Running Science

by Owen Anderson

  Poor Ways to Boost Running Velocity at Lactate Threshold

  Endurance runners and their coaches have been interested in running velocity at lactate threshold since about 1980 when the lactate-threshold concept was first developed by exercise scientists. Over the last 33 years, two popular training techniques have been favored by the majority of runners to advance running velocity at lactate threshold: prolonged moderate exercise and tempo training. Prolonged moderate exercise involves doing a lot of running at submaximal speeds that are actually slower than running velocity at lactate threshold. Tempo training, on the other hand, consists of running steadily for 20 to 30 minutes at a pace that is as close to running velocity at lactate threshold as possible. Both of these techniques have proved to be poor ways to boost this variable.

  Prolonged Moderate Exercise

  Runners and other endurance athletes have traditionally believed that prolonged moderate exercise represents the ultimate way to increase running velocity at lactate threshold. From one perspective, that is somewhat logical thinking. After all, extended, medium-intensity exertions tend to increase the muscles’ abilities to metabolize fat during exercise. If muscle fibers rely more heavily on fat and therefore less heavily on carbohydrate for fuel, less lactate will be produced because lactate is generated primarily from carbohydrate breakdown, not from fat degradation. Thus, at least in theory, less lactate spilling should take place, and running velocity at lactate threshold should not be reached until a relatively high speed is attained.

  There are many problems with this approach, however. As a practical point, moderate training speeds are dissimilar from actual racing speeds from the standpoint of neuromuscular control of gait; therefore, it is difficult for the moderate-intensity runner to develop good economy at race velocities since those higher speeds are deemphasized during training. Moderately paced training is not very specific to racing, and the medium-intensity runner faces a difficult task in developing optimal neuromuscular coordination patterns for high-speed racing.

  In addition, even when an athlete develops a great fat-burning capacity, that capability is seldom used in high-intensity racing situations. One problem is that fat becomes an increasingly minor source of energy at intensities above running velocity at lactate threshold.5 Since most runners reach running velocity at lactate threshold at about 10-mile (16 km) race speed, all shorter distances will be raced at intensities above that threshold.6 This means that fat metabolism is fairly unimportant at race distances of 10 miles (16 km) or less, even in those athletes who have built up prodigious fat-burning furnaces. Thus, the huge training investment in long, moderately paced miles rarely attenuates lactate production above running velocity at lactate threshold since fat can’t replace carbohydrate at those intensities. In fact, high-volume, medium-intensity training may actually increase lactate levels above running velocity at lactate threshold because the muscles of athletes who train in that way are unschooled at clearing and processing lactate and tend to work uneconomically at tempos beyond this threshold.

  If you are a marathon runner, is the situation different? If you simply jog your marathons, moving along easily without stocking up on leg-muscle glycogen before the race and without consuming sports drinks during the event, then fat oxidation will be important, and the high-volume, moderate-intensity training will help raise your fat-oxidation capacity. But, if you are trying to run as fast as you can in the marathon, loading glycogen before the competition and quaffing sports drinks during the event, the marathon itself becomes a carb race; research suggests that up to 80 to 90 percent of the energy needed to run the 26.2 miles (42.2 km) comes from carbohydrate.7 Thus, the high-volume, moderate-intensity training designed to optimize fat oxidation becomes much less useful.

  Tempo Training

  Swedish exercise physiologist Bertil Sjödin and his colleagues Ira Jacobs and Jan Svedenhag published a paper in 1982 that revealed improvements in running velocity at lactate threshold of about .72 kilometers (.45 mi) per hour in eight well-trained runners over a 14-week period.8 The average age of these runners was 20, and mean slow-twitch muscle-fiber composition was 62 percent. A key feature of the training was a weekly continuous 20-minute tempo run at the approximated running velocity at lactate threshold; aside from this tempo session, the athletes trained in their usual ways.

  O2max 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/hr [10.49 mi/hr]) to 4.89 meters per second (17.60 km/hr [10.94 mi/hr]), a change described by the Swedes as being statistically significant. However, no control subjects were involved in the study; the athletes’ running velocities at lactate thresholds after 14 weeks were simply compared with their own results prior to the 14 weeks of training. (This was a risky thing to do given the naturally wide, individual swings in this variable as illustrated by its nonreproducibility in scientific studies.) Overall, not one of the eight runners in Sjödin’s research notched an upgrade to running velocity at lactate threshold as great as 1.6 kilometers per hour (.99 mi/hr); the greatest increase reported was in fact 1.29 kilometers per hour (.80 mi/hr), and this was exceptional. One of the athletes experienced a small dip in running velocity at lactate threshold, and two others nudged this variable upward by only .37 kilometers per hour (.23 mi/hr) or so. In addition, student’s t-test (a method of statistical analysis) for paired observations was used to determine the statistical significance of the differences even though such tests provide no indication of random variation between tests.9

  Despite these many problems, Sjödin’s work has become the foundation of much current training directed toward the goal of improving running velocity at lactate threshold. 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 running velocity at lactate threshold—represents the optimal way to increase running velocity at lactate threshold. As a result, the typical modern runner’s training schedule often revolves around a near-weekly tempo run, which is a carryover from Sjödin’s 1982 big-bang announcement. Given the shaky statistics and more recent evidence that higher-intensity efforts are more potent than exertions at running velocity at lactate threshold for boosting this variable, such reverence for tempo workouts is likely to be suboptimal.

