I asked that somewhere on here, and Kolie said yes. He said you’d still need to go hard, no matter the type of exercise.
1 Like
Interesting, on ramp tests it’s always my legs that quit working
1 Like
Another good graphic on the pathways and timing of changes leading to increased VO2max.
Important clarification. Best way to train VO2max, arguably because it’s less efficient. Best way to race is probably your natural cadence. Your brain is pretty good at finding the path of least resistance for what’s most efficient for you. Just like heat training, altitude training, low-carb, etc. The purpose is to increase the training load and decrease your performance. You’d want to do the opposite for racing/riding. Training makes you slower! Recovery makes you faster. That doesn’t work as well as a slogan though 
Just encountered a study looking at LEG vs LEG+ARM training interventions. Sure enough LEG+ARM showed greater improvements to VO2max, Q, SV, etc. The real question is how will those improved physiological measures relate to actual performance improvements if your sport is cycling? The only performance outcome measure was economy (W/L/min) at the end of a ramp test, which I manually calculated. Both groups improved marginally (94 to 96 and 97 to 98 W/L/min at VO2max for LEG and LEG+ARM, respectively). So while the study concluded that LEG+ARM exercise could improve physiological measures, the effects on performance are equivocal.
My quick answer to this is: “that’s where the action is”
Legs are where most of the contractile and metabolic activity is taking place, and where most of the metabolic milieu is accumulating. Makes sense that the biggest STOP signal is being interpreted by the brain as coming from the same place. But I don’t have a more detailed understanding than that.
Yeah Kolie mentions this in the podcast. An SV plateau can be seen in untrained subjects, but typically SV increases linearly to max in endurance trained athletes
5 Likes
According to this study, SV declines in trained subjects as you approach VO2max.
It appears to have been performed in response to this “Point” article, which summed up a number of other studies showing the same thing.
The Counterpoint article and numerous follow-up letters are also worth reading, at least if CV function during exercise is your bag.
2 Likes
If training using more muscles results in a higher VO2max, then why do the creme de la creme of endurance athletes all have similar VO2max values, regardless of the sport?
Good question. I don’t know. How would you answer that?
1 Like
My answer would be that any large muscle mass activity must place enough demand on the heart that it becomes the limiter. What other answer could there be?
1 Like
That’s not entirely true. Cross-country skiiers and rowers consistently test higher than runners, who test higher than cyclists because, I believe, their testing protocols involve more muscle mass.
If you want to maximize your numbers, make sure to test on an rowing ergometer or treadmill instead of a cycling ergometer.
On another note, would simply concentrating on boosting your stroke volume be a viable strategy for sustained long-term power gains?.. What sort of gains can you make before running up against physiological limits (genetic or otherwise)?
1 Like
what is the point you’re trying to prove? Decline or plateau?
have you checked the referenced studies? They all seem to be on “healthy subjects”, not on “trained subjects”
TL;DR
- there is a conflict of interest here.
- individualised training as suggested by the podcast is certainly an attractive concept, but the claim that it works may be insufficiently supported by evidence.
After having listened to the podcast (once), I want to add some context from my perspective. English is not my native tongue, so I may be missing some nuance here and there. I truly appreciate the mission of this podcast. I think the physiology is explained to a great detail and it is well presented, and I’m sure it takes a ton of time to dig into the literature and present it this way.
Then, I am also very mindful of the fact that there is a major conflict of interest here. This podcast is essentially promoting a coaching service, and as such it may benefit from being presented as having “better insight” than others.
