Is Zone 2 Training Overhyped Or Under Appreciated?
This article is a follow-on from our earlier article on Zone 2 training and the thoughts of Dr Iñigo San Millán, who is coach of Tadej Pogačar, head of performance at UAE Team Emirates, and professor at the University of Colorado School of Medicine.
In this follow-on post, we wanted to discuss some differing perspectives around Zone 2 training and give a balanced viewpoint based on the existing evidence.
As a reminder, San Millán is very much in favour of Zone 2 training (i.e. riding at an intensity very close to the maximum rate of fat oxidation, or the so-called ‘aerobic threshold’). One of the benefits San Millán regularly highlights is an improved capacity for fat oxidation, which contributes to improved fatigue-resistance, and threshold power.
In order to really develop fat oxidation capacity, San Millán repeatedly reinforces the importance of keeping intensity under control during Zone 2 rides, and avoiding power surges. San Millán suggests that this is because when you ride hard, even for a relatively short amount of time, this increases the rate of glycolysis and lactate production. He suggests that an increase in lactate levels is problematic if you’re looking to build fat oxidation capacity for several reasons.
Firstly, lactate is a preferred fuel for muscle cells (preferred over fat). It also inhibits the break down of fats (a process known as ‘lipolysis’) and inhibits the mitochondrial transporter responsible for moving fatty acids into the mitochondria, where they can be combusted for energy. Ultimately, therefore, lactate suppresses fat oxidation, and undermines one of the key goals of Zone 2 rides.
However, it’s important to acknowledge that this perspective isn’t held by everyone and there are some eminent coaches and sports scientists who hold a different view. A key example is Dr Andrew Coggan, who in an interview with Dr Glenn McConell, set out his thoughts on Zone 2 training, which were in fairly strong opposition to the perspectives of San Millán.
In this article, we’ll summarise some of the common criticisms of Iñigo San Millán’s perspectives on Zone 2. It’s worth saying that we are not biologists or biochemists, and some of the very complex mechanistic research in this area is outside our sphere of expertise. However, we hope to provide some practical messages that you might find useful in thinking about your training.
1. Do you need to burn fat to get good at burning fat?
One criticism we see of San Millán’s stance on Zone 2 training is the argument that you don’t need to be burning fat during exercise to get good at fat oxidation.
This is an easy point to corroborate, as there are numerous studies that show, for example, that high-intensity interval training is effective at improving fat oxidation capacity in both trained and untrained athletes (Atakan et al., 2022; Westgarth-Taylor et al., 1997).
However, we don’t think anyone is seriously suggesting Zone 2 riding is the ONLY way to improve fat oxidation capacity.
The more pertinent question is whether Zone 2 riding is a BETTER way to improve this ability vs other types of sessions, which leads to the next common criticism…
2. Is High Intensity Interval (HIIT) training as good as Zone 2 training for developing fat oxidation ability?
Some coaches and academics argue that we get the same increases in the ability to burn fat with high-intensity interval training (HIIT) vs Zone 2 training.
This is a harder point to prove, and we don’t believe enough evidence exists to confirm or discredit this assertion.
However, let’s look at the evidence we do have available…
A good study is by Burgomaster et al. (2008). In this study, 10 untrained participants engaged in a 6-week training intervention, which involved either three weekly sessions of 4-6x 30-second sprints (the HIIT intervention), or five weekly sessions of 40-60 mins riding at 65% VO2peak (the Zone 2 intervention).
The researchers looked at several markers of fat oxidation capacity both before and after this training intervention, and found there was no difference between the HIIT and Zone 2 groups.
Moreover, a recent meta-analysis pooling data from a number of similar studies found no meaningful difference in fat oxidation abilities when comparing HIIT and lower intensity continuous exercise among untrained and often overweight/obese populations (Atakan et al., 2022).
Other studies in untrained population groups have also looked at markers of aerobic capacity and mitochondrial density (which are key components of fat oxidation ability), and found no difference between HIIT and lower-intensity training (Gibala et al., 2006; Gillen et al., 2016).
