Totally non-science response.
I like O/U workouts. For me, they mentally get me ready for the efforts required. If you’re going to race or even ride in pace lines, it’s not always about what numbers you can put out on the front but rather, how rapidly you can recover and go again.
When I do O/U workouts, if my legs aren’t best-part cleared and my breathing under control 30 seconds into the recovery period, I know from experience that I’m in for a rough session.
I’ve been reading up on MCTs for a few months for an upcoming pair of podcasts, and you would not believe how complicated the answer to this question is. Mostly due to the fact that there are a lot of contradictory results. What I gather so far seems to be: both are highly sensitive to training from the untrained state. Later, MCT4 is less sensitive to training and MCT1 is more sensitive and highly correlated with muscle oxidative capacity regardless of MHC type. Both types are bidirectional as determined by gradient, and prevailing theory is MCT1’s higher specificity and lower Vmax (vice versa for MCT4) are for the range of expected metabolic concentrations.
Complications that occur in the Neal study Brennus linked, which had 4 weeks of detraining in chronically low volume cyclists before each intervention. And as expected, MCT4 expression in whole muscle homogenate increased in polarized, my theory being that greater motor unit recruitment trained more fibers. However, MCT1 not changing is a surprise, however the reported lack of change in mitochondrial enzyme activities (CS & HAD) matches with previously established correlations between those variables, so that correlation so far seems incredibly robust so far.
What I haven’t seen yet is any indication that expression changes with exposure to larger or smaller amounts of lactate, though I would imagine there would be small effects there. Seems like MCT4 expression is a sort of cellular “default” in less active fibers, and as fibers become more active they express both relative to certain stimuli, which seem to be our usual suspects like p53 and HIF. Which makes a lot of sense because muscles don’t seem to respond meaningfully (in terms of performance) to substrate exposure, but do respond dramatically to activation of stressors like energy demand and acute “hypoxia”, which trigger an entire host of adaptations.
Turns out that’s another reason that CS & HAD activity is probably so tightly correlated to MCT1 expression, they likely have the same or similar on-switches. But like I said in Watts Doc #40 and many previous podcasts, what oxidizes lactate the most is having large mitochondrial density, and a side note should be large vo2max. I’ve gotten huge improvements in performance in people who have never, ever done an over/under workout. For others, it’s like a default. How I program over/unders will be on one of the podcasts.
A downside of the research here is a lot of studies unfortunately are on cancerous cells too, since cell proliferation pathways are linked to metabolic adaptation pathways they have results that are basically impossible to untangle for a non-expert in these pathway interlinkings like myself. Or seemingly even the experts.
Anyway @Brennus you’re not the first person to notice this and you won’t be the last. Really good observation though, and lots to come on the podcast soon on my theory about how all this works, or doesn’t, and the practical consequences. Odds are pretty good I make some folks pretty upset with the title. Should be fun!
I’m looking forward to the podcast and hoping for some layman’s level take aways. I’m not ashamed to admit the depth of science and chem is frequently over my head. So any basic conclusions and action items are much appreciated.
Hopefully we get to hear clearly how you triage your clients for these interventions.
This is typical of many coaches as well, not just TR. Do we know where did it come from?
Conclusion: A polarised training distribution results in greater systemic adaptation over 6 weeks in already well-trained cyclists. Markers of muscle metabolic adaptation are largely unchanged but metabolomics markers suggest different cellular metabolic stress that requires further investigation.
I’m surprised this changes and the differences happened in as quickly as 6 weeks.
I don’t know if I understand this thread. This paper didn’t look at over-unders.
How are people drawing conclusions about a type of workout when the workout in question wasn’t even studied in the paper?
Well…I don’t know…it makes intuitive sense. But only if you’ve never seen your lactate curve…or any lactate curve. A typical over/under might be…oh, let’s say 4.4mmol on a lactate curve for the ‘over’ and 3.8 for the ‘under’. It’s not ‘on’ or ‘off’ it’s a continuous curve…so right there that’s where you’ve lost me. I don’t think my poor little muscle cells know the difference between 3.8 and 4.4 mmol. They just know whether there is a lot or a little or whether the Kori cycle is really ticking along or whether the Krebs cycle is dominating energy.
So if I want to train lactate production and clearance in a cyclical manner I’m going to do floats where I’m really REALLY producing lactate during the ‘over’…let’s say 130% of FTP…and really clearling lactate on the unders…let’s say 90% of FTP.
Or if I think lactate concentration is the trigger for adaptation of lactate clearance I’m going to do Tmax intervals. Tmax intervals make me feel like somebody scooped out my soul with a dull spoon through my eye socket…but for improving fatigue resistance to repeated anaerobic efforts nothing has been better.
