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Aug 29 22 tweets 7 min read Read on X
VO2Max - How Walking Can Create an Elite VO2Max

Many people think that the only way to raise VO2Max is by doing HIIT.

But you can achieve a high VO2Max just with walking.

Walking is arguably the superior way to build it 🧵
In 2001, there was a landmark paper published. They took a VO2Max measurement at baseline and tracked the cohort for 10.7 years.

What they found was an inverse correlation between VO2max and all cause mortality. Image
This paper has been referenced for years, and many people believe that VO2max is one of the best proxy metrics for longevity?

But the data in this study was collected in the mid 80’s to mid 90’s, before HIIT was ever popularized.

So the way the people achieved high VO2max in the study was from low level aerobic exercise.
In a related analysis from the same KIHD dataset, most of the activity in the low-risk group was below 5.5 METs or too short to count as sustained moderate/vigorous.

Translation: the bulk of it was steady, moderate intensity movement, not HIIT or intense bursts. Image
Image
Subsistence Populations Have High VO2max

The mean VO2max for men ages 20-40 is 56.7. Image
But they achieve this just by walking. Just low and moderate intensity movement.

About 135 minutes of low level movement per day. Image
And while there are athletic benefits of getting a higher VO2max, there are marginal longevity benefits for higher VO2max.

Moving from the top 25% to the top 2% has marginal benefit in terms of survival rate, and risk of death of any cause. Image
Image
But it’s important to note that in hunter gatherer populations, deaths from cardiovascular disease are negligible, even above 60 years of age. Image
They have exceptional bloodwork, low fasting glucose, great blood pressure, low LDL, but wouldn’t be considered elite by modern standards. Image
But even the Tsimane, with modest LDL, and high rates of C reactive protein, a marker associated with increased cardiovascular risk, still have the lowest rates of CAC ever recorded. Image
This likely comes down to how fast they clear LDL.

In a consensus statement from the European Atherosclerosis Society:

“The residence time of LDL in the circulation may be the critical factor in the relationship between plasma LDL subclass level and atherosclerosis risk, as it determines both exposure of arterial tissue to LDL particles and the potential of LDL to undergo proatherogenic intravascular modifications, such as oxidation.”Image
Image
And we see this in kinetic tracer studies. A single weekly supervised aerobic workout in T2D patients resulted in a positive change in mean residence time (MRT) for LDL.

Less exposure = less opportunity for retention. Image
Image
And we see the same thing in a meta analysis.

A new meta-analysis of 19 RCTs in overweight/obese (n=646) shows aerobic exercise improves blood lipids: lower LDL, TG, TC & increased HDL.

Interval training lowered LDL/TC more than continuous, while moderate continuous exercise raised HDL most.

Longer programs had bigger LDL effectsImage
But these RCTs were just 30–60 min on a treadmill/cycle, 3–5x/week.

Compare that to subsistence people walking 12–18 km/day, carrying loads, burning 2–3× more energy every day.

Those volumes shorten LDL residence time dramatically.

Hunter gatherers have much higher clearance
But it’s not just clearance, it’s higher mitochondrial density.

PGC-1a activation -> chronic aerobic movement upregulates mitochondrial biogenesis, oxidative enzymes, capillary density, the machinery that lets you actually oxidize fat/glucose efficiently.
While both HIIT and walking will activate PGC-1a, it comes down to total activation. While HIIT creates a higher amplitude, you can really only perform it twice a week, whereas, with walking, you can do it every day.
This study compared PGC-1a activation between HIIT and steady state.

“A single isocaloric bout of high-intensity cycling (~80% VO₂max) raises skeletal muscle PGC‑1a mRNA ~10×, versus ~3–4× after low-intensity (~40% VO2max), showing that exercise intensity, not just volume, is key for metabolic signaling.”Image
But, when work is matched, there is the same level of PGC-1a activation.

They used oxygen consumption (VO2) as the work proxy, ensuring total oxygen cost (and therefore energy expenditure) of the two trials was the same. Image
And this is where walking absolutely dwarfs VO2max.

Walking 15k steps a day: ~875 L/week
HIIT 2x/week: ~250-300 L/week

Even though your VO2max may be lower than an athlete, you’re getting superior clearance, and superior PGC-1a activation.
And while aerobic exercise can reduce coronary events by ~30%, in this study, there was no difference in all cause mortality between the sedentary group, and the vigorous running group!

The benefits conferred to the lower intensities.

