Cardiorespiratory fitness (CRF) cuts all cause mortality and CVD risk. Every extra MET of CRF reduces risk by 13%

But, lifelong endurance athletes show more coronary atherosclerosis than health non-athletes of similar risk profile, despite having lower events. This seems like a paradox.

Multiple CT cohorts find masters athletes have higher coronary-artery-calcium (CAC) scores and more plaques, especially densely calcified ones. Outcomes are low, but the imaging is scary. Why?

An hour of VO2max work does not equal ten hours of low level movement. If you have spikes of activity, but are otherwise sedentary, this turns out to be kinetic kryptonite. Why?

A stable isotope study showed that after a fat-rich meal the fractional clearance rate (FCR), or the rate at which apoB is cleared, drops ≈ 50%, even though production slows too.

If you think of your lipid system as a sink, the production of lipids is the faucet, the water in the basin is the lipid pool, and FCR is the drain. So in this analogy, this means after a meal, the drain starts clearing more slowly.

The problem is, if these lipids aren’t cleared, then they have more time to either oxidize or enter the intima, and kick off the process of atherosclerosis. It’s the area under the curve (AUC) or exposure time that’s the problem.

Aerobic training chronically increases hepatic LDL-R expression and accelerates LDL removal. However, this upregulation is gradual and doesn’t ramp fast enough to handle an influx.

This is why lower level sustained movement is important. Breaking up sitting with 8 min brisk walks every hour trims next day post prandial lipemia by 11% Translation: micromovement prevents acute LDL-R overload, whereas being sedentary perpetuates it.

Endurance and Micro Injury Back to CAC. Repeated high flow/high pressure coronary pulses during endurance work create endothelial micro tears. The repair of these tears skews toward calcification.

However, these athletic plaques are predominantly dense calcium sheets. They are more like healed scars than soft, rupture prone lesions. This is why event rates stay low despite scary CAC.

Putting it together: - Spikes: heavy fat feeds drive surges - Saturation: clearance slows and AUC rises, increasing exposure time and risk - Injury: Repeated hemodynamic stress seeds micro lesions - Repair: These micro lesions calcify to repair, but these are mostly stable, but

Why one hard run is not better than continuous movement An hour at 90 % VO2max doesn’t offset being sedentary for ten hours. Clearance is continuous, not session based. Low level movement (> 10 k steps) keeps LDL-R flux in the linear range. Being sedentary pushes you onto the

Resolving the Paradox You can be aerobically gifted and atherosclerotic if you: - Load the bloodstream with lipids faster than receptors clear them, and - Repeatedly injure coronaries with extreme hemodynamic stress. Low level movement keeps the drain open and apoB clearing.

Practical Recommendations Even short bouts of steps every hour will mitigate risk. If you walk for 8 minutes every waking hour, you will accumulate between 12-15k steps a day. Put a walking pad under your desk or in front of your TV. Take your dog for more walks. Walk during

@gregmushen Great thread Greg 🙏

@biohacker Thank you!

@gregmushen Part 4? Can we get a mega thread after you finish? 👀

@Juns884 Was just thinking that. Yes! Although putting it in a single thread would be above the thread limit, but I can summarize them and link them out.

@gregmushen Thanks Greg awesome info. I used to walk for 4-6+ miles a night while eating cookies and talking to long distance gf. On top of lots of regular walking. Stayed fit. Biggest problem now is hip pains / labral tears which has reduced how long I can roam for. Bpc incoming

@PoetoftheSun That’s awesome. I had a long distance gf once and did the same thing. Hope your hip pain gets better soon. Can be super painful to walk.

@gregmushen Very interesting post.For those who are concerned about the issue it's worth going through it and considering to apply.👍