Traditional Over/Unders are just hard threshold work. And a lot of athletes really hate them. I just thought it was funny that maybe all of us that hate doing over/unders but slogged them out anyway could maybe just as well have done an hour of tempo.
6x 4min @ 85% PPO followed by 2min rest.
The logical connection is: over/unders are supposed to increase lactate clearance with a putative mechanism being MCT expression, but it turns out other training methods do the same thing, therefore why do over/unders?
It’s like saying 5+5=10, but 1+9=10 and so does 3+7, so if you only care about getting 10 as a result, then there are multiple paths to success.
In the vein of this thread, numerous studies (and my own experience in lactate testing as well) show that the best predictor of lactate clearance during exercise is just muscle contractions, as opposed to something like completely passive rest. My personal experience is that the people who ride the most and have the highest thresholds clear lactate the fastest in all conditions, regardless of just about anything else.
Seems like it comes from the old theories of lactate causing fatigue, so if you work on “tolerance” and “clearance” in theory one would get faster. Doing a consultation with a burned out pro recently, looking at his workouts there were LOTS of over/unders, and the explanation was that this increases lactate clearance, which will increase FTP. Turns out that’s not strictly true, so of course his went nowhere.
That’s a much faster read than any other paper in this thread. 
Standing by…
The logical connection is: over/unders are supposed to increase lactate clearance with a putative mechanism being MCT expression, but it turns out other training methods do the same thing, therefore why do over/unders?
Respectfully, I don’t think that’s a logical conclusion at all.
It’s analogous to saying “I think aspirin saves lives in heart attacks because it has anti-platelet effects and most thrombi that cause heart attacks are platelet-rich. So I did a study that compared the platelet inhibiting effects of ibuprofen to fluoxetine and found that they there was no difference between the two of them! As a result, I’m not going to give patients with heart attacks aspirin anymore, I’ll just give them ibuprofen!”
The background here being that fluoxetine and ibuprofen, like aspirin, both have platelet inhibiting effects. But are not useful to treat heart attacks.
You can’t conclude that over-unders aren’t adding something above and beyond other types of training unless you actually study them. It remains completely possible that they increase MCT expression even more than the training studied in this paper found.
Just like you can’t conclude aspirin is useless in treating heart attacks based on making inferences from other medications that have only vaguely similar mechanisms of action.
(the other problem being that MCT expression is a surrogate outcome, and it’s completely possible over-unders actually improve performance, just via a different mechanism than people have hypothesized… and we care about performance)
@empiricalcycling I just gave you some love.
Consider it a small downpayment on your upcoming monocarboxylase transporter podcasts.
he just wastes that money buying domains of his main competitor. SMH my head
“Shame my head my head?”
Any chance you can expand on your comment about the domains?
Because I have no idea what that’s about?
inside joke with Kolie, he knows
Who has studied them and where’s the output?
I guess that’s fine too, whatever you said, since I know shit about aspirin and don’t follow your metaphor, so I’d appreciate if you dumbed it down for my simple brain if the rest of this missed it.
I think I follow on MCT being a potential surrogate for other adaptations. That was implied in my point about knowing the “switches” that drive their expression, which means we can focus on the bigger picture of what drives the whole host of adaptations rather than something like this.
Also, and I can tell you won’t weigh this meaningful evidence (though I haven’t seen a study on over/unders specifically the way cyclists do them now, but if you know of one please send it my way) in my coaching experience, whatever performance adaptations we’re supposed to get from over/unders (e.g. 8-10min of 1min over/ 1min under) are usually found, and done better, with different interval types.
I haven’t done a TR style over-under in over 3 years now.
FWIW its what I’ve felt and appear to see in my own not-lactate-testing data. When I ask myself “want to stop blowing up on repeated efforts over threshold?” The answer always seems to be ride more and also work on threshold.
in my coaching experience, whatever performance adaptations we’re supposed to get from over/unders (e.g. 8-10min of 1min over/ 1min under) are usually found, and done better, with different interval types
I don’t disagree with this. I don’t have a strong opinion on o/u’s and in domains like this, empiric experience from working with multiple athletes is an important data point. My main thing is I don’t think the conclusions people are trying to make are supported by this study,
I guess that’s fine too, whatever you said, since I know shit about aspirin and don’t follow your metaphor, so I’d appreciate if you dumbed it down for my simple brain if the rest of this missed it.
Lol. Maybe a bad example. Try this - you do a study that compares doing 10 hours a week of z2 work versus 7 hours a week of z3 work, and it shows that they both lead to essentially the same increase in VO2 max by the end of the study.
You can’t conclude that because these things increase VO2max, that there is no role for VO2 max intervals in someone’s training.
Why don’t instead try articulating explicitly what you think is wrong about the conclusions derived from the studies referenced?