March 14, 2012


The interplay of exercise and ketosis – Part II

Read Time 10 minutes

You’ll recall from last week’s post I did a self-experiment to see if I could learn something about the interplay of exercise and ketosis, at least in myself. To understand this discussion, you’ll want to have read Part I of this post.

However, before getting to this, I want to digress and briefly address two unrelated issues:

  1. Some of you (about 67 or 68 as of this writing) have sent me various links to news reports released yesterday reporting on a study out of Harvard’s School of Public Health.  I was planning to eventually write a post about how observational epidemiology is effectively at the heart of the nutritional crises we face – virtually every nutrition-based recommendation (e.g., eat fiber, don’t eat fat, salt is bad for you, red meat is bad for you) we hear is based on this sort of work.  Given this study, and the press it’s getting, I will be writing the post on observational epidemiology next weekHowever, I’m going to ask you all to undertake a little “homework assignment.”  Before next week I would suggest you read this article by Gary Taubes from the New York Times Magazine in 2007 which deals with this exact problem.
  2. I confirmed this week that someone (i.e., me) can actually eat too much of my wife’s ice cream (recipe already posted herepretty please with lard on top no more requests for it).  On two consecutive nights I ate about 4 or 5 bowls of the stuff.  Holy cow did I feel like hell for a few hours.  The amazing part is that I did this on two consecutive nights.  Talk about addictive potential.  Don’t say I didn’t warn you…

OK, back to the purpose of this post: How is ketosis impacting my ability to exercise? Here is the summary of the results from my personal experiment:


Exercise summary data

Let’s take a closer look at what may have been going on in each workout and see what we can learn.



This workout probably produced the most lactate of the three workouts (we don’t know for sure because I only measured immediate pre- and post- levels without measuring in-workout levels).  My glucose level rose by nearly 40% during this workout despite the fact that I did not consume anything.

How does this happen?  Our bodies store glucose in the liver and in muscles in a “storage” form (a long chain of joined glucose molecules) called glycogen.

Whenever our bodies cannot access sufficient cellular oxygen, our metabolism shifts to a less efficient form of energy acquisition called anaerobic catabolism.   During these periods of activity, we cannot oxidize fat or glycogen (i.e., use oxygen to harness the full chemical potential of fat or carbohydrate molecules).  I will be writing in much more detail about these ideas in the next month or so, so don’t worry if these ideas seem a bit foreign right now.  Just know that sometimes our bodies can convert fat or glucose to energy (efficiently), and sometimes we can only convert glucose to energy (inefficiently).

Because of my ketosis, and the metabolic flexibility that accompanies it, I only “require” that my body turn to glucose for energy under the most “stressful” forms of exercise – like I was doing a lot of during this workout.  But keep in mind, my muscles CANNOT export one gram of the glucose they store, so any glucose in my bloodstream is either ingested (which I didn’t do) or coming from my liver, which CAN export glucose.

Furthermore, the stress of a workout like this results in my adrenal glands releasing a set of chemicals called catecholamines, which cause my liver to export even more of its stored glucose via a process called hepatic glucose output (HGO).

[As an aside, one of the major defects in type-2 diabetes is the inability of insulin to suppress HGO.  In other words, even when not under the catecholamine stress that “should” lead to HGO, their livers constantly export glucose, which contributes to elevated blood glucose levels.  The very popular drug, metformin, used often in type-2 diabetes, blocks this process.]

While I did experience a pretty large rise in lactate (almost 3x), my ketones still went up a bit.  This could imply a few things:

  • Elevated lactate levels do not directly inhibit beta-hydroxybutyrate (B-OHB)
  • Mild elevations in glucose do not directly inhibit B-OHB
  • Mild elevations in glucose do not directly inhibit B-OHB, if insulin is being suppressed (as is the case during vigorous exercise)
  • B-OHB was suppressed, but we are only appreciating the net effect, which was a small increase (i.e., because of my MCT oil and activity, B-OHB levels were rising dramatically, but the rise was blunted by some other factor, such as HGO, insulin, and/or lactate)

More questions than answers from this workout, so on to the next workout.



Despite this being a tough ride at several points, on average it was less stressful than the other two workouts and I spent the greater fraction of time in my aerobic to tempo (zone 2 to zone 3) zones.

A ride like this, however, is a great example of the advantages of improved metabolic flexibility that accompanies nutritional ketosis.  My average heart rate during this 6 hour ride was 141.  Prior to becoming ketotic, at a HR of 141 my respiratory quotient (RQ) was about 0.98, which meant I was almost 100% dependent on glycogen (glucose) for energy.  Today, at a HR of 141 (with the same power output), my RQ is about 0.7 to 0.75, which means at the same HR and same power output as prior to ketosis, I now rely on glycogen for only about 10% of my energy needs, and the remaining 90% comes from access to my internal fat stores.

