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Exercise training and diet-resistant obesity

Dante_80
Dante_80 Posts: 479 Member
edited August 2022 in Debate Club
A new interesting study was posted the other day in Lancet. Quoting the summary.
Exercise training enhances muscle mitochondrial metabolism in diet-resistant obesity

Summary

Background
Current paradigms for predicting weight loss in response to energy restriction have general validity but a subset of individuals fail to respond adequately despite documented diet adherence. Patients in the bottom 20% for rate of weight loss following a hypocaloric diet (diet-resistant) have been found to have less type I muscle fibres and lower skeletal muscle mitochondrial function, leading to the hypothesis that physical exercise may be an effective treatment when diet alone is inadequate. In this study, we aimed to assess the efficacy of exercise training on mitochondrial function in women with obesity with a documented history of minimal diet-induced weight loss.

Methods
From over 5000 patient records, 228 files were reviewed to identify baseline characteristics of weight loss response from women with obesity who were previously classified in the top or bottom 20% quintiles based on rate of weight loss in the first 6 weeks during which a 900 kcal/day meal replacement was consumed. A subset of 20 women with obesity were identified based on diet-resistance (n=10) and diet sensitivity (n=10) to undergo a 6-week supervised, progressive, combined aerobic and resistance exercise intervention.

Findings
Diet-sensitive women had lower baseline adiposity, higher fasting insulin and triglycerides, and a greater number of ATP-III criteria for metabolic syndrome. Conversely in diet-resistant women, the exercise intervention improved body composition, skeletal muscle mitochondrial content and metabolism, with minimal effects in diet-sensitive women. In-depth analyses of muscle metabolomes revealed distinct group- and intervention- differences, including lower serine-associated sphingolipid synthesis in diet-resistant women following exercise training.

Interpretation
Exercise preferentially enhances skeletal muscle metabolism and improves body composition in women with a history of minimal diet-induced weight loss. These clinical and metabolic mechanism insights move the field towards better personalised approaches for the treatment of distinct obesity phenotypes.
Generally speaking, it is broadly assumed that you cannot outrun your own fork. Exercise is crucial to your well-being and overall health, but a lot less important than nutrition as far as weight loss is concerned. This is a pretty good article explaining why:
Why you shouldn't exercise to lose weight, explained with 60+ studies
It really seems though that there are some people where exercise seems to help their weight loss goals a lot more than previously suspected. That is very interesting and also indicative of the fact that a "one size fits all" approach in weight loss is at best sub-optimal, if not plain wrong.
Thoughts? I'm willing to bet that some think that "diet-resistant obesity" is not even a thing.


Replies

  • Lietchi
    Lietchi Posts: 6,829 Member
    edited August 2022
    That's my one big question here: what does 'diet resistant' mean in this study? Less weight loss for the same amount of calories, since they mention lower quintiles, but the subset selection is a bit confusing?
    If it's just women who lose less weight on a low calorie diet, it seems to just be a synonym of 'women with a lower base metabolism'?
  • cmriverside
    cmriverside Posts: 34,416 Member
    edited August 2022
    NM, don't even want to get involved. If I could just delete this box I would. (Looking at you, MFP)

    I mean, what's new here?
  • cwolfman13
    cwolfman13 Posts: 41,865 Member
    I remember reading something similar several years ago, though as I recall they called it mitochondrial dysfunction rather than diet resistant obesity. What I got out of it in laymen's terms is that basically with mitochondrial dysfunction, energy and nutrients aren't properly shuffled around the body making weight loss more difficult, weight gain more prevalent, and at the root of many of the diseases associated with obesity.

    From what I remember, it encouraged regular exercise as a means to enhance mitochondrial health by increasing ATP and thus shuffling around energy and nutrients more efficiently making weight loss and healthy weight maintenance easier, beyond the simplicity of the CICO model. It in no way attempted to invalidate the CICO model in that it mentioned that CICO is the overarching principle of weight management, but that mitochondrial health or dysfunction add a layer of nuance that doesn't make things so black and white. It also went into quite a bit on nutrition and how quality nutrition and specific nutrients (can't remember them all) play a pretty important roll here as well.

    Anecdotally I find merit in this in that when I initially started trying to lose weight it was with diet alone and a little walking. When I started exercising regularly with more intensive cardio and weight training things seemed to get much easier after about a month or so of regular exercise though I was in the same calorie deficit.

