An additional factor, also discussed in the book is that there is often an increase…
Training the Obese Beginner: Part 1
So it’s come to my knowledge (based primarily on my Facebook feed) that the Biggest Loser actually concluded this week (with everyone up in arm’s over the relatively anorexic qualities of the winner). And while I’d love to claim that I was intending to run the previous Biggest Loser Feedback to synch with that that’s simply not the case; I don’t have TV and genuinely didn’t know. So call it a happy coincidence.
In any case, following up on that piece, I now want to rerun a 6-part series I wrote a few years back on how I think training the obese beginner should be approached. I’ll be running it over the next few weeks, two pieces each week, once again culminating in a brand new video/rant/blog thingie at the end of the month. I’ve done a bit of tidying up and re-writing, just to smooth out the rougher spots.
Here in Part 1, I want to focus mainly on some of the underlying physiology that occurs in the obese (and make no mistake, what I want to cover won’t be anywhere close to comprehensive; I’ll focus on issues relevant to fat loss); in Part 2-6 I’ll to look at some practical issues that I find many forget when they give advice and/or train the obese hands-on.
Today, what I actually want to do is expand on a comment I made in Fasted Cardio and Fat Loss – Q&A which was this:
At the other extreme, that is in the very obese (here I’m talking about perhaps 35%+ body fat for men and 40%+ for women), the reverse problem is present. There are tons of fatty acids floating around in the bloodstream, but for a variety of reasons, oxidation has become impaired. To fully discuss this issue (along with approaches of fixing it) would require a full article and I won’t say much more about this group here.
While I could simply detail that, I feel that there are other issues worth discussing when looking at the training of the extremely obese and that’s what I’m going to do in this article series.
What Defines Obese?
By extremely obese here, I’m primarily using body fat percentage as the determinant. A male at 30-35%+ body fat and a female at 40%+ are in that category. It’s possible to see even higher numbers; 50-60% isn’t unheard of at the real extremes of obesity.
I won’t mess around with BMI (for discussion of this see Measuring Body Composition Part 1) though it tends to be pretty accurate in this group. That is, while they exist (usually heavier strength/power athletes taking steroids), you don’t see a lot of people at 300+ lbs body weight who aren’t carrying a lot of fat. In general, BMI will track with body fatness, at least in a NON-ATHLETIC population.
I’d also note that it is possible for relatively lighter individuals to carry quite a bit of body fat and much of what I’m going to discuss in terms of underlying physiological “defects” will apply to that group. But for individuals who are carrying both extra weight AND fat, there are issues (mainly issues of programming) that are critical to take into account that I’ll cover later in the series.
Let Me Be Abundantly Clear About the Word “Defect”
As one final pedantic note, so nobody takes me the wrong way, I used the term “defect” above and will continue to use that throughout the article but I want to make it absolutely clear that I’m using it in its literal sense. That is, many physiological systems become impaired (and whether or not this is a cause or a consequence of obesity is still up to debate) in obesity; that is they are defective relative to what is considered ‘normal’ physiology (normal being another loaded word).
But I am NOT using this to try to suggest any sort of negative fashion as if obesity is some sort of defective condition. That is, the word “defect” tends to have very negative connotations (in the same way that the literal meaning of “abnormal” and the connotations that it carries are different) and I am absolutely NOT using the term in that sense. Are we clear? I’m using the term literally here, not connotatively. And that is too a word.
Insulin Resistance/Syndrome X: Part 1
If there is a singular metabolic issue (and it’s really a cluster of issues) that tends to go hand in hand with obesity, it’s what used to be called Syndrome X and is now called the metabolic syndrome. I’d note that while obesity tends to be one of the largest predisposing factors to development, it’s neither a guarantee nor a requirement for this to occur.
That is, there is a proportion of people who despite being obese are metabolically “normal” or “healthy”. It’s also possible to have elements of the Metabolic Syndrome (typically insulin resistance which is what I’ll focus on) and not be overweight. But, with that said, on average, obesity tends to drastically increase the risk of developing the Metabolic Syndrome.
Now, the metabolic syndrome, as noted, is actually a cluster of different things including issues with poorly regulated blood lipid levels, high blood pressure, inflammation and a ton of other things. I’m not going to talk much about those in this series. Instead, what I want to focus on is insulin resistance.
