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"Why Increasing your Aerobic Power Makes You LESS Efficient" - OutsideOnline

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More on the theme of crossovers between elite athletics - and the opportunity for research synergy in M.E. I would so love to see our Silicon Valley, Harvard (Systrom et al), and WorkWell researchers connect with these guys at Silicon Valley Exercise Analytics, that just published an article in Nature on the tradeoff between V02Max and metabolic efficiency. If the way athletes train is critical to their performance, I think we might learn a LOT more about the nuanced details of HOW the lesser affected M.E. patients might be able to selectively train to reduce the devastation of PENE - within the constraints of M.E. (See disclaimer below). This might also help point to targeted pharma treatments.

My interest was first piqued by a fascinating Boxing Day article in OutsideOnline.com entitled, "Why a Higher V02Max isn't Always Better". https://www.outsideonline.com/2407295/why-higher-vo2max-isnt-always-better It's one of their Sweat Science features, written by Alex Hutchinson, who recently wrote a book (intro by Malcolm Gladwell), entitled, Endure: Mind, Body, and the Curiously Elastic Limits of Human Performance. IMO this thinking fits beautifully with what leaders in M.E. research like the WorkWell team, are saying - that training our aerobic systems can be fraught with peril in M.E., and that - if we are lucky enough to be able to do so - we must train with exquisite care and precision, and with a focus on anaerobic performance in the case of M.E. Can we learn from what these Swedish researchers are saying about V02Max vs efficiency?

Hutchinson cites the work of Swedish researchers and Silicon Valley Exercise Analytics (Svexa), specifically their Chief Scientific Officer, Filip Larsen, which was summarized in this blog: "Why Increasing your Aerobic Power Makes You Less Efficinent".
https://www.svexa.com/post/why-increasing-your-aerobic-power-makes-you-less-efficient

This, in turn, is based on what I think might be mandatory reading for metabolic junkies in M.E. research: a November 2019 article in Nature Communications : "Complex I is Bypassed During High Intensity Exercise", https://www.nature.com/articles/s41467-019-12934-8 on which the above blog entry was based.

After all, CPET data supports that mere activities of daily living while living with M.E. are akin to high-intensity exertion. My own V02 Max results from Workwell support that.

What Larsen and his team propose is that, while the Anaerobic Threshold is important in training athletes, the metabolic "switch" that occurs at Complex I might offer a new metric to gauge exercise efficiency. They call this "Complex I Max". Are our M.E. researchers following this, and might this offer an important new metric for M.E.?

Competitive athletes usually perform physiological testing to assess their aerobic threshold, functional threshold power (FTP) and VO2max to optimize their training. The authors now propose a new physiological breaking point where metabolism switches between efficiency mode to power mode, that they term “complex I max” (CImax). In the trained cyclists in this study this occurred around 55-65 % of maximal heart rate. Knowing, and increasing, this breaking point will give athletes and coaches an advantage when designing training protocols and will be valuable from a strategic perspective when racing long endurance events.
Suffice it to say, if you are able, do take a look at this work. I find it fascinating - and hopeful for our understanding of M.E. We know that GET is dangerous for M.E., and that any type of exertion is especially devastating for our severe patients. But we also know that some M.E. patients find incremental improvement with anaerobic exercise, as per Klimas & WorkWell recommendations. Elite athletes are constantly pushing the boundaries of HOW they train to optimize performance in their particular discipline. But they're getting smarter and more precise about how and when they train. I think this nuanced approach could help us understand our own physiological breaking points., and perhaps how to bypass them (at least for efficiency) - and why.

Disclaimer right off the bat - having been pretty much bedbound for the better part of 4 years (23+hours/day) in the past, & mostly housebound/bedbound in the past decade and a half, I am acutely aware that the elite athletics/M.E. crossovers and nuanced training insights may be painfully irrelevant for our severe patients. But I do believe that the metabolic science underpinning this work could be deeply relevant for diagnostics and management (if not ultimate pharma treatment) of M.E.. It kinda excites me.

Would love to write more - this is all my tank allows for now.
 
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Or for a summary, just read this excerpt, from the Nature Abstract: https://www.ncbi.nlm.nih.gov/pubmed/31699973

"Human muscles are tailored towards ATP synthesis. When exercising at high work rates muscles convert glucose to lactate, which is less nutrient efficient than respiration. There is hence a trade-off between endurance and power...."
We know that metabolism in M.E. is exquisitely inefficient, and pathologically tipped towards anaerobic metabolism. Maybe we can slipstream with these athletic researchers?
 

ahmo

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@Joy&K0$ Thanks for this. Not sure I've got much comprehension, the Nature abstract didn't seem to say much. But I've just been considering aerobic/resistance exercise.

