Coaching Information. Article Number2. THE IMPORTANCE OF BLOOD LACTATE THRESHHOLD IN RACE PERFORMANCE. Colin Smith.
You probably believe that the "burn" you feel in your leg muscles when you're running very fast and that the soreness you experience the day after an especially tough workout is produced by lactic acid. You may also cling to the idea that lactic acid is a "waste product" formed in your muscles during strenuous exercise that appears when you've gone into "oxygen debt". In fact the truth is that lactic acid is produced in the body all the time, even when you're at rest, and its concentrations rise when you take a carbohydrate-containing meal. Some understanding of how lactic acid actually functions in your body can improve your running performance tremendously.
Lactic acid (or more accurately, lactate), is the key chemical the body uses to "dispose of” dietary carbohydrate; without it, it would be very difficult to maintain normal blood-sugar levels, or keep your liver and muscles "stockpiled" with carbohydrate. About 50% of the lactate you produce during a tough workout is actually used by your muscles to form glycogen. In fact enhancing your ability to "process" lactate can improve your race times dramatically.
Lactate also helps you from getting too fat. After a high carbohydrate meal much of the carbohydrate enters your bloodstream as glucose, and then heads for your liver. Paradoxically, your liver lets the glucose "slip away" to many parts of the body, including your muscles, which, via glycolysis, quickly break down the glucose to lactate, releasing usable energy. Much of the lactate produced this way can return to the blood, head back to the liver, and finally be used to boost concentrations of glycogen (a key "storage" form of carbohydrate) in this organ. This circuitous process of glycogen formation means that blood levels of both glucose and lactate rise after your high carbohydrate meal. However, lactate levels don't rise nearly as fast as glucose concentrations, primarily because lactate is removed rapidly from the blood, whilst glucose is taken away more sluggishly. By changing some of the absorbed glucose from your meal to lactate, your body quickens the "disposal" of blood carbohydrate, thus controlling the amount of insulin which pours into the blood from the pancreas. This limiting of insulin production helps to prevent wild upswings in fat formation (an undesirable feature of insulin is that it coaxes glucose into adipose cells, where it is converted into "blubber").
To understand what lactate threshold (LT) is, and its significance to training, we need to have an idea of a physiological process - the lactate shuttle. Glucose is converted to pyruvic acid via a complex biological process which is then funnelled into a series of reactions called "the Krebs Cycle", a paramount mechanism in muscle energy production. Pyruvic acid is then converted to lactic acid when it begins to accumulate inside muscle cells. Lactate so formed in tissues, e.g. the leg muscles, (in which glycogen and glucose are being broken down at high rates when you are running at a strenuous pace) can then slip quickly out of the cells engaged in strenuous activity into surrounding tissues and the bloodstream. The muscle cells and tissues receiving the lactate can break it down for fuel (lactate is a vital precursor of adenosine triphosphate (ATP), the key "energy currency" within the cells), or they can use it to form glycogen. Glycogen can hang around quietly in cells until energy is needed at a later time. The ease of diffusibility of lactate prevents glycolysis from shutting down.
When you begin a moderately paced run, lactate levels in the blood initially rise because glycolysis is working away to provide the energy you require. The blood and oxygen flow to the muscles is still minimal (heart rate is beginning to rise, and capillaries leading into the muscles are not yet in the open position), pyruvate is converted to lactate which piles up inside your leg muscle cells and begins spilling out into the blood. Blood lactate levels are surprisingly high considering the modest pace. As heart rate increases and capillaries dilate, oxygen will pour into the muscle cells, oxidising the lactate for energy, the spillover process abates, then the blood lactate levels drop slightly and then stays at a steady level. Even increasing the exercise intensity does not increase the blood lactate level, as long as enough oxygen is moving into the muscle cells to take care of the pyruvate by glycolysis. (i.e. an aerobic process, CWS).
It's only when you get up to a point of speed intensity at which glycolysis is tearing along, so fast that your leg muscles can't convert all the lactate being formed into carbon dioxide and water that the spilling process accelerates. The blood lactate levels rise because not enough oxygen is getting into the cells to handle all of the lactate being produced. The lactate appearance in the blood will exceed the lactate disappearance rate. You have gone above your lactate threshold. (i.e. an anaerobic process, CWS).
