach the LT at about 60% of VO2 max. With training, LT can increase from 60% to above 70% or even higher. Elite endurance athletes and top masters athletes typically have LTs at or above 80% of VO2 max. Values approaching 90% have been reported. The lactate threshold is both responsive to training and influenced by genetics.

Monday, August 20, 2007

There is NO Lactate Threshold

Physiology – There is NO Lactate Threshold – Setting the record straight on lactate
From http://www.powerrunning.com/

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Lactate is a bad guy in the running world. It’s blamed for lots of bad things including fatigue, muscle soreness, and preventing you from running faster. There is even a well known and widely followed training method - tempo runs – that was originated specifically to help you overcome all the bad things lactate was believed to be doing in your body, therefore helping you run faster.


The problem is that none of the bad things you’ve heard about lactate are true. None of them! In fact, exercise physiologists have known for more than 10 years that all the bad things previously believed about lactate are not true. Indeed, quite a bit of the updated information about lactate has been known since the mid-1980s, meaning that some of the updated information on lactate has been known for 20 years. It’s not even a case of controversy amongst exercise physiologists about the negative effects of lactate – it is widely accepted in the exercise physiology world that lactate is NOT responsible for any of the bad things you’ve heard about it.
If the information about lactate is known to be false, and the true nature of lactate has been known and accepted for many years by the exercise physiology world, then why do runners continue to believe all those horrible things about lactate? Why do the negative beliefs about lactate persist in the running community in the face of incontrovertible information to the contrary? I won’t speculate why the long updated information about lactate hasn’t been widely disseminated within the running community. Instead, the purpose of this article is to bring you the latest information about lactate and its role in your body. My goal is to set the record straight on lactate so that at the end of this article any negative beliefs you’ve held about lactate are dispelled, replaced with recent information that gives appropriate credit for the important energy role lactate plays in performance. Considering the depth and width of the negative beliefs about lactate that permeate the running community, this is a big task, so let’s get started.
Note – runners generally use the terms “lactate” and “lactic acid” interchangeably, even though they are not the exact same chemical compound. Though there are chemical differences between lactate and lactic acid these differences are not significant to our discussion. For our purposes we will use the term lactate and lactic acid interchangeably.


Lactate History
In order to properly tackle the various negative beliefs about lactate we begin with a review of the origin of these beliefs about lactate. Why has lactate been considered so important in terms of running performance and just how did lactate become such a villain in the first place? To answer this question requires us to first review the beliefs about the limits of exercise – i.e. why can’t you run faster?


You have probably been exposed to the terms “aerobic” and “anaerobic”. Well, these 2 terms are key to understanding the origin of the villainous beliefs about lactate. In basic terms, aerobic simply means with oxygen and anaerobic means in the absence of oxygen. These terms are talking about 2 ways your body has of producing energy. Your body can produce energy with oxygen, aerobically, or without oxygen, anaerobically.


These methods of producing energy – with and without oxygen – are central to the theory of endurance performance. In the 1920s the British physiologist and Nobel Prize winner A.V. Hill first proposed the exercise theory that has since been termed the cardiovascular/anaerobic model and has been a foundation belief of the running community for more than 70 years. In essence, Hill’s theory was that the reason you can’t run faster is because you can’t get enough oxygen to your working muscles. He suggested that as the intensity of exercise increased the runner reached a point where he was unable to take in and use more oxygen. You have likely heard this belief expressed as the term VO2max. “V” means the volume of flow of oxygen to the body, O2 (correctly written O2) is the chemical symbol for oxygen, and max is the abbreviation for maximum. So, the term VO2max simply means the maximum volume of oxygen being taken in and used by the body. At VO2max, the runner is unable to absorb and use more oxygen. However, and this is key, Hills’ belief was that at VO2max the runner was not running as fast as possible. The runner could run a little bit faster even though he could not take in and use more oxygen.


