Adenosine triphosphate

Some exercise physiologist watching, you can forgive me for oversimplifying things because truly all the energy systems are at work at all times.

So when I talk about the ATP creatine phosphate being exhausted in the first seven seconds, It's very, very, very little contribution if you look at a graph going down to just a bit.

And in a seven-second all-out sprint, there's almost no aerobic system contribution.

But in the background, running background software at all times is the aerobic system, especially as you get around that second curve.

It instantly halts cellular respiration.

Your cells can't make ATP.

So how do you unbind something that has such a high affinity for our vital enzymes?

We use chemical interception.

They do contain very small, rapidly turning over amounts

of ATP.

Drowning is supposed to be very peaceful.

I think that's freezing to death.

not drowning.

They're already in use at the moment circulation stops.

Neurons also contain a small amount of phosphocreatine, which can briefly buffer ATP levels for a few seconds when energy demand suddenly spikes.

In addition, neurons can temporarily rely on anaerobic energy pathways such as glycolysis that do not require oxygen.

GAPDH and PKM2, those are essentially the physical gears of that inefficient glycolysis engine.

Yes, they are absolutely critical for the cancer cell's ability to produce ATP, which is its energy currency.

Right.

So when those enzymes are deactivated by the oxidative damage, ATP production just plummets.

The power grid goes down.

Completely.

The cell runs completely out of energy.

And this severe ATP depletion combined with all that DNA damage we talked about, it activates executioner proteins within the cell.

Yeah.

It's the component of your cells that's responsible for taking the food that has ended up in your and it's broken down to molecules at this point, right, including glucose from your blood and then processing it, converting it into something called ATP, which is the energy source that your cells use.

So fundamentally, if you think, oh, wow, this is the energy source of all of the cells in my body, that sounds kind of important.

Also, mitochondria are responsible for the production of pregnenolone, which is the precursor hormone for our key sex hormones, testosterone and estrogen.

It's taking the resources.

So it's taking that food.

The ATP is processing it, but it's not doing anything.

That would be bad enough.

showing their connection to cognitive decline, to cancers, to mitochondrial issues.

What they seem to be doing is along the inner mitochondrial membrane where your body creates adenosine triphosphate, which is the ATP molecule, what happens is that the electrons need to pass from complex one to complex four cytochrome C oxidase to make adequate amounts of energy, right, but These metals prevent the electrons from doing that and so essentially what they do part of what they do is They cause your body to make less energy.

So you are just more tired all the time and these protein complexes in the inner mitochondrial membrane, they are supposed to be building the proton gradient used to make ATP.

And I found an interesting scientific review, this was at 2025, where they looked at 20 different studies, and they found that the exposure to toxic metals like cadmium lead arsenic all the big ones these metals can disrupt the mitochondrial function in all of these experimental systems and what they seem to do is impair the electron transport chain and they alter the membrane potential And cause oxidative imbalances.

And so when we detoxify, let's say, for example, we get in a sauna, which are incredibly beneficial for sweating, right? Can heavy metals appear in the sweat? And the answer is yes.

And it makes me think on something that our lab is very focused on, sort of the second layer of injury that occurs despite the acetylcholinesterase inhibition that we observed.

So these are other things that our lab is very focused on, other pathways that sort of may intersect with acetylcholinesterase inhibition, things like mitochondrial dysfunction, oxidative stress, calcium dysregulation, which ultimately leads to impaired ATP production.

And obviously, without going into too much depth about this, we all know when you have decreased ADP, the sort of the common energy currency in the cell, that obviously leads to some downstream effects and most likely probably explains the delayed and persistent injury that we see with this type of poisoning.

What translational model have you developed to study acute organophosphate toxicity?

So, you know, based on our sort of what we've seen in various other, uh, injury models, uh, like I kind of mentioned with carbon monoxide organophosphate in this case, uh, traumatic brain injury, post-cardiac arrest stuff is that we are definitely seeing sort of this like convergence, particularly involving the mitochondria.

Cause that's not surprising, right? That's sort of like the powerhouse of the cell.

that regulates ATP production and produces ROS and things like that.

So it's not surprising, I think, to most people that when you have these various different injury models that initiate a cascade of various things, that the final sort of pathway does involve the mitochondria.

Because overall fitness will actually aid with sleep and blood sugar regulation and hormone regulation.

And it would make sense because I remember creatine involves with ATP production and

then

phosphocreatine, which is stored in the bones.