This is an important point.  I will devote future posts to this topic in more detail, but I wanted to use this opportunity to mention it.

So what happened physiologically on this ride?

  • My glucose levels fell, probably because I was slowly accessing glycogen stores for peak efforts (once my HR reaches 162 I become 50% dependent on glycogen) throughout the ride (e.g., peak climbing efforts, hard sections on flats), but my liver was not “called on” to dump out a massive amount of glucose in response to a catecholamine surge (and if it was, at some point during the ride, that amount of glucose had been used up by the time I was finished).
  • B-OHB levels increased by about 2.5x – to 4.4. mM, which is pretty high for me.  My highest recorded B-OHB level was 5.1 mM (also after a long ride).  This confirms what my RQ data indicate — my body almost entirely relies on fat oxidation for energy for activity at this intensity.  In the process, B-OHB is generated in large quantities, both for my brain and also my skeletal muscles (e.g., leg muscles). In reality, cardiac myocytes (heart muscle cells) also “like” B-OHB more than glucose and probably also access it when it is abundant.
  • Lactate levels by the end of the ride were effectively unchanged though. Based on “feel,” I suspect I hit peak lactate levels of 8 to 10 mM on this ride during peak efforts, but I had ample time to clear it.

A few observations:

  • I consumed 67 gm of carbohydrate on this ride (of which 50 gm was Generation UCAN’s super starch), yet this did not appear to negatively impact my ability to generate ketones.  Technically, we can’t be sure this is the case, since I would have needed a “control” to know this (e.g., my metabolic and genetic twin doing and eating everything the same as I did, but without the consumption of super starch and/or without the bike ride).  It’s possible that super starch did slightly inhibit ketosis and that my B-OHB level would have been, say, 5.0 mM instead of 4.4 mM.  Metabolic studies of super starch show that it has a minimal impact on insulin secretion and blood glucose levels, hence the name “super” starch.
  • Whatever impact peak levels of lactate production and hepatic glucose output had during the ride, they seem blunted by the end of the ride (and the ride did finish with a modestly difficult 1.4 mile climb at 6-7% grade, which I rode at a HR of about 150).

Since neither lactate levels nor glucose levels (nor insulin levels by extension) were elevated, I can’t really draw any conclusion about whether one factor, more than any other, suppressed production of B-OHB, so on to the next workout.


High intensity training

This sort of workout spans the creatine-phosphate (CP) system and the anaerobic energy system, and probably involves the aerobic energy system the least. I’ll write a lot about these later, but for now just know the CP system is good for very short bursts of energy (say 10-20 seconds) and recall the previous discussion of aerobic and anaerobic catabolism.  In other words, this is the type of workout where my nutritional state of ketosis offers the least advantage.

  • This workout saw the greatest increase in glucose level, about 70%.  It is important to recall that during this workout I ingested water with a small amount of branched chain amino acids (BCAA’s – valine, leucine, isoleucine) and super starch, about 4 gm and 10 gm, respectively. I do not believe either accounted for the sharp rise in blood glucose and, again, I believe hepatic glucose output in response to a strong catecholamine surge attributed to this increase.
  • Lactate levels also rose, though probably less so than during a peak swim effort.  This suggests more of the effort in this workout was fueled by the CP system (versus the anaerobic system, which probably played a larger role in the swim workout).
  • This was the only workout that saw a fall in B-OHB levels, which now offers some insight into what might be impacting B-OHB production.

Contrasting this workout with the swim workout draws a pleasant contrast: both saw a similar rise in lactate, but one saw twice the rise in blood glucose.  In the former, B-OHB was unchanged (actually rose slightly), while in the latter, B-OHB fell by over a third.

This suggests – but certainly does not prove – that it is not lactate per se that inhibits ketone (B-OHB) production, but rather glucose and/or insulin.  It is possible the BCAA played a role, and if I was thinking straight, I would not have consumed anything during this workout to remove variables. But I have a very hard time believing 3 or 4 gm of BCAA could suppress B-OHB. When you see hoof prints in the sand, you should probably think of horses before you think of zebras.

Conversely, there is some evidence that lactate promotes re-esterification of fatty acids into triglycerides within adipose cells.  What does that mean in English? High levels of lactate take free fatty acids and help promote putting them back into storage form.  This would prevent free fatty acids from making their way to the liver where they could be turned into ketones (e.g., B-OHB). In other words, we may be missing this effect because of my sampling error – I only sampled twice per workout, rather than multiple times throughout the workout.


