Category Archives: Exercise

Artificial light regulates fat mass: no bueno.

“despite not eating more or moving less”

We’ve seen this time and time again: LIGHT IS A DRUG.

 

above quote is extrapolated from this rodent study: “Prolonged daily light exposure increases body fat mass through attenuation of brown adipose tissue activity.”

 

Artificial light impacts nearly every biological system, and it doesn’t even take very much to have an appreciable effect (think: checking your smart phone or watching a television show on your iPad in bed at night).  In this study, adding 4 hours to the usual 12 hours of light slammed the autonomic nervous system, disrupting sympathetic input into brown adipose leading to a significant increase in body fat  “despite not eating more or moving less.”

 

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Ketoadaptation and physiological insulin resistance

This is where the magic happens.

Rat pups, fed a flaxseed oil-based ketogenic diet from weaning onward – note the drop-off in ketones after 2 weeks (Likhodii et al., 2002):

flaxseed ketogenic diet

What happened on day 17?

Patient history: these rats have been “low carb” their whole lives.

Side note: flaxseed oil is very ketogenic! (Likhodii et al., 2000):

ketogenic rodent diets

Flaxseed oil-based ketogenic diet produced higher ketones than 48h fasting; the same can’t be said for butter or lard.  PUFAs in general are more ketogenic than saturated fats in humans, too (eg, Fuehrlein et al., 2004):Saturated polyunsaturated ketones

Crisco keto (adult rats) (Rho et al., 1999):

shortening-based ketogenic diet

suspect those two rogue peaks were experiment days…

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2 New Diet Studies

*ugh* journalists

I’m talking to you, Mandy Oaklander!

Regarding the new low carb vs low fat study, she writes: “Popular diets are pretty much the same for weight loss, study finds.

Effects of low-carbohydrate and low-fat diets: a randomized control trial (Bazzano et al., 2014)

Further, “An earlier study in Annals of Internal Medicine did find that low-carb dieters lost slightly more weight than low-fat dieters after one year. The study today reached similar conclusions, but the differences in weight loss were not significant.”

Perhaps Mandy just doesn’t realize there’s a difference between significant, as in “meaningful,” and significant, as in “P<0.05.”  Pro-tip: you can tell them apart relatively easily, because the latter is usually accompanied by a cute little asterisk.  For example, the differences in weight loss were quite statistically significant (P<0.05):

Bazzano BW
She goes on to say “After a year follow-up, some of those pounds crept back for people on both diets…”

To that I say: yeah, but fat mass continued to decline in those on the low carb diet, meaning some of that weight re-gain was muscle:

Bazzano FM

So, between 6 and 12 months, carbs and calories were creeping up in the LC group, yet fat mass was still declining.  Perhaps this way of eating improved their metabolism, or restored the ability to effectively partition nutrients.

***in real-time: at this point, I realize that Mandy was actually talking about the other study, which she was covering accurately.  Sorry, Mandy!***

Bazzano PA

…so maybe the low-carb (LC) diet improved muscle mass because it was also high protein? …perhaps, but 19% vs 24% (71 vs 85 grams) isn’t a very big difference.  Alternatively, since the LC group really just maintained absolute protein intake (86 grams at baseline, 85 at month 12), whereas low-fat (LF) dieters decreased (86 grams at baseline, 71 at 12 months); perhaps this is why LF lost muscle mass..?  Still, those changes in protein intake are small, and I think people can be too quick to chalk up the benefits of LC to “high protein.”

In sum, this is actually one of the more “pro” LC studies.  And it wasn’t even a huge difference in carbs: 198 vs 127 grams/d at month 12 (54% vs 34%).  Big difference in fat mass; and CRP, a marker of inflammation, even declined in the LC group.

Low fat diet advocates have been giving me headaches for years… the low fat diet caused headaches (P<0.05):

Adverse Events 1

 

 

Adverse Events 2

The study Mandy was actually talking about: Comparison of weight loss among named diet programs in overweight and obese adults: a meta-analysis (Johnston et al., 2014)

It was a meta-analysis, which is just about the only type of study capable of taking down LC.

 

 

…but at least it had this cool chart (modified):

cool chart (modified)

cool chart (modified)

 

*ugh* scientists

crap

The macro’s in “Low fat” overlap with “Moderate,” implying “Low carb” is “EXTREME”  …the authors’ bias is subtle, I’ll give ‘em that, but I’m getting too old for this.