What happens when a runner can’t get enough oxygen to meet the aerobic energy needs of his muscles? When this happens, the body must meet its energy needs via anaerobic methods. As the runner gets closer and closer to VO2max, more and more of his energy is met via anaerobic metabolism. Now we come to the genesis of the negative beliefs about lactate. The cardiovascular/anaerobic model preached that lactate was produced as a result of anaerobic energy production. In accordance with this model, as the intensity of exercise increased oxygen becomes increasingly in short supply, forcing the body to rely more and more on anaerobic metabolism, resulting in an increasing higher level of lactate within the body. This model further suggested that lactate interfered with the muscles’ ability to contract, thus causing fatigue.
In essence, here are the basics of the cardiovascular/anaerobic model, which explains why lactate has been considered so important by the running community for so many years. The cardiovascular/anaerobic model believes:
1. As exercise intensity increases, the body’s energy needs cannot be met entirely through aerobic metabolism – i.e. there is insufficient oxygen available to the working muscles.
2. Due to the increasingly insufficient oxygen supply, the energy needs of the body are instead increasingly met via anaerobic metabolism – i.e. the muscles have become anaerobic.
3. Anaerobic metabolism produces lactate as a by-product.
4. Increasing levels of lactate interfere with muscle contractions, causing fatigue within the muscles.


Now you know the basics of why lactate has been considered important to the running community – it was believed to cause fatigue. This brings us to the concept of lactate threshold.
When scientists first starting measuring changes in blood lactate levels with increasing exercise intensity they noticed something interesting. Lactate seemed to rise very slowly at first, then all of sudden it began to rise precipitously, as illustrated in table 1. The traditional explanation for this sudden rise in lactate levels was that the muscles had become “anaerobic” - meaning that anaerobic energy production had become the primary source of energy within the muscle. The point where lactate levels began increasing rapidly is usually called the lactate threshold, but has also been called the anaerobic threshold and the ventilation threshold.
Table 1: Blood lactate level rising in a precipitous manner - i.e. lactate threshold

The Real Facts About Lactate
Now that you understand why lactate has been considered important by the running community and the origins of the negative beliefs about lactate we turn our attention to the updated information about lactate.


Muscles don’t become anaerobic during exercise
The first thing we need to address is the foundation belief that at high exercise intensity there is insufficient oxygen to meet the energy needs of the body. Despite the widespread belief by many that there is insufficient oxygen to working muscles at high exercise intensity, this has never been proven. In fact, it has always been assumed there is insufficient oxygen, but has never been proven despite years of efforts by physiologists.


McArdle, Katch, and Katch, writing in their well respected exercise physiology textbook have this to say about limited oxygen supply during exercise. “The usual explanation for a lactate increase is based on an assumed relative tissue hypoxia during heavy exercise.”(1) They clearly state that the belief that there is limited oxygen to working muscle (relative tissue hypoxia) is an assumption. It has never been proven.


Despite the fact that this belief has never been proven, it is important to know that it has been treated as a fact for many years by many, and perhaps most, in the scientific community and, consequently, by the lay public.


However, more recent efforts by experts using new techniques to determine if muscles become anaerobic during heavy exercise have shown the opposite to be the case: “these data demonstrate that, during incremental exercise, skeletal muscle cells do not become anaerobic…since intracellular PO2 (the oxygen pressure in the muscles) is well preserved at a constant level, even at maximal exercise.”(2)


So, you now know that muscles do not become anaerobic during exercise.


Why lactate levels increase with exercise intensity
If muscles don’t become anaerobic, then why do lactate levels increase during exercise of increasing intensity? After all, isn’t lactate produced through anaerobic energy production? The short answer to these questions is that lactate is produced during carbohydrate metabolism, irrespective of the availability of oxygen. Here is what Prof. Tim Noakes has to say on this topic in the most recent edition of Lore of Running:
“As the exercise intensity increases, so does the rate of carbohydrate use. When high exercise intensities (greater than 85% to 95% VO2max) are achieved, virtually all the energy comes from carbohydrate oxidation (G.A. Brooks and Mercier 1994; Brooks 1998). This means that the rate of energy flow through the glycolytic pathways increases steeply with increasing exercise intensity. The result is that the rate of lactate production increases inside the muscles.”(3)
In essence, then, lactate is a by-product of carbohydrate metabolism. It is not a matter of the body becoming anaerobic. Instead, as the intensity of exercise increases the body relies increasingly more on carbohydrates to provide the needed energy. More carbohydrates being burned results in a greater volume of lactate being produced and an increase in blood lactate levels. The muscles have not become “anaerobic” - lactate is increasing because the body is burning more and more carbohydrates.