A major criticism that comes forward in this podcast is that the Ronnestad study is not using an “individualised” training recipe, instead it treats the whole intervention group the same. Moreover, the results are said to show inter-individual variation in response (“non-responders”). It is suggested that by individualising training, this may have been prevented. This is also made as a major point in other podcast episodes. Empirical Cycling is portrayed as “we do individualise our training” and “our training works in people who have plateaued over a long time” (i.e., previous non-responders).
this is scientifically termed heterogeneity in treatment effect (HTE). it is often observed that only a part of the people that are treated respond to a drug in a study. there are often many post-hoc ideas and explanations why that is, based on our understanding of physiology (here comes empirical cycling). it’s a sexy idea in science and medicine as it opens the door to personalised interventions (diagnostics and treatments). unfortunately, it is often insufficiently supported by the evidence.
it is very easy in post-hoc analyses to identify variables that seem to determine a treatment effect, when it is actually not true (type I errors). such variables may even seem extremely plausible and fully supported by understanding of the physiology.
essentially, we don’t know if a treatment works 70% of the time in 100% of the individuals, or 100% of the time in 70% of the individuals. moreover, any individual can either respond to an intervention, or not. we only know afterwards, when we look at a group, how often it works and how often it doesn’t (Ronnestad). can we know beforehand (i.e., personalise interventions)? to not make errors, you need to define before a study which variables you think may stratify treatment effects.
the only way scientifically demonstrate HTE is to perform a repeated (randomised) cross-over study, where people are subjected to the different treatments such that intra-individual responses can be compared. an alternative and more useful (yet much more expensive) way can be to design a randomised controlled intervention, where you stratify for a variable that you think is important to determine the treatment effect.
the individualisation of training interventions (here by personalised coaching) is thus, unfortunately, only supported by extrapolation from physiology. such individualization may sometimes work, but sometimes it may not - unless somebody does the study we don’t know.
of course such stratified intervention studies are exponentially more costly, require a larger samples size, and are more laborious to design and perform than the “simple” studies, like the Ronnestad study. that is precisely why they are often not performed. it doesn’t mean that scientists are ignorant, it means that there are real-world constrains to what we can do with the money and time at hand. I don’t think we should blame the scientists for such constrains.
references on HTE:
- Statistical pitfalls of personalized medicine
- Individual response to treatment: is it a valid assumption?
- Viewpoints on Heterogeneity of Treatment Effect and Precision Medicine
Where this podcast really goes over the top for me is when the authors of the Ronnestad study are said to be “disingenuous” and “don’t understand what they are doing” [my memory]. this is put forward in a public way without giving the authors a chance to comment.
so I think at least for this part of the podcast, the criticism is insufficiently based on data supporting individualised intervention, is made against the background of a big conflict of interest, and is unnecessarily critical of the authors of this study. make of that what you want.
18 Likes
You’ve been misled. XC skiers often have high VO2max values because they are “right-sized”. If you apply allometric scaling instead of using a per ratio (i.e., per kg) approach, there is no difference across sports.
(Note that in cardiology, we routinely normalize cardiac dimensions to estimated body surface area, not body mass.)
Trained cyclists can achieve true VO2max when cycling. Even highly-trained swimmers can come very close, even though swimming is mostly an upper-body sport, and the arms can’t normally demand as much blood flow and oxygen as the legs.
Finally, the way to “concentrate on increasing SV” is just to do a lot of hard training. There is no need, and really no ability, to try to be any more specific than that. (Elsewhere I joked about doing intervals while immersed in cold water, in an attempt to maximize cardiac adaptations by enhancing LVEDP. It’s actually been tried, and it doesn’t help.)
That the question still seems to be rather unsettled, even among the true experts.
BTW, that’s a plot of Q, not SV, that you posted. Assuming HR is still increasing quasi-linearly, it means that SV has peaked and is decreasing.
1 Like
The entire basis of the podcast is to show people the underlying physiology of performance to make their own training decisions on the factors that they consider important after learning about them. It’s why we spent so long setting up the episode with the previous episodes. That episode’s structure began with my approach, and then explained what I felt would be the next obvious question “where do 30/15s fit in?” For improvement of long term structural VO2max limiters, they do not, hence the preceding several hours of podcast on avO2diff, hemoglobin and respiration, ramp testing and anaerobic capacity, etc. If the Ronnestad study and intervals weren’t so popular, and I were not absolutely certain it’s a question I’d get 1000x, I would not have even given the study a second thought, and never would have mentioned it, because I’d much rather be constructive than destructive. I just didn’t see there was just nothing to be constructive about with that study. The sheer number of studies that leave something to be desired in methodology outnumbers the high quality ones. For instance, there’s a study that shows that a-vo2 difference explains the entire variation in vo2max between various levels of trained or untrained population, but they don’t even look at SV or BV. I’ll never include that study on the podcast unless it becomes popular and I feel it warrants discussion.
