Running Science

by Owen Anderson

  At the end of the experimental period, endurance time during a challenging incremental test was 29 percent longer in the trained leg compared with the control, and MCT1 levels in the trained thigh had shot up by 15 percent. Interestingly enough, the amount of lactate removed from the blood during the demanding incremental test was 63 millimoles per liter (1.1 gm/dl) for the trained leg versus just 16 millimoles (288 mg/dl) in the untrained leg with poorer MCT1. Only about 29 percent of this difference could be accounted for by the longer time to exhaustion in the trained leg, indicating that a probable reason for the enhanced endurance in the trained leg was its increased ability to use lactate for fuel. Supporting this assumption, the trained thigh had lower levels of intramuscular lactate at the exhaustion point even though it had removed much more lactate from the blood compared with the untrained leg.

  An earlier investigation, also carried out at the Copenhagen Muscle Research Centre and the August Krogh Institute, revealed that 8 weeks of intense cycling workouts boosted MCT1 concentrations by 76 percent.17 In this study, the intense training consisted of interval workouts with three to five sets of (2 × 30 seconds and 3 × 60 seconds), with top-of-the-line intensities and 2-minute recoveries. No other training was completed during the 8-week period.

  Taken together, the available research strongly supports the notion that intense training is best for boosting MCT1 content and the rates of lactate uptake and use—and thus greater resistance to fatigue during hard exercise and a higher running velocity at lactate threshold. It is logical that this would be the case. The most potent stimulus for increasing MCT1 levels may be high blood and muscle lactate levels just as the best stimulus for improving O2max may involve pushing the oxygen envelope by training at high speeds that evoke high rates of oxygen consumption. Of course, you can’t have consistently high lactate levels if you carry out the bulk of your training at a speed that is below your running velocity at lactate threshold. It is doubtful that carrying out the majority of your training at intensities associated with low lactate levels will stimulate your muscles to suddenly embark on a frenzied MCT1 construction project.

  In one study, a runner who trained from 90 to 120 minutes each day at an intensity below lactate threshold developed a decent aerobic capacity (i.e., O2max), but his MCT1 content and lactate-transport capacity were poor, and thus his resistance to fatigue during high-quality running was inferior to that of athletes who trained in higher-quality ways.3

  In another important study, the highest lactate-transport capacity was found in an Olympic medal winner, who carried out the greatest amount of training at high intensities.18 The researchers in this investigation concluded that “a large volume of training is not sufficient to improve the ability to transport lactate” and that “regular high-intensity sessions must be included.” A corollary research project with laboratory rats revealed that training at about 50 percent of O2max had no effect on lactate-transport capacity; however, working at 90 percent of O2max lifted lactate transport by 58 percent, and training at an intensity of 112 percent of O2max caused lactate-transport ability to soar by 76 percent.19

  vO2max Training

  Science has shown that vO2max training—carrying out work intervals at the intensity of vO2max itself—is great for optimizing running velocity at lactate threshold. This may seem a bit confusing. After all, isn’t vO2max training designed to enhance vO2max but not running velocity at lactate threshold? How can one form of training accomplish both things simultaneously?

  To answer these questions, one need only look at the research carried out by Veronique Billat and her colleagues at the University of Lille, the Center of Sport Medicine, and the National Center of Health in France. Billat and her co-workers asked a group of experienced runners to take part in 4 weeks of training that included one interval session at vO2max each week. The athletes were specialists in middle- and long-distance running (1,500 meters to half marathon), their mean age was 24, and their average O2max was a very good 71.2 ml • kg-1 • min-1.20

  After just 4 weeks of training with four total vO2max workouts, vO2max was up by 3 percent from 20.5 kilometers (12.7 mi) per hour to 21.1 kilometers (13.1) per hour (i.e., from about 4:43 per mile to 4:34 per mile). In addition, running economy improved by an astounding 6 percent, and heart rates at typical training speeds dipped by 4 percent. Running velocity at lactate threshold also increased by about 3 percent! (See chapters 9 and 26 for additional details.) The reason for this is most likely that the high vO2max training intensity stimulated an increased capacity of lactate oxidation in the muscles and—by promoting high blood lactate levels—forced muscles to maximize their MCT1 concentrations.

  Sprint Training

  Traditionally, runners have used sprint work to heighten maximal running speed. What many runners don’t know is that sprint training can also help optimize running velocity at lactate threshold. Researchers from Imperial College in London, Deakin University, the University of New South Wales, and Queensland University worked with seven endurance-trained runners.21 This septet was reasonably fit (O2max = 58 ml • kg-1 • min-1), and their average age was 27.7 years; the seven athletes had no history of prior sprint training.

