Posted: December 10, 2004

Science of Sport: Bad News For Lactate Lovers

By Owen Anderson, Ph. D. - Copyright © 2002-2004

Little Lactate-Level Readers Reveal Lactate Of The Moment Accurately But May Fail To Foretell Finer Fitness

Whether you are a runner, cyclist, rower, cross-country skier, swimmer, or triathlete, your lactate-threshold velocity - the movement speed at which blood-lactate concentrations begin to increase fairly dramatically - is a great predictor of your performance capacity. The reason for this is that lactate is a tremendously important muscle fuel during sustained activity; thus, if lactate begins piling up in the blood at fairly low speeds (i. e., if an athlete has a low lactate-threshold velocity), the muscles have a poor capacity for utilizing a key source of energy, and thus work output will be slight and fatigue will occur relatively early. If lactate doesn't accumulate until an athlete reaches a very high speed, the athlete's muscles must have a great capacity to use lactate for fuel, and so performances will be higher in quality and fatigue will occur later.

Naturally, athletes have focused on lactate-threshold velocity as a key physiological variable which should be improved during training. Logically, it follows that if training is going well, lactate-threshold speed should improve, and performances should also get better. But how can one determine if lactate-threshold velocity is really advancing?

Enter the lactate monitors. Fairly inexpensive, portable devices like the LactatePro have proven to be remarkably accurate little fellows. That is, at any specific point in time, they will produce a reading for blood lactate which is remarkably close to the true lactate level in your blood. This accuracy has been very exciting to many coaches and athletes. After all, they have reasoned, with just a few "finger sticks" they could tell very reliably which way lactate-threshold velocity was heading. Once lactate-threshold velocity was established for an athlete, he/she could carry out workouts at that intensity every two to four weeks or so; if lactate levels were down at the established lactate-threshold speed, then training must be going well, and true lactate-threshold speed must be higher than the previously established lactate-threshold velocity. Similarly, if lactate levels were up, training must be going badly, and adjustments would need to be made to ensure that changes in lactate threshold would reverse course.

Indeed, validations of certain kinds of "lactate-threshold training" have depended on measured changes in lactate readings. For example, in the early 1980s renowned Swedish exercise physiologist Bertil Sjodin uncovered a .72 km/hour "increase" in lactate-threshold velocity (LTV) over a 14-week period in the athletes he was studying and concluded that the training the athletes had utilized was particularly beneficial for lactate-threshold-speed development (1).

However, there is a key element missing in such a conclusion - and in current beliefs about lactate training and the use of lactate monitors. That element is simply the reproducibility of blood-lactate levels - the propensity of blood-lactate concentrations to remain the same at a specific exercise intensity, unless an athlete has achieved a real change in fitness. If blood-lactate levels tend to vary to a great extent in individual athletes as a result of non-fitness-related factors, even when exercise intensity remains the same, then it can be very difficult to argue that a change in observed blood lactate is truly the result of altered fitness.

In fact, the lactate levels in an athlete's blood at any specific moment in time during exercise are a function of the intensity of exercise and also the length of time over which the exercise has been conducted. Lactate is also sensitive to a variety of other factors, including the nutritional and psychological status of an athlete. The consumption of a high-carbohydrate meal during the hours leading up to a workout, for example, can drive up blood-lactate levels during exercise, while a fattier diet can make plasma-lactate concentrations more modest. In addition, increased states of tension and/or anxiety can lead to augmented blood-lactate levels, while calmer psychological conditions tend to keep lactate at more minimal readings. Mild states of dehydration can make lactate levels appear to be loftier than they really are, compared with a euhydrated state. Finally, even time of day can have an effect on lactate concentrations (blood lactate follows a circadian rhythm).

The problem, then, is very basic and easy to understand. If you are a runner, for example, and your lactate-threshold velocity is measured at 4.47 meters per second (6:00 per mile), is that speed at which lactate begins cresting completely determined by your fitness? How much depends on other factors (the small measurement errors of the lactate monitor, the "interpolation" mistakes when LT speed is estimated from a graph which plots lactate levels against running speed, and the potentially big "skews" associated with nutritional, hydration, and psychological status)? And, when you re-measure your LTV after four weeks or so and find that it is 4.60 meters per second (5:50 per mile), is that a real change in lactate-threshold velocity, or does it simply reflect the natural variation which is produced by non-fitness-related factors?

Until now, we haven't really been sure. Previous studies have suggested that lactate readings are reasonably reproducible (1 & 2), but these investigations have been characterized by deep flaws in the statistical analyses (3). As athletes and coaches, this uncertainty leaves us in a very precarious position: We simply don't know by how much a lactate reading has to change in order for us to assume that it represents a real upgrade or downgrade in fitness. If a measured lactate-threshold running speed changes from 17 km/hour to 17.75 km/hour, for example, can we trust it? If LTV falls from 17 to 16.5 km/hour, should we be perturbed - or should we acknowledge that this drop-off may simply be part of the natural variation in measured LTV?

