Category Archives: Exercise

Insulin, sympathetic nervous system, and nutrient timing.

Insulin secretion is attenuated by sympathetic nervous system activity; eg, via exercise.  Theoretically, exercising after a meal should blunt insulin secretion and I don’t think this will lessen the benefits of exercise, but rather enhance nutrient partitioning.   And this isn’t about the [mythical?] post-workout “anabolic window.”

Sympathetic innervation of pancreas: norepinephrine –> adrenergic receptor activation = decreased insulin secretion & increased lipolysis (Stich et al., 1999):

Stich insulin

Stich CAS

note how quickly catecholamines are cleared upon exercise cessation

Stich NEFA

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Implications of the circadian nature of ketones.

Ketosis.  Happens during starvation and also by restricting carbohydrates (and protein, to a lesser degree)… might be important for epilepsy and bipolar disorder, too.

ketogenesis

Ketostix measure urinary acetoacetate (AcAc) and reflect the degree of ketosis in the blood probably about 2-4 hours ago.  Blood ketone meters measure beta-hydroxybutyrate (bHB) right now.  bHB fluctuates to a greater degree, eg, it plummets after a meal whereas AcAc takes longer to decline.  AcAc/bHB is usually around 1, but increases after a meal (Mori et al., 1990):Ketone body ratio

Conversely, when glucose levels decline and fatty acid oxidation increases, liver redox potential drops which reduces AcAc/bHB.

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Sarcopenia has little to do with aging

It has to do with the duration of time spent being sedentary.

They say a picture is worth a thousand words, but luckily enough today you get both.

Sarcopenia: “poverty of flesh,” or the age-induced loss of skeletal muscle mass, strength, and function = reduced quality of life.  Sorry old-timers, but I hereby officially revise the definition from “aging-induced” to “sedentary-induced.”  Herein, I present evidence that sarcopenia is not a phenomenon of aging per se, but rather of disuse atrophy.  Dear Webster’s & Britannica, please revise accordingly.

Skeletal muscles: use ‘em or lose ‘em #TPMC

Thanks to Julianne Taylor & Skyler Tanner for directing me to these images.

divide and conquer

Exhibit A. Chronic exercise preserves lean muscle mass in masters athletes (Wroblewski et al., 2011)

This study evaluated “high-level recreational athletes.”  “Masters” just means they were over 40.  And “high-level” doesn’t mean “elite,” it just means they exercised 4-5 times per week.  These weren’t super-obsessed gym rats… it’s probably who I’ll be in 7 years [sigh].

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Look AHEAD – Nutrition Disinformation 2.0

The day you’ve all been waiting for has finally arrived.  Results from the Look AHEAD study have been published.  When I first wrote about this study (HERE), it had been prematurely halted because the intervention was providing no benefits.  Everybody was in a state of shock and awe because Low Fat didn’t save lives.  But that was before we even had the data.  

Reminder: the “intensive lifestyle intervention” consisted of a Low Fat Diet & exercise.  The results?  Yes, they lost more weight than control, but they also took more Orlistat (of which I’m not a fan, see HERE for why):

orlistat

Orlistat = pharmaceutically enhanced low fat diet. 

Their normal diets were not healthy, but neither was low fat –>

med use

Medication use increased drastically in both groups.  The pundits have gone wild because medication use was lower in the intensive Low Fat group at the end of the study, but this is Nutrition Disinformation 2.0.  Eerily reminiscent of the recent Mediterranean Diet study, the conclusions are the same: keep eating poorly and the need for medications will increase.  You can call it a lot of things, but not “healthy.”  The alternative –>  How to define a “healthy” diet.  Period.


Significant adverse events:SAE

The only thing to reach statistical significance was more fractures in the intensive Low Fat group, but you didn’t read any headlines that said “Low Fat breaks bones.”  Imagine if that happened on low carb [sigh]  The next closest thing to statistical significance was increased amputations in the intensive Low Fat group :/

gem:History of CVD

Translation: if you were healthy at baseline, then you could tolerate a low fat diet.  Otherwise, not so much.  This is exactly what happened in the Women’s Health Initiative.

Ha

needless to say, none of the “possible explanations” they considered were Low fat diet Fail.

calories proper

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Westside Barbell, Hormesis, and Antifragility

Some people think Westside makes some of the strongest athletes in the world because unlike most other training regimes, they are constantly lifting very heavy weight.  Other protocols restrict heavy lifting to certain times of the year, in-season / off-season, etc.  At Westside, you’re going heavy on an exercise that changes very frequently (every 1 – 3 weeks).  And it’s this latter point that provides the basis for why other people think Westside works.  By constantly changing which exercise is lifted at maximal intensity, the body never fully adapts, or gets into a rut – this is part of Westside’s ‘Conjugate Method.’

