Dieting While Injured
Question: Hi Lyle, I am a big fan of your work and I have an important question. So I have ulnar nerve subluxation in my left arm and I am restricted in my training. I choose to avoid any pressing movements such as any bench press, any tricep movement, and any shoulder press. Every other lift I can do, I am cutting now and I am wondering what is the best way to go about preserving my muscle mass without bench press/shoulder press/tricep movements? Should I stick to heavy chest flies and Heavy shoulder raises? What about triceps? Thanks so much Lyle.
Answer: I wouldn’t diet while injured would be my suggestion unless you can find something workable for those muscles group. You will lose muscle in them without some type of training stimulus. If you’re determined to diet either accept the muscle loss or, I dunno, maybe isometrics of some sort. It’s better than nothing. Or see if what I’m going to talk about in the next question is workable.
Osteogenesis Imperfecta Type I
Question: Dear Mr. McDonald, I´m writing this e-mail to you because I don´t know what to do anymore and neither do the “specialists” that I´ve already consulted. I was born with a gene deficiency called “Osteogenesis Imperfecta Type 1” or brittle bone disease. Luckily, it´s only Type 1, the mildest of all types (if I had any of the other types training in general would probably be off the table…). In short this means that my body has a malfunction regarding the production of collagen tissues (type 1) which pretty much can be found in almost all types of structures the human body consists of, but most of it can be found in the bones – that´s why they break easier and also why it´s called brittle bone disease.
Answer: The above question was much longer but mostly a reiteration of the above so I cut it for length. First and foremost, I’m not a doctor and I don’t even play one on television so take my comments under that clarification. However, I do think I can offer a bit of input on this.
In recent years, there has been a progressive amount of research showing that lighter load, higher repetition work can be as effective (but not better) than heavy training for growth and this is true in both untrained and trained individuals.
Now, for the most part, I don’t think too highly of this type of training (or Blood Flow Restriction/Kaaaaatsuuuu training despite it’s current faddish popularity) for hypertrophy, at least not as a primary training method. It’s painful as hell (in several subjects threw up), it doesn’t generate more growth, doesn’t improve strength and there is another issue I’ll mention in a second.
However, there are a handful of situations where I do think it can be useful. In older folks, where a lot of this was first trialed, it can offer a training stimulus that deliberately reduces joint and bone loading. The same holds for injuries (after a low back injury, I once limited myself to single set Superslow training for a while to get a muscular stimulus without putting high peak forces through my spine). And I think in this specific situation it might play a role. Since OI is a disease of brittle bones, this type of training should allow a sufficient muscular stimulus while deliberately reducing bone loading forces.
But this brings up the issue I said I’d mention which is actually strengthening the bones. This requires fairly high absolute or peak loading (athletes who do a lot of jumping or sprinting have higher bone density than even powerlifters who generate high but more extended forces; endurance athletes are the worst off) and I don’t think low load/BFR training will generate that.
And I don’t know what the solution here is except perhaps to take the VERY long approach of starting with light load training and gradually reducing the repetition range. I’m talking over months and months with the repetitions gradually coming down and it might take longer than that. Bone mineral density (BMD) develops very slowly and I don’t even know if it can occur at all in OI. It might realistically take a year or more to gain even a few percent although I might expect this to be faster in already brittle bones.
So 25-35 reps to failure for 3-4 months or until joint or bone pain stops. Now move to 20-25 reps for 3-4 months or until joint or bone pain stops. Now move to 15-20 reps for 3-4 months. The 10-15 repetitions. By the time you get to the 8-12 range, it’s heavy enough to have a benefit on bones (and note that muscular pull, using different angles plays a role in this).
Hopefully with each gradual increase in loading and decrease in repetitions there will be slightly more bone loading. This should go along with proper nutrition which includes sufficient dietary protein, calcium, Vitamin D, Vitamins K1 and K2 and veggies. I also know that they have been trialing various drugs, often anabolic steroids for increasing bone density but this is beyond what I can talk about meaningfully.
Building Muscle Without Carbs
Question: Hello Lyle. I’m an avid (“student”) reader of yours. I wanted to throw a question at you on building muscle on a diet with very little carbs. From what I have gathered, the body burns a certain percentage of fat and carbs for energy. For example: as you are reading this your body, supposedly, is burning around 60% fat and 40% carbs. At rest, the body burns roughly 33% carbs and the rest fat.