On the face of things, these studies support the view that HIIT and Zone 2 give similar fat oxidation benefits. However, all of these studies involved untrained populations, who have a very large potential for improvement, and in whom simply exercising at any intensity will bring about improvements in a whole host of aerobic attributes. In particular, the key rate-limiter for fat oxidation in these athletes is likely to be muscular mitochondrial content, which we know is stimulated by both intensity and volume.
However, there are other factors that limit fat oxidation capacity, including the levels of fatty acid transport proteins (e.g. CD36 and CPT-1), the levels of stored triglycerides in the muscles and the levels of certain hormones (e.g. HSL and LPL) (Purdom et al., 2018). It’s unclear whether these factors might be the rate-limiters in more well-trained athletes, and whether higher-level athletes need to be more selective in their choice of training session if they are looking to really optimise fat oxidation capacity.
Ultimately, we just don’t know with complete certainty whether one style of training is better than any other in improving fat oxidation in people who are already training regularly on the bike. As per San Millán’s arguments, it does make logical sense that training at an intensity that maximally activates fat oxidation should be one of the best ways to develop this ability, but we don’t know this for sure.
3. Lactate doesn’t suppress fat oxidation?
Finally, there is a view held by a minority of people that lactate doesn’t suppress fat oxidation.
These people typically acknowledge that, as exercise intensity increases then lipolysis (the break-down of long-chain fat molecules into glycerol and free fatty acids, which are used for fuel) is suppressed. However, just because there’s a correlation between lactate levels and suppression of lipolysis, this doesn’t automatically imply cause and effect.
Studies used to support argument that lactate doesn’t suppress fat oxidation
We’ve come across a couple of studies cited in support of the argument that lactate doesn’t suppress fat oxidation or lipolysis. One is a study by George Brooks and colleagues (Miller et al., 2002). It’s worth noting from the outset that this study was not primarily designed to investigate the impact of elevated lactate levels during exercise on fat oxidation/lipolysis rates, so the study design isn’t great for answering this question (as you’ll see shortly…).
In this study, participants underwent a 10-week training intervention. Before the intervention, the participants had the levels of glycerol and free fatty acids (markers of the rate of lipolysis) measured under two conditions. In both conditions, the participants were at rest, however, in one condition, lactate was maintained at an elevated level of 4mmol/L via infusion.
It was shown that there was no difference in the levels of circulating glycerol or free fatty acids, nor was there any difference in substrate utilisation when at rest, despite the elevated lactate levels.
On the face of things, this finding indicates that lactate doesn’t suppress fat oxidation.
However, in this instance, as all participants were resting, the total energy demands would have been very low, and therefore any change in substrate utilisation or markers of lipolysis would likely have been small and hard to detect. Moreover, it’s well known that metabolism at rest is quite different from metabolism during exercise…
Fortunately, there was another arm of the investigation, which took place after the 10-week training intervention. In this arm, the participants exercised at 60% of VO2max, and lactate levels were either (A) allowed to settle at their normal level or (B) lactate was infused to hold lactate levels pre-training levels (i.e. the level they reached when riding at 60% of VO2max before the 10-week intervention). In effect, therefore, this arm of the study compared markers of fat oxidation at two different lactate levels, while exercising at the same intensity.
In this arm of the study, there were again no differences in fat oxidation rate or markers of lipolysis in the blood, despite differing lactate levels.
However, crucially, the level of lactate in the A and B conditions is likely to have been really quite similar, because a 10-week training intervention won’t change lactate levels by a particularly large amount. Indeed, the researchers commented that in some cases they even had to turn off the lactate infusion to ensure the target lactate level wasn’t exceeded. Thus, given the very small difference in lactate levels, it would have been impossible to detect any subtle differences in fat oxidation rates without recruiting a very high number of participants.
Ultimately, the study was never designed to answer the question of whether fat oxidation or lipolysis rates are impacted by lactate during exercise, and we don’t believe we can use this study to answer this question!
