Category Archives: muscle

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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Energy Balance > CICO

The regulation of energy balance is a long-term process, and it can’t be maintained by counting calories on a day-to-day basis.  Taubes once wrote that exercise doesn’t cause weight loss because it builds up an appetite, so you end up sucking down a Starbuck’s Jumbo Calorie Bomb on the way home from doing Yoga at the gym.  This is probably somewhat true, but this little gem from 1955 exposes some very interesting nuances.

Edholm(Edholm et al., 1955)

These researchers rigorously measured food intake and did a comprehensive assessment of energy expenditure during a wide variety of activities – lying down, standing, walking, gun cleaning, stair climbing, dressing, etc., etc.

Divide and conquer

The individual differences: big people expend more energy on life.  most of the time.

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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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Pocket Guide to Intermittent Fasting

Intermittent Fasting (IF) is all the rage these days, and there are a variety of different protocols out there, pioneered by people ranging from Ori Hofmekler (The Warrior Diet), Kate Harrison (The 5:2 Diet), Michael Mosley (The Fast Diet), Bert Herring (Fast-5), John Daugirdas (The QOD Diet), and Martin Berkhan (LeanGains), all the way to Jack Kruse (Epi-paleo Rx).  Chances are you’re probably unwittingly already doing one of them, at least intermittently.  The theoretical benefits are seemingly endless (albeit via few human trials), beyond the scope of my brain.

Tl;dr:

Non-IF: grazing; 6-8 meals per day.  Only significantly fasting duration occurs while asleep.
Normal-ish?: 3 squares.  Two 5-hour fasts, then fasting while asleep.
Eat Stop Eat or The 5/2 Bikini Diet: Eat only a small dinner 2 days/wk (600 kcal), eat normally other 5 days.
ADF: Alternate Day Fasting – 75% restriction on day 1; 25% surplus on day 2.
Leangains: Skip breakfast.
The Warrior Diet: Skip breakfast & lunch. (+1)
EOD: eat only Every Other Day.  36 hour fasts – from dinner on day 1 until breakfast on day 3.

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Fat mitochondria

No, not heavyweight powerhouses.  Mitochondria IN fat cells.
electricity is required for your space heater, not your long johns.

mito

At first glance, the mere presence of mitochondria in adipocytes seems perplexing.  On one hand, there’s tons of fat to burn, so why not have the capacity to do it?  Well yeah, but on the other hand, adipose doesn’t do very much.  It doesn’t contract like skeletal muscle or crank out glucose like liver.  Mitochondria in BAT is understandable, to generate heat and what not.  electricity is required for your space heater, not your long johns.

My best guess is that adipose tissue mitochondria are there to do something else – make shorter acyl chained FA’s, or free radicals, etc., to signal something.  Just not primarily to generate energy.

But drop an anvil on adipose tissue mitochondria and you get some interesting mice indeed.  Impossible mice.

TFAM – in brief, the enzyme that goes by the acronym TFAM makes mitochondria work.  Global TFAM KO is lethal.  But adipose tissue (AT)-specific KO is interesting.  Uncoupling goes through the roof and fat literally burns away.  kind of***.

Adipose-specific deletion of TFAM increases mitochondrial oxidation and protects mice against obesity and insulin resistance (Vernochet et al., 2012)

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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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Philosophy of the faux-low carb mouse and others like it

The Laws of Energy Balance are always maintained.  Here are some insights into how this is accomplished from a mouse perspective.  A hormonal milieu which is unfriendly for fat storage will make you lean, but not by magic.  We’ve got: 1) reduced food intake; and/or 2) increased energy expenditure.

Recall the faux-low carb mouse (Ins1+/-; Ins2-/- aka InsKO; Mehran et al., 2012).  They can’t get fat because of an inability to develop hyperinsulinemia.  Food intake isn’t reduced, so energy expenditure goes up.  Since the fat isn’t stored, it needs an “out,” so it either inhibits food intake or ramps up energy expenditure; InsKO gives us the latter.

While not hormonally-mediated, PPARg+/- mice can’t get fat because of defective adipogenesis and they handle this problem both ways; by reducing food intake and increasing energy expenditure (Kubota et al., 1999).  Similar to InsKO, PPARg+/- have lower insulin, but the primary defect in these mice is defective adipogenesis.  They can’t store fat, so this unstored fat: 1) tells the brain there’s plenty of fuel around so stop eating; and 2) ramps up energy expenditure to burn itself off:

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Sir Philip Randle and the effects of blocking fat oxidation

The Randle Cycle, put forth in 1963, dictates that increased fatty acid oxidation inhibits glucose uptake and increased glucose oxidation inhibits fatty acid oxidation – it just makes sense.  Insulin enhances glucose uptake and oxidation while suppressing lipolysis; growth hormone, cortisol, and adrenaline enhance lipolysis and fatty acid oxidation which suppresses glucose oxidation.  Low carbohydrate diets reduce insulin, and the reduced glucose oxidation is metabolically irrelevant because of reduced glucose intake (by definition).  This is critical information.  And as a student of basic intermediary metabolism, I prefer the Randle Cycle over any number of alphabet soup recipes to explain metabolic phenotypes (eg, fat and carbs as opposed to IRS, Akt, Jnk, ERK, etc., etc.).  Many valuable lessons can be learned from understanding permutations of the Randle Cycle.

For example,

Inhibition of carnitine palmitoyltransferase-1 activity alleviates insulin resistance in diet-induced obese mice (Keung et al., 2012)

divide and conquer

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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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