Now, insulin resistance, in rather simple terms, refers to a situation where various tissues in the body including skeletal muscle, liver and fat cells no longer respond appropriately to the signal sent by the hormone insulin. This has a number of consequences not the least of which is that blood sugar levels tend to become poorly regulated.
There is not only typically an increase in fasting blood sugar levels (which is actually diagnostic for the syndrome/pre diabetes) but some strange things can occur in response to the ingestion of carbohydrates. Usually there is an overproduction of insulin in response to their consumption which can drive blood sugar too low and cause reactive hypoglycemia and/or hunger.
As well, because the liver is no longer responding appropriately to the signal sent by insulin, other bad things happen that I’m not going to detail here. Of some importance, and I’d note that the causes of insulin resistance are very involved, is the fact that, when whole body insulin resistance develops, fat cells become resistant to the effects of insulin. This has a couple of consequences one of which is that insulin no longer inhibits fatty acid release which is part of what I was alluding to in the section I quoted myself on above.
Insulin Resistance: Part 2
That is, under normal conditions, in response to an increase in insulin levels (due to carbohydrate or protein consumption), the body will reduce fatty acid levels. But in the obese, this pathway is inhibited (this is also part of why drugs that cause insulin resistance such as growth hormone, clenbuterol or ephedrine, often improve fat loss; they prevent insulin from inhibiting fat release). But insulin resistance at the fat cell is part of why there tend to be lots of fatty acids floating around in the bloodstream all the time in folks with metabolic syndrome.
This is actually part of what causes further insulin resistance (especially at skeletal muscle cells): chronically elevated blood fatty acids. Of course, in that insulin is involved in fat storage, this also means that incoming calories no longer have anywhere to ‘go’ since insulin is no longer playing its storage role. This is part of what leads to the increase in blood levels of glucose, fatty acids, etc. they can’t be stored where they belong.
In a very real sense, this is an adaptation to obesity that attempts to push calories away from fat cells (towards burning elsewhere). I’ve talked about in my books (especially The Ultimate Diet 2.0) that, in this sense, under certain conditions, being insulin resistant can be a “good” thing.
Tangentially, insulin resistance appears to have developed as a positive adaptation to low-carbohydrate conditions during our evolution most likely to spare glucose for use by the brain; it’s only under high-carbohydrate intake conditions that insulin resistance becomes a bad thing. Keep this in mind when you read articles talking about how low-carbohydrate/ketogenic diets induce insulin resistance; they do but it’s for a good reason.
That insulin resistance is actually a “good thing” is especially true under both low-carbohydrate and low-calorie dieting conditions. If the fat cells are trying to keep calories out (and push them to burning elsewhere), this can facilitate fat loss. In this vein, one of the major adaptations to getting leaner is a massive increase in insulin sensitivity, which is part of what makes further fat mobilization more difficult as folks get leaner. I’d mention that this is exactly the opposite of how most people think it works (insulin sensitivity actually predicts weight gain, not the other way around).
But going back to the obese, this adaptation is only beneficial IF other tissues are able to optimally burn those fatty acids off. That is, having plenty of fatty acids floating around only helps fat loss if they can be burned off for energy. But I’m getting ahead of myself.
I’ll finish up this section by pointing out that insulin resistance has some practical implications in terms of the choice of diets. Whether or not they have an actual “metabolic advantage” in terms of fat loss, it’s become clear that reduced carbohydrate (and increased protein/fat) diets improve a variety of metabolic parameters associated with the metabolic syndrome. This is even more the case if weight/fat loss occurs.
I’ll come back to this topic later in the series and I’d refer readers to Insulin Sensitivity and Fat Loss on the site. I’d also refer readers to Insulin Levels and Fat Loss – Q&A for more information about the issue of insulin and fat loss. Moving on.
RER, RQ, and NPRQ
No, not the talk-radio station. First off, RER refers to respiratory exchange ratio, RQ to respiratory quotient and NPRQ to non-protein respiratory quotient. All three refer to basically the same thing and I’ll use RER from here on out. And what they refer to is the mix of fuel being used by the body both at rest and during activity. I won’t bore you with the details, basically these three things are all a measure of the ratio of oxygen being consumed and carbon dioxide being produced and this is used as a proxy for fuel use in the body.