If I really wanted to make the case for the necessity of my coaching services, I would be taking a different approach, and not giving people the knowledge to make these improvements in their training without me. But I can’t train everyone, I don’t want a coaching empire like some. I want to pay my bills and retire (if I’m fortunate enough to live that long), and I want everyone to know what’s beneath their intervals and why, so they can train better. My case for individualization of intervals themselves here pretty much only extends to duration and execution, and I provided suggestions for ways in which people can do that as well.
Here’s the big reason we need an individualized approach in training: people vary, and perhaps more in sport than in medicine but I don’t know much about medicine so I can’t say that for sure. But here’s a few thoughts on variation in people that need individualization. Peak power relative to FTP, FTP relative to vo2max, etc. When studies do things like assign a work rate as a % of final ramp test power, it doesn’t take into account the variability in anaerobic capacity, which can go from 8kJ to 50kJ. It also doesn’t take into account where FTP is relative to vo2max, so a group working at 80% vo2max (in L/min) may be working over or under threshold, particularly if they’re not too well trained, and even if they are many athletes have an FTP below 80% vo2max. Even blood lactate concentration at MLSS varies, with values as high as 8-10mmol, despite that a population average tends to be around 3.8-4mmol but can also be lower. Where athletes are in-season and their training matters with this too. These are things we spent hours discussing on the podcast so people can not only interpret studies better, but also make better training decisions for themselves. In the Ronnestad study I would love it if they had done an MLSS test and looked at variation on where athletes were in relation to that, and that could be a good discussion on communication and expectations between researchers and subjects.
So yes, I very much think that an individualized approach is necessary in sport. Imagine if we looked at the population average of FTP in men with 5 years of endurance training and competing, and we find a population average of 300w. Assigning 2x20min at 300w should yield the same training result, right? No, we failed to individualize it to an important physiologic point. But what you haven’t ever heard me do is tie something that varies in people to such a physiologic point unless I am absolutely certain people don’t vary. Intervals at 90% FTP for example. People do vary in how long they can hold this power, both continuously and intermittently, but my recommendation is to look at how long you can hold it and then extend it. That’s what I mean by individualized, I’m sorry if that hasn’t been made sufficiently explicit.
I’ll give you one more. An article by two of the best right now, Lundby and Montero. When they don’t see a training response, increase the stimulus (more workouts per week) and then there is no more non-responders. And because they’re looking at vo2max as the response in untrained individuals, they measured all the major factors that influence vo2max, as we discussed in many episodes. That’s also individualization. It can take many forms.
The entire point of this podcast series on vo2max was to show people how various types of training affect different aspects of vo2max in both the short and long term, and my suggestion for how to improve everyone’s long term limiter of stroke volume, and why I think my approach to this works and accounts for individual variation in SV plateau or not. Nobody has to sit through ads for the podcast, agree with me, hire me, or take my suggestions, or listen to a word I have to say. Ronnestad is free to answer my criticisms. He is welcome to comment and defend the methodology. I said I felt it was disingenuous or there was a lack of understanding, not both. The mere fact that we need to question the instructions, training intervention, or testing protocol instead of just debate the mechanism of the results is, at the very least, to me, very poorly thought out at best. I’m happy to apologize for being critical of his character, but I stand behind my various criticisms of the study design, for whatever reason it was badly done.
18 Likes
There are problems with the methodology of the Ronnested study that are just basic bad science. I fully appreciate the difficulties of doing good science, money, recruiting participants, time scale of fitting it into a grant or someone’s thesis research… (I work in science too, even though this isn’t my field). I wouldn’t call the study disingineous or anything like that, I just think they didn’t mitigate against a few factors that are influencing their results to a degree that makes them nearly meaningless.
