report on blood lactate

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When Marc Rogers travelled to St. Louis back in July, 1984 to begin post-graduate research in exercise physiology at Washington University, he also commenced training for the St. Louis Marathon, which was scheduled for November. Before getting into his hard-core marathon preparations, Marc underwent an exercise test in the St. Louis lab and learned that his VO2max was 70 ml/kg/min, while his lactate-threshold (LT) velocity was reached at 78 per cent of VO2max, or at 54.6 ml/kg/min.

Marc proceeded to train very aggressively, combining high-intensity work with high mileage (about 80 miles per week) and was re-tested in early November. Despite the heavy-duty training, Marc's VO2max had moved upward by nary a millilitre of oxygen, clinging stubbornly to the same 70-ml mark of mid-summer. Fortunately, though, Marc's LT had gone through the roof, climbing from 78 to a lusty 90 per cent of VO2max (or 63 ml/kg/min). And yes - Marc won the St. Louis Marathon that autumn, primarily because of his huge advance in LT.

To understand what actually happened to Marc, and to discover how you, too, can make major gains in LT and performance, we need to tell a tale about something called lactate. The first chapter of this lactate parable will centre around a key physiological process called glycolysis.

Glycolysis is so important that if your muscles lost their ability to carry it out, you would not be able to compete in any athletic event lasting more than a few seconds. In glycolysis, glucose is broken down inside your muscle cells - via a series of 10 different chemical reactions - into something called pyruvic acid, releasing some of the energy needed for muscular contractions. The pyruvic acid can then be funnelled into a complex series of reactions called the Krebs cycle, which furnishes over 90 per cent of the energy you need to run, cycle, or swim. Since glycolysis provides your muscles with quick energy and also 'jump-starts' the Krebs cycle, it is a paramount player in muscular energy production. In fact, without gycolysis your muscles would grind to a halt after only 10 to 15 seconds of your workout or race - with your legs feeling as though they had bounced up against the mother of all 'walls'.

Fortunately, glycolysis usually proceeds normally, without your having to think about it, and it also tends to 'keep pace' with your exertions; the more intensely you exercise, the 'hotter' the glycolysis fires burn. One very important consequence of this is that if glucose is broken down to pyruvic acid at very high rates, pyruvic acid can begin to accumulate inside your muscle cells, and an enzyme called lactic dehydrogenase can promptly convert much of the pyruvic acid to lactic acid.

Bad stuff?
As an athlete, you're probably no stranger to the idea that lactic acid forms rather readily in your muscle cells, especially when you are exerting yourself quite strenuously. In fact, you probably believe that the 'burn' you feel in your leg muscles when you're running, cycling, or swimming very fast is caused by lactic acid - and that the soreness you experience the day after an especially tough workout is produced by the same 'troublesome' compound. You may also cling to the idea that lactic acid is a 'waste product' formed in your muscles during strenuous exercise, and that lactic acid appears in your muscles when you 'run out' of oxygen, or because you've gone into 'oxygen debt'. In short, you probably believe that lactic acid is really bad stuff!

Well, it isn't! All of the above statements are untrue: lactic acid doesn't produce burning sensations, it does not induce soreness, and it's not a form of metabolic 'rubbish' which must be eliminated from your cells as quickly as possible. In addition, oxygen shortfalls are not required in order to make lactic acid appear in your muscles and blood: The truth is that lactic acid is produced in your body all the time, around the clock, even when you're at rest, and its concentrations rise whenever you take in a carbohydrate-containing meal. Fortunately, we're not telling you all this to improve your chances of gaining a PhD in cell physiology: We're giving you the straight scoop because an understanding of how lactic acid actually functions in your body can improve your performances tremendously!

You see, instead of being a dangerous compound which wreaks havoc inside muscle cells, lactic acid (or more accurately, lactate) is actually the key chemical your 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 per cent of the lactate you produce during a very tough workout is actually used by your muscles to form glycogen; far from damaging your tissues or inducing soreness, this glycogen provides you with the energy you need to carry out subsequent quality workouts ('Disposal of Lactate during and after Strenuous Exercise in Humans,' Journal of Applied Physiology, vol. 61(1), pp. 338-343, 1986). During exercise, lactate is an irreplaceable source of energy for muscles and other tissues, so much so that enhancing your ability to 'process' lactate can improve your race times rather dramatically. If you're a typical runner, the 'lactate training techniques' outlined in this article should hasten your 10-K clockings by at least a minute.

As if that weren't enough, lactate also helps keep you from getting fat. To understand how that happens, let's pretend that you have just finished a high-carbohydrate meal. Much of the carbohydrate in that repast enters your bloodstream as glucose - and heads straight for your liver. Paradoxically enough, your liver refrains from picking up this train-load of glucose, preferring instead to let it 'slip away' to the rest of the body. Once the glucose eludes your liver, it goes to many places, including your muscles, which can - via glycolysis - quickly break down the glucose to lactate, releasing usable energy in the process. Much of the lactate produced by glycolysis 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 the liver.