These questions are key, and the coach or athlete who ignores them is employing lactate-measuring devices in an illogical way. To find out how reproducible lactate readings really are, scientists at the Institute of Biomedical and Life Sciences at the University of Glasgow and the National University of Ireland in Galway recently studied 20 men and 16 women (4). All of the subjects were physically active, taking part in at least two aerobic-dance, cross-country-running, volleyball, soccer, or rugby workouts each week. The active individuals completed two treadmill lactate-profile tests; almost all of the tests were completed one week apart and at approximately the same time of day (we forgot to mention that LTV - in addition to depending on hydration, psychological status, dietary factors, and caffeine consumption - is also influenced by the time of day at which it is measured). LTV, defined as the treadmill velocity which produced the first significant elevation of blood-lactate concentration above the level measured at rest, was determined for each athlete on the two separate occasions. The heart rate and perceived effort (using Borg's 6-20 category scale) associated with LTV were also measured. To determine whether fitness level has an impact on LTV reproducibility, the subjects were divided into two groups - those with an LTV equal to or greater than 10.5 kilometers per hour (the moderate-fitness group) and those with an LTV slower than 10.5 km/hour (the low-fitness group). 10.5 km/hour equates with a tempo of about 9:12 per mile.

As it turned out, fitness and reproducibility were linked; the two LTV readings for the moderate-fitness-group members tended to be closer together than the two separate recordings for the low-fitness individuals. This makes sense: As fitness levels increase, fitness should become a stronger factor with respect to LTV and should be less likely to be "swamped" by vicissitudes in other variables.

Gender did not have a significant effect on reproducibility of LTV. However, the Glasgow-Galway research revealed that it is natural for LTV to vary in an athlete by more than one kilometer per hour in either direction. To put it another way, if "true" LTV was initially measured in the laboratory at 15 km/hour, future readings of 16 km/hour - or 14 km/hour - would be reasonably interpreted as normal variations around the average LTV, rather than significantly different speeds associated with lactate threshold. To put it another way, a conclusion that 16 represented an upswing in fitness or that 14 was associated with a drop-off in capacity would be very tenuous.

Similarly, heart rate at LTV exhibited a rather large natural variation. In fact, the research suggested that athletes should expect the heart rate associated with a specific LTV to vary by up to 12 to 18 beats per minute from one day to the next! This rather large natural variation in heart rate presents problems for those who believe they have identified a "lactate-threshold heart rate" and who are carrying out training at that specific heart rate, believing it will be beneficial for LTV enhancement. In fact, it would not be unreasonable to expect that the heart rate which the athlete had "tied" to LTV might be up to 18 beats "off" the true LTV ticker rate!

Overall, the Glasgow-Galway investigation revealed that athletes would have to make large improvements in LTV before the change could confidently be ascribed to be outside natural day-to-day variability in measured LTV. For example, a member of the higher-fitness group would have to boost (or decrease) LTV by 1.62 kilometers per hour (27 meters per minute!) in order to be certain that a change in fitness status had actually been achieved! For example, an endurance runner with an established LTV of 16 km/hour would have to achieve a new reading of 17.62 km/hour to be confident that his/her LTV had really improved. This is in effect a change in lactate-threshold tempo from 6:03 per mile to 5:30 per mile, a 33-second per mile advance! This is a huge alteration, especially when one considers that most cross-country and distance runners do not hope for more than a 16-second per mile improvement in race pace over the course of a three-month season. As the researchers calmly pointed out, "These figures cast doubt on the sensitivity of the blood lactate test to a change of fitness in this population."

In addition, things get even shakier when one realizes that an original estimate for LTV determined in the laboratory for an athlete might be far off true LTV. Take an athlete with a true LTV of 16 km/hour, for example. He/she may visit the lab and come home with an LTV determination 17 km/hour, instead of 16, because of the natural variation we have been talking about. Then the athlete might work very hard for eight weeks, undergo a re-test, and find that measured LTV has moved up to 18 km/hour. Since it is a move of only one km/hour, the athlete believes it is simply a reflection of natural variation in LTV, even though in this case it is a real improvement.

As mentioned, heart rate at LTV was also not highly reproducible. Unfortunately, the story for RPE (rating of perceived effort) was not much better. In the Glasgow research, RPE at LTV was found to average 14.1, while RPE at a blood-lactate level of 4 mmol/Liter (a blood-lactate concentration which is often recommended for "lactate-threshold-improvement" training) settled at 17.2 (out of a max score of 20). However, there was again a rather grandiose variability, suggesting that the use of RPE to prescribe workout intensity would be unwise. Overall, an athlete would have to lower RPE at a specific LTV by about three Borg-scale units (!) in order to assume that a real change in LTV had taken place. As the researchers pointed out, "This wide range highlights that the use of RPE to prescribe intensity at (lactate-threshold velocity) has severe limitations."