Another study cited in support of the viewpoint that lactate doesn’t suppress lipolysis/fat oxidation is by Coggan (1987). The study involved repeated bouts of riding for 15-mins at 80% VO2max, followed by 15-mins at 60% VO2max. The respiratory exchange ratio (RER) was measured in the last last 5-mins of each 15-min block. RER tells us about the relative contribution of fats and carbohydrates to energy production.
It’s been pointed out that in this study, the RER in the final 5-mins of each lower intensity block looked exactly the same irrespective of whether it was or was not preceded by a high-intensity block. It’s argued therefore that the lactate produced in the high-intensity blocks was having no impact on fat oxidation rates during the low-intensity blocks.
One concern with this interpretation of the data is that lactate levels in the high-intensity blocks only reached 5mmol/L, which is not particularly high. It’s therefore wholly possible that (i) lactate levels were not high enough to notably impact fat oxidation rates or (ii) lactate levels had fallen back to baseline by the time the RER measurement was taken, but fat oxidation may have been suppressed earlier within each low-intensity block.
In relation to this latter theory, the participants in the study were described as ‘trained’, which might mean that these cyclists were particularly good at clearing lactate from their blood during the low intensity blocks, and that less well-trained cyclists would have had a measurable suppression of fat oxidation during the final 5-mins of each block.
Overall therefore, we don’t believe the studies above provide convincing evidence that lactate DOES NOT suppress fat oxidation or lipolysis.
So what evidence is there that it DOES?
Other Scientific Literature
A key study is that of Boyd et al. (1974), where 6 untrained men exercised at 40% VO2max for 1.5 hours. In the last 30-mins of the exercise bout, lactate was infused to raise blood lactate levels to an average of 8.8 mmol/L. In response the levels of circulating free fatty acids and glycerol were found to be suppressed, indicating a reduction in lipolysis caused by lactate infusion.
However, other studies following a similar design have failed to detect an impact of lactate infusion on markers of lipolysis and fat oxidation (Ferrannini et al., 1993; Trudeau et al., 1999). Notably though, these studies used relatively low lactate levels (2mmol/L and 6.4mmol/L respectively). It could therefore be suggested that lactate only suppresses lipolysis and/or fat oxidation when lactate levels are high.
This theory is supported by research conducted in dogs (Fredholm, 1971), where lactate was observed to suppress free fatty acid release from subcutaneous adipose tissue when lactate levels were in the region of 10-14mmol/L, but there was no observable suppression at 5-7mmol/L and below. [Note this study helps explain why there was no suppression of fat oxidation shown in Coggan (1987), as described above!]
More recent studies have also found mechanistic evidence looking at the impact of lactate on receptors in adipose tissue suggesting lactate inhibits lipolysis (e.g. Liu et al., 2009). Moreover, as well as suppressing lipolysis, lactate might also act to reduce fat oxidation in other ways. For example, there is some evidence that hydrogen ions (which are produced alongside lactate) may interfere with CPT1, which is a key enzyme in fatty acid metabolism (Achten & Jeukendrup, 2004). It’s also thought that lactate potentially acts in conjunction with pyruvate to stop the transfer of free fatty acids into the mitochondrial reticulum (Brooks, 2020).
Overall, therefore, we think that there’s some good evidence that lactate does inhibit fat oxidation during exercise. However, what doesn’t seem to be acknowledged very often is that lactate levels may need to be quite high (e.g. 8mmol/L or above) to have a meaningful impact.
Summary and Practical Recommendations
In summary, we agree that training at a Zone 2 intensity is not the only way to improve fat oxidation capacity. However, we don’t believe there’s enough evidence to say whether Zone 2 is better, worse or equal to other types of training for improving fat oxidation capacity among trained cyclists.
In the absence of any other evidence to guide us, then it seems logical that working at a Zone 2 intensity, where fat oxidation rates are high, is probably a good approach to take if looking to maximise fat oxidation rates. Anecdotally, we find that the athletes who do the highest amounts of this type of training tend to have a fitness profile suggesting a strong capacity to oxidise fats.
