-: Now we're gonna look at specifically
how we use glucose in this.
You guys already understand the mechanics,
but there are some conditional things on whether or not
that glucose actually even makes it into the mitochondria.
So, if we look at the fate of glucose when there's,
everything's good, we're pretty much at rest,
if we even need to burn any, we have glucose,
and we're going to divide this into basically two halves.
So, over here on the left side, this is what's going on
in the cytosol, and over here on the right side,
that's what's gonna happen inside the mitochondria.
So if you imagine this as like a flow down a ramp,
so right now, it's at a small incline,
so there's not gonna be much pressure,
but there is a little bit of pressure to take the glucose,
make some ATP in the cytosol through that anaerobic
glycolysis, and then get a bunch of ATP from it
once those pyruvate actually enter the mitochondria,
so once we've metabolized that glucose all the way.
So at rest, there's a small drive for this.
But what about when we actually
create a demand for more energy?
We're gonna drive this guy up.
So now, the, you know, the urge to get that glucose
into the ATP, that's gonna happen
at a much more accelerated rate, right?
So now this glucose really wants to go through that process,
and the thing that's going to do that
is gonna be activation of the AMPK.
Quick refresher, what's gonna get that AMPK going?
Well, we've got calcium
being released from muscle contractions.
We've got high AMP from high-intensity metabolic work,
so burning through a lot of ATP.
So as ATP and AMP climb, that ratio of those
to the ATP affectivates how much AMPK in on.
So the lower ATP and the higher AMP,
the more AMPK that's gonna be activated;
therefore, the higher this is gonna go.
So think of this as it's not just on or off,
but it's like, well, it could be here,
it could be here, it could be here,
it could be here, depending on the rate
at which the energy is being depleted and how much actual
AMP there is in relationship to how much ATP there is.
The other thing that gets AMPK activated
is a little bit of low glycogen.
So the lower your glycogen, the more this thing
is going to act on really fast.
And the reason it does that,
even though this is burning the glucose,
the reason it's gonna do that is because remember,
AMPK is also gonna open the door
to get glucose in from the blood.
So the lower glycogen, the more you're likely going to open
the doors to get glucose into that muscle cell
from the blood once you start training.
That doesn't mean that if you have full glycogen,
you don't also do that; it just means
your cell's gonna panic and do it really early
if it's already depleted going in.
But, you're still gonna be limited by actually
getting that glucose from there, because that's gotta
come all the way from the liver or the digestive tract.
So obviously from a performance perspective,
glycogen is gonna be a better, faster available fuel source
whereas this is kind of like panic mode.
So, in these conditions, if everything is functioning well,
this glucose is going to make a small amount of ATP
in the cytosol, but it's gonna get metabolized
all the way down into the mitochondria
and create a ton of ATP down there.
So, easily, you know, there's, so, if you look at like,
the rough numbers, if we were to compare, you know,
it's like, okay, you get two ATP out here,
and then I get like 36, 32 to 36 down here.
So significantly more ATP if we can take that glucose
all the way to complete metabolism.
That doesn't always happen.
So let's look at what is actually needed for this to happen.
We looked at that small chart, and I said,
okay, we get this two ATP, but in the process of doing that,
we also need to take this NAD+ to NADH.
We need this conversion in order to allow this process
to go, for us to get the pyruvate that is gonna
go into the mitochondria and then be metabolized
all the way down into that big bulk of 32, 36 ATP.
In the mitochondria, we have the reverse happen.
We actually take the NADH,
so this thing over here that we made,
the mitochondria uses that and recycles it to NAD+.
So, if this and this are happening at the same rate,
I have going to NADH, recycled back, everybody's happy,
because they're basically fueling each other,
and that works really well.
So, we have this stuff needed for this part,
and we have this stuff needed for this part.
As long as it's balanced, we're okay.
But if something were to happen on that side,
so, say your mitochondria weren't healthy
or something like that, if anything that happens,
what's gonna happen to this side of the equation
if it's no longer getting the NAD+
in order to be able to run this process?