That is, biochemically we know that the burning of carbohydrates has an RER of 1.0 (1 molecule of O2 metabolized for each molecule of CO2). The burning of fat has an RER of 0.7. Protein is somewhere in the middle (about 0.86 or so depending on the protein source).
So given that a whole bunch of conditions that I’m not going to bore you with are met (one critical one is steady state conditions so that means rest or aerobic activity, measuring RER during anaerobic activity is problematic), a measurement of RER tells you what the body is using for fuel. I’d mention that since protein rarely contributes massively to fuel use in the body, protein is typically ignored. That’s what NPRQ refers to: it’s the non-protein respiratory quotient. I’ll ignore protein here, too.
In any case, an RER of 0.7 would indicate 100% fat use, an RER of 1.0 would indicate 100% carb use. Every value in-between those two extremes means a mix of fuels (lower equals more fat oxidation, higher more carb oxidation) and charts can be Googled if you care. I’d note that some odd situations will cause an RER of below 0.7 to show up, it’s an oddity to do with carbon dioxide metabolism with ketogenic diets and you needn’t worry about it.
So what determines RER? Well a bunch of things. Gender (RER can change throughout the cycle), training status (more training tends to lower RER), and probably genetics all play a role. Of some importance, habitual diet can affect things massively, in at least two ways.
As I discussed in Nutrient Intake, Nutrient Storage and Nutrient Oxidation and then expounded upon in How We Get Fat the body adjusts fuel use to intake; ignoring protein carbohydrate intake tends to influence things the most. Eat more carbs and you burn more carbs and less fat (RER goes up).
As well, the status of muscle glycogen influences RER profoundly; high muscle glycogen tends to impair fat burning at the expense of carbohydrate oxidation. That is, when muscle glycogen is perpetually raised, the body burns more carbs and burns less fat. Keep this in mind when I talk about diet in Part 2.
So what’s my point? Well, two points actually. The first is that many studies have found that the obese have a higher resting RER on average; that is they tend to preferentially burn carbohydrates for fuel. A study that just came out found that resting RER was predictive of RER during activity; that is folks who burn more carbs at rest burn more during exercise and vice-versa.
The second is that habitual diet (and a diet high in both carbohydrates and fats, and I’m talking about a diet that is, by definition, in excess of maintenance calories) can be a cause of further problems such as impaired fat burning and a preferential usage of carbohydrates. Again, I’ll talk more about this in Part 2.
And this brings me in a roundabout way to my original quote from last Friday’s piece, the fact that the obese tend to have lots of fatty acids floating around but an impaired ability to burn them. Which brings me to the next metabolic “defect”.
Impaired Mitochondrial Function
A number of studies over the past years have found evidence of impaired mitochondrial function in the obese. Now, for background, as everyone learned and promptly forgot in high-school science, mitochondria are specialized bits of the cell where things are burned, especially fatty acids.
There’s actually a fascinating history to how we gained the use of mitochondria that even I am not nerdy enough to detail here. Oh yeah, I’d be remiss in not mentioning that the mitochondria are THE POWERHOUSE OF THE CELL (an in-joke for biochem nerds).
But study after study after study finds impaired function of mitochondria in both obesity and diabetes (I’d say more of the research has been done on the latter group) and this has a number of metabolic consequences not the least of which is impaired fat oxidation. Some studies also find that the obese don’t increase fat oxidation during activity as well as lean people; essentially they have lost a metabolic flexibility to switch between fuel sources.
Another consequence is that, because fatty acids can’t be burned in muscle cell (or liver) they are often deposited in inappropriate places or converted to things like ceramide inside cells that cause further problems. But that’s getting a bit deeper than I want to go here.
Now a question that always raises its ugly head here is what’s causing what. That is, does impaired mitochondrial function help to cause obesity, or does developing obesity cause the mitochondrial impairment? You can replace those terms with just about anything else you want; there’s always a big question surrounding causation here. That is, when you see any type of metabolic “defect” associated with obesity you always have to wonder whether it helped to cause the obesity or was caused by the obesity.