  Effective Ways to Boost Running Velocity at Lactate Threshold

  Recent research has disclosed that there are three key ways to upgrade running velocity at lactate threshold: intense training, vO2max training, and sprint training for endurance runners. In addition, several other training modalities, including circuit training, lactate-stacker sessions, super sets, and even running intervals at 5K speed have a positive impact on this variable. All of these training methods are described in the upcoming sections.

  Intense Training

  Scientific research actually reveals that fairly intense training, not high-volume work at moderate intensities, is the best booster of running velocity at lactate threshold.10 In a study carried out at the University of North Carolina at Greensboro, runners who suddenly raised their average training intensity by completing two fartlek sessions and one interval workout per week boosted running velocity at lactate threshold significantly in just 8 weeks and as a result shaved more than a minute from their average 10K times. The fartlek work involved 2- to 5-minute bursts at 10K pace, which is about 2 to 3 percent faster than running velocity at lactate threshold; the intervals were completed at about 5K speed, which can be around 5 to 6 percent quicker than running velocity at lactate threshold.11

  The idea that intense workouts are best for raising running velocity at lactate threshold was reinforced in research carried out at York University by Stephen Keith and Ira Jacobs.12 In the York investigations, one group of athletes trained exactly at lactate-threshold intensity for 30 minutes per workout. Training at lactate threshold (tempo training as noted earlier)
is perhaps the most popular modality used by runners in their attempts to advance running velocity at lactate threshold. A second group of exercisers divided their 30-minute workouts into four intervals, each of which lasted for 7.5 minutes. Two of the intervals were completed at an intensity above lactate threshold, while the other two were carried out below threshold. Each group of athletes worked out four times per each of the 8 weeks of the study.

  In the second group, the below-threshold exertions, which were used for two of the four 7.5-minute intervals per workout, corresponded with an intensity of about 60 to 73 percent of O2max. The above-threshold intensity, also employed for two 7.5-minute intervals per workout, was set at about 30 percent of the difference between lactate threshold and actual O2max. Thirty percent of the threshold-O2max difference would usually represent an intensity of up to 87 percent of O2max, or about 88 to 93 percent of maximal heart rate. In terms of actual running velocity, it would correspond with a running speed that is almost exactly the same as 10K pace.

  After 8 weeks of training, the two sets of athletes had achieved similar increases in O2max and lactate threshold. The gains in threshold were impressive, averaging 14 percent in both groups. Advances in aerobic enzymes were also notable and nearly identical in the two groups of athletes. In an endurance test in which group members exercised for as long as possible at an intensity corresponding to their pretraining lactate threshold, the above-threshold athletes seemed to hold an edge, sustaining their exercise for a total of 71 minutes, while the at-threshold subjects lasted for 64 minutes.

  At first glance, these results seem to suggest that there is not a huge advantage to be gained by surging through highly demanding workouts above lactate threshold. Note, however, that the above-threshold athletes really logged only 60 minutes of quality work per week (4 × 15 minutes per exertion), while the at-threshold subjects put in 120 weekly minutes of quality effort (4 × 30 minutes). The above-threshold athletes achieved the same gains in lactate threshold and O2max—and perhaps enjoyed a slight advantage in endurance—as the at-threshold individuals, with only half the total quality-training time. It is reasonable to assume that had the above-threshold athletes stepped up their volume of above-threshold work just a little bit, they would have outdistanced the at-threshold subjects.

  Why does moving above running velocity at lactate threshold during training seem to be so effective at lifting this variable? Three primary reasons are responsible for the changes: muscles improve their ability to use lactate and pyruvate, aerobic enzyme production increases, and the amount of MCT1 increases.

  Teaching Muscles to Use Lactate and Pyruvate

  For one thing, work done at faster than running velocity at lactate threshold seems to be particularly important for improving the lactate profiles of fast-twitch muscle fibers. In research carried out at the University of Missouri, several groups of rats hustled along on laboratory treadmills at a variety of different paces ranging from 15 to 37 meters per minute (43-100 min/mi). The faster velocities—by rat standards—that averaged 30 meters per minute and above produced flood tides of lactate in the rodents’ bloodstreams, as expected, but the researchers also noticed something very interesting. High lactate levels were linked with glycogen depletion of the rats’ fast-twitch muscle fibers, not their slow-twitch cells. In other words, fast-twitch fibers were primarily responsible for the huge upswing in blood lactate.13

  Of course, fast-twitch fibers are not heavily used during moderately paced exertions but play a larger role as movement speeds increase beyond running velocity at lactate threshold. Compared to slow-twitch cells, fast-twitch fibers are ordinarily somewhat low on mitochondria and aerobic enzymes, and so it is logical that they would release relatively large quantities of lactate into the blood during intense running. If the fast-twitch fibers are poor at oxidizing pyruvate, a closely related chemical precursor to lactate, massive amounts of lactate will be produced, and running velocity at lactate threshold will be reached at a very mediocre pace. As the fast-twitch fibers get better at breaking down pyruvate, less lactate will be produced, and running velocity at lactate threshold will increase. There is only one way to stimulate the fast-twitchers to get better: Use them during training, specifically at tough, fast paces. To put it another way, fast-twitch muscle cells can be the culprits underlying a poor running velocity at lactate threshold, and the only way to upgrade their lactate-processing machinery is to engage them and force them to adapt with aerobic enzyme and mitochondrial production.

