Ketones, carbs, and physical performance.

Or more specifically, ketone monoesters and carbs.  Literally, this study was a high-dose ketone monoester supp sans caloric or carb restriction.  I know, weird right?

 

Ketone ester

 

Non sequiter nutrition notes, #context, etc.:

1) ketone esters =/= ketone salts.  Ketone salts are either sodium or potassium-dominant.  Ketone esters are essentially salt-free.  Possibly helpful background reading here.

2) nutritional ketosis =/= starvation ketosis =/= ketone supp ketosis.  Because #context.

Starvation ketosis, but not nutritional ketosis, is muscle-sparing.  Ketone supps sans carb restriction might be.

3) the theory of ketone supps for sport is: 1) ketones are an energetically favorable fuel; and 2) they’ll spare glycogen, theoretically allowing prolonged duration of moderate-to-high intensity performance.  Adding in carbs will likely further this.

4) I have no studies to support this, but the idea of ketone supps in the #context of high carb doesn’t sit will with me.  Seems like high levels of both substrates = mitochondrial overload and oxidative stress.  Maybe.

5) there’s a gradient of fuel use during exercise:

-explosive power: creatine, anaerobic

-high intensity: glycogen, anaerobic

-low intensity: fatty acid oxidation, aerobic

But it’s a gradient with a lot of overlap, and ketoadaptation further blurs the lines.

 

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Circadian timing with REV-ERB and PERIOD

The circadian proteins Bmal and casein kinase (CK) enhance and degrade Period (PER), respectively, by completely different mechanisms.  Both are necessary, but at different times of day… #context

Gross oversimplification: the Bmal party is kicked off in the morning by LIGHT, and acts to increase PER by night (among many, many other things).  As the day progresses, REV-ERB the Repressor slowly shuts down Bmal, so that peak PER occurs in the evening and doesn’t carry over until the next morning.  GSK3b activates REV-ERB the Repressor.  Lithium puts the system in fast forward, leading to phase advance* and ZZZ’s when timed right, at night… I think

 

Lithium GSK3b image

 

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Long-term fat adaptation

Recent comments about FASTER have upgraded this study to “the only long-term study on fat-adaptation.”  Needless to say, I disagree.  Again.

Side note: FASTER had no randomization or intervention (ie, confounded by selection bias, among others); they basically recruited long-term low carb & high carb ultra-endurance runners and measured the stuffings out of ’em.

Ultimately, they showed a very high maximal fat oxidation rate in low carb ultra-runners, 1.5 grams per minute.  This is important because MAXIMAL HUMAN FAT BURNING CAPACITY

 

TROGDOR the BURNiNATOR

 

In previous studies on SAD (Standard Athletic Diet haha), maximal fat oxidation at similar VO2max% has been reported to be much lower, <1 g/min (eg, Hetlid et al., 2015 and Volek et al., 2016).

 

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Gypped by GIP

Dr. Johnson’s recent paper is nothing short of a monster.  They did a TON of experiments.  Here, I only want to focus on one aspect.

The insulin-obesity hypothesis in a nutshell (very oversimplified): more insulin = more fat mass and vice versa.

I know I know, it was mice fed standard rodent chow, but also included models relevant to human biology like reduced insulin and caloric restriction, which may reflect certain aspects of ketogenic diets and intermittent fasting… and some of the results actually do reflect what happens to humans.  Some.

 

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Keto-Crossfit

Study: a handful of average-bodied Crossfitters in their mid-30’s were recruited and told to either: 1) keep doing what they’re doing; or 2) go full keto.  Crossfit 4x/week.   Strength testing before and after 6 weeks (Gregory et al., 2017).

I’ll start with the best part: KETOADAPTATION IS A REAL TRUE THING THAT WORKS (P<0.05).  Otherwise, this group’s performance would’ve plummeted.  It is known.

The performance test was time to complete a 500-meter row, 40 body weight squats, 30 abdominal mat sit-ups, 20 hand release pushups, and 10 pull-ups.

Tl;dr: both groups knocked about a half a minute off their time!

The key here is duration: 6 weeks of ketogenic dieting is adequate to restore performance back to baseline.  <3 weeks is not.

 

performance

 

Here’s the downside (sort of):

 

body comp

Basically, the keto group dropped carbs and failed to compensate by upping other calories.  I know I know, spontaneous ad lib appetite reduction, but this is a study on PHYSICAL PERFORMANCE.