There is NO lactate threshold
Okay, now we know that the muscles don’t go anaerobic during heavy exercise and lactate production is due to carbohydrate being burned to produce energy. This brings us to the topic of “lactate threshold”. Recall that the theory of lactate threshold was that at some exercise intensity blood lactate levels increase dramatically, i.e. crosses a threshold, due to anaerobic metabolism. We already know that lactate is being produced in increasing high amounts for reasons other than the muscles becoming “anaerobic”, but is lactate increasing after crossing some “threshold”? Again, the answer is no.


Lactate increases exponentially with increases in exercise intensity and does NOT exhibit a threshold. This being the case, why did exercise physiologists believe there was a lactate threshold? Going back to Prof. Noakes again:
“This mistaken conclusion resulted from at least 2 errors. First, too few blood samples were measured. For example, if only 4 blood samples had been drawn at running speeds of 10, 14, 16, and 20 km per hour, then a fictitious anaerobic threshold would have been identified at 15.5 km per hour. But measuring blood lactate concentrations repeatedly – for example every km per hour – shows that blood lactate concentrations rise exponentially without any evidence of a threshold phenomenon.”

“It is clear that the blood lactate concentrations do not show a clearly defined, abrupt threshold response during exercise of progressively increasing intensity. Rather, blood lactate concentrations begin to rise as soon as progressive exercise commences. However, at low intensities, the rate of the increase is so low that it is barely noticeable. Only when the exercise becomes more intense does the rise become apparent, which perhaps explains the erroneous impression that blood lactate concentrations increase abruptly when the lactate threshold is reached.”

“For these reasons, the term anaerobic threshold, lactate threshold, and lactate turnpoint are no longer justifiable”(4)


So, you see, there is not a lactate threshold. Lactate increases exponentially with increases in exercise intensity and exhibits no evidence of a “threshold”.


Lactate doesn’t cause fatigue – it helps prevent fatigue
You might say at this point that whether lactate is produced by anaerobic metabolism or not, or increases in a "threshold" manner or not is immaterial if increasing amounts of lactate cause fatigue. After all, it doesn't really matter how the level of lactate increases if lactate is the cause of fatigue. (Recall that it has long been believed by the running community that lactate causes fatigue.) It is this core belief that has caused runners to focus so intently on lactate threshold - lactate causes fatigue and the lactate threshold is the point where there is suddenly enough lactate in the body to cause fatigue to increase rapidly. There is no doubt that blood lactate levels increase with increasing exercise intensity. If lactate causes fatigue then it wouldn't matter if muscles become anaerobic or how lactate increases in the body - these points do not negate the idea that lactate causes fatigue. Lactate does increase with increasing exercise intensity and if it causes fatigue, then the other points are ancillary. Therefore, the most important question to ask is, Does lactate cause fatigue? Absolutely not!
"Lactate is a totally innocuous substance that, if infused into the bloodstream, has no noticeable effects."(5)


That's right - you could inject your muscles with lactate and you would experience NO additional fatigue because lactate does not cause fatigue.


To top off the facts about lactate is this kicker – lactate not only does not cause fatigue as it has long been believed to, but there is reason to believe it actually helps prevent fatigue. How’s that for a complete turnaround of everything you ever believed about lactate?
Researchers examining muscle fatigue in rats caused by a reduced pH and loss of potassium found that the “subsequent addition of…lactic acid led, however, to an almost complete force recovery.” These researchers write:
“In contrast to the often suggested role for acidosis as a cause of muscle fatigue, it is shown that in muscles where force was depressed by high (potassium), acidification by lactic acid produced a pronounced recovery of force. Since intense exercise is associated with increased (potassium), this indicates that acidosis may protect against fatigue rather than being a cause of fatigue.”(6)
What they are saying in the above quote is that lactic acid in the muscles is likely to protect against fatigue, allowing the muscle to work longer and/or harder before fatigue sets in.