What you're gonna get is you're gonna get your two ATP
still, but once you've gotten your two ATP,
you're not gonna get that pyruvate, that next couple steps
that actually you need to get that glucose
into the molecule that's gonna enter the mitochondria.
It still requires this.
If that's not there, we are actually
going to do something else.
We are going to take that glucose molecule,
we're gonna break it down, and instead of making pyruvate,
it is gonna get shoved towards lactic acid.
The reason it's gonna do that is to take this
and make lactic acid, so it's actually,
instead of that pyruvate going here,
what happens is that we take that pyruvate,
we convert it to lactic acid.
That process does the same thing that this does.
It's actually gonna take the NADH
and recycle it back to NAD+.
So, here's where that starts to happen.
When energy demand is so high that this guy
is functioning at max capacity, so let's go like RPMs.
So, the mitochondria's running at 60 RPMs.
It doesn't really work in a traffic circle,
but bear with me.
So that thing's going at 60 RPMs.
This thing's going at 60 RPMs.
They're feeding each other.
Everything's working perfect.
What happens if I need to go faster than that?
So if you think of like those cars that have two engines,
like they have a gas-powered engine and then they have
like an extra electric engine, let's look at it that way.
Like, this is the gas-powered engine.
It can run and just go and go and go and go,
and this is the electric one.
So this guy recharges that, everything's good.
But when you need even a little bit more horsepower,
what the body will do or the car will do
is they'll use both engines to maximal capacity.
So, imagine this guy's going at 70 RPMs,
and this guy's going at 60, because you just,
you need the horsepower, because the intensity of work,
the energy demand is that high.
But what that means is you are going
to start depleting some of this NAD+
faster than you can regenerate it down here.
And what's gonna happen is you're making pyruvate
at 70 RPMs here, but you're only able
to take it in at 60 RPMs, meaning every minute,
there's an extra 10 pyruvate that can't make it in there.
So, what happens is you have this pyruvate
that's just like, sitting out here, like, I don't,
I can get into the mitochondria,
and it's starting to build up.
Your body wants more ATP.
One way it can get ATP, one way it can get energy faster
and get some of that pyruvate that's building up
is actually to take that extra pyruvate and convert it
to lactic acid, and then it can get more of this,
'cause over time, if you imagine that this is going at 60
and this is going at 70, what would happen
is that when there's no longer enough of this
is this process would actually start to slow down,
meaning that I would start to actually be able to do less
of the front-end of glycolysis,
because the backend was too slow.
I'd be waiting on another NAD+.
So this would start to get sluggish.
I'd have this buildup of pyruvate.
Both of those things are gonna create
this concentration gradient where, in order
to be able to continually produce ATP outside the cell,
the body's going to reuse that pyruvate to recharge
and continue being able to run this process
independent of the mitochondria.
So it's gonna be like, okay, well, the mitochondria
can take what it can take, but we need more energy,
and in order to do that, we're gonna have to use
the pyruvate for something else for short-term energy.
Now, remember, this is a small amount of ATP.
This is the big one.
But, this happens like, really fast
with very limited resources needed.
This is limited by the number of mitochondria
and how well they work and a lot of, a lot of nutritional
status things in order for that to function.
So, this, this essentially can go,
so like imagine that like, that thing
has a rate limiter that's really, really low.
So, 60 RPMs is its max, but maybe this guy
can go to a thousand RPMs before it explodes.
So what it'll do is it'll do that extra work,
but it's very inefficient work.
When I say inefficient, what I mean is because we're
recycling that pyruvate, instead of that pyruvate
being able to make a ton of ATP later,
it's gonna get shoved to lactic acid
and actually leave the cell.
So we're essentially, we're only getting
a little bit of energy out of that glucose,
and then we're losing, we're losing the byproduct
instead of being able to get all the energy
we could have gotten out of that glucose.
But, we are able to get the energy we needed
in that moment of high demand.
So, from a performance perspective, this is awesome.
From a fuel efficiency perspective,
from getting every ATP molecule
out of glucose that's possible, it's not very efficient.