I've now spent 3 months recovering some flexibility and mobility, thanks to a good physio and a commitment to change my downward trajectory. Initially I just worked on stretching. Once I got the correct targets and exercises, I finally could make gradual improvement. And then I began some pool exercises, beginning w/ walking, since my legs were too weak and bound up to walk my way through my restrictions. And I've worked my way up to 7 laps in the pool, about half using my arms, and half only legs and kickboard.

I've been thinking about what next. Physio suggested an exercise bike, which I got, but that doesn't give me nearly the aerobic experience as the pool. But I don't think I'll stick to the pool when the weather gets cool, even though it's indoor. So your post makes me consider the idea of combining the bike, which is good for my knees, w/ some mini-tramp, which gets me puffing. And something approaching resistance, not with weights, but just body, Pilates style. I think I'll get over the desire for aerobic training, be very circumspect about pushing myself. I consider myself moderate ME, spend a lot of time resting, ok w/ caring for myself. cheers, Happy New Year.
 
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Thank you ahmo!

To be clear, my understanding is that we need to avoid stressing our already-taxed aerobic systems, and work on AN-aerobic conditioning, or VERY, very careful aerobic work below a carefully determined heartrate. I would encourage you to take a look at the WorkWell Foundation's website, where they have excellent videos that outline what we can do to increase our functionality, without precipitating PEM or long-term crashes. https://workwellfoundation.org/resources/

For example, from the section "Resources" they have Part 1 and 2 of "Expanding Physical Capability in ME/CFS":
and

Many patients (myself included, and I'm a former physiotherapist, have gotten MUCH worse from attempts at aerobic conditioning, so I would urge caution with any aerobic work (bike, pool), if you dont first have data on your own V02 Max - or the cliff, where you crash into unsustainable metabolism.

Workwell have (somewhere?) a case report of a lady who did progressive aerobic conditioning, and set herself badly back. They also have recommendations on how to proceed with an-aerobic conditioning.

This is why I'm so interested in how different types of athletes use specific conditioning techniques to target specific muscle types and specific metabolic pathways. I believe the work of this team featured in Nature could be important for our researchers.

Hope this helps!
 

sb4

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@Joy&K0$ I haven't read the articles but it sounds interesting. Am I right in thinking the CFS metabolism is like the athletes when they are going all out. Ie, the mito focus purely on maxing out ATP production using "all" fat and then the cytosol maxes out its ATP production using all glucose.

This would explain why some CFS people notice worsening with carbs, indeed I have significant increase in symptoms post carb meal.

I am thinking what happens is the mito are running as maxed out as they can on mainly fat when I am at rest. Then when I eat glucose meal insulin and the randle cycle presents my cells with a lower ratio of fat and higher ratio of carbs. Then something mysterious happens where I can't use carbs properly so they get dumped into lactate and indeed I get a lactic acid build up from doing mimimal tasks despite my muscles not really being all that small nor deconditioned. Anyway, this leaves the cell with less energy than it had before and a build up of lactate in the cell / blood causing heart to pump harder in order to try and get O2 and nutrients to cells to help them generate energy.

Wheras if I eat a VLC high fat meal I don't get anywhere near as bad heart symptoms because the cell is producing more or less the same energy as fasting. It seems my cells are set up to use fat for some reason. Possibly because they are going all out to produce energy, like the athletes despite the fact I am just sitting in a chair.

Makes me think about metformin. I originally dismissed the idea because I already have a lactic acid problem and other CFSers reported getting worse on it, but recently someone reported getting better. Supposedly metformin works by inhibiting glucose electrons entry into complex 2 of the mito. This means there is less reverse electron flow on the ECT. Reverse Electron flow generates super oxide which then makes the cell more insulin resistant (a good thing if the cell is full of energy).
The glucose then gets wasted as lactic acid but less insulin resistance means the fat cells release more fat, and this means cells will use more fat as energy.

I figure if we are wasting glucose as lactic acid anyway then we might benefit from avoiding the problem I speculated on earlier which was after eating glucose meal our cells take up less fat and more (relatively) useless glucose. If our insulin signalling is normal then some of this glucose will enter complex 2 and signal cell full and insulin resistance despite the cell struggling for energy. If we stop glucose from entering complex 2 with metformin then maybe our cells will see roughly the same amount of fat that they did when fasting.

I realise I haven't explained this well nor thought it through that well so I apologies for that. Just the thing that is bugging me is why are my cells running on fat okish (actually pretty bad) yet when I add glucose they seem to run even worse. This is taking into account the extra blood flow required for digestion as the same thing doesn't happen with low glucose meal. Why can't the cell be supplied with the same amount of fat for energy and just waste the glucose as lactic acid. I can only think that either the cell recieves less fat after glucose or the lactic acid itself is causing issues.
 

sb4

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One more thing I will add. I notice that if I eat carbs in the day when insulin sensitivity is the highest I get the worst post carb symptoms. However if I eat carbs after it has been dark for a while (sun gone down) I get significantly less post carb symptoms. This is when insulin resistance is highest.