Hydrogen Ions & Muscle Acidity
Some physiologists, knowing that lactate does not cause fatigue, have suggested an alternate theory for muscle fatigue. They suggest that hydrogen ions (H+), which are produced during the conversion of lactic acid to lactate, are the true cause of muscle fatigue. This theory holds that the H+ changes the pH within the muscle, increasing muscle acidity, which interferes with the muscles’ ability to contract. As more and more lactate is produced, so too are more H+ produced, leading to an increasing acidic muscle and an increasing level of fatigue. This theory explains why increases in lactate correlate with increased fatigue. H+ is produced as a result of lactate metabolism, the H+ makes the muscle cell acidic, and the acidity interferes with muscle contraction (in effect, causes fatigue) - more lactate means more H+, producing greater acidity, resulting in more fatigue.


However, this theory has been challenged. Dr. Bruce Gladden, in his 2004 review of lactate metabolism writes,
“...lactic acid is more than 99% dissociated at physiological pH. This has led to the incorrect notion that the donation of a proton by each lactic acid molecule causes a decreased pH during conditions such as exercise.(7)


A research update by Stackhouse, et al addresses this topic:
“In addition, many textbooks report that muscle fatigue is mainly the result of a decrease in pH within the muscle cell due to a rise in hydrogen ion concentration ([H+]) resulting from anaerobic metabolism and the accumulation of lactic acid. Recent literature, however, contradicts this assertion.”(8)


These 2 quotes mean that lactate derived H+ does not play a major role in changing muscle pH levels. H+ does increase in the muscles, but it is not a primary player in creating muscle acidity.
Finally, a research paper by Westerblad et al says this:
“…the increase in H+ (i.e. reduced pH or acidosis) is the classic cause of skeletal muscle fatigue. However, the role of reduced pH as an important cause of fatigue is now being challenged, and several recent studies show that reduced pH may have little effect on contraction in mammalian muscle at physiological temperatures.”(9)


What Westerblad is saying here is that recent research indicates that increased muscle acidity is NOT a cause of fatigue. Though it is too soon to dismiss the idea that muscle acidity contributes to fatigue, the theory is certainly being challenged and recent evidence on this topic suggests the H+ are not the primary cause of muscle acidity.


Lactate is Actually A Potent Energy Source
Instead of being a source of fatigue, exercise physiologists now know that lactate is a potent fuel source for the body, and some have suggested it may be the most important fuel available to the muscle. Research shows that about 75-80% of lactate is used to produce energy through oxidation, with the remainder converted to glucose and glycogen. Working muscles oxidize the lactate for fuel. Blood lactate is absorbed by the liver, the heart, and inactive muscle. The liver converts uses lactate to produce glucose and glycogen, the heart uses lactate as a preferred fuel, and inactive muscle stores lactate.


More recently leading lactate researcher George Brooks has pioneered the concept of a "lactate shuttle". The importance of the lactate shuttle is that it is the mechanism that allows carbohydrates to be moved from one muscle group to another. Muscles do not have the ability to send their stored carbohydrates (glycogen) to other parts of the body, so, for example, a resting group of muscles can't send their stored glycogen to working muscles that may be low on glycogen. Dr. Brooks has shown that the lactate shuttle is the way in which the body's store of carbohydrates can be transferred to working muscles during and after exercise. For example, during a run workout glycogen stores in your inactive arm muscles can be converted to lactate and shuttled to your leg muscles, providing an additional and important source of energy for your working leg muscles.


Summary
In summary, it has long been held by the running community that lactate was the primary culprit in lots of metabolic “crimes”. These beliefs are now known to be false. Muscles do not become anaerobic during exercise, lactate does not cause fatigue, and there is NO lactate threshold. Instead lactate is produced as a result of carbohydrate metabolism and may actually delay fatigue. Lactate is accepted as an important and potent source of fuel for working muscles. In his 2004 review of the current state of knowledge about lactate Prof. Bruce Gladden sums it up best. He writes:
“For much of the 20th Century, lactate was largely considered a dead-end waste product of glycolysis due to hypoxia, the primary cause of the O2 debt following exercise, a major cause of muscle fatigue, and a key factor in acidosis-induced tissue damage...

