Alan Couzens, MS (Sports Science), CSCS, PES.

So, what is lactate? In general terms, lactate is simply a by-product of anaerobic metabolism. When insufficient O2 is available for complete fuel breakdown, a small amount of energy can be released with glucose conversion to an intermediate substance – pyruvic acid. In turn, this pyruvic acid can either be metabolized (in the presence of sufficient oxygen) via aerobic glycolysis or it can be further disassociated into lactic acid and H+ ions. In the context of “anaerobic” athletic events, it is the accumulation of these H+ ions that ultimately limits performance. In the context of typical aerobic athletic events, the power of the athlete to oxidize this pyruvate via aerobic processes becomes an important factor in limiting performance.

For the ironman athlete, there are a couple of important physiological implications to consider when we see elevated lactate values:

#1 Blood lactate can be indicative of a greater reliance on anaerobic processes for the production of energy.

#2 Blood lactate can be indicative of a shift from fat-burning to carbohydrate burning.

This implication is much more important for an Ironman athlete than the first because glycogen depletion is a primary limiter in Ironman racing. If you can reduce the proportion of energy that is coming from glycolytic processes and maximize that coming from lipolytic processes, your glycogen stores will last longer for the same given workload. Because these are a much more finite store than your lipids, it behoves the Ironman athlete to do all that he/she can to maximize this adaptation.

Without going into too much depth, for the science guys out there, the increased lactate exhibited from carbohydrate oxidation can be explained by the increased acidity of the carbohydrate molecule when compared to the fatty acid molecule. This increased acidity ultimately results in greater CO2 production when energy is liberated from Glucose as opposed to FFA’s (~25% more CO2 for the same net energy yield). Ultimately, this extra CO2 has to go somewhere. Typically it combines with H20 to form H2CO3 (carbonic acid), which in turn dissociates into H+ ions and bicarbonate (HCO3). It is the conversion of H+ ions & Pyruvate into Lactate via it’s interaction with Lactic Dehydrogenase that ultimately results in increased lactate within the muscle.

Now, it is important to note that slow twitch fibers utilize a different form of lactic dehydrogenase (H-LDH) that maintains the equilibrium preferentially shifted toward pyruvate, NOT lactate (this in turn favors lipolysis over glycolysis). Thus, if slowtwitch fibers are being exclusively used & the body is primarily reliant on fat as a substrate, muscle lactate production is negligible.

So, what does this all mean in a practical sense to you as an athlete?

Curve 1 (Alan) represents a traditional lactate profile. The subject’s first deflection point (AeT)occurs at a speed of ~ 7.0 miles per hour and a lactate level of 2mmol/L. If you draw a straight line from this first deflection point along the curve, you will see that at the 4th data point (~4mmol/L), the curve breaks away from this second straight line and becomes more steep. We term this deflection VT2 or the anaerobic threshold. It is these two ‘breakpoints’ in the curve that provide the most information on recommendations for assigning training zones and recommendations on changes to training methodologies in the coming phase.

Before we go into the practical implications for Alan’s training program, first a quick recap on what is going on, biochemically at each of the points on the curve:

When Alan begins the test and gradually increases his pace to a comfortable aerobic level, arterial blood lactate remains relatively unchanged from resting levels (1.4mmol/L in Alan’s case) despite an increase in pace. The first workload intensity that represents a jump in the lactate level is termed the aerobic threshold. Both ventilatory and blood lactate rises can be observed at this level. The ventilatory rise is explainable as previously mentioned on the basis of blood HCO3 buffering mechanisms, in which the additional CO2 produced with the recruitment of FOG (type IIa) fibers via their preference for aerobic glycolysis (sugar burning) over lipolysis (fat burning) results in temporary buffering with NaHCO3 to form Carbonic acid, which eventually is expelled (as CO2 gas) via increased ventilation when it reaches the lungs. Even if you don’t 100% get the rationale, the important thing to note is that an increase in lactate response & an increase in ventilation are signalling a change in muscle fiber recruitment from slow twitch fibers (fat-burners) to FOG fibers (sugar-burners) (Skinner & McLellan, 1980). As Ironman athletes, the longer we can stave off this switch, the better.

As FG fibers begin to be recruited and the anaerobic load goes up, at workloads greater than those described (~75-90% VO2max), the blood lactate level then begins a more rapid rise. In Alan’s case this can be seen at 8.0mph (~82% VO2max). The threshold at which this rise takes place can be termed the anaerobic threshold. Both ventilatory (panting) and blood lactate changes occur at this threshold as well. At the work intensity where the blood lactate concentration begins to accumulate and blood acidity begins to rise, the rising H+ ion accumulation provides a powerful stimulus for NaHCO3 buffering and a consequent rise in expired CO2.