  The subjects performed three sessions per week of sprint training for 6 weeks. Each workout involved four sets of nearly maximal sprints that were 40 to 100 meters in length. The total number of sprints per session increased from 14 during the first week of training to 30 reps during the sixth week, and the lengths of the reps also expanded from an initial range of 40 to 80 meters during the first week to 80 to 100 meters during the sixth week. To make matters even tougher, recovery times between sprints were gradually tightened: The work-to-rest ratio started at 1:5 during week one but gradually evolved to 1:3 during the final week; recovery between sets of sprints held fast at 5 minutes across the 42 days. In addition to the sprint training, the seven athletes also logged about 50K per week of moderate running at below running velocity at lactate threshold.

  To get a feeling for how the sprint sessions developed over time, Session 1, the first sprint workout carried out in the first week of the study, included four sets:

  4 × 40 meters

  4 × 50 meters

  4 × 60 meters

  2 × 80 meters

  Each rep in the four sets was carried out at 90 percent of maximal effort. For this inaugural sprint session, the work-to-recovery ratio was 1:5; between reps were 5 seconds of recovery for each second of sprinting, and total rest between each set was 5 minutes.

  In contrast, Session 18, the final sprint workout of the sixth week, included these sets:

  8 × 100 meters

  6 × 100 meters

  8 × 80 meters

  6 × 80 meters

  These 28 reps were all struck at 90 to 100 percent of maximal effort with a work-to-recovery ratio of only 1:3, but there were still 5-minute recoveries between sets. From sprint session 1 to 18, the number of reps had risen from 14 to 28, and the total sprinting distance had increased from 760 to 2,520 meters (.5-1.6 mi).

  The Australian and English researchers involved in this study had asked the seven endurance runners to run as far as possible at an intensity of 110 percent of vO2max before and after the 6 weeks of sprint training. Prior to the 6-week period, the runners were able to hang in there at that intensity for a total of 140 seconds before complete exhaustion set in; they covered 745 meters (.46 mi) during this 140 seconds of red-hot running. In contrast, after the sprint training, even though the longest sprint-training rep was just 100 meters, the runners kept going for 157.7 seconds at 110 percent of vO2max, an 11 percent upgrade, and also covered 838 meters (.52 mi), another 11 percent increase, before falling prostrate on the ground.

  In addition to focusing on performance times, the investigators were also quite interested in MCT1. In this study, MCT1 levels in muscles increased by about 50 percent after the 6 weeks of sprint training, an effect that should significantly boost running velocity at lactate threshold.

>   Other Training Methods

  In addition to vO2max and sprint training, other high-quality sessions (defined as being above running velocity at lactate threshold) should also improve running velocity at lactate threshold. Circuit training has been linked with lactate-threshold improvements, probably because of the high oxygen-consumption rates and lactate outputs that can be achieved during such training.22 Similarly, lactate-stacker sessions, in which a runner alternates 1-minute intervals at faster than vO2max with 2-minute jog recoveries, should be excellent for upgrading both lactate-oxidation rates and MCT1 concentrations—and thus running velocity at lactate threshold. In addition, superset training, in which a runner takes no recovery between high-speed intervals with the first interval being faster than the second, should also bolster running velocity at lactate threshold. In fact, there are an almost infinite number of workouts that would have a positive effect on running velocity at lactate threshold. The key is that sessions to enhance this variable should be conducted at speeds faster than running velocity at lactate threshold. This means that workouts carried out at 10K pace, 5K pace, 3200-meter speed, 3K tempo, mile pace, 1500-meter velocity, and 800-meter should all be productive from the standpoint of increasing running velocity at lactate threshold.

  Lactate Monitors

  If training is going well, running velocity at lactate threshold should continue to move upward, and performances should also get better, but how can it be determined if running velocity at lactate threshold is really advancing? Some runners are tempted to use lactate monitors. Many fairly inexpensive, portable devices have proven to be remarkably accurate. That is, at any specific point in time, one of these devices will produce a reading for blood lactate that is remarkably close to the true lactate level in the person’s blood. This accuracy has excited many coaches and runners. After all, they have reasoned, with just a few finger sticks they can tell very reliably which way running velocity at lactate threshold is heading.

  Indeed, validations of certain kinds of training to increase lactate threshold have depended on measured changes in lactate readings. For example, Sjödin’s research in the early 1980s (see the Tempo Training section earlier in this chapter) used this sort of lactate reading. However, there is a key element missing in such a conclusion and in current beliefs about lactate training and the use of lactate monitors. The missing element is the reproducibility of blood lactate levels. In other words, for lactate monitors to work, blood lactate concentrations need to remain the same at a specific exercise intensity unless an athlete has achieved a real change in fitness. If blood lactate levels vary to a great extent in individual athletes as a result of factors unrelated to fitness, 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 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 blood lactate concentrations more modest. In addition, increased states of tension or anxiety can lead to augmented blood lactate levels, while calmer psychological conditions tend to keep lactate levels at more minimal readings. Mild states of dehydration can make lactate levels appear to be higher than they really are compared with levels in a well-hydrated state. Finally, even time of day can have an effect on lactate concentrations since blood lactate follows a circadian rhythm.