We believe there’s good evidence to suggest that lactate does suppress fat oxidation, but only at high lactate levels. Therefore, very short power surges (<30-seconds), or extended efforts performed at or just below threshold probably don’t have a long-term impact on fat oxidation, and are safe to include within a Zone 2 ride, where improved fat oxidation is a key goal.
Care probably needs to be taken to avoid repeated hard efforts above threshold lasting ~30-seconds and upwards, as these are more likely to cause a more significant jump in lactate levels that may suppress fat oxidation for a period of time after each surge. Of course, there’s still the argument that you don’t need to be burning fat in order to get better at burning fat. Nevertheless, until we get a better understanding of what’s ‘optimal’ in terms of developing this ability, we’d be inclined to steer clear of hard efforts like these within a Zone 2 ride if you really are trying to work on your fat oxidation capacity as a priority.
What’s often lost from the debate around Zone 2 rides and power control is a discussion of wider reasons why power control is important. In our view, the most compelling reason to keep a lid on power output comes down to fatigue-management and recovery. It’s important to keep Zone 2 rides well-regulated in terms of intensity simply because this fosters better recovery between key high-intensity sessions. Put simply, there’s no point riding harder than you need to!
Another point of note is that we think athletes and coaches are potentially getting tied up in trying to isolate specific physiological adaptations (e.g. fat oxidation). The adaptations that contribute to improved fat oxidation (e.g. increased mitochondrial density) also contribute to abilities like improved VO2max and anaerobic capacity, so it’s difficult to say one form of training is good for one specific ability, and there’s always a high degree of overlap.
What’s most important is that you’re doing a mixture of different types/intensities of training across the medium/longer term (e.g. across a period of several weeks), and importantly including sufficient recovery between key high-intensity sessions, so that these can be performed to a high standard. This will challenge the body in different ways to help avoid fitness stagnation.
References
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Atakan, M. M., Guzel, Y., Shrestha, N., Kosar, S. N., Grgic, J., Astorino, T. A., ... & Pedisic, Z. (2022). Effects of high-intensity interval training (HIIT) and sprint interval training (SIT) on fat oxidation during exercise: a systematic review and meta-analysis. British Journal of Sports Medicine, 56(17), 988-996.
Boyd III, A. E., Giamber, S. R., Mager, M., & Lebovitz, H. E. (1974). Lactate inhibition of lipolysis in exercising man. Metabolism, 23(6), 531-542.
Brooks, G. A. (2020). Lactate as a fulcrum of metabolism. Redox biology, 35, 101454.
Coggan, A. (1987). Effect of carbohydrate supplementation on metabolism and performance during prolonged exercise.
Burgomaster, K. A., Howarth, K. R., Phillips, S. M., Rakobowchuk, M., MacDonald, M. J., McGee, S. L., & Gibala, M. J. (2008). Similar metabolic adaptations during exercise after low volume sprint interval and traditional endurance training in humans. The Journal of physiology, 586(1), 151-160.
Purdom, T., Kravitz, L., Dokladny, K., & Mermier, C. (2018). Understanding the factors that effect maximal fat oxidation. Journal of the International Society of Sports Nutrition, 15(1), 3.
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Gillen, J. B., Martin, B. J., MacInnis, M. J., Skelly, L. E., Tarnopolsky, M. A., & Gibala, M. J. (2016). Twelve weeks of sprint interval training improves indices of cardiometabolic health similar to traditional endurance training despite a five-fold lower exercise volume and time commitment. PloS one, 11(4), e0154075.
Liu, C., Wu, J., Zhu, J., Kuei, C., Yu, J., Shelton, J., ... & Lovenberg, T. W. (2009). Lactate inhibits lipolysis in fat cells through activation of an orphan G-protein-coupled receptor, GPR81. Journal of Biological Chemistry, 284(5), 2811-2822.
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