It can be a hard question to answer sometimes and there’s a third possibility that many tend to ignore: perhaps a sub-clinical mitochondrial impairment predisposes folks towards obesity and when that’s combined with the modern diet and lifestyle, as they become obese, the problem just gets worse. Usually the truth is that third one for most of this stuff.
Usually this question is at least partially answered by seeing if weight loss and/or an increase in activity helps to reverse the “defect”. In the case of most aspects of the metabolic syndrome, both exercise and weight loss tend to improve things and reverse most parts of the syndrome. Note that improve is not necessarily the same as eliminate.
I would at least point people to the Biggest Loser Feedback for the improvements he saw in heart rate, blood pressure and blood glucose in a mere 14 days. He got essentially normalization in a miniscule period of time secondary to a massive increase in activity and equally massive weight loss.
In the case of defective mitochondria, I can only think of one or two recent papers that have examined the issue but the answer is that, yes, the “defect” appears to go away with an increase in activity. We have known for decades that one adaptation to regular aerobic activity is an increase in both mitochondrial number and activity and it would be strange that this would be unable to occur unless there were some massive pathophysiology occurring.
A Grab Bag of Practical Stuff
The above doesn’t even begin to scratch the surface of everything that’s going on in the obese individual physiologically but, as I said, I’m not trying to be comprehensive here. Moving away from all of the physiological issues that can be part of training obese beginners, I want to address a couple of practical issues that folks working with this population should really consider (but, by and large, seem not to).
The first is really specific to commercial gyms but I find that the very obese are often intimidated as hell going into the gym. It can be tough surrounded by a bunch of skinny/fit folks when you’re just getting started (this is something I’m going to come back to in my forthcoming video piece at the end of this series) and this is certainly not helped by the fairly shitty attitude that many who are in shape take towards them. As a sterling example, you can look at the spate of “Oh No Here Come the New Years Resolutioner” graphics, basically criticizing people for joining a gym and starting to work out.
Related to the general intimidation factor, it also seems common for obese folks to have had bad early exercise experiences that certainly don’t help with their desire to be there. These things frequently lead to a hesitancy to enter the typical commercial gym, filled with fit, buff (and frequently judgmental) people.
Practically this means that trainers working with this population MUST ensure that their client have a positive experience from the outset of the program. This is something I’ll come back to a number of times during this series but I really don’t think it can be mentioned too many times. I’d note in this vein that studies show that having a positive experience from activity is a huge key in long-term adherence. How surprising.
A second issue is that, by and large, the obese often have a very low tolerance for any type of exercise. Sure, sure, you’ve watched The Biggest Loser and they jump them into hours of activity from the get-go. It makes for great TV but it also causes problems. Many of the contestants have gotten overuse/impact injuries right out of the gate and, many years ago, one guy on BL Australia several years back threw a blood clot. Afterwards he was limited to nothing but low volumes of low intensity activity afterwards. Amusingly, he lost the most weight. There might be a lesson there but that’s a topic for another day.
Getting off-topic briefly, I fully expect one of these TV exercise programs to kill someone with this silly bullshit. I’ve seen it happen locally (the Austin Gold’s Gym killed a guy many years ago by running him through intense activity right off the bat; he dropped dead of a heart attack) and it will happen on prime-time TVd. Of course, when this causes ratings to soar, we’ll be just one step closer to The Running Man and true TV death sports.
But in general, without the incentive of $250,000 pushing them, the typical obese beginner isn’t going to put themselves through massive amounts of exercise, at least not initially. If they get wrecked out of the gate, they are unlikely to even try exercising a second time. In keeping with the idea of “ensuring a positive experience” I mentioned above starting gradually and ramping up makes more sense then throwing than into the grinder. The second approach may generate better short-term results but the long-term results are more at risk in my opinion.
Finally, there are the simple realities of a larger individual moving their body during activity (both weights and cardio). There are joint impact issues to consider, the realities of coordination that a 120 lb female personal trainer has no clue about, etc. This has implications for exercise choice and what can or should be done with the obese beginner. Again, a topic I’ll cover in much detail later in this series.
And, again I’m sure I’ve left stuff out but between the look at physiological issues and the above, this is as good a place as any to stop for today. I’ll pick it up next week in Part 2 and start looking at some of the practical implications (and how to apply it) then.