But, from performance, like, when you need horsepower,
you need horsepower.
You're not concerned about gas mileage.
So that's what this whole process is for.
And what happens, we talked systemically.
Where's that lactic acid gonna go?
Well, it's gonna leave this cell.
It's gonna go into the bloodstream.
The liver will then take that lactic acid,
recycle it into glucose, send it back around.
Maybe it gets uptaken by that cell again later,
and then I have the glucose again.
So I didn't lose the glucose forever,
but what I did do is I wasted some energy
to do that whole recycling process.
An easy way to think about it is that in this process
of going from glucose to lactic acid,
I get two ATP, but the recycling process
from the lactic acid to the glucose and back
is gonna take six.
So it's a negative four.
So I lose, I lose energy overall.
It's catabolic to my body as a whole,
but I provided fuel where I needed it
to be able to perform when there was a high demand.
Now, if you think about this, I got performance
where I needed it, but I technically created
an energy-negative situation.
Can you think of a specific goal that a person might have
where being able to perform at a high level
but also burning a lot of calories,
burning a lot of nutrients, would be a good idea?
That's why lactic acid training can work very well
for body composition, is you are, you're essentially
creating the demand for a high performance energy system
that's very inefficient, which, when my goal is to get rid
of excess energy, burning it inefficiently is actually good.
Like, bad gas mileage is good
when you just wanna burn gas faster.
It's not good, efficiency is bad when you're trying
to waste fuel, and that's essentially what we're trying
to do, right, when we're trying to burn off pounds
of body fat, is we're trying to get people
to be burning through more fuel.
This is a way of, like, a healthy way,
of being able to promote essentially an inefficient
metabolic process, because we're actually,
this is very inefficient in terms of the net energy I get,
but it allows me to perform well.
So, it takes something that's good and fun to do in the gym,
something where I can actually control an outcome.
So instead of restricted feeding to create
a negative energy balance,
I'm actually using high-performance exercise
to create a negative energy balance.
That's when it's good, when I do that from training.
What if this isn't from training?
What if this is happening simply
because my mitochondria suck,
because they haven't been given the nutrition they need,
they've been under too much stress, they've been inflamed
or whatever it may be, that citric acid cycle
or that electron transport chain
is missing nutrients or damaged?
We're gonna end up with the same thing, right?
We're gonna be, oh, lactic acid.
We're gonna be making lactic acid because my ability
to run the mitochondria for it,
so instead of this guy running at 60 RPMs,
it runs at a sad, sluggish 20 RPMs.
So now, it's a totally different scenario.
Instead of a higher performance thing being
what shuttles this lactic acid thing, so,
this is a way of me training my body for performance,
but losing some metabolic efficiency,
now it's like, well, I just suck at making energy,
which means the cell just has an awful life,
because it's got low energy all the time,
and its energy system that it's using is very inefficient.
So this is essentially like it's a tax,
a parasite to the body almost,
because now it's creating all this lactic acid when it
shouldn't be, because its energy metabolism is so poor.
So it's essentially like, putting this load
on the rest of the body to support it.
When that is the case, now, this is a situation,
if we have a lot of tissue like that,
it's gonna stress out the liver.
It's gonna affect your cortisol levels.
It's gonna affect your stress hormones.
It's gonna affect your nervous system.
It's gonna affect the glucose and insulin sensitivity
of these tissues, so that you're gonna start to see
a link to of negative impacts systemically,
because you have these cells that are essentially
a drain on the body, 'cause their energy metabolism is poor,
and they're constantly creating metabolic waste,
and in order to deal with that,
instead of this being like you would think,
like, well, if we're wasting a bunch of energy,
wouldn't that just help me get shredded?
No, it won't, because what your body will do
is it will adapt to this stress by lowering things
like thyroid hormone and elevating your stress hormones
to try and compensate.
So because this cell sucks at life,
what your body's gonna do is it's gonna tell
all of the other cells that they get to burn less energy,
because we have this stressful situation
that we're dealing with, because of these other cells.