So, based on the above data, how do we calculate appropriate training zones for Alan?
Let’s begin by considering our physiological objectives:

Increase fat oxidation
Knowing that, in Alan’s event (Ironman Triathlon), glycogen depletion is a primary limiter (esp for those in the 10-12hr bracket), it is of utmost importance to maximally train those fibers that can produce energy without consuming large quantities of carbohydrate, i.e. the slow twitch fibers. We can see from the chart that in Alan’s case, the transition from slow-FOG fibers occurs at ~2mmol/L or 7mph. Therefore, for our runs that aim to improve this ability we should be training @ or below ~7mph or, this can be prescribed according to the heart rate that corresponded with this level during the test, in Alan’s case ~155bpm (from lab data not shown).

Increase aerobic capacity of FOG fibers.
A secondary objective for the sub-elite Ironman, and perhaps a primary objective for the elite Ironman is to improve the oxidative capacity of the athlete’s type II fibers. It is likely, in the course of the competition that pace or terrain changes, along with fatigue will force the athlete to produce more power than can be provided by ST fibers alone. Therefore, it is important that the athlete improves the oxidative potential and efficiency of any fibers he/she is likely to recruit come race day. For the intermediate IMer, this means lower threshold FOG fibers, for the elite IMer, this means the full spectrum of FOG fibers. From a training zone perspective, we could delineate these zones as 2-3mmol/L (Zone 2) and 3-4mmol/L (Zone 3) for Alan, or, 155-166bpm & 166-172bpm resp.

3. Increase oxidative potential of FG fibers,
i.e. transform your fast twitch fibers into more FOG-like fibers. In muscle biopsies of elite endurance athletes it is frequently hard to discover any fibers that resemble traditional fast twitch fibers. The reason for this is that the athlete improves the oxidative potential of his white fibers that they begin to take on the aerobic characteristics of red fibers. This has big implications for the elite athlete in terms of power output, esp on the bike. If the elite IMer is able to recruit 90% of his fibers aerobically and the novice is only able to recruit 60%, you don’t have to be a professor to deduce the performance implications. At Alan’s performance level, I wouldn’t prescribe this level of training, but for illustrative purposes this zone (Zone 4) would be 4-6mmol/L or 172-182bpm.

4. Increase VO2max
For the super-elite athlete that has fully maximized their ability to oxidize as much fat as possible (to produce energy), i.e. in practical terms, raised their aerobic threshold to 70% or more of VO2max, and has raised the oxidative potential of their FOG fibers to 90% of VO2max, the limiter now becomes oxygen delivery. This is best improved by very hard sessions that are at or very close to the intensity corresponding to the athlete’s VO2max. There will come a time in the elite athlete’s development that they will need to oscillate between periods of “speedwork”, i.e. VO2max and periods of “volume” or aerobic development, with each phase providing the small but necessary extra stimulus to ratchet the other capacity up a couple more notches. It needs to be noted, however, that this is very elite stuff. For the sake of argument, Alan’s zone for this intensity (Zone 5) would be 6-9mmol/L or 182-194bpm.

So, that’s how we calculate the training zones, now what does the curve tell us about what our training priorities should be for the coming phase?

Let’s begin by looking at the first point, what we are terming the aerobic threshold.
The point best correlated to Ironman performance among the curves is the first point, i.e. speed at AeT. In order of Ironman performance we have:

Gordo AeT = 9.2mph
Jeff AeT = 8.0mph
John AeT = 8.0mph
Mat AeT = 8.0mph
Alan AeT = 7.1mph

This is important to note. While, the profile of the curves is quite different beyond the AeT point, with some being more steep than others after AeT (e.g. Gordo & Alan vs. Mat, John, Jeff), the best predictor of Ironman performance is not the profile of the curve, but rather the speed at AeT (the other factors come into play, as discussed below but moving your curve as far ‘right’ as possible should be priority #1).

So, how do we move the curve to the right? Well, we could try to ‘push it’ with a high volume of work at or below the AeT or ‘drag it’ by elevating our VO2max as high as possible and hoping that the subsequent points will fall into line. The former method, i.e. ‘pushing the curve’ has received the most empirical support as the best method for long term adaptation (e.g. Touretski & Pyne, 1994) and makes the most logical sense when we break VO2max into it’s two constituent components: Cardiac output and Arterio-venous oxygen difference. The first of these is maximized in a very short period of time: 12-14 weeks (Seiler, 1998). Therefore, if continued top end improvement is desired, one must undertake training that addresses peripheral limiters which have a much greater time course of training adaptation (Seiler, 1998).