 




 

And in further support of “muscle growth sans carbs,” keto dieters upped protein by 15% and this still wasn’t enough to compensate for the reduction in carbs/insulin: they still lost a bit of lean mass (NS).  Imagine if they hadn’t increased the brotein? yikes

 

food

 

so basically, they lost body fat because CICO and retained lean mass because exercise and protein haha jk

 

Admittedly, it was cool to see the body comp changes, but we know fat loss eventually plateaus and people start eating maintenance calories again (maybe a bit more if Ebbeling can be believed).  And this is where they remain for the rest of their lives (hopefully).  So at 6 weeks, they were still losing weight, nowhere near where they’re going to be for the rest of their lives, but THAT’s where I’d like to see performance testing (ie, at a stable body weight).  Don’t get me wrong, I hate myself in advance for making this critique: the researchers should’ve pushed more calories in the keto dieters bc this is a confounder in a study on PHYSICAL PERFORMANCE…  but this doesn’t really matter in the big scheme of things because Blackburn’s group did that and showed the results were the same haha

 




 

On another note, I don’t think people should expect an additional performance boost from being more ketoadapted (or more fat-adapted or whatever), primarily because whether the study is 3 weeks or 6, performance never really gets better than baseline in experienced athletes.  With more advanced training techniques, sure (and I think this is common), but not more keto- or fat-adaptation.

 

calories proper

 

 

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LIGHT timing for circadian entrainment

Basically, this much is pretty obvious now: LIGHT and food in the morning + darkness after sunset = proper circadian entrainment.  But the how is pretty cool; LIGHT affects different biochemical pathways at different times of the day, which is how it can either advance or delay your circadian phase.

LIGHT entering the eyes is perceived by ipRGCs which then dish out glutamate and PACAP.  These mediators go on to activate receptors in the SCN (the “Master Clock”).

Depending on the time of day, glutamate and PACAP affect different pathways.

 

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Insulin resistance and obesity

Some people believe insulin resistance (IR) causes obesity, and they are not pleased when I say this is actually a controversial topic in the field…

“Bill isn’t toeing the company line.  Again.”

So I asked a simple question: if IR causes obesity, how?

 

 

The Common Response: 1) IR -> 2) hyperinsulinemia -> 3) more insulin = more fat mass. 

However, this is flawed.

Easiest rebuttal (somewhat of a strawman, but whatevs): Barbara Corkey and her group has done a lot of work showing that insulin hypersecretion (caused by dietary additives, preservatives, weird chemicals, etc.) may actually precede & causes IR… not enough insulin hypersecretion to induce hypoglycemia, just enough to induce IR.

So that basically breaks the 1st step in the Common Response, but doesn’t really disprove the possibility that IR still causes obesity (or can cause obesity).

In any case, check out Corkey’s 2011 Banting Lecture.  Highly recommended, a lot of food for thought.

 

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Hey CICO, I’m playing by your rules.

Brief background: the notorious Ebbeling study of 2012 showed an apparent metabolic advantage of a ketogenic diet.  After losing some weight, participants were assigned to low fat (LF), low GI, or ketogenic diets.  As expected, energy expenditure (EE) declined in all groups after weight loss.

 

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Dopamine and breakfast

While opining on her latest protein-rich breakfast experiment, Jane Plain mentioned ghrelin as an important mediator of the circadian component (more on this below).

T.S. Wiley wrote a lot about the protein-rich breakfast; here’s my understanding of her take on it.

N.B. I highly recommend her book, Lights out: sleep, sugar, and survival.

 

Quotes are mainly taken from the text. I’ve tracked down some of the cites; the rest are in the back of the book, albeit somewhat unorganized :/

 

Part 1. We naturally have a cortisol spike first thing in the morning, known as the Cortisol Awakening Response (CAR).  This peak, which can be screwed up by artificial light at night or a big evening dinner, helps support morning light-induced dopamine.

 

CAR

 

Dopamine is great, but may induce impulsivity if it’s unfettered.

Enter: the protein-rich breakfast. It provides tryptophan and a bit of insulin to promote serotonin synthesis (eg, Manjarrez-Gutierrez et al., 1999).

Not enough serotonin to make you crazy, just enough to balance the dopamine = impulse control.

~ circadian balance achieved ~

 

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Vasopressin’ me again

I’ve been following the links between blood pressure modulatory hormones and circadian rhythms for a while now — and while it’s a fascinating overall picture, this nut hasn’t been cracked [yet].  A paper published in Science may have brought us one step closer.  (And some potential biohacks.)

Background reading (probably important, because my thoughts on this aren’t very coherent [yet]):

LIGHT, Leptin, and Environmental Mismatch (skip down to Part 2)

Circadian phase delays and metabolism

Circadian biology: jet lag, mood, & potential role of BP regulatory peptides

 

The new study: Changes in the composition of brain interstitial ions control the sleep-wake cycle (Ding et al., 2016)

It was a study on mouse brain, but the #context is very relevant here.

Tl;dr: they showed that changes in extracellular ions, independent from neuronal activity, can induce sleep or wakefulness.  “Independent from neuronal activity” was accomplished by silencing the neurons with tetrodotoxin.

 

Pufferfish

 

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