So it appears that insulin could be the factor that is causing the cells to struggle with carbs which strenghens the idea in my previous post that the reason I get symptoms after carbs is because the carbs replace some of the fats that where originally going to the cell and generate lactic acid instead of useful mitochondrial oxidation.

So maybe metformin would allow my cells to still receive adequate energy from fat even in the presence of glucose?
 

Wishful

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This would explain why some CFS people notice worsening with carbs, indeed I have significant increase in symptoms post carb meal.
I had worsening 20 minutes after a quickly-digestible carb meal. Taking BCAA's with the meal blocked the worsening (or maybe delayed it and spread it out until it was unnoticeable). That implies that insulin's ability to increase TRP transport to the brain was responsible.

If you have BCAA's available, test whether they affect your response to carbs. I didn't notice a worsening if the carbs were high-fibre.
 
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Wow @sb4 and @Wishful, what thought-provoking replies. SB, I think you're spot on with the following:

YES! (I think) to the following:

Am I right in thinking the CFS metabolism is like the athletes when they are going all out. Ie, the mito focus purely on maxing out ATP production using "all" fat and then the cytosol maxes out its ATP production using all glucose
.

Then something mysterious happens where I can't use carbs properly so they get dumped into lactate and indeed I get a lactic acid build up from doing mimimal tasks despite my muscles not really being all that small nor deconditioned.
At the best of times, I struggle with the complexity of metabolic science, so I'm working with a painfully broad-brush understanding, & I think you guys might be at Version 4.0, while I'm still at 1.1 LOL. But I'd hazard a guess that the "something mysterious in your above quote" MIGHT be this bypass of Complex 1, which the sports scientists are finding during high intensity exercise.

The authors now propose a new physiological breaking point where metabolism switches between efficiency mode to power mode, that they term “complex I max” (CImax).
The question might be - how to prevent this bypassing of Complex 1, this new physiological breaking point? What are the molecular triggers? How might we inhibit or delay this bypass? (You can bet the sports scientists will be looking at this too). I think it would be worthwhile for our M.E. scientists to learn how to measure this bypass, and then track it in M.E. patients. We have been looking at the Anaerobic Threshold as our "canary in the coal mine:". Could this “complex I max”, or CImax be a LEADING indicator, or even a biomarker for PEM if happening at trivial levels of activity for M.E. patients (but metabolically equivalent to intense athletic exertion)? Might ingestion of carbs or BCAA affect where this "switch" kicks in? (One of possibly many hacks that could be judiciously tried, while we wait for better studies). If Dr Davis & OMI collaborators could find an easy way to measure this in real-time, then we might get the kind of biological feedback that could support smart strategies like @Wishful's.

FWIW I definitely have post-prandrial energy issues, also worse in the a.m.. And I'm still experimenting with ketone ester supplementation, although the cost of the cadillac version (IMO HVMN's Keton esters - see the thread on it) is limiting me to laughably rare use. But my N of 1 is leaning towards a tentative feeling that it gives me more in the tank. Now am trying to biohack with wearable technology to figure out how to quantify when I hit my AT, and if/how ketone supplementation is affecting my gas tank, PEM etc. Will write more on that later.

@Wishful - your comment on high-fibre carbs. Is that like creating a slow-release of carbs? I'm wondering if taking fibre supplementation might help when taking any carbs??

Once again, thanks for your replies, very thought provoking.
 
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sb4

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@Wishful Unfortunately, I have tried BCAA and didn't notice any difference. Perhaps I need a much bigger dose.

@Joy&K0$ I tried Ketone Salts but didn't notice much difference in glucose tolerance however it seems MCTs (C8) did produce a noticable difference. I also found emulsifying in eggs helped less GI symptoms induced by the MCTs.
 

Wishful

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@Wishful Unfortunately, I have tried BCAA and didn't notice any difference. Perhaps I need a much bigger dose.
Oh well, maybe it's one of those 'just me' things: my sensitivity to TRP in my brain may be unusual. I think I used less than a level tsp which provided full blocking, and it worked the first time, so it's not a 'need to take it for x weeks' treatment. If it didn't work for you, taking more for longer is unlikely to work, at least via the mechanism it uses for me.
 