So, that’s step 1: Push the curve as far to the right as possible by performing a very high volume of exercise slightly below the AeT:

Clearly, all of the crew, irrespective of what their lactate profile does after that first deflection point, could benefit from continued emphasis in this area. This begs the question, how much is enough? Mark Allen got to the point that he was able to run 5:19/mi at this point (11.3mph). He accomplished this with repeated bouts of 12 week base periods over the course of 10+ years where ALL of his training was done below this point (Noakes, 2003). This is not too far from the first break-point of Gelindo Bordin and may represent a near optimal value for lipolytic power. In short, as an endurance athlete, until you are running 11.3mph w/ a lactate level very close to your resting level, you have some serious upside to improve all levels of performance @ & above AeT by devoting a high volume of training to an intensity at or below your first deflection point (~2mmol/L).

When comparing the next section of the curves (from 2-4mmol/L), some notable differences can be observed. It is fairly clear that John, Mat and Jeff all exhibit a fairly tame gradient from 2-4 mmol/L. This is indicative of a very well trained aerobic glycolytic system or, from a muscle fiber perspective, their FOG fibers are very well trained to produce work. In fact, you will notice that at the 4mmol/L mark, their curves begin to approach Gordo’s curve. The only problem is, when you look at the area between their curves and Gordo’s, this represents a high glycolytic cost to do so. My hunch is that they have been spending a good amount of time (perhaps unintentionally) training above their AeT’s. While this may be a good thing in terms of specific preparation for a 10hr IM, comparison of their grades with Gordo’s indicates a much greater upside to moving their first point closer to his via training at or below the 2mmol/L mark.

On the other side of the coin, for a curve like Alan’s that represents a fairly steep rise after AeT, IF he gets to the point that AeT endurance is no longer a specific limiter to Ironman performance, a short specific phase of training designed to flatten his 2-4mmol/L line prior to racing an IM may be prudent. This is accomplished with dedicated “key sessions” that are slightly above his AeT:

Looking beyond the 4mmol/L mark, it is clear that Alan and Gordo’s curves exhibit a second deflection point. This is indicative of the individual Anaerobic Threshold, which, as previously mentioned, indicates the period of exercise in which lactate dissipation and clearance can no longer match the rate of accumulation. Because of the anaerobic nature of Fast Glycolytic (FG) fibers, this also tends to indicate a shift in recruitment pattern from FOG to FG fibers. It is not uncommon in elite endurance athletes to notice an absence of this second deflection point (Martin and Coe, 1991). Frequently, these athletes are very efficient at clearing lactate and also taking it up and using it as a substrate. In addition, frequently,elite athletes do not exhibit traditional FG fibers under conditions of a biopsy, i.e. they have converted fibers that were previously inept at using oxygen into fibers that can produce work under oxidative conditions, i.e. with minimal lactate output.

Gordo’s lactate curve is a little atypical of elite long course athletes in this regard. If I were to hypothesize on this, it may be due to more emphasis on higher intensity speed work during this year compared to last, or a consistent emphasis on strength training. In the context of IM racing, this difference may be a bit of a red herring. It is unlikely that he will be spending significant periods of time at 4mmol/L esp during the run. If we were to see a similar profile on the bike and, particularly on the swim, it may indicate a potential area for improvement in the context of a tactical race. In this case, greater emphasis on Zone 3 training may prove useful (to flatten out the 3-4mmol/L) aspect of the curve.

Zone 4 training, as previously mentioned may be useful at the super-elite level to ‘peak up’ oxygen delivery mechanisms which will ultimately allow higher threshold fibers to be saturated with O2 and trained, i.e. as a corollary to Zone 3 training. It is important to note that VO2max is rarely a limiter to Zone 1 & 2 intensities and therefore, it’s use in the training of sub-elite long course athletes needs to be seriously questioned.

Hopefully, I have conveyed the importance of regular lactate testing for the endurance athlete. Hopefully, I have also conveyed the importance of having a coach or sports scientist who is very familiar with Ironman-specific lactate interpretation to advise you on training implications arising from such a test.

To enquire about our testing packages here at our Endurance Corner Lab in Boulder, Colorado, or to ask any questions about lactate testing in general, please contact me at alan@endurancecorner.com.

References available on request.