Dear Obesity Researchers,

If you want to design a study showing a low fat diet is as good as low carb for fat loss, here’s your best bet: recruit young, exercise-tolerant overweight patients who aren’t on any meds.  PROOF (see Ebbeling study).  Or find 10 similar ones and write up a pro-LF meta.

If you want to show low carb is better, recruit patients with obesity.

 

calories proper

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Cyclical ketosis, glycogen depletion, and nutrient partitioning

Meal & exercise timing in the contexts of “damage control” and nutrient partitioning are frequent topics on this blog.  I generally opt for a pre-workout meal, but nutrient timing hasn’t panned out very well in the literature.  That’s probably why I’m open to the idea of resistance exercise in the fasted state.  A lot of pseudoscientific arguments can be made for both fed and fasted exercise, and since a few blog posts have already been dedicated to the former, this one will focus on the latter.

The pseudoscience explanation is something like this: since fatty acids are elevated when fasting, exercise in this condition will burn more fat; and chronically doing so will increase mitochondria #.  The lack of dietary carbs might enhance exercise-induced glycogen depletion, which itself would bias more post-workout calories toward glycogen synthesis / supercompensation.  Much of this is actually true, but has really only been validated for endurance training (eg, Stannard 2010, Van Proeyen 2011, & Trabelsi 2012; but not here Paoli 2011)… and the few times it’s been studied in the context of resistance exercise, no effect (eg, Moore 2007 & Trabelsi 2013).  However, there are some pretty interesting tidbits (beyond the pseudoscience) which suggest how/why it might work, in the right context.

Exercising fasted or fed for fat loss?  Influence of food intake on RER and EPOC after a bout of endurance training (Paoli et al., 2011)

John Kiefer, an advocate of resistance exercise in the fasted state, mentioned: “the sympathetic nervous system responds quicker to fasted-exercise. You release adrenaline faster. Your body is more sensitive particularly to the fat burning properties of adrenaline and you get bigger rushes of adrenaline.”

Much of this is spot on.  That is, ketogenic dieting and glycogen depletion increase exercise-induced sympathetic activation and fat oxidation (eg, Jansson 1982, Langfort 1996, & Weltan 1998).

The question is: can this improve nutrient partitioning and physical performance?  Magic 8-Ball says: “Signs point to yes.”  I concur.

Contrary to popular beliefs, glycogen depletion per se doesn’t harm many aspects of physical performance.  A lot of fuel systems are at play; you don’t need a full tank of glycogen.

Effect of low-carbohydrate-ketogenic diet on metabolic and hormonal responses to graded exercise in men (Langfort et al., 1996)

High-intensity exercise performance is not impaired by low intramuscular glycogen (Symons & Jacobs, 1989)

Increased fat oxidation compensates for reduced glycogen at lower exercise intensities (eg, Zderic 2004), and ketoadaptation may do the same at higher intensities.

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Ketosis in an evolutionary context

Humans are unique in their remarkable ability to enter ketosis.  They’re also situated near the top of the food chain.  Coincidence?

During starvation, humans rapidly enter ketosis; they do this better than king penguins, and bears don’t do it at all.

Starvation ketosis

 

Starvation ketosis

Humans maintain a high level of functionality during starvation.  We can still hunt & plan; some would even argue it’s a more finely tuned state, cognitively.  And that’s important, because if we became progressively weaker and slower, chances of acquiring food would rapidly decline.

Perhaps this is why fasting bears just sleep most of the time: no ketones = no bueno..?

Observation: chronic ketosis is relatively rare in nature.  Angelo Coppola interpreted that to mean animals may have evolved a protective mechanism against ketosis (if you were following along, please let me know if this is a misrepresentation).

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Carb Back-Loading, take II

I recently had the pleasure of speaking with John Kiefer and his crew about Carb Back-Loading proper; we discussed the protocol and many other hormonal effects associated with this pattern of nutrient & exercise timing.  Interesting stuff; plenty of fodder for future blog posts…

Brief refresher: skeletal muscle insulin sensitivity is higher in the morning than in the evening.  Exercise boosts insulin sensitivity selectively in muscle, which is relatively more important in the evening.  Thus, an evening carb-load may benefit from exercise to effectively partition the energy influx into skeletal muscle [and away from adipose tissue].

