What the latest research says about your lactate threshold and lactate training
When I wrote the book Lactate Lift-Off in 1998, research concerning lactate production and utilization during exercise was really beginning to take off in an exciting way. One of the key thrusts of the new research was that lactate threshold, i.e., the exercise intensity at which lactate begins to build up rather precipitously in the blood, is a function not just of lactate production by muscle cells (as we once tended to believe) but is also highly dependent on the ability of muscle cells to clear lactate from tissue spaces and blood plasma.
While that new 'thrust' may seem either pedestrian or esoteric, depending on your background and personality, it actually has exciting implications for training. Basically, it means that the endurance athlete should no longer attempt to optimize lactate threshold simply by developing rather stolid muscle cells which stubbornly stay away from the practice of producing significant quantities of lactate. Although that is not a bad idea, it is also necessary to train muscle fibres in the fine art of clearing lactate from interstitial fluids and the blood. To do that, it is essential to expose those fibres to rather lofty lactate levels. Tempo training, i.e., working continuously for 20 to 30 minutes at lactate-threshold intensity, won't do, since it takes place at the precise level of effort at which lactate production is JUST BEGINNING to take off. Instead, one must burn along at higher-than-lactate-threshold speeds during workouts in order to set a fire under the lactate-clearing process and lift lactate threshold as much as possible.
Since my fingers tapped the words of Lactate Lift-Off on to my PowerMac's hard drive, even more exciting research has been carried out in scientific laboratories around the world. Before we delve into that new research, though, let's spend a few moments reviewing some lactate basics, so that you'll be up to speed when we get to the new stuff.
Remember that for your muscles to contract and propel you forward as you move along, your muscles require energy (how's that for an easy opener?). One of the key energy-producing processes inside your muscle cells is called oxygen-independent glycolysis.
During oxygen-independent glycolysis (the word glycolysis literally means the 'breaking' of glucose), glucose molecules are broken down inside the muscle cells; for each molecule of glucose degraded, two molecules of lactic acid are produced (lactic acid consists of a proton and our good friend lactate). This breakdown of glucose to lactic acid produces a fair amount of energy for contractions, and no oxygen is needed or utilized in the process.
Fatigue and feedback
As is the case with most cellular processes, feedback mechanisms can come into play. Specifically, if large quantities of lactate build up within a muscle cell, glycolysis is inhibited and the muscle fibre fatigues (the fatigue is not caused by lactate ions, however, but by the protons associated with them).
This fatigue can be prevented in two ways. A muscle cell can funnel lactate into 'oxidative phosphorylation', an oxygen-dependent process which breaks down the lactate and creates a substantial amount of usable energy.
Alternatively, the cell can dump lactate into its surroundings, pushing it out through its cell membrane and letting the lactate fend for itself in the cruel world of tissue fluids and capillary blood.
That 'push', however, is dependent on the presence of 'monocarboxylate transporters' (MCTs) which reside in the membranes of the muscle cells. These transporters actually 'grab' lactate and move it through the protein-lipid membrane grid, allowing lactate to escape. Without the transporters, lactate movement would proceed at a considerably slower pace.
The MCTs are like lactate doors, and scientists have discovered that the doors can function in a 'two-way' manner. When lactate levels are high within a muscle cell, MCTs can thrust a good portion of that lactate outside the cell. On the other hand, when lactate levels are soaring on the exterior, MCTs can bring the lactate inward. At this point in time, it's not exactly clear whether a single type of MCT can be both inward- and outward-directed, or whether different MCTs are needed for these opposing movements.
How the muscle fibres cooperate
At any rate, the MCTs' propensities to move lactate lead to some very interesting phenomena. For one thing, MCTs allow muscle cells to 'communicate' with each other, with lactate being the 'text' of the conversation. For example, your quadriceps muscles in your thighs are often a mix of 'fast-twitch' and 'slow-twitch' muscle cells. When you run, cycle, or swim at a hard pace, the fast-twitch fibres may begin emitting lactate at high rates (fast twitchers tend to have a high glycolytic capacity and thus can produce a lot of lactate, but they're not set up very well for oxidative phosphorylation, and so instead of breaking down lactate they tend to get rid of it). The neighbouring slow-twitch fibers may then begin plucking this lactate out of the muscle fluids. It all works out very nicely; the fast-twitchers can't use the lactate, so they give it to their neighbours, the slow-twitchers, who greedily break it down for energy.
What if the quads contain only slow-twitch fibres? That's no problem, because some of the slow fibres will be working harder than others (in any particular muscle, there can be great variation in force production between cells), and the intense toilers can spill their lactate to the more easygoing cells (slow-twitch fibres can produce lactate, in spite of their 'slowness').