The correct thing do is actually to get these guys
to metabolism up, because if this guy's able
to burn more fuel the appropriate way, that's good,
because then he's able to fuel more metabolic processes.
He might actually consume more energy
and be less of a tax on the body that way than being stuck
in this like, inefficient form of metabolism
where it's only running on the anaerobic glycolysis
that happens outside of the cell
and being a drain on the rest of the body.
So, this can be from missing cofactors in the citric acid
cycle, oxidative stress, you know, training,
training oxidative stress too long,
which is a really popular training mechanism,
especially for like, metabolic stuff.
People like to do training for oxidative stress,
because it's associated with hard work, because it requires
you, like, doing long sets and things like that.
So, whatever the, this could be from poor oxygen delivery,
could be from missing cofactors in the electron
transport chain, lots of different things,
but ultimately, this is unhealthy mitochondria.
In some way, shape, or form, regardless of the result,
unhealthy mitochondria create eventually
a systemic stress response, lowering of metabolism,
lowering of positive hormones.
So, when we look at that slow citric acid cycle,
we're gonna look at a couple other things
in terms of how that's gonna affect us systemically.
So if I have AMPK, I have glycolysis,
I have all this stuff that's supposed to be stimulating
this guy, but he just can't run as fast as he should,
what I'll actually get is, say like this guy can do
the first step just fine, but the second or third
or whatever, there's kinks in the chain.
So I'll actually start to build up some of these products.
So, as this, whatever rate this cycle completes,
it'll fuel the electron transport chain.
Whatever extra, like, wherever there's bottlenecks,
there's gonna be overflow of a byproduct
of whatever's happening at that particular point.
So let's say there's a point right here
where going from then this step to the next one,
it's inefficient.
So what I'll have is I'll have some things leaving
the citric acid cycle, actually leaving the mitochondria,
and one of those things in citrate.
And when citrate gets pushed out of the mitochondria
into the rest of the cell, that is the stimulus
that hey, we have tons of energy,
and we should go into fat storage.
Now, under normal conditions, that would happen
because there's no longer a pull on this end.
There's no longer ADP coming in, to the electron
transport chain is going to no longer have the pull.
It would only have the push from fuel coming in,
but if there's no pull, now that push is gonna get slowed
down because we don't actually need to make a lot of ADP.
So instead of just burning all of the fuel for no reason,
what we would actually do is say, hey, let's stop that.
If you've got some extra stuff, send it out here,
and we will restore it.
When that situation is not because energy demands
have been replenished, what you get in is this state
where maybe your cell senses it's starving,
so AMPK stays high, or glycogen is still low,
or whatever, whatever happens out there,
where the ATP is still low.
So the signal for fuel to be coming in is still being there,
but there's this, I can't quite actually get
that electron transport chain functioning,
so I'm gonna start exiting some of this citrate out here.
So essentially what I'm doing
is even though I have low energy,
I'm telling my body that it should be storing fat,
at this particular cell, right?
I'm telling, I'm telling yeah, this cell, we're good,
we have enough.
We should be storing fat.
And so that's where you get into a situation
where simply not being able to function
at a mitochondrial level, if this, if these two things,
if both of your gas pedals are not functioning well
because you're either missing nutrients over here
or missing nutrients over here,
there's that disparity.
There's this break of communication between the energy
that's needed and what we should be doing
with the fuel source to produce that energy.
So, then, we actually start using that fuel source
to refatten ourselves, so you can literally,
in this case, be taking carbohydrates or fatty acids
and then recycling them into fatty acids.
So, once you get in here, like,
this can't recycle anything back into glycogen.
Once glucose is broken down, right,
here at the muscle cell, we're not gonna re-engineer that,
reverse engineer that into glucose,
so the one thing that we will do is we will take
those extra resources, the broken-down fatty acids
or the broken-down parts of glucose, and we will build
fatty acids out of those within that muscle tissue.
If you guys aren't very familiar, as we build up fat
and muscle tissue, it's correlated with this,
but that high citrate level creates the state
where this muscle then becomes insulin resistant.