So on, and so on . . . I had read through biology that the body cannot burn 100% fat. So, if there are very little to no carbs, then the body burns the amino acids in its place. (Yes? No?) Do you have any info that explains how the body is able to not only keep the muscle but build it through weightlifting if it is burning all of those amino acids??? From a biological point of view, it just doesn’t make sense. Unless the body does indeed burn at or near 100% fat. But I could not find any sources on that. Maybe people just need to eat 50-100 more grams of protein, especially when on a ketosis diet???
Answer: The actual subject line of this question was “Question on how the body builds muscle without carbs?” and my short answer answer to that is “poorly.” based on the overall hormonal profile that occurs with very low-carbohydrate diets.
You see increased cortisol, increased binding of testosterone to SHBG and a host of others and here’s an amusing bit of trivia. In the only study I’m aware of, women with intractable epilepsy were put on a maintenance level ketogenic diet. And every single one of them, I mean 100% developed menstrual cycle disorders. Because even at maintenance calories, a ketogenic diet is still biologically a starvation state no matter how you cut it.
But clearly there’s a bit more to his question (and note that all of this is discussed in painful detail in my first book The Ketogenic Diet).
The problem with what is written above is the idea that the body is burning nearly that much body protein for energy simply because carbs aren’t available. Certainly, it is true that the production of glucose from protein increases when carbohydrate intake is very low (below about 100-120 grams per day which is the cutoff for the development of ketosis). In fact, during complete starvation (the ultimately low-carbohydrate state), the loss of body protein is extremely high.
For about three weeks anyhow.
Before expanding on that, let me back up a bit. Most tissues in the body can use glucose or fatty acids for fuel (and the switch back and forth is called metabolic flexibility) although glucose is the preferred fuel by most if it is available. There are a few exceptions. The heart uses fatty acids and this is to ensure that there is enough fuel available.
A few odd others like the eye and some part of the kidney and one other that I can’t remember right now can only use glucose (but it comes from the recycling of things like lactate). But muscle and most other tissues in the body can switch back and forth as needed (requirements also change during exercise).
And then there is the brain. It’s usually stated that the brain can only use glucose for fuel (to the tune of about 80-120 grams per day) but it’s more accurate to say that it can’t use fatty acids. Which seems like the same thing but isn’t because there is an alternate fuel that is available: ketones (aka ketone bodies, aka ketoacids).
Ketones are made in the liver when fat oxidation goes up beyond a certain degree and this generally happens when carbohydrate is extremely low (other nutrients also play a role). The cutoff is the same 80-120 grams/day that defines the brains normal carbohydrate requirements and this is what defines a ketogenic diet.
Yes, most low-carbohydrate diets set carb intake levels lower, 30-50 grams of carbohydrate but this is more of a practical issue than a biological issue. Physiologically, any carb intake below ~100 grams per day will induce some degree of ketosis (defined as a blood concentration of ketones above a certain point that I don’t recall at the moment) with more ketones being produced if carbohydrate intake is lower.
And the entire point of ketones is to spare body protein in the situation where carbohydrates aren’t available. So imagine someone is starving completely, eating nothing. For about 3 weeks their use of body protein for the production of glucose will be enormous and they will be losing a lot of body protein (note that this is impacted on enormously by body fat percentage, the more fat someone is carrying the less protein they use for fuel which is why I always scale my dietary recommendations based on body fat percentage).
If that body protein loss continued unabated, they’d lose a lot of muscle, their bodies would start to eat their organs and they would eventually die. And that would be bad. So the body shifts its metabolism, primarily the brain to using ketones. Over roughly three weeks, the brain will use more and more ketones until it derives roughly 75% of it’s total fuel from them, the other 25% has to come from glucose and this will come from protein breakdown.
Under starvation conditions, that means body protein will still be broken down for energy. But the energy can also come from dietary protein; this is a big part of why protein requirements go UP when someone is dieting: some of the protein is being used for energy so more has to be eaten.
And by that point, the grand majority of energy in the body will be coming from fatty acids (in most tissues), ketones (in the brain) with some glucose still being used by the brain and a few other odd tissues that can’t use fatty acids or ketones. So the idea that an enormous amount of protein is being used for energy under these conditions is only true for a little while.
So long as someone increases dietary protein, this offsets the bodies need to use body protein for fuel. Which still isn’t to say that I think a ketogenic diet, even on high calories is optimal for mass gains. It’s still biologically a starvation state in a hormonal sense even if you’re eating lots of food and the overall hormonal profile for mass gains will be superior even on moderate carbohydrates comparatively speaking (there are also cyclical ketogenic diets but that’s beyond the scope of this).