So what did I learn, overall?

I think it’s safe to say I did not definitively answer any questions, which is not surprising given the number of confounding factors, lack of controls, and sample size of one.  However, I think I did learn a few things.


Lesson 1

The metabolic advantages of nutritional ketosis seemed most apparent during my bike ride, evidenced by my ability to access internal fat stores across a much broader range of physiologic stress than a non-ketotic individual.  (More on this in Lesson 4.)


Lesson 2

The swim and high intensity dry-land workouts suggested that my state of nutritional ketosis did not completely impair my ability to store or export hepatic glucose.  This is a very important point!  Why?  Because, it runs counter to the “conventional wisdom” of low-carb (or ketotic) nutrition with respect to physical performance.  We are “told” that without carbohydrates we can’t synthesize glycogen (i.e., we can’t store glucose).  However, those who promote this idea fail to realize that glycerol (the backbone of triglycerides) is turned into glycogen, along with amino acids, not to mention the 20 to 40 gm of carbohydrates I consume each day (since my brain doesn’t need them).  We know muscles still store glycogen in ketosis, as this has been well studied and documented via muscle biopsies by Phinney, Volek, and others.  But, my little self-experiment actually adds a layer to this.  Because muscle can’t export glucose (muscle lacks the enzyme glucose-1-phosphatase), we know that the increase in my blood glucose was accounted for by HGO – my liver exporting its glycogen.  In other words, ketosis does not appear to completely impair hepatic glycogen formation or export.  Again, we’d need controls to try to assess how much, if any, hepatic glycogen formation and/or export is inhibited.  It’s hard to make the argument that being in ketosis is allowing me to swim and do high intensity training with greater aptitude, and as I’ve commented in the past, I feel I’m about 5-10% “off” where I was prior to ketosis for these specific activities, but at the same time, I could be doing more to optimize around them (e.g., spend less time on my bike which invariably detracts from them, supplement with creatine which may support shorter, more explosive movements), which I am not.


Lesson 3

Consuming “massive” amounts of super starch (50 gm on the ride), did not seem to adversely affect my ketotic state.  My total carbohydrate intake for that day, including what I consumed for the other 18 hours of the day, was probably close to 90 gm (50 gm of super starch plus 40 gm of carbs from the other food I ate).  This suggests one or two possibilities:

  • Because of the molecular structure of super starch (I’ll be discussing this in the future, so please hold questions) and the concomitant metabolic profile that follows from this structure, it may not inhibit ketosis like other carbohydrate, and/or
  • During periods of profound physical stress insulin secretion is being sufficiently inhibited that higher-than-normal amounts of carbohydrate can be tolerated without negatively impacting ketone production.

This is pretty straightforward to test, even in myself.  I just haven’t done so yet.


Lesson 4

While it’s probably the case that my liver has less glycogen (i.e., stored glucose) at any point in time, relative to what would be present if I were eating a high-carb diet, it’s not clear this matters, at least for some types of workouts.  Why? Take the following example:

  • Someone my size can probably store about 100 gm of hepatic (liver) glycogen and about 300 gm of muscle glycogen at “full” capacity. This represents about 1600 calories worth of glucose – the most I can store at any one time.
  • Before I was ketotic, my RQ at 60% max VO2 (about 2,500 mL of O2 per min consumption) was nearly 1.00, so at that level of power output (a pace I can hold for hours from a cardiovascular fitness standpoint) I required 95% of my energy to come from glycogen.  So, how long do my glycogen stores last?  2,500 mL of O2 per minute translates to about 750 calories per hour, so I would be good for about 2 hours and 15 minutes on my glycogen stores.
  • Contrast this with my ketotic state.  Let’s assume my glycogen stores are now only half what they were before.  Muscle biopsy data suggests this is probably an overly conservative estimate, but let us assume this to be the case. Now I only store 50 mg of hepatic glycogen and 150 gm of muscle glycogen, about 800 calories worth of glucose.
  • In ketosis, my RQ at 60% max VO2 is 0.77 (at last check), telling me I am getting only 22% of my energy from glucose and the remaining 78% from fat.  So, how long do my depleted glycogen stores last? Nearly 5 hours.  Why?  Because I barely access glucose at the SAME level of oxygen consumption and the same power output. 

I know what you’re thinking…why is this an advantage? Just consume more glucose as you ride! It’s not that simple, but you’ll have to wait until my upcoming post, “What does exercise have to do with being in the ICU” to find out.