This somewhat circuitous process of glycogen formation means that blood levels of both glucose and lactate rise after you've had your high-carbo meal. However, lactate levels don't rise nearly as fast as glucose concentrations, primarily because lactate is rather rapidly removed from the blood once it appears, while glucose is taken away only sluggishly. By changing some of the absorbed glucose from your meal over to lactate, your body quickens the 'disposal' of blood carbohydrate, thus controlling the amount of insulin which pours into the blood from your pancreas (the higher the glucose level, the greater the insulin response). This limiting of insulin production helps to prevent wild upswings in fat formation (one of the 'bad' points about insulin is that it coaxes glucose into adipose cells, where it is converted into blubber).

The lactate shuttle
Lactate is also the primary player in an important process which occurs in your body - and which may be called the 'lactate shuttle.' Described by George Brooks and his colleagues at the University of California-Berkeley, the lactate shuttle involves the following chain of events:
1. Lactate is formed in ample amounts in tissues in which glycogen and glucose are being broken down at high rates (for example, in your leg muscles when you are running at a strenuous pace). As we indicated, pyruvate is actually formed first; as pyruvate 'piles up', it is readily converted to lactate.

2. After pyruvate is converted to lactate, the lactate can slip quickly and quietly out of cells and into surrounding tissues and the blood. This 'lactate escape' in effect prevents glycolysis (the conversion of glucose into pyruvate) from shutting down (if pyruvate built up to overly generous levels, glycolysis might 'back up', thwarting energy production). As lactate leaves hard-working muscle cells, it can be 'picked up' by other muscle cells and tissues. This departure of lactate from cells engaged in strenuous activity is sometimes called the 'spilling' of excess lactic acid into the blood.

3. The muscle cells and tissues receiving the lactate have the option of either breaking down lactate for fuel (lactate is a rich source of ATP, the key 'energy currency' within cells) - or else using lactate as a building block for the formation of glycogen. The glycogen created from lactate can simply hang around quietly in cells until energy is needed at a later time.

Knowledge of the lactate shuttle helps you understand how important lactate really is: its easy diffusibility prevents glycolysis from shutting down, and its 'high-octane' fuel status helps a variety of cells to satisfy their immediate energy requirements or else store energy for future use.

An understanding of the lactate shuttle also helps you make sense of those curious Scandinavian studies which have shown that vigorous training carried out with only the right leg can also upgrade the fitness of the left leg - and even that vigorous leg exercise can improve the fitness of the arms! Sure, there's a cardiovascular effect going on in such research (a heart strengthened by exercise will do a better job of getting blood and oxygen to the whole body), but the other part of the story is that the non-working tissues learn how to process the lactate 'spilled' in their direction by the hard-working cells (from one leg to the other or from the legs to the arms). As the non-exercising 'lactate-recipient cells' get better at using lactate, they have more energy available to sustain activity when they are actually called upon to exercise.

What is the lactate threshold?
The lactate shuttle also helps you comprehend that mysterious phenomenon called the lactate threshold, or LT. When you begin a fairly moderate workout, lactate levels in your blood initially rise, simply because glycolysis is working away to provide quite a bit of the energy you require. If there were plenty of oxygen around, the pyruvate formed from glycolysis could 'be broken down all the way' to carbon dioxide and water, releasing a lot of important energy in the process. However, because you've just started your workout and therefore the blood and oxygen flow to your muscles is still somewhat minimal (heart rate is just beginning to rise, and capillaries leading into the muscle are not yet in the full-open position), pyruvate will be converted to lactate, and lactate will pile up inside your leg-muscle cells and begin spilling out into the blood. If we measured your blood-lactate levels at this early stage of your workout, we might find surprisingly high concentrations of lactate, even though you were ambling along at a pretty modest pace.

If you keep moving along at a temperate pace, your blood lactate will quickly simmer down, however. As heart rate increases and capillaries dilate, oxygen will pour into your muscle cells, lactate will be oxidized for energy, and the spill-over process will abate. Your blood-lactate levels will drop a bit and then hold steady, which simply means that the entry and exit rates of lactate into and out of the blood are equal.

And lactate levels may hold steady, even as you gradually increase your exercise intensity. As long as you're not going too fast, eg, as long as enough oxygen is moving into your muscle cells to take care of the pyruvate produced by glycolysis and thus control the lactate spillage, your blood lactate will appear to be as calm as a small Scottish pond on a windless day.

It's only when you get up to a point (actually to a speed or exercise intensity) at which glycolysis is tearing along so fast that your leg muscles can't convert all the lactate being formed to carbon dioxide and water that the spilling process may accelerate - so much so that lactate levels in the blood may really begin to lift off. This point may be reached because not enough oxygen is getting into the cells to 'handle' all the lactate (pyruvate) being produced, or because there are not enough enzymes available to guide along the pyruvate-oxidation process, or even because your tissues are not very good at 'clearing' large amounts of lactate from the blood. Whatever the reason, the lactate-appearance rate in the blood may suddenly exceed the lactate-disappearance rate, and so blood-lactate levels begin to climb. You have gone above your lactate threshold!

