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Which exercise is important to reversing/managing Insulin Resistance and Diabetes?

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  • Which exercise is important to reversing/managing Insulin Resistance and Diabetes?

    This is one topic that I hope Dr. Brewer sees and looks into as I think that it is meaningful. Peter Attia recently released a podcast with Inigo San Milian about how the mitochondria function in people with insulin resistance/pre-diabetes/diabetes vs. elite athletes, in particular cyclists. It is pretty clear that mitochondria function/efficiency is a major factor in maintaining metabolic health. We know clearly that mitochondria function/efficiency decreases with age, and that is one of the biggest drivers of insulin resistance. So what can we do whether we are young or old and have significant insulin resistance?

    First thing is to recall that insulin resistance is due to the accumulation of fat (actually free fatty acids) in the muscles and liver; primarily in the muscle. Second thing is that our subcutaneous fat in particular is critical for metabolic health; people with little subcutaneous fat (aka thin fat folks) can have as much insulin resistance as somebody who is obese. Both of these topics were covered in Banting Award (annual American Diabetes Association award to those who contribute to the science of diabetes) videos that I posted in the not too distant past. How does this information help us understand what is exactly going on in the mitochondria as we drift from metabolic health through insulin resistance to diabetes? Well it turns out that it is all about fat burning while we are in a fasted state (not fasting in the sense many people think but just haven't eaten for the last couple of hours or more).

    Inigo San Milian's research indicates that in that fasted state a metabolically healthy person will burn those free fatty acids sent from the subcutaneous tissue to the muscle mitochondria through oxidative phosphorylation to produce ATP efficiently. When a person has insulin resistance that is increasing towards diabetes, the mitochondria burn less free fatty acids and the body uses glucose through glycolysis to produce pyruvate and then lactate. There is a visible fat droplet in the skeletal muscle cells because that fat is not being burned. At this point it isn’t that the mitochondria aren’t as efficient, it is that the mitochondria aren’t being used. This has profound effects on metabolism. How can we tell when a person’s skeletal muscle is not burning fatty acids properly? When the lactate levels in the blood are higher than normal. It is possible to measure lactate levels at home using a lactate meter and strips, but from the quick search I did it costs about 10x more than using a glucometer.

    Beyond obviously dieting what can a person do to reverse insulin resistance/pre-diabetes/diabetes? Exercise which results in using mitochondria and importantly zone 2 exercise which increases the number of mitochondria. From many tests it was found that 60-90 minutes at least 2x weekly to maintain mitochondria function was necessary and more sessions weekly resulted in increased number of mitochondria. Zone 2 exercise for an elite athlete is not the same as it is for a metabolically unhealthy person who is overweight as an example. For a person who has significant insulin resistance, a brisk walk might be enough.

    The goal is to stress the zone 2 response to the extent possible as at higher exercise levels the body turns increasingly towards glycolysis in order to meet the growing demand for ATP with eventual use of stored glycogen and ATP in pockets of the muscle tissue itself to produce the quick bursts that some sports require. We now know why we get insulin resistance (beyond poor diet and lifestyle), and what to do to prevent or reverse it (especially in younger people).

    I have attached the Peter Attia podcast I mentioned above. In the podcast they talk about a lot of things related to elite athletes that may or may not be of interest, and so look at the show notes if you want to just hear the parts I described. Also near the end there is an interesting discussion about metformin and how that relates to prevention of cancer vs. mitochondrial disfunction from insulin resistance/diabetes. I also list a couple of articles related to how to make sense of this topic without necessarily getting into the details.
    https://peterattiamd.com/inigosanmillan/
    https://www.endocrineweb.com/profess...abolic-disease
    https://www.washingtonpost.com/natio...829_story.html
    Last edited by Tom; 12-28-2019, 02:04 AM.

  • #2
    In case anyone wonders, I still believe in the value of HIIT (high intensity training) and resistance training in addition to the zone 2 exercise. I have been doing a forty minute or so brisk walk three days a week after dinner, and it appears like I need to get that up to at least 60 minutes.

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    • #3
      Re: the ability to burn the fat within muscle fibers. Yes, I saw that on the Banting lecture as well. I think that contains a key to the next level of management in improving care of IR and T2DM. I have swung from a total aerobic guy years ago to mostly HIIT and resistance training now. But I am re-incorporating Zone 2. There are different levels of aerobic. 1 is equivalent to walking. That has shown undeniable benefit in the science. And I never stopped that, even when focusing more on HIIT and resistance. However, what I've dropped for short times is that Zone 2 in between a walking equivalent and HIIT. I do that level mostly in road cycling and Nordic track. Nordic track was my major form of aerobic mileage base in the past for the marathons and ultra. Back to the Banting lecture and burning fat in muscle fibers. There is also an old school medication that was mentioned as a key to that: pioglitzone (Actos). Brad Bale's taken it for years. I personally started it a couple of months ago. I take it several times/month, not every day. And I have several patients on it. It's mostly patients with IR or T2DM that don't want to take metformin due to poor kidney function. I have a couple of folks (myself included) that are combining met and pio.

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      • #4
        I'll have a look at this. I do a mix of HIIT, active recovery on days after HIIT with resistance training on all but legs on those days and another day or two of what would be zone 2. I use a mix of a spinning bike, elliptical and treadmill based on how my legs and joints feel from my 1 day of leg resistance training prior. I may remove a HIIT day and remove an active recovery day and change them to zone 2 days.

        Need to research this first

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        • #5
          Originally posted by Ford Brewer View Post
          Re: the ability to burn the fat within muscle fibers. Yes, I saw that on the Banting lecture as well. I think that contains a key to the next level of management in improving care of IR and T2DM. I have swung from a total aerobic guy years ago to mostly HIIT and resistance training now. But I am re-incorporating Zone 2. There are different levels of aerobic. 1 is equivalent to walking. That has shown undeniable benefit in the science. And I never stopped that, even when focusing more on HIIT and resistance. However, what I've dropped for short times is that Zone 2 in between a walking equivalent and HIIT. I do that level mostly in road cycling and Nordic track. Nordic track was my major form of aerobic mileage base in the past for the marathons and ultra. Back to the Banting lecture and burning fat in muscle fibers. There is also an old school medication that was mentioned as a key to that: pioglitzone (Actos). Brad Bale's taken it for years. I personally started it a couple of months ago. I take it several times/month, not every day. And I have several patients on it. It's mostly patients with IR or T2DM that don't want to take metformin due to poor kidney function. I have a couple of folks (myself included) that are combining met and pio.
          I've actually been taking Pioglitazone as well despite now not even being prediabetic.

          I also mentioned it in another post on the Cardiac forum but what do you think about finofibrate for cardiac inflammation? It's a different ppar, α as opposed to γ and the PPAR agonists/mixed/antagonists seem very interesting.

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