Summary of Part 1 of my CBL review: studies on nutrient timing sans exercise aren’t entirely consistent, in part, due to reciprocal regulation of insulin sensitivity in skeletal muscle and adipose tissue.  That is, excess energy from an evening carb-load, without the exercise-induced, skeletal muscle-specific boost in insulin sensitivity, may be biased less toward muscle growth and more toward fat storage, because unlike skeletal muscle, the sensitivity of adipose tissue to insulin appears to improve as the day progresses… and without exercise to offset this, as in the studies discussed below, this may lead to suboptimal results.

*one thing Kiefer stressed, and I agree, is that the effects of any given intervention may be population-specific.  For example, he pointed out that diurnal insulin sensitivity is less robust in obese and aged populations.  So if two findings aren’t in full agreement, click the link to the study and check this first… context matters!

 

 

Tl;dr: I think high intensity exercise and possibly the time of day it’s performed, and regular bouts of fasting, are important factors that mediate the efficacy of CBL and similar protocols. Continue reading

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Carb Back-Loading and the Circadian Regulation of Metabolism

Carb Back-Loading (CBL) redux, part I

Step 1: eat little in the morning (maybe some fat+protein; definitely no carb)
Step 2: exercise in the afternoon/evening
Step 3: eat the carbs, all of them.  Preferably high glycemic carbs.
Other: no dietary fat post-workout; protein periodically throughout the day.

What makes CBL different from its predecessors is the stress on the timing – exercise and carbs in the evening.  John Berardi’s “Massive Eating” dietary guidelines are similar: protein+fat meals all day except pre- and post-workout, which are protein+carb meals.  Martin Berkan’s “LeanGains” is fasting most of the time (including pre-workout), exercise in the afternoon, then a big post-workout meal (quite similar to CBL).  My only tweak, as discussed below (and previously here and here), would be a pre- rather than post-workout meal [in some contexts].

There’s a summary of this blog post at the bottom… it might be helpful to read that first (see: “Tl;dr:”).  Also, please note that much of this post is about the fringe of theoretically optimizing nutrient partitioning, like improving from 85 to 90%, or 40 to 45%, not 40 to 90%…  I’m not that deluded.

My initial take, in general, is that this book is loaded with gems about nutrition, exercise, biochemistry, and physiology.  It’s also very readable and has a lot of good recommendations.  In this post, I want to discuss one specific aspect of CBL: tissue-specific circadian regulation of metabolism.

 

nutrient timing

 

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Lipid Hypothesis 2.0: Eat Butter

The original lipid hypothesis stated, more or less, that lowering blood cholesterol would reduce premature mortality from heart disease.  At the time, it was thought that dietary cholesterol and saturated fat increased the ‘bad’ type of blood cholesterol, so the advice was to restrict those foods.  All of that was wrong.

Time

Lipid Hypothesis 2.0: Eat Butter

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Fasting, circadian biology, and epigenetics

From the best I can gather, one of the more immediate players in circadian biology is the coenzyme nicotinamide adenine dinucleotide (NAD), which participates in a variety of redox reactions.  Fasting increases the intracellular NAD/NADH ratio, setting off a cascade of events involving epigenetics and the regulation of metabolism.  HT to Jack Kruse for really cracking into this nut.

NAD activates sirtuins, a family of deacetylase enzymes.  This is epigenetics.

SIRT1

 

SIRT1 regulates the activity of BMAL1 and CLOCK, two circadian transcription factors, which target NAMPT, an enzyme that synthesizes NAD.  And in a curious feed-forward mechanism, CLOCK and BMAL1 enhance SIRT1 expression… genetic deletion of any of these players induces insulin resistance (Zhou et al., 2014), and this can be recapitulated with constant darkness: reduced BMAL1 and SIRT1, hepatic insulin resistance; the latter can be reversed with resveratrol (which may or may not be acting through SIRT1; this is controversial).  While alcohol does no great favors for circadian biology, if you’re going to imbibe, perhaps a resveratrol-rich Argentinian malbec served, and this might be the important part, at night, when all of this stuff is going on… coincidentally [fortunately], that’s precisely when most choose to imbibe.

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Nutrient Partitioning: …a *very* high protein diet.

Or: what happens when you eat a ton of protein?

RDA: 0.8 g/kg

Active individuals: 1.2-2.0 g/kg (via ISSN)
Comment (1): I think sedentary, physically inactive, and non-exercisers should be in this range to offset disuse atrophy.  And they should exercise.
Comment (2): Do athletes really need more protein than non-athletes?  They have exercise, a powerful anabolic stimulus.  More protein may improve performance or body composition, but they might not *need* it, in terms of nitrogen retention… there’s probably a study on this.

NEED =/= OPTIMIZATION

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