    On the flip side of that, after a few years of regular, daily exercise I was injured and had to take a good 3 months off from doing much of anything. I didn't really change my diet or how much I was eating and just figured I'd gain weight and lose it later...I like to eat and didn't really want to cut back. I kept waiting to see the scale start to creep up, but it took around 6 weeks before I saw any weight gain and from that point on, it was pretty steady gain of about 10 Lbs in a couple of months. At the time I recalled the study I had read and wondered if I was just "running hot" with a fired up mitochondrial function from years of regular exercise and it took 6 weeks to start to go back into dysfunction...IDK
  • Hiawassee88
    Hiawassee88 Posts: 35,754 Member
    edited August 2022
    @cwolfman13
    I surmise you're familiar with the old phlogiston theory of weight management, 1669 by J. J. Becher. Food is burned and phlogiston is released. Theory: Restore phlogiston by eating and eventually you will reach your dream weight. Scientists found items weighed more after the burning process. It's an old theory about metabolism's oxidative component. Food burned = phlogiston released = increase in weight.
    https://www.encyclopedia.com/science/encyclopedias-almanacs-transcripts-and-maps/rise-and-fall-phlogiston-theory-fire

  • NorthCascades
    NorthCascades Posts: 10,968 Member
    Dante_80 wrote: »
    A new interesting study was posted the other day in Lancet. Quoting the summary.
    Exercise training enhances muscle mitochondrial metabolism in diet-resistant obesity

    Summary

    Background
    Current paradigms for predicting weight loss in response to energy restriction have general validity but a subset of individuals fail to respond adequately despite documented diet adherence. Patients in the bottom 20% for rate of weight loss following a hypocaloric diet (diet-resistant) have been found to have less type I muscle fibres and lower skeletal muscle mitochondrial function, leading to the hypothesis that physical exercise may be an effective treatment when diet alone is inadequate. In this study, we aimed to assess the efficacy of exercise training on mitochondrial function in women with obesity with a documented history of minimal diet-induced weight loss.

    Methods
    From over 5000 patient records, 228 files were reviewed to identify baseline characteristics of weight loss response from women with obesity who were previously classified in the top or bottom 20% quintiles based on rate of weight loss in the first 6 weeks during which a 900 kcal/day meal replacement was consumed. A subset of 20 women with obesity were identified based on diet-resistance (n=10) and diet sensitivity (n=10) to undergo a 6-week supervised, progressive, combined aerobic and resistance exercise intervention.

    Findings
    Diet-sensitive women had lower baseline adiposity, higher fasting insulin and triglycerides, and a greater number of ATP-III criteria for metabolic syndrome. Conversely in diet-resistant women, the exercise intervention improved body composition, skeletal muscle mitochondrial content and metabolism, with minimal effects in diet-sensitive women. In-depth analyses of muscle metabolomes revealed distinct group- and intervention- differences, including lower serine-associated sphingolipid synthesis in diet-resistant women following exercise training.

    Interpretation
    Exercise preferentially enhances skeletal muscle metabolism and improves body composition in women with a history of minimal diet-induced weight loss. These clinical and metabolic mechanism insights move the field towards better personalised approaches for the treatment of distinct obesity phenotypes.
    Generally speaking, it is broadly assumed that you cannot outrun your own fork. Exercise is crucial to your well-being and overall health, but a lot less important than nutrition as far as weight loss is concerned. This is a pretty good article explaining why:
    Why you shouldn't exercise to lose weight, explained with 60+ studies
    It really seems though that there are some people where exercise seems to help their weight loss goals a lot more than previously suspected. That is very interesting and also indicative of the fact that a "one size fits all" approach in weight loss is at best sub-optimal, if not plain wrong.
    Thoughts? I'm willing to bet that some think that "diet-resistant obesity" is not even a thing.


    If this is broadly assumed, it's only by people who don't understand math.
  • AnnPT77
    AnnPT77 Posts: 34,216 Member
    This is a big speculative reach, but if we are talking about mitochondrial dysfunction here, it may be interesting that there seems to be a good bit going on with research into the effects on mitochondria of creatine monohydrate (a supplement commonly used, and well regarded, to enhance certain kinds of exercise performance . . . also regarded as quite safe to use, i.e. not a scary PED). There doesn't seem - in what I've read - to be much benefit to body composition absent strength training alongside, or much benefit to weight loss per se (in fact, it tends to add water weight).