In practical terms you want to progressively move your LT to higher running speeds because doing so will mean your oxidative energy systems are improving and that your muscles are getting better at pulling lactate out of the blood and using it for energy. Lactate threshold is the single best predictor of endurance performance, better even than that much vaunted physiological variable VO2max. LT is very responsive to training, if you have been training for several years VO2max may not have moved up upward significantly at all, whereas LT might soar by up to 20% in a single year of hard work. This correlation of increased LT (yet stable VO2max) after a training period versus high athletic achievement has been measured in the improved performance of many elite athletes.
LT is so dynamic because the skeletal muscles can adapt to training and this LT improvement is less limited by the ageing process than VO2max. VO2max is largely dependent on the size of the left ventricle - the key heart chamber that pumps blood out to the body, and this does not change very much in volume after you have been training for a number of years. In fact as we get older maximal heart rate tends to decline by an average of 1 heart beat per year, and the strength and flexibility of the left ventricle also tends to diminish - factors that lower maximal cardiac output, important components of VO2max. Conversely, mitochondria, which play a large part in boosting LT, and also the aerobic enzymes which give LT a kick start, are not necessarily reduced by the ageing process. This was graphically illustrated in a recent comparative study of veteran runners versus young runners of comparable LT's - both groups produced similar 10km times even though the former group had an average VO2max of 10% lower than the latter group.
So how do we improve LT? Studies show that intense training is the best LT booster, because such workouts improve the heart's capacity to deliver oxygen, and improve the ability of the muscles to use oxygen. They also increase the ability of the heart and other muscles to clear lactate from blood. Intense training sessions that cause a body to exceed LT, produce a flood tide of lactate in the blood stream: this is linked with glycogen depletion of "fast-twitch" muscle fibres (not "slow-twitch"), which are responsible for the huge upswings in blood lactate. Fast-twitch fibres play a larger role as running speeds increase beyond LT pace, than the low-twitch fibres. Fast-twitch fibres are low on mitochondria and aerobic enzymes, so these would belch out lactate as they are called into play because these fibres are very poor at oxidising pyruvate. To stimulate fast twitch fibres and increase LT speed you have to use them during training, specifically at fairly sustained paces. Studies have shown that this works because the concentration of a mitochondrial enzyme in fast twitch fibres - cytochrome C, increases by about 1% per minute of daily training as long as the intensity is set at 85 to 100% VO2max.
Overall, research suggests that the range of intensities from 5km to 10 mile pace is great for improving LT, with faster pace within this zone being particularly effective. However, the advantage of a slower pace within this zone is that it can be used for many more minutes of weekly training, even overcoming the per minute disadvantage; e.g., it is much easier to complete 40 minutes of training at your 10 mile race pace than it is to charge through 40 minutes at 5 km pace, and the risk of overtraining and injury is lower.
It is important to note that paces closer to your 10 mile than your 5km velocity, with heart rates nearer to 85% of VO2max rather than 95%, seem to work best when they are sustained in a continuous manner for periods of 20 minutes or more. When such a 20 minute session was added to the 14 weeks training routine of a group of athletes the average LT's improved by 4%, and 10 km times were trimmed by over a minute. Other studies have also established that 20 minutes may just be a threshold needed to heighten LT significantly.
Additional research has indicated that strength training (circuits) can have a positive impact on LT, probably because the power of individual muscle cells had been increased and not so many lactate producing fast twitch fibres needed to be recruited during exercise. The reduced activation of fast twitch cells would lead to lower lactate outputs, and thus a potentially higher lactate threshold.
The importance of rest was also investigated. Studies have found that at least every 6 weeks, training should be reduced for 6 to 7 days to allow muscles to recover from strenuous training and create the new structures and enzymes that will raise LT, i.e. constant hard training can be detrimental to LT improvement.
In order to optimise LT, workouts should involve heavy lactate production, to "teach" muscles to break down lactate as fuel and enhance their lactate clearance capabilities. Workouts should also improve the "buffering capacity" of muscles, i.e. their ability to cope with the upward zooms in acidity associated with intense efforts (kicks to the finish line etc.). An example of such a workout would include a good warm-up then a number of 2 minute intervals carried out at very close to maximal intensity, tempered with 4 minute recoveries. The 2 minute blasts produce lots of lactate, the 4 minute recoveries coax the muscle cells into increasing their ability to metabolise the lactate produced as well as provide downtime so that the next 2 minute work interval can again be conducted at a very hard intensity.
Ideally, an optimal 7 week period should include 6 weeks of work and 1 week of rest. The 6 weeks of work should include quality workouts; the rest of the weekly training should involve easy efforts. The LT workouts should increase in difficulty over the 6 week period.
Abstracted from an article in Peak Performance by Owen Anderson.