Going back to the black sheep example I open Part I of this post with, we know that at least one person in nutritional ketosis seems to make enough liver and muscle glycogen to support even the most demanding of his energetic needs.


Photo by Troy Oldham on Unsplash

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  1. Hi Peter. I wrote to you a few weeks ago about the use of superstarch for long distance running. I didn’t have time to get my hands on some and try it out prior to my last race and so just went without. But am happy to report running the Boston Marathon in 4:01 on VLC diet. Pre-race dinner was roast chicken and dark meat, spinach salad with eggs, bacon, avocado. Breakfast of 3 eggs plus extra yolk cooked in butter 5 hours pre-race with an avocado 2 hours pre-race. Tried to “salt-load” in anticipation of heat/dehydration factor. Honestly, I felt horrible throughout the race but so did almost everyone else (who had not been training in a warm climate).. We we waiting around for the race to start in the sun in Athlete’s Village for 90 minutes before the start and I felt dehydrated by mile 3. If you didn’t hear, temperature soared to near 90 by the finish. Wanted to prove I could run a decent race on VLC and I’m pretty satisfied. Time last year at Boston was 3:37 in ideal weather on more typical diet and using carb supplements (GU, Gatorade, etc) Q45 minutes thru the race. My weight is the same. Have been doing more intense strength training this year. Started training for Boston later this year so less sessions of speed work. Hard to know if diet, weather, or training differences (or combo) slowed me down. But in any case, will take slightly slower time in exchange for feeling great, satisfied and less food-obsessed since lowering my carb intake. Off to run the Big Sur Marathon this weekend. Although still recovering and on a very different course, will be interesting to see how my time compares without the heat-wave factor. As a physician with an MPH, I love reading your blogs. Your are doing a fantastic job of teaching readers how to look at the medical liit with educated skepticism. Thanks for all of you effort! Signed, another n of 1

    • Jessica, hard to make a comparison, I’m sure. Conditions in Boston were pretty tough this year if the lead runner’s times were any indication.

  2. Hello Dr Attia! I have been on a ketogenic diet for approx. 6 weeks now. I went on it to see if it would help my migraines (which are exceptionally chronic, often silent, and sometimes basilar-type) and it worked so well I was able to ditch the propranolol and verapimil. But so many on this diet seem to disregard exercise, which means finding information on exercise and low carb diets extremely difficult to find! Personally I do quite a bit of exercise, lots of swimming and lifting. I’m finding swimming to be easier than ever on this diet, but lifting is generally more difficult.

    I have a question. Do you think there is a correlation between people who tend to have good endurance abilities (vs sprinter types) and their ability to easily transition to a ketogenic diet? I didn’t get the infamous carb flu and my body generally seems to prefer this diet to the traditional low fat “healthy” diet I was on before. Also whenever I eat a bit too much carbs (or drink too much) and I transition back into ketosis the next morning, my body tends to get really shaky for an hour. Do you know what causes this?

    Thank you so much for this article! I find it fascinating no one talks about the glycerol part of triglycerides, it makes sense your body would make do with replenishing the glycogen stores by using fat instead of sugar. Maybe instead of people recommending carb loading we should be recommending eating more coconut oil instead.

    • Great question, Karin. I do not know the answer and have not seen any data suggesting this to be the case. One could make a teleological argument, though.

  3. Thanks so much for this terrific resource. I am a Lecturer in Physiology at an Irish medical school and full time research scientist so really appreciate the rigorous hypothesis driven approach you take . Its convincing, realistic and scientifically justifiable which it much appreciated!
    My question is related to my personal situation- In 10 weeks time I take on Ironman UK—Goal is to ‘ just finish’ and the race will likely take me 15h +. I have been ( like many it now seems) unable to drop body fat since starting IM journey in January, despite hours of good quality training & eating a mainly organic high quality diet. I completed a Half Ironman in training yesterday and there is no question I need to drop as many kgs as possible before race on July 22 ( in order to make hilly race bike leg and marathon tolerable). Some weeks ago,a local nutritionist suggested I go ketogenic which I have resisted ( as I do > 16h training per week) but your site has me convinced.
    My questions:
    1. With 10 weeks to go is it too risky ( re training performance) to go ketogenic ?—I will supplement electrolytes & keep protein down to minimize side effects
    2. If I take in high GI carbs on long bike rides only will this completely negate the efforts of going ketogenic for the rest of the week—I don’t think there is enough time for me to acclimitize to the keto approach to long sessions
    3. On keto diet is the concept of a ‘ cheat meal’ completely off limits ?
    Many, many thanks

    • 1. In my opinion, 10 weeks is probably feasible. It took me about 12 weeks to feel 100%++
      2. Yes, you should avoid high GI carbs, even on the bike, if you’re ketotic. Low GI carbs (e.g., cashews, Super Starch) are much preferred.
      3. Correct, no cheating in ketosis. It takes days to get right back in.