What a low LT speed really means
To put it another way, your lactate threshold (LT) is the running, cycling, or swimming speed above which lactate begins to accumulate in your blood. As mentioned, in one sense, that sudden lactate pile-up is normal: Every single endurance athlete in the world has an LT; everyone eventually reaches an intensity at which lactate begins to burgeon in the blood. However, if your LT is reached at a somewhat low exercise intensity, it often means that the 'oxidative energy systems' in your muscles are not working very well. If they were performing at a high level, they would use oxygen to break lactate down to carbon dioxide and water, preventing lactate from pouring into the blood. If your LT occurs at an inchmeal pace, it may mean that you're not getting enough oxygen inside your muscle cells where it really matters, or that you don't have adequate concentrations of the enzymes necessary to oxidize pyruvate at high rates - or enough mitochondria in your muscle cells (mitochondria are the small grain-like structures which are the actual sites for the oxidation of pyruvate; without mitochondria, pyruvate simply can't release its energy to the cell). As mentioned, since blood lactate depends not only on lactate formation but also on how well your tissues can utilize lactate once it appears, a low LT can also mean that your muscles, heart, and other tissues are not very good at extracting lactate from the blood.

In practical terms, you want to progressively move your LT to higher and higher running, cycling, or swimming speeds, because doing so will mean that 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. In effect, having a low LT is not bad in itself (the lactate won't hurt you) but is a symptom that all is not well with your muscles' 'machinery' for breaking down pyruvate, using oxygen, and/or processing lactate.

It's important to note that for many endurance athletes improving lactate threshold is the key to better performances. A variety of different scientific studies have shown that lactate threshold is the single best predictor of endurance performance - better even than that vaunted physiological variable - VO2max, aka maximal aerobic capacity ('Blood Lactate: Implications for Training and Sports Performance,' Sports Medicine, vol. 3, pp. 10-25, 1986, and also 'A Longitudinal Assessment of Anaerobic Threshold and Distance-Running Performance,' Medicine and Science in Sports and Exercise, vol. 16(3), pp. 278-282, 1984).

It responds well to training
There's also great news (and certainly great news should be very welcome now that you've waded through all this physiology): not only is LT the best predictor of performance, but it is also very responsive to training - much more responsive than VO2max. If you've been training for several years, VO2max may not move upward at all over the course of a single year of hard work, while LT might soar by up to 20 per cent!

Remember Marc Rogers - our St.-Louis-Marathon winner? You'll recall that he won the race not because of a big move in VO2max, which actually was static despite a very impressive training regime, but because of a huge lift-off in LT. Marc's 'machinery' for oxidizing pyruvate and processing lactate improved dramatically, lifting his LT from 78 to 90 per cent of VO2max in less than four months of training, so he was the one who took home the first-place trophy!

Why is LT so dynamic? 'The skeletal muscles can adapt rather suddenly and strikingly to training, producing major gains in LT,' says Marc, who is currently an exercise physiologist at the University of Maryland. 'In contrast, VO2max is a fairly stable cardiovascular variable in experienced endurance athletes. To understand that, bear in mind that VO2max is to a large degree dependent on the size of the left ventricle (the key heart chamber which pumps oxygenated blood out to the body), and the left ventricle just doesn't change very much in volume after you've been training for a number of years. That's why VO2max values may not rise at all - or may only increase by a couple of percent, even with a high volume and/or intensity of training. Meanwhile, LT can be expected to increase from 5 to 20 per cent - given the appropriate training stimulus.'

And research agrees
Marc's comments are well supported by scientific research. For example, when scientists at Georgia State University and the Emory University School of Medicine followed nine elite distance runners over a two and a-half year period during which the athletes prepared for the 1984 Summer Olympic Games in Los Angeles, they found that VO2max remained unchanged over the entire 30-month period, while LT advanced by an average of 6 per cent. The LT upswing corresponded with either improved PBs or higher competitive rankings for the runners involved in the study ('Physiological Changes in Elite Male Distance Runners,' The Physician and Sportsmedicine, vol. 14(1), pp. 152-171, 1986).

Another exciting aspect of LT improvement is that it seems to be much less limited by the ageing process, compared with upswings in VO2max, economy and power ('Effects of Physical Training on Skeletal Muscle Metabolism and Ultrastructure in 70- to 75-Year-Old Men,' Acta Physiologica Scandinavica, vol. 109, pp. 149-156, 1980, and also 'Maintenance of the Adaptation of Skeletal Muscle Mitochondria to Exercise in Old Rats,' Medicine and Science in Sports and Exercise, vol. 15, pp. 243-251, 1983). To put it another way, as you get older, your best opportunity for improving your performances may come from LT-type training.

That should not be a big shock. Remember that as you get older, maximal heart rate tends to decline by an average of one beat per year, and the strength and flexibility of the left ventricle also tend to diminish. These factors lower maximal cardiac output, a key component of VO2max. Meanwhile, those pesky little mitochondria which play a large role in boosting LT, and also the aerobic enzymes which give LT a kick-start, are not necessarily reduced by the ageing process ('The Ageing Muscle,' Clinical Physiology, vol. 3, pp. 209-218, 1983).

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