Category Archives: Uncategorized

The impact of keto-adaptation on exercise performance and yada yada yada

New review out of Pittsburgh, Pennsylvania, gets some things right (Sherrier and Li, 2019).

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… takes some things out of context, too, like saying “beneficial effects of ketogenic diets on cancer,” as if that’s an established fact.

It’s not… but still, let’s focus on the positive

Some ground rules:

  1. ketogenic diet =/= fasting
  2. nutritional ketosis =/= exercise
  3. carbs =/= obesity
  4. the opposite of intermittent fasting isn’t diabetes

Another ground rule, or maybe a disclaimer: I’ve read and blogged about nearly every study on ketoadaptation & physical performance that’s out there. My 30000-foot view is: “it’s fine.”

Given adequate time to adapt (~3 weeks), keto doesn’t wreck physical performance. Some studies show a little positive, some a little negative; net sum = neutral.

Other energy systems kick in and performance is maintained. Any further gains from training are just that: gains from training (not gainz from moar ketoadaptation).

Keto isn’t muscle-sparing or anything like that, and you likely need more protein (not less) to maintain muscle, but this also isn’t really that big of a deal.

This article is pretty good, imo. Covers a lot of topics ranging from glycogen on keto to fat balance to exercise efficiency and more.

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5/2, ADF, and eTRF: place your bets!

Three studies. Predicted effects on body composition & glucose tolerance?

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5/2 (Panizza et al., 2019): this is a form of intermittent fasting (IF). Two consecutive days you eat 70% less than usual; the other five days you eat at maintenance. It’s not ‘ad lib;’ there’s some calorie counting involved.

This study design was a little odd, but it’s cool that it came out around the same time as the other two (ADF & new eTRF) so we can cover a lot of ground in a short amount of time.

Is it fair to compare 5/2, higher protein, lower carb, Mediterranean diet to a lower protein, higher carb DASH diet? Predicted effects on body composition?

And I even say some nice things about fasting 🙂


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Physiological insulin resistance: benevolent pseudo-diabetes

The mystery of the ketogenic diet: benevolent pseudo-diabetes (Blagosklonny, 2019)

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“studies in rodents have found that the ketogenic diet causes diabetes”

Narrator: No, they don’t. In fact, rodent keto studies are all over the board.

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Sometimes glucose tolerance is up, sometimes it’s down, sometimes it depends on what you’re actually comparing it to — is the control group low fat or the notoriously misnamed high fat diet (it should just be called an obesogenic diet imo).

off topic — just found these and they’re awesome. Check out the digits.

OK, in some studies, keto mice are insulin resistant. Sometimes it correlates with body weight. See all the ‘somes’ here? You can’t make broad statements about rodent keto studies.

And you definitely can’t use them to support recommendations for human diabetes/obesity.

this probably isn’t even keto’s strongest suit anyway…

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Tell me again, how skipping breakfast unlocks a secret anabolic potential of skeletal muscle

SMH

Time-restricted feeding plus resistance training in active females: a randomized trial (Tinsley et al., 2019)

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Hate to be a buzzkill because this was actually a well-designed and well-conducted study.

I’m not a huge fan of intermittent fasting (IR) because it’s usually shown to be no better than continuous energy restriction (CER) yet also require prolonged periods of severe energy restriction.

Also, if forced, I’d recommend starting with eTRF or an early dinner; the point being to extend the fasting window by starting it earlier in the day rather than ending it later — there might actually be some metabolic benefits of this over isocaloric CER.

And in this case especially, athletes, who benefit from increased protein-feeding frequency which is removed from IF by design (although the authors attempted to partially bypass this by adding some HMB to an IF group).

#context: this wasn’t eTRF. It was skipping breakfast. These weren’t older insulin resistant people. They were young females with resistant training experience.

So, tell me again, how fasting induces growth hormone secretion which promotes the anabolic potential of skeletal muscle?

Breakfast and a late lunch instead?


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Short- and long-term regulation of appetite

The energy expenditure and food intake of individual men.

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So, this study has been making the rounds: Skipping Breakfast Before Exercise Creates a More Negative 24-hour Energy Balance: A Randomized Controlled Trial in Healthy Physically Active Young Men (Edinburgh et al., 2019)

I didn’t want to comment on it because critics could easily say I was just biased (many studies support breakfast from a variety of angles therefore so do I).

Does skipping breakfast allow your to maintain an energy deficit and lose excess body fat? If so, GO FOR IT. Skipping breakfast may not be optimal long-term wrt health & general well-being, but it’s better than carrying around excess body fat for decades.

I don’t buy intermittent fasting does much beyond that — with the exception of a few studies on eTRF (early Time-Restricted Feeding) which showed favorable effects on weight loss, insulin sensitivity, and fasting blood glucose. Not entirely sure why this happens with skipping dinner and not skipping breakfast but it is what it is. Probably has something to do with, ya know, circadian rhythms.

Regulation of energy balance –

1) I think the Edhold 1955 study on the short- vs. long-term regulation of appetite is great. Both what they did and their discussion.


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Circadian rhythms and ketosis in migraines

Ask almost anyone who experiences chronic migraines and they’ll almost always say their latest attack was preceded by a period of poor quality or short duration sleep.