But the idea that the body is burning tons and tons of protein, which was the real gist of your question, isn’t correct due to the overall shift in metabolism from glucose to fatty acids/ketones over about 3 weeks of adaptation. I still don’t think ketogenic diets are OPTIMAL for building muscle growth. They can work (especially if they are used cyclicall) but even moderate carb diets tend to produce a better/more anabolic hormonal response in this regard.
Anxiety, Low-Carb Diets and BCAA Supplements
Question: Hi Lyle. I happened upon your site while researching the connection of dieting leading to anxiety. I am prone to anxiety and panic attacks and have been on zoloft 50mg for years. As of mid November I did Isagenix 30 day program with one day a week of a cleanse.
The cleanse days were horrible for me as I don’t do well on not eating. Anywhoo…after I completed the month of cutting out a lot of carbs and drinking their whey protein shakes 1-2x a day, drinking BCAA’s and eating healthy, I had a major panic attack about a week and a half later. It was odd. I hadn’t had one in years. I am very active.
I teach Cycle, Boot Camp and am a long distance runner. I workout 5-7 days a week. This panic attack was about 4 weeks ago. Since then, I have had to increase the Zoloft to 75mg and I’m trying to get through the upstart side effects (ironically, agitation and anxiety increased) that I can’t seem to shake just yet (4-6 weeks to feel a difference. I am on week 3).
I just wanted to get your opinion on the correlation between dieting and anxiety. I am curious if the addition of adding Whey protein with amino acids and BCAA’s once / twice a day caused this issue. I am SO frustrated to not feel normal again and it has definitely hindered my outlet – running. Thoughts would be greatly appreciated! Thanks!
Answer: Ok, I swear this will be a short one. I addressed this a lot of this within the context of depression as well and you can go read that for most of what you need to know. Tangentially, re-reading that piece, I couldn’t honestly write it today. I suspect I was mired in a bunch of research on the topic because most of those details are completely wiped from my brain. In any case, reading that will give at least some background to this question along with some general concepts of how to address it.
Now, first let me state that anxiety spans a lot of different types of things; interestingly, and suggesting that serotonin plays a role in many of them is the fact that Selective Serotonin Reuptake Inhitibors (SSRI’s), drugs that raise serotonin in the nerve space by preventing it’s re-uptake appear to have major benefit for treatment of anxiety. Zoloft which you mentioned being on is an SSRI (and note that SSRI’s take 3-4 weeks to really kick in for some reason). As well you didn’t mention if you’re still on a low-carbohydrate diet.
But let me talk briefly about anxiety. Years ago when I was way up my butt into neurochemistry, serotonin gave me the worst problem in terms of figuring out what in the hell it actually did and here’s why. Low serotonin levels can be associated with depression but also mania (which trust me are at opposite ends of the continuum), anxiety, aggression and a whole host of conditions that have absolutely nothing to do with one another. But low serotonin is frequently present (and the treatments are broadly the same) in all of them. But why?
The reason is that serotonin per se isn’t causing any of these conditions. Rather, it’s either inhibiting or allowing them to occur. Serotonin turns out to be a general inhibitory neurochemical. When it’s high it tends to generally inhibit behaviors; when it drops it stops doing this.
Of some interest, when prey animals are put in front of their predator, they get a huge burst of serotonin and freeze in place (note that this depends on how close they are to the predator; if they are far enough away they run, if they are too close they fight). But serotonin is attempting to inhibit movement.
This actually raises the question of why serotonin seems to be so involved in sleep and half of me thinks it’s that serotonin is actually paralyzing people in an odd way (the other half of me thinks I’m an absolute idiot for thinking that and note that sleep is insanely complicated neurochemically). Mind you, serotonin converts to melatonin which is probably the mechanism at work here.
And the same appears to be what’s going on here. If someone is prone to aggression and serotonin drops, their aggression manifests. IF someone is prone to depression and serotonin drops, their depression manifests (note that high serotonin can also be associated with depression). If they are prone to mania and serotonin drops…. And the same would occur with anxiety. If someone is prone to anxiety and serotonin drops…well, I think you can finish this sentence.
So broadly speaking, if you’re prone to this type of thing, either
a. Don’t go on low carbs (generally less then 100 g/day is where issues start)
b. Find one of those high tryptophan proteins I mentioned in the depression piece
c. Take either L-trypotphan or 5-HTP to boost serotonin levels
So far as the whey and BCAA, let me address them in reverse order. It is conceivable that the BCAA (which I personally think is useless if protein intake is sufficient) could be having an issue for the reasons discussed in the article on depression. BCAA compete with tryptophan for uptake into the brain since they share the same transporter.