One of the problems is with the two tests before and after the training intervention. What is the uncertainty of those two data points? If one of the tests is out, it has a big influence on the result. For example, a participant could have hold back on the first test because of unfamiliarity with the test protocol or even the equipment. Doing it a second time, there suddenly is an improvement. It is off course difficult to repeat these tests, because of scheduling, timing, and even the training effect of the test itself. But the authors could have at least discussed this error source, and tried to estimate the magnitude. How big could it be, and how does that compare to the expected change from the test protocol?
Another problem is that these were trained subjects, and they continued some training in addition to the training intervals. Was this other training in line with something that would normally keep their fitness ‘steady’? If for example, they suddenly trained significantly less, their fitness would decrease, regardless of the miracle intervals they did for the study. Were is the attempt to quantify this outside effect?
It is off course incredibly hard to control all these factors, or even being aware of them, especially for researchers that see the participants maybe once a week.
Maybe a different approach would be to design studies where researchers worked closer with coaches and their athletes, and go alongside the training the athletes do anyway.
3 Likes
I had two TR pages open. I meant to post on the Kolie Moore podcast wisdom post
Sorry
Ill still stand by TR and Kolie Moore podcast together are answering many question i have about training.
1 Like
Why match for power? If the athletes could tolerate 410 seconds at >90% of VO2max, shouldn’t they have cranked up the intensity of constant intervals?
Edit to add: Based on this graph from the paper, it certainly should have been possible. Regardless of the format, average VO2 was only 4.4-4.5 L/min during the on periods, or only about 85% of VO2max. Counting seconds above 90% therefore seems rather disingenuous when the overall intensity was actually only moderate.
FWIW, the one time they had me do 6 x 5 min intervals hooked up to the metabolic cart, I hit VO2max at the end of each interval.
Edit to add 2: The more I read the study, the lower my opinion of it. Basically they had folks doing 5 minute intervals at approximately FTP, and make a big deal out of the fact that throwing in the occasional 30 second surge increased the demand a bit. So what?!?
1 Like
Strawman intervals again but they’re not even trying to hide it.
Varied-intensity work intervals consisted of three 30-second
surges at 100%MAP, interspersed with two 1-minute blocks,
and a final 1.5 minutes at 77%MAP. Constant-intensity work
intervals consisted of 5 minutes at 84%MAP
So… those who intermittently worked harder than 84% MAP saw more time over 90% vo2max? There’s no equivalence between those intervals, which were probably below LT for some (poor measurement of that btw) and a little above it for others, but plenty of headroom to go harder. I’m not sure what this study is really supposed to show. Spurious assessment of FTP as well, no way to tell where athletes were working relative to it, so a little below for a few and probably a little above for some too. They didn’t publish L O2 per interval either, just % vo2max. Not egregious here, but that’s statistical sweeping under the rug. So… Not long enough at, oh, let’s say 95-105% FTP, with slight bias to over FTP to be generous, to elicit much time at 90% vo2max. Lots of flashy numbers in here to distract from more strawman intervals.
In comparison with a HIIT session with constant-intensity work
intervals, well-trained cyclists sustain higher fractions of VO˙ 2max
when power output is repeatedly varied within the work intervals.
That’s the conclusion. I think anyone can understand why it irks me. Honestly, I’m most disappointed in *Stephen Cheung for lauding this design and methodology (we’ve already had words elsewhere so that won’t come as a surprise) but appreciate he’s not over-interpreting the results.
1 Like
WRT to studies on the topic, what would be a better approach than power-matched intervals? IF matched? Just go as hard as you can for the duration, regardless of if its 5 mins steady, or 5 mins variable, and let power and IF fall where they may?
WRT training, at what point (I.e. recreational → semi serious → semi-pro → pro cyclist; or maybe hours per week of training) does the distinction on the kind of VO2max interval you do matter more than consistency
of doing your chosen interval style?
Or is there a certain athlete physiology that responds better to certain kinds of VO2max intervals, regardless of training volume?
2 Likes