  4. Hi Peter,

    Thank you for another excellent post! I did experience lose of explosive power during my basketball play but my endurance has improved dramatically and made me a second half monster. My weight lifting sessions have been less than ideal until I fixed other related variables you mentioned and my progress in weight room has been progressive and steady.

    However, I do have a question about eating. When I was on a high carb diet, my appetite is huge and I am constantly hungry. After switching to high fat diet (around 40g carb per day), My appetite became a non-issue and I rarely feel hungry. However, if I eat only when I am hungry, then I might eat only two meals a day. I currently eat every three to four hours even though I am not hungry. So my question is: if I eat the same amount of food everyday, does it make a physiological difference if I consume them in three meals or five meals? Or do you think scheduled feeding is a bad idea and it is best to eat whenever one is hungry? Really appreciate your time.



    • There is a lot of discussion about this, and I have not yet had the time to do my own research, so I can’t really comment on it with credibility. Hope to soon.

  5. Hi I’ve seen around the place, esp. in the bodybuilding arena that a carb-up day is recommended if not essential to replenish glycogen stores in the body esp. if you are exercising.
    Do you recommend a carb-up day?
    There will be issues with trying to get back into ketosis which will take several days, but can your body make sufficient glycogen stores to replenish your muscles?
    your thoughts?

  6. Peter,
    You say that one is either in a state of ketosis or not – with no shades of grey. How does this affect the ratio of fat to glucose used during aerobic exercise? Is there a switch or a continuum? I like your ratios, where you conserve glycogen. Perhaps I’m asking whether you think fat utilisation increases on a low carb diet whether or not you happen to be in ketosis? The reason I ask is that I am on a low carb regimen and can manage 5 or 6 hour hilly bike rides ( albeit nothing like your pace) without bonking and (mainly) resisting the cake at coffee breaks, but don’tknow how close I am to the edge. Maybe it doesn’t matter, but I’m curious. Also I suspect I may eat more protein than required to be in ketosis. Any thoughts?
    Thanks. Keep up the good work.

  7. Thanks I understand that but I was really asking about the fat to glucose ratio of fuel during moderate aerobic exercise and the effect of ketosis on that. I’ve seen your data and wondered how critical ketosis is to the high fat usage compared with just a low carb diet but not quite in Ketosis.
    Sorry for being unclear before. Thanks

    • RQ, which is the ratio of VCO2 to VO2, is a continuous variable, so again the ratio of fat to glucose oxidation (and glycolysis to fat oxidation) is continuous, not discrete. What ketosis does it “shift” the RQ curve. I hope this helps.

  8. Hi Peter,
    don’t know if this is the rigth place to post this question.

    Can there be a correlation between knee pain (in the joint) and a very low carb diet ?
    Since going very low carb I have experienced pain in my knees during my long training runs (>15 miles) and was just wondering if I migth need some special supplement when training for ultra runs and going LowCarb ?

    As for now I’m not taking anything apart from ekstra salt and occasionally bouillion.

    Apart from this little problem, I’ve only experienced positive changes during the 2 months below 40g of Carbs / day – I feel very good in training, especially during runs that exceeds 2 hours.

    Great blog and can’t wait for the Nusi to start

  9. Love the blog Peter!

    I am someone who is out to win an Olympic medal, in a sport (biathlon) where my races are typically 20-35 minutes long so I mostly race just above anaerobic threshold, with sprints needed for surges during the race and at the finish. I see the benefits in keto-adaptation but I also see possible drawbacks in my performance and I am trying to find a balance between the two by consuming a low carbohydrate diet (but not below 50g/day) and low-glycemic diet. However will this just put me in the state where I’m not fully keto-adapted but not consuming enough carbohydrates to fuel my body, i.e. nutritional hell?

    • My guess would be that full-blown ketosis is not idea for your race. Rather, you’re probably better in a sugar-reduced, but non-ketotic state, primarily for the sake of training.