If BCAA are chronically elevated, this might further lower serotonin in addition to the low-carbohydrate intake. Whey has the highest BCAA content of any dietary protein and the same might occur. That said, both BCAA and whey raise insulin and, as discussed in the depression article, that works to lower blood BCAA content. So I suspect that it’s primarily the low-carbohydrates at work here. Raise them and I think the problem will go away.
Damn, I did it, that actually was pretty short.
Lag Time Between Drop in Leptin and Metabolic Adaptation
Question: You wrote at some point that there is a lag time between the drop in leptin and the drop in metabolic rate (i.e. lowered thyroid/SNS output) and I’d be surprised if 12 or even 24 hours is sufficient to reverse this and to email you if I must know the answer why. Well I must know.
Answer: Ok, so I’ll assume folks know more or less about leptin and what it does, if not, read this series. I’ll wait. If you can’t be bothered, here’s the short course. Leptin is a hormone released primarily from fat cells (But also in smaller amounts from places like stomach and muscle) that sends the brain a signal about two things: how much fat you’re carrying and how much you’re eating. When you eat less, leptin drops rapidly, with 7 days of dieting it can drop by 50% but clearly you haven’t lost 50% of your body fat. After that, it drops more slowly along with actual losses in fat.
The drop in leptin coordinates the adaptations to starvation, lowering SNS output, thyroid, metabolic rate, increasing hunger, etc. Quite in fact, replacing leptin (with injections) to pre-diet levels reverses all of these adaptations. But that said, adaptations in response to leptin show a lag time. For example, looking indirectly, there is no real increase in hunger to dieting for 3-4 days. A very recent study showed that eating 25% of maintenance for one day had no impact on appetite or food intake over the next 48 hours. As well, some studies actually show a small increase in energy expenditure by day 4 of total starvation.
Tangentially, this is part of why the whole “if you skip a meal you go into starvation mode” is nonsense. Unlike rats and mice, who’s short life span means that a single meal is very important for them, humans have plenty of body fat and a long life span. A meal doesn’t matter to us, a day of not eating doesn’t matter for us.
We’ve got plenty of body fat to cover the difference. Rats and mice don’t usually store fat and if they don’t eat for a little while they can flat out die so they adapt faster and there is at least one small animal (I forget which) that can die if it misses a meal.
It makes no sense for the human body to adapt to changes on a meal-to-meal or even day-to-day fashion as it wouldn’t signal anything of relevance, in terms of the available food supply, to a human body. So if there is plenty of food for a day, meh. It might go away tomorrow. If there’s no food today, there might be food tomorrow. I think you get the idea.
But by the time food has been unavailable (and dieting is just starvation on a longer time scale) for 4 days, presumably this indicates that there is a problem with the food supply or whatever the brain is parsing this as. Ok, time to start adapting (I’d note in this regard that women can cause their bodies to start to adapt metabolism with 5 days of hard dieting) now. But that’s the lag time.
And I’d expect the system to work identically in the opposite direction. Yes, years ago I wrote about using 5 or 24 hour refeeds and was overly optimistic about their potential impact on raising leptin and reversing the dieting adaptations but now I’m sure that it doesn’t work that way (in contrast, the 2.5 days of overfeeding in the Ultimate Diet 2.0 does). I’ll also present some fascinating data in the Women’s book on this topic that support that overall conclusion but I gotta keep a couple of secrets.
Basically, if the system doesn’t downregulate in 12-24 hours to reduced food intake, I wouldn’t expect it to adapt back to normal in that time frame. The lag should work both ways. Which isn’t to say that short refeeds can’t still be valuable in terms of refilling muscle glycogen or what not. But on a low frequency, they probably don’t do much to reverse metabolic adaptation (it is possible that a one day refeed more frequently, perhaps every 3-4 days might work, however and some fascinating work on Intermittent Caloric Restriction or ICR is pointing towards this as having a lot of benefits).
Now you know. And knowing is half the battle.
Dehydrated vs. Hydrated Muscle Gains
Question: I have a friend was arguing with me about the definition of muscle you mentioned in your article. He thinks the muscle you are talking about in the article is dehydrated muscle, which he thinks impossible to gain 50 lbs in human life time. I think this is ridiculous to view it that way. So what do you actually mean “50 lbs muscle” in your article? Thanks
Answer: Proving that people will argue about anything. I am talking about whole muscle in terms of protein, water, glycogen, minerals, etc. and can’t imagine why anybody would think I was talking about dehydrated muscle (muscle is about 75% water). I can’t imagine why that wasn’t fairly obvious but, hey….
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