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That, in itself, is a hint circadian rhythms may be involved.

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Can circadian dysregulation exacerbate migraines? (Ong et al., 2018)

In this study, sleep characteristics and circadian rhythms were evaluated in 20 chronic migraine sufferers and 20 healthy controls.

They found that, despite similar sleep duration, later sleep timing and circadian dysregulation (as per salivary melatonin) were associated with higher migraine frequency and severity.

It is seriously unpleasant, but migraines can be experimentally induced in otherwise healthy people (eg, Amin et al., 2012).

PACAP. We’ve talked about this before. It’s a pretty big player in regulating circadian rhythms.

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Have circadian arrhythmia long enough, Type 2 then Type 3 Diabetes

ApoE4: The door to insulin resistant dyslipidemia and brain fog? a case report (Stoykovich and Gibas, 2019).

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A retired business who was exposed to artificial light, day and night, his entire adult life. Insomnia. Last 15 years had T2D. Now, foggy thinking, forgetfulness, and impaired verbal fluency.

We aren’t given many details about his 10-week hypocaloric ketogenic diet but that’s OK in this case, as ‘hypocaloric’ was confirmed via weight loss, ketosis was confirmed via ketometer, and, well, this:

A little weight loss goes a long way. And those ketones may have helped, too…

Flash forward and we get this:

Ketones improves apolipoprotein E4-related memory deficiency via sirtuin 3 (Yin et al., 2019)

Wait, is it Sirt3 -> ketones or vice versa?

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The studies on high carb, high fibre diets for T2DM

40 years late, sue me 🙂

These small, short duration studies suggest switching people from an ADA diet to a high carb, high fibre, whole food-based diet (HCF) would be of benefit in T2DM (Kiehm et al., 1976 and Anderson and Ward, 1979) (and longer-term follow-up with similar results).

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These studies have been blogged about. Like, a lot.

The diets were approximately isocaloric (not much weight loss on either); lower protein in the first study, same protein in the second.

Study design: relatively weak — 1 week on ADA diet, followed by 2 weeks HCF.

Strengths: the second study was in a metabolic ward and controlled for protein, and the long-term follow-up was at 15 months. Weight stable for the most part.

Here’s the rub:

  1. HCF didn’t work in the most insulin resistant group. Fasting glucose actually seemed to improve a bit on ADA and then appeared to deteriorate in some individuals on HCF.

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Gluconeogenic precursors on LCHF

Metabolic advantage (MA): theoretical boost in energy expenditure induced by a diet. Some studies show it exists, others don’t. In any case, ask any keto proponent about MA and they’ll surely say something like, “if it exists, gluconeogenesis (GNG) may be one of the main drivers.”

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I can get behind that because GNG is an energetically expensive process and is likely increased when you’re not eating carbs. Ie, keto.

Disclaimer: this may be another demonstration of how nutritional ketosis isn’t muscle sparing.

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[sorry for the poor image quality, here’s the source for a better version]

This brings us to the relevance of substrate. In general, the main gluconeogenic substrates are glycerol (from adipose), lactate (from glucose metabolism), and amino acids (eg, alanine & glutamine from skeletal muscle).

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If we’re doing more GNG, we need more GNG substrate/precursors.

Lactate: the contribution of lactate to GNG doesn’t even budge during prolonged starvation, in a #context when we’re trying to do anything & everything to preserve GNG precursors… boring.

Next up: glycerol, then amino acids (it’s good!).

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Protein & sarcopenia

Unless otherwise requested, this will be my last post on protein for a while. I promise. Maybe.

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Came upon another review that went over some of the nuances of different protein sources, amino acid profiles, etc., and lean mass (Gorissen and Witard, 2018).

While I don’t think this really matters that much, most people on Earth get their protein 60% from plants, 40% from animals. Flip those values for the Americas and Europe.

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Wrt protein: I think quantity from diverse sources is more important than shooting for some specific amino acid score. It’s more practical and less guesswork, imo.

  • Sarcopenia sucks (P<0.05). It’s one of the leading causes of reduced quality of life.
  • Anabolic resistance: dietary protein intake usually stimulates muscle protein synthesis. This is reduced in inflammation and aging. There are a few steps to get around this.
  • Protein balance is muscle protein synthesis (MPS) AND muscle protein breakdown (MPB). The authors acknowledged this in the intro (YAY!), but the whole review focused on the former.
  • In general, it is thought that dietary protein supports MPS while insulin blunts MPB (over-simplified).

As detailed below, strategies to augment muscle protein synthesis (MPS) to the anabolic effects of dietary protein:

  • increase the dose (moar protein) — added protein provides more substrate to support MPS. Protein-induced insulin secretion helps blunt MPB
  • exercise can sensitize skeletal muscle to the anabolic effects of protein
  • seafood/DHA may have a similar sensitizing effect (2 or 3 studies support this)
  • cheat code LEUCINE (supported by many studies) – the gymbroni’s got this one right. It’s why whey, soy, and lean chicken are go-to’s: most leucine per calorie. Steak, nuts, and eggs have it too, but much less per calorie.

#context

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