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Are AGEs and Lipofuscin related? Could ALT-711 eliminate lipofuscin?

Aubrey de Grey ag24 at mole.bio.cam.ac.uk
Tue Jan 12 09:52:53 EST 1999


Robert Ames wrote:

> Nice theory, but what about weightlifters?  They have an average
> longevity greater than normal if somewhat less than runners.  Yet
> the high intensity exercise produces calcium levels toxic to
> mitochondria, resulting in reduced mitochondrial densities.

but Hazel wrote:

> From what I've seen and read, weightlifters don't live longer than
> normal.  They die young.

and I know of neither correlation.  I'd be grateful for references;
numerous interpretations are possible on the limited data so far
discussed.

William wrote:

> So do you think it would be good for all of us to get lots and lots
> of excersise so that we can accumilate many more mitochondria that
> are really needed in our cells, so that eventually, when we grow old,
> mitochondrial DNA deletions will not be too much of a problem because
> we will have plenty of mitochondria to spare?

Not exactly.  We have plenty of mitochondria to spare anyway, since
less than 1% (probably much less) of them suffer mutations at all.  The
reason those few may be a problem is by being much more toxic than
would arise just from their lack of function.  A fair interpretation
of the benefit of exercise in this regard is that mitochondrial DNA
mutations happen a little less frequently, because their increased
mitochondrial complement is on average doing less respiration.  (This
comes about because athletes use no more energy when they're asleep
that the rest of us.)  The effect is slight, though: quite hard to
separate from e.g. the tendency of athletes to eat right.

rjk3 wrote:

> There is some evidence that exercised mitochondria tend to use more
> efficient energy pathways than otherwise, and being more efficient
> produce fewer free radicals.

That's not exactly how I'd put it: "efficiency" denotes how much of
the energy from turning oxygen and hydrogen (sort of) into water is
transferred into making ATP from ADP, and most of the energy that is
lost just becomes heat, not superoxide.  Perhaps more precise is to
say that in some conditions non-respiring mitochondria make more free
radicals than respiring ones.  However, these conditions are not what
mitochondria normally experience in the body: they involve metabolism
of succinate, which enters the respiratory chain at a different place
than most things, and that is now known to be crucial.  See Herrero and
Barja, J. Bioenergetics and Biomembranes 29(3):241-249.

> Also, I seem to recall that the mitochondria in exercisers, aerobic
> and weightlifters alike (do both) are also LARGER than sedentary
> mitochondria.

The best-established result is that exercise causes increased numbers
of mitochondria in younger people and bigger ones in older people.  The
important number is the total mitochondrial inner membrane surface area,
though, which is increased by either.

> Bird mitochondria are more efficient than that of mammals.  Birds
> live longer proportionately to their size.

Absolutely.  The rate of superoxide production by bird mitochondria is
so low that they suffer less free radical damage than mammals even
though they have LOWER levels of antioxidant enzymes and a higher
metabolic rate.  Not to mention huge blood glucose levels.  No one knows
how they do it; studies are continuing, but not nearly enough of them.

Aubrey de Grey




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