  Due to all of these influences, a runner whose running velocity at lactate threshold is measured at 4.47 meters per second (6:00 per mile) does not know if the speed at which lactate begins cresting is determined completely by fitness. How much depends on other factors, such as the small measurement errors of the lactate monitor and the potentially big skews associated with nutritional, hydration, and psychological status? And if running velocity at lactate threshold is measured again after 4 weeks or so and is 4.60 meters per second (5:50 per mile), is that a real change in running velocity at lactate threshold? Or does it simply reflect the natural variation that is produced by factors not related to fitness?

  For these reasons, lactate monitors cannot be recommended as effective tools for monitoring changes in running velocity at lactate threshold. Because readings can’t usually be reproduced for running velocity at lactate threshold, 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 or she was in much better or worse shape—thanks to perceived exertion during intense runs—without piercing a digit to take a lactate measurement.

  Some studies have suggested that lactate readings are reasonably reproducible,23, 24 but these investigations have been characterized by deep flaws in their statistical analyses.25 As a result, 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 running velocity at lactate threshold changes from 17 kilometers (10.6 mi) per hour to 17.75 kilometers (11.03 mi) per hour, for example, can we trust it? If running velocity at lactate threshold falls from 17 to 16.5 kilometers (10.6-10.3 mi) per hour, should we be perturbed—or should we acknowledge that this drop-off may simply be part of the natural variation in measured running velocity at lactate threshold? These questions are key, and the coach or athlete who ignores them while employing lactate-measuring devices is proceeding in an illogical manner.

  Reproducibility of Lactate Levels

  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 studied 20 men and 16 women.26 All the subjects were physically active, taking part in at least two aerobic dance, cross-country running, volleyball, soccer, or rugby workouts each week. These subjects completed two treadmill lactate-profile tests; almost all the tests were completed 1 week apart and at approximately the same time of day.

  Running velocity at lactate threshold was determined for each athlete on those two occasions. The heart rate and perceived effort (using Borg’s 6-20 category scale) associated with running velocity at lactate threshold were also measured. To determine whether fitness level has an impact on running velocity at lactate threshold reproducibility, the subjects were divided into two groups: those with a running velocity at lactate threshold equal to or greater than 10.5 kilometers (6.5 mi) per hour (the moderate-fitness group), or a pace of about 9:12 per mile, and those with a running velocity at lactate threshold slower than 10.5 kilometers (6.5 mi) per hour (the lower-fitness group).

  As it turned out, fitness and reproducibility were linked: The two running velocity at lactate threshold readings for the moderate-fitness group tended to be closer together than the two separate recordings for the lower-fitness group. This makes sense: As fitness levels increase, fitness should become a stronger factor with respect to running velocity at lactate threshold and should be less likely to be swamped by vicissitudes in other variables.

  The sex of the runner did not have a significant effect on the reproducibility of running velocity at lactate threshold. However, the Glasgow-Galway research revealed that it is natural for running velocity at lactate threshold to vary in an athlete by more than 1 kilometer (.62 mi) per hour in either direction. For example, if true running velocity at lactate threshold was initially measured in the laboratory at 15 kilometers (9.3 mi) per hour, future readings of 14 or 16 kilometers (8.7 or 9.9 mi) per hour would be reasonably interpreted as normal variations around the average running velocity at lactate threshold rather than as significantly different speeds associated with lactate threshold. 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 running velocity at lactate threshold exhibited a rather large natural variation. In fact, the research suggested that athletes should expect the heart rate associated with a specific running velocity at lactate threshold 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 enhancing running velocity at lactate threshold. In fact, it would not be unreasonable to expect that the heart rate an athlete had tied to running velocity at lactate threshold might be up to 18 beats off the true rate!

  Overall, the Glasgow-Galway investigation revealed that athletes would have to make large improvements in running velocity at lactate threshold before the change could confidently be ascribed to be outside natural variability in measured running velocity at lactate threshold. For example, a member of the moderate-fitness group would have to boost or decrease running velocity at lactate threshold by 1.62 kilometers (1.01 mi) per hour (27 meters per minute) in order to be certain that a change in fitness status had actually been achieved! As an example, an endurance runner with an established running velocity at lactate threshold of 16 kilometers (9.94 mi) per hour would have to achieve a new reading of 17.62 kilometers (10.95 mi) per hour to be confident that his or her running velocity at lactate threshold had really improved. This is in effect a change in tempo at lactate threshold from 6:03 per mile to 5:30 per mile, a 33-second per mile improvement! This is a huge alteration, especially when considering 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.”