The bulk of the evidence suggests that lactate is an important intermediary in numerous metabolic processes, a particularly mobile fuel for aerobic metabolism, and perhaps a mediator of redox state among various compartments both within and between cells. Lactate can no longer be considered the usual suspect for metabolic ‘crimes’, but is instead a central player in cellular, regional, and whole body metabolism.”(6)


Reference:
McArdle, Katch, Katch, Exercise Physiology: energy, nutrition, and human performance, 4th edition, 1996, pg. 123
Richardson R, Noyszewski E, Leigh J, Wagner P. Lactate efflux from exercising human skeletal muscle: role of intracellular PO2, J Appl Phsiol 1998, 85(2), 627-634
Noakes, T Lore of Running, 4th edition, 2004, pg 160
Noakes, T Lore of Running, 4th edition, 2004, pg 158-159
Noakes, T Lore of Running, 4th edition, 2004, pg 163
Nielsen O, Paoli F, Overgaard K. Protective Effects of lactic acid on force production in rat skeletal muscle J of Physiol 2001, 536.1, 161-166
Gladden L. B., Lactate Metabolism: a new paradigm for the third millennium J Physiol 2004 558(1), 5-30
Stackhouse SK, Reisman DS, Binder-Macleod SA., Challenging the role of pH in skeletal muscle, Phys Ther 2001, 81(12), 1897-903
Westerblad H, Allen D, Jannergren J. Muscle Fatigue: Lactic Acid or Inorganic Phosphate the Major Cause? News Physiol Sci 2002, 17, 17-21

Tuesday, May 8, 2007

5 Critical Tasks

5 Critical Tasks
By Owen Anderson.
From www.pponline.co.uk
-
If you want to reach your peak level of performance and be a winner, especially in an endurance sport, you must accomplish five critical tasks:

I . Maximise your aerobic capacity (V02max) so that more energy is available to sustain your exercise
2. Raise your lactate threshold as high as possible, so that intense efforts can be maintained with a minimum of fatigue
3. Become more efficient at carrying out the exact activities required in your particular sport, so that less energy is wasted during competition and hard exertions feel less stressful
4. Fortify yourself psychologically, so that the vicissitudes of training and competing can be handled more easily
5. Learn how to rest, so that your hard training is perfectly balanced with adequate amounts of recovery

1. Maximal aerobic capacity
Hoisting this is probably the easiest of the five tasks, since just engaging in your sport for expanded periods of time can heighten V02max. If you're a runner, for example, and currently training 40 miles per week, you can earn a nice V02max upgrade simply by expanding your weekly schedule to 50-60 miles, without increasing the actual intensity of your work-outs.

However, beyond a certain point, increasing your quantity of training no longer boosts V02max. Once that point is reached, INTENSITY of training becomes the key factor: you'll have to cycle, run, row or swim at speeds which lift your heart rate to at least 95 per cent of maximal in order to push V02max as high as possible. To make things more difficult, attaining such high heart rates for brief periods of time won't work. If you're really interested in sending V02max to the stratosphere, your 'intensity needle' will have to point to 95 per cent of maximal heart rate for four-to-five minute stretches several times during selected workouts.

2. Lactate threshold
Lifting lactate threshold (LT) - the exercise intensity above which lactic acid begins to increase appreciably in your blood - is fairly straightforward. If you fatten up your V02max, you will usually raise your threshold as well, since LT is often a fixed percentage of aerobic capacity.

However, it is also possible to raise LT independently, which is lucky in those cases where V02max refuses to budge. Training continuously at about 85-90 per cent of maximal heart rate for 20- to 25-minute periods will generally have a profound effect on LT. If you don't own a heart monitor or hate checking your pulse, a good LT-raising intensity is one which feels as though it would be impossible to sustain for longer than 30 minutes during a workout.

3. Efficiency
The key to improving your efficiency of movement is to recognise that each muscle in your body is composed of collections of individual muscle cells. If you make a particular muscle stronger, then fewer of the individual cells within that muscle will be required to sustain a certain level of effort. In other words, more muscle cells within the strengthened muscle are allowed to rest while you're engaging in your sport, and other muscles which assist your power-boosted muscle are less likely to be called into play. Since you'll need to activate fewer individual muscle cells to pedal a bicycle at 20 miles per hour, swim at 1.5 metres per second or row a boat at a particular velocity, your overall energy demand will be lower - you'll be more efficient! As a result, you'll be able to step up to higher than expected intensities of exercise, or else conserve large quantities of precious muscle fuel if you prefer to remain at your traditional work rate.

