Lactate and lipolysis/zone 2 "mania"

Training
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(Wasn’t sure where to stick this, so moderators, feel free to move if appropriate.)

One of the justifications offered for avoiding excursions to higher intensities during endurance workouts is to avoid suppression of lipolysis by lactate. The unstated assumption is that to get better at oxidizing fat you need to oxidize fat. However, as I have pointed out here and on the Inside Exercise podcast, neither of the above are true (something that has been known for a half century). First, the reduction in fatty acid concentration during high intensity exercise is not due to lactate-mediated suppression of lipolysis, but rather “entrapment” of fatty acid within adipose tissue due to diversion of blood flow to exercising muscle. This is why there is a massive “overshoot” in plasma fatty acid concentrations when exercise is over, despite the fact that lipolysis itself rapidly decreases. Second, the increased ability to oxidize fat after training is primarily the result of a training-induced increase in mitochondrial respiratory capacity, which is stimulated by contractile activity itself, regardless of the fuel source (i.e., fat or carbohydrate).

Nonetheless, there are apparently coaches and sports scientists who continue to promote these false ideas. That led to somebody emailing me, asking for references. I pointed them towards studies by Issekutz and by Bulow in the 1970s, but then got digging around in the literature to refresh my own memory. In doing so, I came across this study, which I don’t recall seeing before:

In addition to directly testing the hypothesis that lactate suppresses exercise-stimulated lipolysis in human adipose tissue in vivo, perhaps most noteworthy is the fact that they tested the effect of lactate at a higher concentration than Miller, Brooks, et al., who “clamped” lactate at a plasma (and therefore lower interstitial) concentration of “only” 4-5 mmol/L (and also found no effect).

TL,DR:

Elevated lactate concentrations do not suppress lipolysis in exercising humans. This is a falsehood that needs to be buried once and for all.

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Just wanted to say thanks for engaging on this platform. There’s so much bro science and anecdata out there that it’s refreshing to have someone who has spent his career studying the facts weigh in from time to time. And now I’m not going to worry about going VO2 max occasionally on these Appalachian hills during my z2 rides.

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Thanks for this!

One of the benefits that I’ve heard about endurance training is that it promotes mitochondrial adaptation (is that the term?) with limited fatigue penalty - basically, it’s the most adaptation for the least amount of cumulative fatigue.
Has that been tested? Is it accurate?

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Warning! Long-winded answer agead, but I promise I will get there…

As I have been pointing out to people for a long time, the muscular adaptations to exercise training are both exceedingly complicated, yet rather simple. That is, while repeated bouts of exercise influence the expression of thousands of genes, at the end of the day these changes (and the accompanying post-translational modification of proteins, etc.) result in only one of two things:

  1. An increase in the ability of muscle to produce greater maximal force or power output, or

  2. An increase in the ability of to sustain an already submaximal force or power output for a longer period of time, i.e., greater resistance to fatigue (failure).

The latter set of adaptations could then be subdivided into adaptations that result in greater fatigue resistance during very high intensity, non-sustainable exercise (e.g., an increase in muscle buffer capacity) vs. those that contribute to fatigue resistance during lower intensity, more sustainable exercise (e.g., an increase in the capacity to transport fatty acid across the sarcolemma), with some overlap between these subcategories (e.g., an increase in capillarization would both enhance delivery of substrates during lower intensity exercise and removal of potentially fatiguing waste products during higher intensity exercise).

Viewed from this perspective, I think it far easier to understand why you don’t really need to train at very specific intensities to induce specific adaptations. The body really has only one of two “programs” by which it can respond, which belies the notion that you can directly target just one thing (e.g., an increase in MCT). It is also important to recognize that 1) the idea of exercise “intensity” is a bit nebulous at the level of the individual motor unit (since by and large they are either “on” or “off” and don’t really care much about what their neighbors are doing), and 2) although during exercise ATP can be supplied both anaerobically and aerobically, recovery from exercise is essentially a completely aerobic process. This further blurs the lines between training “zones”, and explains why something like HIIT leads to the same outcomes as continuous exercise at a much lower intensity.

TL, DR: It’s all good! In particular, training at a VERY wide range of intensities leads to an increase in mitochondrial respiratory capacity. There is absolutely nothing special about so-called “zone 2” in this regard, except perhaps the fact that you can do more of it, resulting in a greater overall “dose” of training (i.e., combination of volume and intensity).* Anybody touting the “magical” nature of zone 2 and mitochondria simply doesn’t know what they’re talking about (this includes folks like ISM and Attia).

*With that said, the studies in the literature demonstrating the largest increases in mitochondrial marker enzymes that have had individuals train the hardest, not the most, with initially untrained individuals achieving comparable to elite athletes after just a few months of training. So at the end of the day, it may not really matter, i.e., “all roads lead to Rome”. Instead, it may simply come down to the individual, how much time and motivation they have, how durable they are, etc.

Don’t say I didn’t warn you about a long answer! :slight_smile:

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You’re welcome.