The principle is embraced by Crossfit, as per their random workouts-of-the-day, and also follows a tangent of the Hormesis theory: small doses of individual exercises, eg, conventional deadlifts one week, good mornings the next, sumo deads the next week, and so on and so forth – will improve your squats; the body never knows what’s coming (even though you might have planned it weeks in advance, or at least planned to check The WOD Shop).  Also discussed albeit briefly, in Taleb’s Antifragile, wherein being prepared for “random” shocks seem to benefit the system as a whole, or make it stronger.  Sedentary makes you fragile, weak, and soft; exercise makes you robust; Westside is Antifragile.

Antifragile

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Ketoadaptation

Athletes who drop carbs cold turkey suddenly suck.  It is known.  

But with a smidge of stick-to-it-iveness, performance completely recovers, in virtually every.  measurable.  aspect.  

This was shown years and years ago, in a seminal study by Drs Phinney, Bistrian, Evans, Gervino, and Blackburn.

The human metabolic response to chronic ketosis without caloric restriction: preservation of submaximal exercise capability with reduced carbohydrate oxidation (1983)

Normally, fatty acids fuel low intensity exercise and carbs fuel high.  This is because high intensity exercise requires a high rate of ATP production, and glycogen to lactate generates ATP faster than a speeding bullet.  This is what makes power.  Getting ATP from fatty acids is like draining maple syrup from trees [at first].

mito pic

However, go low carb for long enough and the syrup begins to flow like water.  I lack the time to show what “long enough” entails, but  4 out of 5 studies on low carb diets and performance that only last a few days will show this.  Ketoadaptation takes time; ~3 weeks.

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Biohacking holiday weight gain

What should you eat before the big feast?  (hint: eggs.)  And don’t try to compensate in advance by eating less, this will only make you hungrier.  Furthermore, foods in your regular diet are probably healthier than holiday fare, so you definitely don’t want to eat fewer healthy foods to make room for empty calories.

Tip 1. 

Variation in the effects of three different breakfast meals on subjective satiety and subsequent intake of energy at lunch and evening meal (Fallaize et al., 2012)

Participants were served only one of these for breakfast:

And given unlimited amounts of these for lunch and dinner:

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The faux-low carb mouse and a diatribe

The faux-low carb mouse

Hyperinsulinemia drives diet-induced obesity blah blah blah (Mehran et al., 2012)

The researchers generated a mouse with half as much insulin as normal mice.  Physiological insulin levels remain intact, but hyperinsulinemia is genetically inhibited.  For the sake of simplicity, we’ll call them “InsKO.”

When fed a high fat diet, normal mice become markedly hyperinsulinemic (pink line) whereas InsKO mice maintain relatively normal insulin levels (red line).  Blue lines are chow-fed mice; similar trend but less interesting.

divide and conquer

InsKO mice don’t get fat,

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Milo of Croton vs. concurrent training

Lesson 1.  Milo of Croton

Every day since a very young age, Milo would drape his calf over his shoulders and do his daily exercises.  As his calf grew, so did Milo’s strength.  Many years passed and by the time of the Olympic games, Milo’s calf had become a full-grown bull and Milo’s strength became unparalleled in all the land (or so the story goes).

This is how strength-training works.  Increasing the amount of weight you lift progressively, consistently, and frequently makes you stronger.

Lesson 2.  Concurrent training

Resistance training builds muscle and strength.  Endurance exercise is good for the heart, burns fat and muscle, but doesn’t make you stronger.  Endurance exercise hinders the gains reaped from resistance exercise, not vice versa.  Interpretation: runners should lift; lifters shouldn’t run (sprints don’t count).

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Metabolic rate per se

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Admittedly, the effect of diet on metabolic rate is small (i.e. statistically non-significant in most cases), but its incredible consistency across space and time suggest it could be true.  And given the difficulty of maintaining a reduced body weight after dieting, it might even be important.  The following studies are examples of widely differing subject populations in various metabolic conditions; yet the effects of diet on metabolic rate exhibit a phenomenal degree of similarity.

disclaimer: I don’t know what’s more important – metabolic rate per se, the diet behind it, or the resulting hormonal adaptations.  All of the diets that are associated with a higher metabolic rate are also predicted to result in lower insulin levels and higher fat oxidation.  Thus, we are left with a triumvirate of diet, hormonal milieu, and energy expenditure… all of which are important for body composition and quality of life.

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