  10. CrossFitter, although right now I’m in a season of OLY lifting and lots of strength/percentage training at lower volumes/higher loads. I eat a mostly keto diet with the exception of lifting meets and high intenisty metcons where I consume a little pre-workout (medium chain triglycerides, fructose, and electrolytes) about 12g sugar pre workout during weight lifting sessions and metcons or days of multiple workouts…also replenish glycogen with coconut water/sweet potatos…would you save the pre just for the higher intensity wods? Wanting to compete in the future at the games! Mostly hitting high fat, moderate protein otherwise, with a little IF until post 10:30am training sessions which go until noon! Cheers

  11. Hi Dr Attia

    Thank you for the amazing information, I am learning so much.
    I am a chiropractor practicing in Stockholm Sweden. I am doing my 2nd masters degree. I am doing it at the Swedish school of Sports and Health Science and am about to decide on a study for my masters thesis.
    After reading your info I am really inspired and intrested in the adaptation from carbs to fat/ketone based fuel sources – what you decribed in “How a low carb diet affected my athletic performance (Part 4)”. Also based on my own experience.
    There seems to be alot of conventional wisdom to break through when I talk to people at the university about this concept.

    I know you must be very busy but wondered if you have any advice on the following 2 areas.
    1. As a study, would it be worth doing a comparason study of one or a few cyclists going from carb to fat as fuel source. Or would it be better comparing fat adapted with carb based cyclists? I thought of measuring the parameters you used in “How a low carb diet affected my athletic performance (Part 4)” Do you have any other suggestions for a study.

    2. I need to try to “sell” the concept to a tutor, as I said: break through some conventional wisdome. Any sources of literature you can recommend. I understand that Jeff Volek and Steve Phinney should be read, anything else?

    Kind regards

    • Steve Phinney did a great study while at MIT in the early 80’s where a group of highly trained cyclists, in a crossover design, did standard diet vs. ketogenic diet. Take a look at that. Repeating this study with recreational (vs. highly competitive) cyclists would be very interesting. With a crossover design you could adequately power this study with far fewer subjects. As far as other sources, looking at the references in their book is a great place to go.

  12. Peter,

    Awesome blog.

    I am in week 2 of keto adaptation after being inspired by the Volek and Phinney book. I am still wondering how much of an advantage (if any) keto adaptation is for endurance exercise. You calculated (in “Lesson 4”) that you would last 5h instead of 2h15min on carbs. But in Phinney’s 1983 paper that studied the 5 cyclists, their time to exhaustion did not actually increase significantly, despite a much lower RQ. In addition, they didn’t consume carbs in the pre-keto test, as they would have in a race, so keto comes out looking like a pretty poor choice there (I realize there are other advantages, and I care about those too!).

    I am also surprised that they (and you!) used such a low intensity level, 65% of VO2max. Is *any* kind of race done at this level of intensity? It would be really interesting to see RQ numbers in, say 5% increments for a keto-adapted person vs a non-keto-adapted person. At what intensity or at what race distance do you think keto adaptation provides a benefit, for us mere mortals (as opposed to elite athletes)?

    • Ketosis may not provide any benefit for a 400 IM (5 minute all out), but the point about RQ is for events lasting over ~3 hours. The longer the event, the more benefit to keto-adaptation.

  13. I was curious as to why you only last 5hrs whilst exercising.
    If you body still had stores of fat, do they convert to ketones as you exercise, replacing what you had lost?
    So then is it possible to keep going until you’ve exhausted all the fat stores in your body?

    • This point is only looking at stored glycogen capacity, not the aerobic utilization of fat, which, as you suggest is nearly infinite. This is a complex topic and worthy of its own series (or book, actually). I’ll address this in the coming year.

  14. Peter,
    I’m heading up to the Sierras for a week-long off-trail high-altitude carry-everything-in-and-out hike, in a week. It’s around 80 miles, mostly up between 11- 13,000 feet, with lots of up and down. (i’m 55, 190 lbs, fit.)

    Last year I took the normal stuff (Clif bars, etc.) and did fine. But I’ve been experimenting with your high-fat diet for the past few months; I feel great, and am fascinated with trying it out in a remote, sort of survivalist adventure. Is this a really dumb idea? (Once I get up there, there’s no turning back for the week.) I love your whole basic idea about not “hitting the wall” through burning fat, and thought that up there I could rely on my stored body fat as a fuel I don’t have to carry in my pack.

    Can you recommend some portable nutrients to take? So far I have:
    Coconut oil
    MTC oil
    boullion cubes
    mag/potass suppliments
    fish oil
    tuna or salmon packets
    chicken packets
    nuts (?)
    Jerky (?)

    Can you suggest anything else? Whey protein? Super starch?

    All the backpacking nutrition sites I found online, and there are many, take the carbs=good/fat=bad line. But I love your story, your research, and my experience with it. So I’m looking to you.

    Bruce Caward

  15. Peter,
    Do you use sodium or other electrolyte supplements *during* prolonged exercise, particularly in the heat? Or do you feel that it is enough to add the extra sodium as bouillon etc at other times during the day?