Maybe it’s different with HIIT, but we don’t know.Image
So in summary:

1) You can achieve an elite VO2max from walking alone

2) The biggest benefit comes from being in the top quartile of VO2max

3) Continuous movement helps clear LDL (and glucose)

4) Vigorous exercise may have negative benefit

5) Walking long distances daily trumps HIIT in both clearance, and PGC-1a activation.

6) ~15k steps a day will put you in hunter gatherer range.
@Mark_Sisson @Alan_Couzens and I are going to make walking cool again.

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More from @gregmushen

Aug 22
Many people report their health improving after removing fiber.

Why is this, and are they really improving their long term health?

Is this proof that fiber is “non-essential”?

Short answer: no
Long answer: 🧵
You could think of our microbiome as a fermentation vessel.

The fermentation feeds the 10^13 organisms living in your gut.

We have 3x10^13 human cells.

In that sense, we are at least as much microbe as we are human.
But we have about 20k human protein coding genes vs. millions of microbial genes.

So from this sense, we are more microbe than human.

Like a mechanical Swiss watch, or a transmission. Conceptually clean, functionally baffling in the details.
Read 25 tweets
Aug 15
Why Don’t Hunter Gatherers Have Heart Disease? (Part 10)

We know what happens when you move subsistence populations to the city. They start developing disease.

But what happens when you move them back? 🧵
In the 70’s and early 80’s, health surveys in remote Aboriginal villages showed a disturbing trend:

- T2D was exploding in prevalence
- The onset was very rapid, occurring within a decade or two of lifestyle change
At the time, a popular viewpoint was this was genetic, that Aboriginals were prone to T2D aka “thrifty gene” ideas were very popular back then.
Read 12 tweets
Aug 15
Why Don’t Hunter Gatherers Have Heart Disease? (Part 9)

In parts six we evaluated several groups with hepatic insulin resistance.

In part seven, we evaluated how this could happen with VAT being the likely culprit.

But what is VAT and how does it lead to insulin resistance?🧵
What are SAT and VAT?

SAT = subcutaneous adipose tissue
VAT = visceral adipose tissue

SAT (also SCAT) is the primary, low risk storage depot. It has the ability to expand but expansion is limited (hypertrophy, fibrosis, inflammation), then it starts spilling over into VAT. Image
VAT is tissue that sits inside the abdomen.

Parts of it connect to the liver via the portal vein.

The Portal Hypothesis explains how this might lead to hepatic insulin resistance. Image
Read 20 tweets
Aug 14
Why Don’t Hunter Gatherers Have Heart Disease? (Part 8)

We have learned a lot in this series. Before going further, let’s build a model for what we are seeing.

The model will help explain why hunter gatherers aren’t getting chronic disease

Could this be a unified theory? 🧵
Before we start, it’s important to realize that all models are wrong, but some are useful.

Science has many examples of wrong but useful models. Bohr’s model is a good example of this. It was wrong, but led to quantum mechanics.

So our goal is to be wrong but useful.
I believe we’ve learned enough to do this.

The goal isn’t to be perfect, but at least explain what we’ve seen so far. It will help us test it once new information arrives.

Better to iterate on an imperfect model than not build a model at all.
Read 26 tweets
Aug 11
Why Don’t Hunter Gathers Have Heart Disease? (Part 6c)

The Maasai taught us the case:

Hepatic dominant IR can be low risk until urbanization pushes it to multi-axis

Can the Pima prove the law?

What happens when you hold genes constant, but change lifestyle? 🧵
First, a little background about the Pima. This may seem like a bit of a detour, but it provides important context for how we ended up with such a perfect natural experiment…
The Pima historically inhabited the Gila and Salt River valleys straddling what is now southern Arizona, and northern Sonora.

In 1848, the US annexed large swaths of northern Mexico. Then in 1853, the Gadsden Purchase added more, driving a hard border through ancestral lands. Image
Read 16 tweets
Aug 8
Why Don’t Hunter Gathers Have Heart Disease? (Part 5)

Hunter gatherers have VO2max > 50

VO2max is strongly correlated with longevity.

So raise VO2Max fast with HIIT and you should be able to skip the walking, right?

Not so fast🧵
VO2Max Correlation is from Population Data

In 2001, there was a landmark paper published. They took a VO2Max measurement at baseline and tracked the cohort for 10.7 years.

What they found was an inverse correlation between VO2max and all cause mortality.

But there’s a problem Image
The baseline measurements were taken between 1984-1989. Follow up was in 1997, before HIIT was popularized for the general public.

Early intervention protocols existed (e.g. T in abata), but the VO2max-mortality cohorts were not built on HIIT blocks.
Read 18 tweets

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