    I just started reading some of this (in context of deciding to supplement creatine as an n=1 experiment), so I don't have a lot to offer. A couple of things that may be provocative:

    * A meta analysis suggesting more body fat loss in 50+ folks when supplementing creatine alongside resistance training:
    In summary, this meta-analysis showed that creatine supplementation during resistance training has the potential to decrease body fat in adults ≥50 years of age. Decreasing fat mass is important for reducing the risk of disease (cardiovascular, type II diabetes, obesity), morbidity and premature mortality. While the mechanisms explaining the potential decrease in fat mass remain to be determined in humans, preliminary rodent data suggests creatine influences fat bioenergetics, metabolism, and energy expenditure.

    from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7739317/

    * A narrative review of some of the areas of research concerning mitochondrial dysfunction and creatine (not very consumer-friendly because very technical):

    https://www.mdpi.com/2072-6643/14/3/529/htm#B104-nutrients-14-00529

    Examine.com seems skeptical about the results so far in this area, but sees positives in other respects:

    https://www.mdpi.com/2072-6643/14/3/529/htm#B104-nutrients-14-00529 (<= effects matrix)
    https://examine.com/supplements/creatine/research/ (<= background info)

    Please don't ask me any questions, because I'm still trying to figure this out myself.
  • Dante_80
    Dante_80 Posts: 479 Member
    edited August 2022
    If this is broadly assumed, it's only by people who don't understand math.

    Would you care to elaborate? My understanding is that "outrunning your own fork" means it is very difficult to balance out a bad nutrition with exercise for weight loss. Especially long term. This is the specific definition I was trying to communicate when posting the Vox article.

    Did you mean something different?

  • cmriverside
    cmriverside Posts: 34,416 Member
    edited August 2022
    .
    Dante_80 wrote: »
    If this is broadly assumed, it's only by people who don't understand math.

    Would you care to elaborate? My understanding is that "outrunning your own fork" means it is very difficult to balance out a bad nutrition with exercise for weight loss. Especially long term. This is the specific definition I was trying to communicate when posting the Vox article.

    Did you mean something different?

    It's just you posted this as "New" information. I don't want to speak for NorthCascades, but anyone who has lost weight using calorie counting knows this...which would be people who are using this site.

    If I do a moderate 6 mile walk (as I do daily) I only use about 200-300 extra calories. That's *a* cookie or two. A slice of cheese on a piece of toast. A handful of nuts. I don't get a lot more to eat. I know this because math and I've tested it over time.

    However the benefits of exercise are great, not the least of which being that daily exercise allows me to stay in my calories comfortably. For whatever reason, when I don't exercise I tend to seriously over-eat (like by several hundred calories - not just that 200-300) and when I do exercise I can be happy with my calories. I don't think it's psychological, I think there are greater biological forces at work.
  • Dante_80
    Dante_80 Posts: 479 Member
    edited August 2022
    .
    Dante_80 wrote: »
    If this is broadly assumed, it's only by people who don't understand math.

    Would you care to elaborate? My understanding is that "outrunning your own fork" means it is very difficult to balance out a bad nutrition with exercise for weight loss. Especially long term. This is the specific definition I was trying to communicate when posting the Vox article.

    Did you mean something different?

    It's just you posted this as "New" information.

    But I didn't? The only "new" information in the OP is the new study about exercise and muscle mitochondrial metabolism in diet-resistant obesity. ;)

    The part about "outrunning your fork" is very well known (and the old Vox article I linked explains the reasons for it through studies). But NorthCascades was somewhat disagreeing with it (I think?) so I asked for some clarification.

  • sijomial
    sijomial Posts: 19,809 Member
    edited August 2022
    Dante_80 wrote: »
    If this is broadly assumed, it's only by people who don't understand math.

    Would you care to elaborate? My understanding is that "outrunning your own fork" means it is very difficult to balance out a bad nutrition with exercise for weight loss. Especially long term. This is the specific definition I was trying to communicate when posting the Vox article.

    Did you mean something different?
    Not @NorthCascades but I agree with him.

    Why do you assume bad nutrition though? That seems a huge reach. Serious exercisers tend to be pretty nutritionally aware.

    Personally I could very easily use exercise to create a sustainable and significant deficit (I don't need to though). I could create an excessive short term deficit from exercise if I really wanted to!
    Cut my weight to an unusually low level this year as a performance experiment and it was a damn sight easier when I'm eating 3000 - 4000cals than if I was restricted to a sedentary allowance.

    In the past I also simply changed my commute swapping one leg of my journey from public transport to walking and saw a gradual loss of weight.

    To me "you can't outrun your fork" is one of the dumb phrases that have passed into common usage and adds very little benefit or insight. It's much more nuanced than that.
    The number of people who could benefit health-wise from adding more movement (including exercise) is growing all the time and this dopey phrase does nothing to encourage them.