    • Only REALLY long stuff. Anything up to about 6 hours and I’m fine with just water +/- some super starch or nuts (both of which do contain sodium).

    • You’ve got to very careful drawing conclusions from any study that feeds fat to mice. Mice are herbivores, so their metabolism of fat is very different from ours. Just because cats are harmful to mice, doesn’t mean they’re harmful to humans.

    • Thanks! I wonder how expensive a serum LPS test would be, say along with a C-reactive protein screen if one were interested in a base line at the beginning of going paleo and then again in six months to a year? I was just thinking about the “leaky intestine” hypothesis that Cordain mentions a lot in his book. With the vast amount of microflora in the the gut, one might expect a basal level of LPS getting through.

      Or as you say, just another example of a fine mouse study with little relevance to humans.

  16. Hi Peter. I’m doing boxing and I have been in ketosis for a few months. What is your opinion on boxing in ketosis? Also, I’m currently doing the super slow workout once a week for conditioning and the rest of the days, I practice sparring. What is your opinion on my training methods?

  17. Hi Peter!

    Im doing a lot of exercise and I have found out that I can still be in the optimum ketosis range while consuming both creatin and BCAA intake during my heavy weightlfting. When finished with my weightlifting-workout I tend to wait for some hour before I eat, not to go to hight with the protein intake under too short of timespan. The days Im doing more of a endurance exercise, I don´t take BCAA nor Creatine. I also do IF and “cykle” my intake of carbs (mostly round 5-15 g/day) and protein (higher but not too high on weightlifting days). I daily eat MCT-oil and coconutoil. It would be interesting testing the Superstarch UCAN when i do my weightlifting but as far I can see, it´s not for sale in Sweden. My question is if you have any opinion on intake of acetyl-L-carnitine, training in a ketonic state? Is there any benefit or disadvantage whit this supplement?

  18. I know Peter gets inundated with questions from half the would-be keto-questers in the world, so if *anyone* has any information to share with me, I’d really appreciate it. I’m going through a bit of a cancer scare; to be honest, really freaking out, and trying to get into keto and lower my blood glucose levels as rapidly as possible. I’ve been emulating Peter’s diet as closely as I can – almost zero carbs, moderate protein, and always the cleanest foods possible. I’ve been supplementing with generous helpings of omega-3 rich oils as well.

    Problem is, after more than a week of this, I just seem to be losing muscle mass, power, and energy, and my glucose levels, if anything, are *higher* on average than they were prior to my zero carb diet. I’m pretty lean and athletic already, so this kind of weight loss is not really desirable. I’m afraid my body is cannibalizing itself to maintain constant glucose levels, and if that’s the case, how is one supposed to deny blood sugar to hungry tumors?

    I know it’s a little off-topic, but if *anyone* has any advice of any kind, I’d really appreciate it. I’m kinda’ terrified, and desperate for quality information. Thanks to anyone looking!

    ps – …y’know, I think a forum would be really nice on this site. Seems as though a lot of people that visit would like the chance to talk with one another. I’ll bet it would attract a really nice, quality community, no?

    • Tristan, sorry to hear about the scare you’re enduring right now. Yes, I agree, a forum would be a good idea, and I’m trying to figure out a way to do it, where it will be maximally helpful and minimally annoying (e.g., rude, disruptive, destructive). If you’re feeling this way you’re likely off on one or two fronts: 1) too much protein, and/or 2) not enough sodium. Others can chime in with details and if you go through comments in other posts (e.g., What I eat), you’ll get all the guidance you need.

    • Hi Tristan,

      The thing that really got me keto-adapted was fasted exercise in the morning before breakfast. I think most people are using ketones to some extent when they wake up since it is some time since the last meal. Try taking some coconut oil, some other fat or MCT when you get up, have a strong coffee and then exercise. Maybe this will help convince your body to use ketones more.


    • Thomas Seyfried — As a whole protocol to treat cancer as a Metabolic Disease using Calorie restricted Ketogenic Diet and two drugs to further restrict fermentable fuels to the cancer cells. Which are Glucose and Glutamine .

      “Pauline Davies: So what does it actually mean for a patient? How much do they have to restrict their diet?

      Thomas Seyfried: Well this is an important point and this is one of the reasons it’s a stumbling block. Some patients have to realize they have to stop eating for several days, and get their blood sugar down to 55 to 65 milligrams per deciliter and their ketones up to about 3 to 7 millimolar and then they know they’re in the state.