So, it basically, as the citrate goes up here,
so, this guy, so we get citrate coming out of there
because the citric acid cycle is not functioning well.
AMPK is gonna get shut down,
and GLUT4 is gonna get pulled away.
So it's gonna compete with the effects of insulin,
'cause essentially, the citrate tells the cell, we're full.
There's no room for anything else.
We are so full that we are actually
now storing fuel within ourselves.
So it's gonna close the doors to incoming fuel sources,
which then, if this is muscle tissue and you've been
stressing it out like this and you've broken the system,
you've now created a place where it's, now I can't get
energy created in that muscle very efficiently,
and I can't get glucose in there to replenish
the glycogen levels and to recover from training.
So mitochondrial health is gonna be a huge factor
in determining how you tax tissue
from a metabolic standpoint.
How trainable are your muscle cells from a metabolic phase
is gonna have a lot to do
with how trainable are your mitochondria.
How trainable are your energy systems?
How much stress can they have,
because that's gonna affect your recoverability
from any sort of metabolic stimulus.
So, the key thing that we talked about,
in terms of systemic here, is the lactic acid,
in terms of the positive from training
or the negative from, you know,
poor mitchondrial function.
In order to produce lactic acid,
we have to have glucose.
So, if we're looking at setting that benefit
from training, you could not do it in a,
like, in a low-glycogen, low carbohydrate state.
If you wanna get that, you know, you wanna create
that negative energy balance, that recycling effect
of the liver, which systemically, remember, that's gonna
lead to growth hormone and all these other benefits,
we have to have glucose to burn in some way,
shape, or form, either in stored glycogen
or incoming nutrients.
Remember, glycogen's way more efficient, though,
than any carbohydrates that would be delivered
from the diet at that particular point in time.
We need a high rate of energy consumption.
So if you're not burning through energy fast,
which is why if you do low-intensity cardio,
you don't make a lot of lactic acid,
but if you do high-intensity cardio
or you do high-intensity metabolic training with weights,
you get a lot of lactic acid.
The more energy the mitochondria can produce, right,
the higher the threshold is needed to make lactic acid.
So, remember, I was saying, like, okay,
if we have the mitochondria running at 60 RPMs
and we have then, we need to run the exterior
or the extra cellular glycolysis at 70 RPMs
to then start making some lactic acid.
Well, if I get more mitochondria or I get them more
efficiently so that I can be running them at, say,
100 RPMs, well, now, in order to make lactic acid,
I need to tax the energy system enough
to where I would need to tax the outside portion
to 120 RPMs, right.
So the better my mitochondrial health,
the faster, the more intense the energy demand
needs to be for it to produce lactic acid.
So that's one of those trainability things
where the threshold is gonna go up.
As you get adaptations, so if you get adaptations
to your mitochondria, and they reproduce,
or, you know, they become more efficient,
then guess what, in order to get the same
lactic acid stimulus, you're going to need to have
to increase the intensity of that metabolic training.
And if you keep doing that over and over and over again,
guess what, it gets to the point where it's like,
man, that all becomes really hard to do this.
But you let that system detrain a little bit,
and then all of the sudden, you'll be ready to,
you know, be ready to enter a lower threshold for that
and be able to get the lactic acid a little bit easier.
You let those energy systems detrain just a couple weeks,
and all of the sudden, boom, you can hit that again.
The poorer the mitochondrial function, the lower
the threshold to be able to produce lactic acid,
but that's not a good thing,
because what it's gonna do is it's going to lead
to this chronic stress on the body that is going to cause
a systemic imbalance in hormones.
We're gonna get lowering of thyroid,
increased levels of stress hormones, and ultimately,
if the synergy between the citric acid cycle
and the electron transport chain,
they're not good, we can actually get to the point
where we are getting an insulin resistance
for those particular cells, which is going to drastically
decrease their ability to recover and fuel themselves.
So we're gonna see loss of performance
and dysregulation of systemic hormones
that would otherwise improve our metabolism.
We'll see a lowering of total body metabolism if we have
a lot of cells that have poor mitochondrial function.