Wishful

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@Wishful - your comment on high-fibre carbs. Is that like creating a slow-release of carbs? I'm wondering if taking fibre supplementation might help when taking any carbs??
I haven't experimented a lot with adding fibre. I'm not sure whether white flour + wheat bran is as effective as whole wheat flour. For that matter, I don't know whether typical whole wheat flour isn't just regular white flour that had some 'waste product' bran added back in. :rolleyes:

What I can say is that rolled oats didn't trigger the effect, and neither did whole wheat flour. Regular pasta did trigger the reaction, but high-fibre pasta doesn't. I found only a few brands of snacks (crackers, etc) that didn't cause me problems, and they had 'whole wheat flour' as the main ingredient. Ones marketed as 'whole grain' or 'high fibre' with regular wheat flour as the main ingredient did cause problems.

I haven't noticed the worsening of ME symptoms from quickly-digested carbs for a while. More recently the quickly-digested carbs caused insomnia. I'm not sure whether that's still an issue; I just don't buy the regular flour products anymore.
 

Wishful

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We have been looking at the Anaerobic Threshold as our "canary in the coal mine:". Could this “complex I max”, or CImax be a LEADING indicator, or even a biomarker for PEM if happening at trivial levels of activity for M.E. patients (but metabolically equivalent to intense athletic exertion)?
I believe that anaerobic activity problems are a secondary symptom of ME. I have ME and don't have any muscle problems. I can do a six-hour bike ride without even triggering PEM, but just a few minutes of activity that I'm not used to doing, such as washing a window above my head, does trigger PEM. Would that indicate a difference in thresholds between often-used and little-used muscle tissue, or something else. I did think that the difference was in how much damage those muscles acquired in those activities, thus triggering different levels of immune system activation (to clean up damaged cells). I came up with a new hypothesis yesterday, which I'm looking into. It seems that there are significant changes in cerebral activity due to physical exertion. It takes more 'cerebral effort' to push your muscles harder. I know that certain types of cerebral effort can trigger my PEM, so maybe 'pushing' oneself physically causes similar cerebral changes that trigger PEM. Alternatively, maybe the cerebral changes due to ME makes it harder to make those certain brain cells send adequate signals to the muscles. More research required...
 

ljimbo423

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Unfortunately, I have tried BCAA and didn't notice any difference. Perhaps I need a much bigger dose.
When I first tried BCAA's I thought I wasn't going to get any benefit from them. I started with 1-2 grams a day and worked up to 8 grams a day and noticed just a slight increase in energy.

When I got to 12-15 grams a day, the difference in my energy levels was undeniable! I've been taking 12-13 grams a day ever since, I won't be without them.
 

ljimbo423

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Maybe you're blocking TRP transport all the time. :thumbsup: Might be hard to notice changes in post-carb symptoms if you're saturated.
I'm not sure how the BCAA's are helping me. First I thought they were bypassing a dysfunctional PDH enzyme in the mito. and creating more energy that way.

Then I found research that says they cause a switch in activated microglia, from a M1-proinflammatory state, to a M2, anti-inflammatory state. Then theirs the Tryptophan angle! I get dizzy just thinking about it!

Maybe it's all 3? Whatever the reason is, I'm happy to have found another arrow to put in my quiver.:)
 

panckage

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I've been thinking about what next. Physio suggested an exercise bike, which I got, but that doesn't give me nearly the aerobic experience as the pool. But I don't think I'll stick to the pool when the weather gets cool, even though it's indoor.
FWIW I find I can use an exercise bike pretty fine but swimming gives me a lot of PEM. As you alluded to an exercise bike is very limiting in terms of ROM so it is not enough by itself. If swimming is fine for you i would encourage you to keep trying even when its cold. Exposure to cold (as well as hot) seems to be important for health, just as ROM are for the body. Wim Hof has been formally studied and there is evidence to support this. I am still a newbie to cold exposure but it seems to be helping me with proper movement
 

Wishful

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FWIW I find I can use an exercise bike pretty fine but swimming gives me a lot of PEM.
For me it's not the level or duration of exertion that results in PEM; it's the use of muscles beyond their normal movement range. Riding a bicycle for 6 hrs (after gradually building up to it) didn't cause PEM, but climbing a ladder once (different motion/stress) did trigger it. My guess is that swimming would trigger my PEM too, even if bike riding doesn't.

If you are thinking of buying exercise equipment, I suggest something that best matches the activity that you are most accustomed to. If you weren't a bicycle rider for a long time, that might not be the best choice. If you're used to swimming, look for something that uses similar movements.
 

ahmo

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I've just decided to give up swimming twice a week. Maybe if I go to once a week I'll have a bit more energy to do things like cleaning tasks.:rolleyes: Feels good to finally exercise, but I don't know that it's the best for my body.
 

panckage

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I'm still trying to find out why "swimming" (mostly just water exercise) is so bad for me. I'm doing the Wim hof cold immersion now and generally having the same type of crashing after a short period. I am investigating whether it is actually my body's response to the cold/cool water (and subsequent rewarming) as opposed to the exercise that is causing the crashing