      So we have clear biomarkers for patients to get into this particular metabolic state. The problem is a lot of patients are reluctant, they have other thoughts, the issue of cachexia always comes up and they say, “How could you have a patient who’s losing weight stop eating?” And as I said, they’re losing weight because the tumor cells are mobilizing glucose from their tissues of fats and protein. ”

      “But you know if I had cancer, if I had a glioblastoma, I would stop eating for at least fourteen days and then I would take the drug protocol that we advocate because I know this would be my only chance of survival.”

      “Pauline Davies: Have you ever tried this yourself?

      Thomas Seyfried: Yeah people ask me that and the answer is I’ve tried it. How far can I go? Maybe two days, I’m still working. My students have gone a lot longer than I have. But you know if I had cancer, if I had a glioblastoma, I would stop eating for at least fourteen days and then I would take the drug protocol that we advocate because I know this would be my only chance of survival.

      And I know exactly what we have to do, how low we have to get the blood glucose down. But if you don’t need to do that, why would you do that? I know what to do if I had to do this. It’s like having the tire changer in your car, if you get a flat tire you know how to use it, but you wouldn’t just go out and change tires just for the sake of changing tires. I know what to do and we’re still working to it, but I think it’s generally a healthy thing to do anyway.

      Pauline Davies: Thank you.”

      More details here

      and here .

    • Peter and Paleo, thank you so much for your replies! I can’t tell you how much it means to have any kind advice right now – I can’t go to a doctor yet as my personal insurance policy just started on the 1st, and I’m terrified they’ll claim the condition existed prior to my coverage and drop me… but I digress.

      I did fasting HIIT the first two days of the diet, and have tried to stay moderately active since. I’m feeling better about energy and muscle loss now, but I still wake up with a blood glucose ~90mg/dL – higher than when I went to bed. I’m being very careful to not eat to much protein, nor too much at once, but… it’s hard to strike the right balance, I think.

      Peter, if you have time, I see that *your* blood sugar isn’t really much lower than “average”, even in a state of full-on ketosis. If ketosis doesn’t precipitate a drop in blood glucose, how is it supposed to deny food to glucose-hungry tumors? I’ve read that people on a combination of extreme calorie restriction AND keto can get the their blood glucose down around 50-60mg/dL for the purposes of fighting cancer, but those reports describe diets of 600 calories per day… with the associated side-effects. I’m not trying to play devil’s advocate, but it does seem to be a legitimate question.

      Again, thank you both so, so much for taking the time to talk with me. It’s been a very rough couple of weeks. :-p

      • Great question. It probably has more to do with insulin levels and IGF-1 than glucose levels. I do plan, in the next year or so, to do a very detailed series of posts on cancer.

    • Raymund, that’s a lot of food for thought – forgive the pun. Ugh, terrible… 😉 Thanks very much for those links; I’ll look at them in detail, but I wanted to give you my appreciation first. It’s very kind of you to show interest, and I hope someone else out there might eventually benefit as well.

      Peter, thanks to you again for taking the time. I’ll also thank you for a friend of mine who went keto after discovering this site and isn’t looking back. 🙂 I look forward to reading more here, cancer-related or no. Much gratitude.


    • Tristan , You can look inside that book on Amazon..

      He especially mentions caffeine in the form of Coffee as something that will not allow the blood glucose levels to fall . Even after 6 days of fasting and elevated Ketones.

      it is on page 381 .

      From Jimmy Moore’s Site –>

      “. Seyfried noted that a cancer-preventing fast should probably be done using distilled water only and nothing else”

      “A therapeutic fast should not contain any nutrients. The body will release vitamins from fat and minerals from bones during the fast.”

      “He explained that the weight loss on a one-week fast like this is mostly water weight because the fasting process depletes glycogen stores which retain most of the water in the body.”

      “Dr. Seyfried noted that there is some “minor” protein loss “especially if fat is mobilized”

      “If your blood ketone levels are elevated then you are definitely burning fat.”

      When I asked what this weeklong fasting does to cancer cells, he said the “damage to mitochondrial respiration is the origin of all cancers.”

      “Fasting will induce cellular autophagy thus allowing the cells of the body to consume damaged or defective mitochondria. Metabolism of ketone bodies will reduce damaging oxygen radicals while enhancing the metabolic efficiency of the mitochondria. Fasting prevents cancer by enhancing the metabolic efficiency of mitochondria and by eliminating damaged mitochondria.”

      “He recommended a book Herbert M. Shelton called Fasting for Renewal of Life that gets into the nitty gritty of what is happening when you fast.

      “He reiterated the importance of consuming only distilled water or a small amount of non-caffeinated green tea. As for the vitamins I took during my fast, he said they are “not needed for short fasts (less than 20 days).”

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