Lactate level readers are great little gadgets – but don’t rely on them to reflect changes in fitness. Whether you are a cyclist, rower, runner, cross-country skier, swimmer, or triathlete, your lactate-threshold velocity (LTV) – the speed at which blood lactate concentrations begin to increase fairly dramatically – is a great predictor of your performance capacity. Lactate is a tremendously important muscle fuel during sustained activity, and if it begins piling up in the blood at fairly low speeds the muscles must have a poor capacity for utilising 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 individual must have a great capacity to use lactate for fuel, and so performances will be higher in quality and fatigue will occur later. Naturally, then, 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 be consequently enhanced. But how can one determine if lactate-threshold velocity really is improving? Enter the lactate monitors: fairly inexpensive little devices like the LactatePro have been shown to be remarkably accurate in that, at any specific point in time, they can produce a reading for blood lactate which is remarkably close to the true lactate level in your blood. The idea that a little ‘finger stick’ can show which way LTV is heading has proved very exciting to many coaches and athletes. They reasoned that once lactate-threshold velocity was established for an athlete, he/she could carry out workouts at that intensity every 2-4 weeks to see if the readings changed; if lactate levels were down at the established lactate-threshold speed, then training must be going well and vice versa. Validations of certain kinds of ‘lactate-threshold training’ have depended on such changes in lactate readings. For example, in the early 1980s renowned Swedish exercise physiologist Bertil Sjodin uncovered a 0.72 k/hour ‘increase’ in LTV in the athletes he was studying over a 14-week period and concluded that their training was particularly beneficial for lactate-threshold speed development.

However, a key element in such a conclusion – and in current beliefs about lactate training and the use of lactate monitors – is the assumption that lactate levels are highly reproducible. What if they are not? The lactate levels in an athlete’s blood at any specific moment in time during exercise are undoubtedly a function of the intensity and duration of that exercise. However, lactate is also sensitive to a variety of other factors, including nutritional and psychological status. For example, consuming a high-carbohydrate meal during the hours leading up to a workout can drive up blood lactate levels during exercise, while a fattier diet can reduce them. Similarly, states of tension and/or anxiety can lead to augmented blood lactate levels, while calmer states tend to keep them down. Mild states of dehydration can make lactate levels appear higher than they really are and even the time of day can be a factor, since blood lactate follows a circadian rhythm.

Is the change real or illusory?

The problem, then, is a basic one: if you are a cyclist, for example, and your LTV is measured at 35k/hour, is that speed 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 cycling speed, and the potentially big ‘skews’ associated with nutritional, hydration, and psychological status)? And, when you re-measure your LTV and find that it is 36k/hour, is that a real change or simply a reflection of a variation in factors unrelated to fitness? Until now, we haven’t really been sure. Previous studies have suggested that lactate readings are reasonably reproducible, but these have also been characterised by flaws in the statistical analyses. As athletes and coaches, this 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 change in fitness. If a measured lactate-threshold running speed changes from 17 to 17.75 k/hour, for example, can we trust it? If LTV falls from 17 to 16.5 k/hour, should we be perturbed? 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 University of Glasgow and the National University of Ireland, in Galway, recently studied 20 men and 16 women, all of whom were taking part in at least two sessions of aerobic dance, cross-country running, volleyball, football or rugby each week. The subjects completed two treadmill lactate-profile tests spaced one week apart and carried out at the same time of day to remove circadian rhythms as a variable. 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 each occasion, and 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 10.5k per hour (the moderate-fitness group) and those with a slower LTV (the low-fitness group).

As it turned out, fitness and reproducibility were linked; the two lactate readings for the moderate-fitness-group members tended to be closer together than those of the low-fitness group. This makes sense: as fitness levels increase, fitness should become a stronger determinant of LTV and less liable to be ‘swamped’ by changes 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 by more than one kilometre per hour in either direction. In other words, if LTV was initially measured in the laboratory at 15 k/hour, future readings of either 16 or 14 k/hour could be reasonably interpreted as normal variations rather than significant changes. Heart rate at LTV also exhibited a rather large natural variation, varying by up to 12-18 beats per minute from one day to the next! This wide variability presents problems for those who believe they have identified a ‘lactate-threshold heart rate’ and are carrying out training at this specific rate in the belief that it will enhance LTV. In fact, it would not be unreasonable to expect that the heart rate ‘tied’ to LTV might be up to 18 beats ‘off’ the true LTV ticker rate.

Lactate test lacks sensitivity

Overall, the Glasgow-Galway investigation revealed that athletes would have to make large improvements in LTV before the change could confidently be ascribed to their training rather than extraneous factors. For example, a member of the higher-fitness group would have to boost (or decrease) LTV by as much as 1.62k per hour (27m per minute!) to be certain that a change in fitness status had actually been achieved! In the case of an endurance runner with an established LTV of 16 k/hour, this would mean an increase to 17.62 k/hour. 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 change, which is obviously huge, especially given that most cross-country runners do not hope for more than a 16-second per mile improvement in race pace over the course of a 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’. Things get even shakier when you realise that an original estimate for LTV determined in the laboratory might be far from the true reading. Take an athlete with a true LTV of 16k/hour, for example: he/she visits the lab and comes home with a determination of LTV at 17 k/hour because of the natural variation we have been talking about; the athlete works very hard for eight weeks, re-tests, and finds that measured LTV has moved up to 18k/hour. Since this is a small change, the athlete believes it simply reflects natural variation, even though in this case it is a real improvement. One can get around this problem to some extent by taking three different LTV readings over a relatively short period of time and then averaging the three data points to reach a ‘ballpark’ figure. As you can see, although the lactate monitors are precise at any one moment in time, the interpretation of their readings is far from straightforward. As mentioned, heart rate at LTV was also not highly reproducible in the study, and the story for RPE (rating of perceived effort) was not much better. RPE at LTV was found to average 14.1 (out of a max score of 20), while RPE at a blood lactate level of 4mmol/litre – which is often recommended for ‘lactate-threshold improvement’ training – settled at 17.2. However, there was a large degree of variability between subjects, 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 be sure 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’. RPE is an interesting story in its own right: like lactate, it varies according to emotional state and diet (high-carbohydrate diets tending to produce lower RPE scores). Interestingly, gender appears to have no significant repeatable effect on RPE, but it is influenced by the interaction between the gender of the athlete and the gender of the experimenter; this is why scientists or lab assistants almost always take RPEs from athletes of the same sex. In addition, RPE seems to be influenced by personality type, with extroverts, for example, tending to have lower RPEs than introverts.

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 élite 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 the truth of the proposition, however, and we cannot merely assume it. The bottom line, unfortunately, is that lactate monitors cannot be recommended as effective tools for monitoring changes in fitness. This does not mean that lactate-threshold-style training is out; it simply means that changes in lactate readings picked up by the monitors must be so large to be considered ‘real’ that an athlete could not fail to be aware that he was in much better/worse shape than before (without piercing his skin and taking a lactate measurement). Other tests of fitness (sprints, hopping tests, six-minute efforts etc) may work better, although some of these alternatives will also have to undergo the same scrutiny as lactate monitoring. For now, the best fitness exam any athlete has is a fixed-distance (or fixed-time) maximal effort during training – or an actual competition.

Owen Anderson