If the quads are completely fast-twitch, things get more interesting. There will be lots of cells belching out lactate, but there won't be any cells standing by within the muscle with a high lactate-pick-up capacity (fast-twitchers are very poor at picking up lactate, for good reason; if they hold on to too much of the stuff, glycolysis will shut down). This is one reason why fast-twitch muscle fibres are not good for the long haul; by getting rid of lactate, they are throwing away a huge reservoir of useful energy. The lactate they give off usually ends up being used for energy by some other tissues in the body.
What you have in common with hamsters
The lactate can travel fairly far before it is gobbled up. The heart, for example, is a huge lactate 'sink'; it loves to pick up lactate which the muscles have carelessly discarded, and the heart is quite proficient at using that lactate for energy. Other destinations for lactate are possible, too. For example, the lactate pouring out of a pair of hard-charging legs may be carried by the circulatory system to the upper body, where arm, shoulder, abdominal, and even low-back muscles can chomp away steadily on the lactate as an individual moves along at an intense pace (MCTs in those upper-body muscles will bring the lactate to the interiors of the cells).
When I wrote Lactate Lift-Off, exercise scientists had uncovered just a few MCTs, but now eight different transporters have been identified in human tissues. All of the eight MCTs fit into cell membranes. All have 12 transmembrane-spanning helices (loops), six on the inside of the membrane and six outside. For endurance athletes, the most important monocarboxylate transporter is unquestionably MCT1, which is the key lactate mover in muscle cells. MCT1 was actually discovered in Chinese hamsters; researchers discovered that a single point mutation in the compound greatly enhanced the transport of mevalonate (a cholesterol precursor) into hamster ovaries. They realized they must have uncovered a transporter of some kind, and subsequently MCT1 was identified in mice, rats, and humans. Interestingly enough, human MCT1 is almost exactly the same as the Chinese-hamster version. The origin of MCT1 has also been traced to a specific region of human chromosome No. 1, and this MCT1 'mapping' has some exciting implications. There is no doubt variation in human MCT1 - variation which is under genetic control. This variation will unquestionably have an effect on lactate threshold and therefore endurance performance. Thus, it's safe to say that we are on the threshold of understanding at least one small part of the genetic basis underlying differences in endurance-performance capacity. Slow-twitch muscle fibres tend to have sizeable quantities of MCT1 in their membranes, while fast-twitch cells do not. In the lower part of the human leg, for example, the soleus muscle (located below and beneath the gastrocnemius muscle in the calf area), which is primarily composed of slow-twitch fibres, has lots of MCT1. Move up to the hamstring area, however, where fast-twitch cells tend to occur with higher frequency, and MCT1 concentrations are considerably lower. As it turns out, the human heart - an endurance muscle extraordinaire - is rich in MCT1s.
Basically, the occurrence of lots of MCT1 in slow-twitch and cardiac muscle cells tells us that MCT1 probably does a great job clearing lactate from the blood and tissue spaces, bringing the lactate into cells so that it can be rushed - kicking and screaming - toward oxidative phosphorylation.
And now, MCT4
MCT4 is the other transporter which appears to be important for human athletes. Although there is some debate about its exact role, it seems to be present in higher concentrations in fast-twitch muscle cells and is probably able to help pump lactate out of such cells, thus helping to prevent glycolysis from shutting down. Interestingly enough, MCT1 and MCT4 have different sensitivities to lactate. Basically, MCT1 can transport lactate inward at high rates even when lactate concentrations are rather modest, perhaps a reflection of how anxious slow-twitch cells are to use energy-rich lactate for fuel. On the other hand, MCT4 doesn't begin to truly get in gear with the outward pushing until lactate levels build up rather appreciably.
Prolonged inactivity causes concentrations of both MCT1 and MCT4 to fall, while regular physical activity causes both to increase. The key question for athletes is of course 'Which type of activity is optimal for MCT promotion?' - and the answer continues to be that intense exercise is better than moderate exertion. In fact, intense training can produce sizeable upswings in MCT concentrations very rapidly. In a recent study in which athletes trained intensely on bicycles for seven consecutive days, MCT1 levels in the quads advanced by 18 per cent over the same time period. Such a change would mean that lactate could be brought into muscle cells much more quickly and thus could be used to create energy at a higher rate than before the seven days of training, an effect which should improve lactate threshold and enhance performance.
The importance of intensity for boosting lactate threshold is one reason why Sports Performance Bulletin recommends fairly non-traditional workouts like the 'lactate-doser' session for improving lactate threshold. To carry out the doser, you simply warm up thoroughly and then alternate two-minute blasts at close to max intensity with four- to five-minute recoveries at a modest pace. As you have already realised, the blasts bathe muscle cells in lactate, and the recovery jogs allow muscle fibres to clear the lactate which has been produced. Over time, this kind of workout should dramatically hike MCT concentrations, lactate clearance, lactate threshold, and performance capacity.
Owen Anderson