Here is a lovely article about mitochondrial dysfunction and “scienceploitation” from the team at McGill University.
Quick fixes aren’t. Addressing mitochondrial dysfunction is hard in the real world, he says. “ If you want to keep your mitochondria from getting gummed up, I’m afraid that the best advice remains as unsexy and dull as ever: eat well, get enough sleep, and exercise regularly. Your mitochondria will thank you later.” Read the article to find out why….
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Here’s the referenced lecture on “How mitochondria contribute to health and disease”. This chart on metabolism illustrates the stunning complication of just the known functions involved in metabolism. Mitochondria are at the heart of this subway chart but there are many components.
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This article does not mention the fact that metabolism gradually damages mitochondria and this changes gene expression
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Are you describing a lifetime accumulation of damage? Is this “aging”? It can’t be linear as the mitochondria make an effort to remain functional. … the decline is slow but accelerating over time until it is fast. This represents the pace / rate of aging? Slower for a healthier person.
I understand mitochondria use fusion and fission to do maintenance (keep the good parts & dump the old bad stuff). They don’t have the robust DNA protection that our nuclear DNA has but they have these other mechanisms.
I think aging is mainly two things
a) Damage to mitochondrial DNA which makes them less efficient
b) The presence of senescent cells (which becomes an issue).
There is an interesting paper which basically says if you rely on a number of things in series then you end up with an exponential curve for a failure rate.
This paper references the original paper which is not free to air.
https://www.osti.gov/servlets/purl/1479952
What happens with mitochondria is that as they go wrong different proteins are produced (or not produced) and the normal systems of homeostasis go wrong accelerating damage.
It is not linear. The damage rate increases and also you cannot be certain exactly how damage correlates to function. Hence it is quite likely that further damage reduces efficiency at a further rate.
I looked at the detailed subunits recently and wrote a post about this.
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https://journals.biologists.com/jeb/article/219/2/243/33487/Mitochondria-to-motion-optimizing-oxidative
Mitochondria oxidize substrates to generate the ATP that fuels muscle contraction and locomotion. This review focuses on three steps in oxidative phosphorylation that have independent roles in setting the overall mitochondrial ATP flux and thereby have direct impact on locomotion. The first is the electron transport chain, which sets the pace for oxidation. New studies indicate that the electron transport chain capacity per mitochondria declines with age and disease, but can be revived by both acute and chronic treatments. The resulting higher ATP production is reflected in improved muscle power output and locomotory performance. The second step is the coupling of ATP supply from O2 uptake (mitochondrial coupling efficiency). Treatments that elevate mitochondrial coupling raise both exercise efficiency and the capacity for sustained exercise in both young and old muscle. The final step is ATP synthesis itself, which is under dynamic control at multiple sites to provide the 50-fold range of ATP flux between resting muscle and exercise at the mitochondrial capacity. Thus, malleability at sites in these subsystems of oxidative phosphorylation has an impact on ATP flux, with direct effects on exercise performance. Interventions are emerging that target these three independent subsystems to provide many paths to improve ATP flux and elevate the muscle performance lost to inactivity, age or disease.
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