To get more powerful, and therefore more efficient, you'll need to carry out some training at levels of effort which are actually higher than your usual competitive intensities. Obviously such exertions can't be sustained for long, so the usual plan -for the endurance-oriented athlete is to employ 3090 second intervals at close to top capacity. The recipe for the correct recovery interval during such workouts is a bit ambiguous. Utilising recoveries that are equal in duration to the work intervals can be good, because it helps an athlete's muscles to develop 'lactate tolerance' - the ability to control increases in acidity and sustain high power outputs for longer periods of time. On the other hand, longer rest intervals allow more work to be done during each work interval so it's probably best to have some workouts with short recoveries and others with more extended rest periods. Sprinters, of course, usually won't want the 90-second work intervals; for a 400m sprinter, for example, 10- and 20-second intervals at faster than 400m pace would be ideal.

An additional way to become more efficient is to make use of an esteemed tenet of training called the 'specificity principle'. There's no special magic here; the idea is simply to do some training at the exact intensity one hopes to use during an important competition.

For example, the top-level runner who wants to sizzle through a 5K in 13:10 should complete some 1000m intervals in 2:38 each, the 10K competitor shooting for a 30-minute race should carry out 2000m intervals in six minutes, and the marathoner hoping for a 2:11 clocking should cruise through 10-miles runs in 50 minutes. In each case, these runners are practising the exact tempo which will be required for the race. Likewise the rower who wants to hustle a boat through the water at a particular cruising velocity, the cyclist shooting for a goal time, and the skier needing a specific pace to win a race, must all practise that particular intensity during training.

The bottom line is that competition is not just a muscular event; an athlete's nervous system must learn to CONTROL muscular activity at the precise exertion level required for the race. Specific training allows the nervous and muscular systems to come together in a coordinated way.

4. Fortify yourself psychologically
Compared to the physiological requirements of a winning performance, the exact psychological needs of the top-level athlete are less clear, but it is certain that superior performers are able to concentrate almost totally on their bodies during workouts and competitions, blocking out extraneous thoughts and negative information which might impede their performances. The best athletes also tend to be somewhat self-critical, but not overly so, and they often engage in 'positive self-talk', giving themselves encouragement both during exercise and throughout the course of an average day.

Supreme competitors also have the ability to let bad performances roll off their backs; in fact, they tend to regard poor outings as opportunities to learn more about themselves and to make necessary changes in both their physical and mental preparations for competitions. The best athletes also seem to form mental images of themselves moving powerfully and quickly, and they tune in these images before major competitions.Finally, almost all great athletes have the apparently paradoxical ability to both relax and remain somewhat tense. Their muscles are untaut and ready for maximally powerful efforts during competition, yet within their minds keen fires burn which are ready to ignite almost superhuman physical exertion.

5. Learn how to rest
Although severe workouts are necessary to get to the top, rest is equally important but is all too often missing from a potentially great athlete's schedule. Attuned to the idea that high-level workouts produce winning performances, the majority of athletes go overboard, pushing themselves to the brink of fatigue and overtraining. Top athletes have learned that optimal training involves exercising and resting; it's not possible to reach supreme performance levels unless fierce exertions are balanced with restoration and recovery.

Even the seemingly fatigue-proof Kenyan runners take two-month respites each year during which they do very little training. As they put it so simply: 'Our bodies need to take a rest, so that we can train hard the rest of the year'. All competitive athletes should have at least one annual six- to eight-week period in which very little training is done, and should avoid the temptation to carry out too many high-intensity workouts during the training year.

True, not every athlete needs to reach the five goals which I've outlined above. Sprinters and throwers, for example, don't require high V02max levels or lofty lactate thresholds, and they may in fact lose some of their raw muscle power if they focus on V02max-building training. Sprinters and throwers need to enhance the anaerobic capacities of their muscles, not the aerobic, so the maximum amount of force can be exerted in the shortest possible time. However, for athletes involved in activities which last for more than a couple of minutes, hitting all five targets should lead to the biggest pay-off of all: a winning performance.

Owen Anderson