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Thanks! I appreciate the long winded, more specific answer!
Ok, so would the bulleted version of this be:

  1. An increase in the ability of muscle to produce greater maximal force or power output, or
  2. An increase in the ability of to sustain an already submaximal force or power output for a longer period of time, i.e., greater resistance to fatigue (failure).
    2.1. greater fatigue resistance during very high intensity, non-sustainable exercise (e.g., an increase in muscle buffer capacity)
    2.2. fatigue resistance during lower intensity, more sustainable exercise (e.g., an increase in the capacity to transport fatty acid across the sarcolemma),
    2.3. Both: increase in capillarization would both enhance delivery of substrates during lower intensity exercise and removal of potentially fatiguing waste products during higher intensity exercise).
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Yes, and in fact I have verbally referred to “type 2a” and “type 2b” adaptations before - e.g., on Inside Exercise - but that’s risky because it might lead people to think I am referring to fiber types.

It’s also important to keep in mind that this is a high level/conceptual perspective - if you get into the weeds you could almost certainly find exceptions to my generalizations.

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The Cog = Andrew Coggan ? You did an episode on Inside Training, it must be you.

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Correct.

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So if I want to combine sprint training with long endurance ride there is no reason to have to wait for the end of the ride to do the sprints, but i can do them whenever i want? Without fear of “ruining” my “clean” Z2 ride and adaptations.

Also with regard of your later comments, the best intensity to train for general fitness (“base”) is the highest you can sustain for the time available? So for me currently 4 rides a week 6 to 9 hours a week is mostly tempo (3/wk) with some filler endurance and occasionally a sprint/intensity session.

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Thank you for taking the time to engage with us, mere mortals!

Is there anything, at all, special to low intensity training, like higher mitochondrial biogenesis, or capillarization ?

Maybe a more interesting question: in your interview, you seemed to agree that beyond 10h a week is when you would recommend adding low intensity rides at the expense of harder ones. You mentioned your son’s swimming lessons. In your experience, how does that number vary for different age groups or fitness levels ? I imagine the first rule is to listen for signs of overtraining?

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Absolutely no reason to wait. In fact, it’s generally best to do sprint (neuromuscular power) training when you’re freshest, and can hit the highest numbers. Yes, you won’t be as fresh as the end of a race (especially if you haven’t made sure to rest up the last several minutes), but I can’t think of any physiological benefits to doing sprint training while tired (there could be psychological benefits).

Beyond 10 h/wk is when (where?) I would guesstimate that most people would need to dial back the intensity of their “moderate intensity filler workouts” to maintain the intensity of their harder ones. Everyone’s different, though, and I don’t think that being fully recovered all the time is necessarily the optimal approach.

IOW, sometimes it’s about the quantity of the quality, but other times it’s about the quality of the quantity.

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I’m not sure if I understand your reasoning here. Sure, lactate doesn’t inhibit lipolysis.

But are you also suggesting that:

  1. Lipolysis continues unabated even at very high exercise intensities? Like, that during a 30s anaerobic effort, fat oxidation is just going brrrr?
  2. That the absence of lactate causing a reduction in lipolysis means that there is no reduction in lipolysis? How does this argue against the presence of some other humoral or maybe neural mediator of lipolysis rate?
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Yes, lipolysis proceeds at a very high rate during intense exercise. In the classic study below, for example, the rate of appearance of glycerol (considered the overall best measure of the whole body rate of lipolysis) was essentially just as high after 30 min of exercise at 85% of VO2max as it was after 2 h at 65% of VO2max. As I have mentioned before, Larry Sprint has even published data showing significant utilization of IMTG during electrical stimulation of rodent muscle, in which metabolic rate is as high as it can be.

(BTW, take the absolute rates of substrate oxidation in the above study with a grain of salt. At the time, there was an issue with the CO2 analyzer providing a non-linear response, something I know because I originally built/rebuilt/validated the metabolic cart. During his dissertation defense, poor Jeff Horowitz had to sit through Ed and I discussing this, until Ed admitted he’d lost our $20 bet.)

See above. It’s certainly possible that some other factor (e.g., the hyperglycemia that develops during high intensity exercise) plays a role in limiting release of fatty acid from adipose tissue (in this case, by stimulating reesterification). However, the primary issue seems to be diversion of blood flow, leading to entrapment of fatty acids (but not glycerol, or at least not to the same extent, since it doesn’t require albumin for transport). Again, this is why there is such a large overshoot in fatty acid appearance and concentration post-exercise, when the appearance and concentration of glycerol start decreasing immediately. (See the study above for an example.)

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So, ride your bike as often as you can, as hard as you can, for as long as you can whilst making sure you get enough recovery so you can continue doing it with no ill effects.

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That summarizes everything

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So how does one get better at oxidizing fat? If training intensity is not the main factor, what is left, dietary interventions?

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Probably answer is - ride more and let the body do their thing.

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By performing endurance (vs. resistance) exercise training and thereby increasing your muscle respiratory capacity:

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I have no idea how this should impact my training?

Please advise:
Should I use a structured training plan?
Is the athletes training age and level an important constituent?
If so what type of periodisation should be used?
Is the event type/duration an important constituent, ie, how, why, etc?