  What if your muscle fibers are primarily slow-twitch? The key problem associated with a low running velocity at lactate threshold is that a low level of this variable is a symptom of a poor lactate-processing capability. From the standpoint of creating energy for faster running, it’s suboptimal when lactate is drifting around in the blood, unused, and it’s good if the lactate is being broken down at high rates inside muscles and also being pulled into muscles at high rates so that it can be metabolized. Thus, the key problem with a low running velocity at lactate threshold is the inability of muscle cells to create the energy they need by clearing lactate and breaking it down. The only way to teach muscle cells to handle lactate and pyruvate quickly is to expose them to higher concentrations of the two compounds, and that means fast-paced training whether leg-muscle cells are primarily fast-twitch or slow-twitch.

  Increasing Aerobic Enzyme Production

  Intense running has a dramatic impact on the production of the aerobic enzymes required to break down lactate as illustrated by research completed at the State University of New York at Syracuse.14 In this study, which was carried out over an 8-week period, the concentration of a key mitochondrial enzyme called cytochrome c increased by about 1 percent per minute of daily training as long as training intensity was set at 85 to 100 percent of O2max, or approximately 92 to 100 percent of maximal heart rate. This means that by carrying out 10 minutes of daily training within this intensity zone, subjects boosted cytochrome c by 10 percent after 8 weeks; with 27 minutes of daily training within the high-intensity zone, cytochrome c increased by 27 percent in 8 weeks. In contrast, working at a lower intensity of only 70 to 75 percent of O2max increased cytochrome c by only 18 percent. Since cytochrome c is a critically important oxidative enzyme found within the mitochondria, upswings in cytochrome c should be linked with improvements in running velocity at lactate threshold.

  In this study, the gains associated with faster training were even more impressive from the standpoint of the fast-twitch muscle fibers. Ten minutes of daily training at 100 percent of O2max roughly tripled cytochrome c concentrations within fast-twitch cells, while running 27 minutes per day at 85 percent of O2max increased cytochrome c by just 80 percent, and 90 daily minutes at 70 percent of O2max raised cytochrome c by just 74 percent. In other words, decreases in training intensity were linked with smaller aerobic enzyme adaptations even when the total volume of training was increased ninefold from 10 to 90 minutes per day.

  Increasing MCT1

  What kind of training is best for studding muscle and mitochondrial membranes with maximal outcroppings of MCT1? In research carried out by lactate expert Arend Bonen and his colleagues at the University of Waterloo in Ontario, Canada, laboratory rats were divided into two different groups, both of which trained for 3 weeks.15 One group exercised moderately, working at a pace of 21 meters per minute on a treadmill with an incline of 8 percent. The second group of rats trained more intensely at the relatively sizzling speed of 31 meters per minute and with a treadmill angle of 15 percent.

  After 3 weeks, the moderately trained rodents had failed to raise their leg-muscle concentrations of MCT1 at all! Not surprisingly, lactate-uptake rate was also no better than before the training began. In contrast, the more intensely trained rats had augmented MCT1 levels in key leg muscles by 70 to 94 percent and had boosted average lactate-uptake rate by around 80 percent!

  The more intense training also benefited the hearts of the exercising rats. After 3 weeks of moderate tr
aining, heart-muscle cells in the medium-intensity rodents did react by firing up MCT1 content by 36 percent; the rate at which the heart swallowed up blood lactate also increased after the moderate training. Once again, however, intense training provided the ticket for considerably stronger MCT1 improvement. Total heart MCT1 expanded by 44 percent in the intensely trained rats, and lactate-uptake rate increased by 173 percent!

  Separate research carried out by Carsten Juel and his colleagues at the Copenhagen Muscle Research Centre and the August Krogh Institute in Denmark reveals that intense exercise is a potent MCT1 booster.16 In this Danish study, six human male subjects performed vigorous one-leg knee-extensor training at a rate of 60 kicks per minute on an ergometer; the other leg served as a control. Each training session consisted of a 5-minute warm-up and then 15 1-minute work intervals at an incredible intensity of 150 percent of thigh O2max with 3-minute recoveries (if you are troubled by the phrase “thigh O2max,” remember that just as the whole body has a O2max, each appendage, region, and muscle within the body has its own unique O2max, too). This workout was completed three times a week for 2 weeks, four times a week for 2 more weeks, and then five times a week for 3 to 4 weeks. No other training was completed during the 7- to 8-week period.