The "RPE story" is very interesting in its own right. Like lactate, RPE varies according to emotional state and diet (high-carbohydrate diets tend to produce lower RPE scores, for example, while high-fat eating shoots RPE upward). Interestingly, gender appears to have no significant, repeatable effect on RPE, but RPE is influenced by the interaction between the gender of the athlete and the sex of the experimenter; this is why female scientists or lab assistants almost always take RPEs from female athletes, while male whitecoats jot down the RPEs of male exercisers. In addition, RPE seems to depend to some extent on personality type: Extroverts, for example, generally have lower RPEs during strenuous exercise, compared with introverts (the theory underlying this phenomenon is that introverts are bothered to a greater extent by sensory information flowing into their central nervous systems, including the sensations associated with strenuous exercise).

One caveat is in order: Although blood-lactate tests do not appear to be sensitive indicators of changes in fitness, remember that the Glasgow-Galway research did find an apparent link between LTV reproducibility and high fitness. Thus, truly elite athletes may have fairly low natural variations in LTV, and consequently their blood-lactate tests might have greater power. Further research will have to establish this, however; we can not merely assume that it is the case.

One key addendum to our story is in order, too. As we have mentioned, vaunted Viking exercise physiologist Bertil Sjodin (and his not-too-shabby colleagues, Ira Jacobs and Jan Svedenhag) published a paper in 1982 which revealed improvements in lactate-threshold running speed of about .72 km/hour in eight well-trained runners over a 14-week period (1). The average age of these runners was 20, and mean slow-twitch muscle-fiber composition was 62%. A key feature of the training carried out during the 14-week period was a weekly, continuous, 20-minute tempo run at the approximated lactate-threshold running velocity; aside from this tempo session, the athletes trained in their usual ways.

VO2max failed to move upward during the 14 weeks of training, but average velocity at lactate threshold seemed to improve from 4.69 meters per second (16.88 km/hour) to 4.89 meters per second (17.60 km/hr), a change which was described by the Swedes as being statistically significant. However, no control subjects were involved in the study; the athletes' LTVs after 14 weeks were simply compared with their own LTVs prior to the 14 weeks of training (a risky thing to do, given the wide, natural, individual swings in LTV, i. e., the non-reproducibility of LTV, reported by the Glasgow scientists). Overall, not one of the eight runners in Bertil's baby notched up an LTV upgrade as great as 1.6 km/hour; the greatest increase reported was in fact 1.29, and this was exceptional - one of the athletes experienced a small dip in LTV, and two others nudged upward by only .37 km/hr or so. In addition, student's t-test for paired observations was used to determine the statistical significance of the LTV differences, even though such tests provide no indication of random variation between tests (5).

Despite these many problems, Bertil's work has become the foundation of much current training which is directed toward the goal of improving lactate-threshold speed. Shortly after the publication of the Swedish investigation, coaches and endurance athletes "seized on" the study, citing it as validation of the notion that "tempo training" - exercising for about 20 minutes or so at lactate-threshold speed - represents the optimal way to hearten LTV. As a result, the typical modern-runner's training schedule often revolves around a near-weekly tempo run, which is a carry-over from Bertil's "big bang" from 1982. Given the shaky statistics and more recent evidence that higher-intensity efforts may be more potent than at-LTV exertions for boosting LTV (6), such reverence for tempo workouts may well be sub-optimal.

Our additional bottom line is that lactate monitors can not be recommended as effective tools for the monitoring of changes of fitness. This does not mean that lactate-threshold-style training is out, however; it simply means that - because of a lack of reproducibility of LTV - changes in lactate readings picked up by the monitors must be so large to be considered "real" that an athlete would already know that he was in much better/worse shape without piercing his skin and taking a lactate measurement. Other tests of fitness (sprints, hopping tests, six-minute efforts, etc.) may work better than lactate inspections, although these alternatives will also have to undergo the same scrutiny which has now been placed on lactate monitoring. For now, the best fitness exam any athlete can hope for is a fixed-distance (or fixed-time) maximal effort during training - or an actual competition.

		  
References

(1) European Journal of Applied Physiology, Vol. 49, pp. 45-57, 1982
(2) International Journal of Sports Medicine, Vol. 11, pp. 26-32, 1990
(3) International Journal of Sports Medicine, Vol. 12, pp. 363-368, 1991
(4) Sports Medicine, Vol. 26, pp. 217-238, 1998
(5) European Journal of Applied Physiology, Vol. 87, pp. 159-166, 2002
(6) Lactate Lift-Off.  (1998). Lansing: SSS Publishing Inc.