-: Another important regulator of this
whole mitochondrial metabolism thing
is going to be oxidative stress.
So if we look at where our energy status was
when AMPK is activated, we have that driving up
the metabolism of the mitochondria,
so glucose is gonna be coming in,
there's gonna be a high drive of getting energy
into the mitochondria for ATP regeneration.
If we add oxidative stress into that mix,
especially a significant amount,
it's going to slow it down.
And that's because oxidative stress
is going to inhibit incoming glucose,
which simply just means there's not enough
glucose to fuel this process.
It's also going to decrease the activity of AMPK.
Now that is important.
If you look at the, you know when we were
looking at the mitochondria,
we're getting fed into the citric acid cycle,
and then the electron transport chain,
we had those two gas pedals.
The gas pedal one was the nutrients
coming in on this side.
Gas pedal two was the demand of energy.
If you are producing a ton of free radicals,
a ton of oxidative stress,
and you keep feeding that mitochondria
it's going to continue making more free radicals,
making more oxidants and that is going
to have the potential to damage the cell.
As those oxidants build up,
if we can't keep up with that in terms
of making our own antioxidants to neutralize those
they will start scavenging around
and attaching to the cell membrane,
and organelles, and proteins reeking havoc
and creating damage to those parts of the cell,
to those other molecules in the cell.
And that can essentially lead to the point
where the cell needs to terminate itself.
So as a protective mechanism you can only
tolerate so much oxidative stress before
the cell has to protect itself in an additional fashion,
which is essentially choking off
the energy source for the mitochondria.
So it's going to do that by decreasing the fuel
that's coming into the cell and then decreasing AMPK,
which is going to decrease the amount
of fuel that's in the cell from actually
getting into the mitochondria.
So glycogen is going to stop being broken down,
fatty acids are going to stop being
broken down at the same rate.
And everything is going to not come in as much.
It can also inhibit the citric acid cycle.
Just like its ability to take up fuel period.
So it can affect within the mitochondria
the ability for it to take in the nutrients
form the cytosol, from within the cell.
So that's an important protective mechanism to have
so that we don't do extensive damage to our cells.
If we created so much oxidative stress
it could even go out and attack things.
Like the membrane of the nucleus
and stuff like that and really cause long term damage
to the cells if there was nothing
to keep this under control.
A little bit of oxidative stress,
as you'll see in the upcoming units,
could be a good thing when that's
the training stimulus we're going for.
But chronic oxidative stress is not a good idea,
or prolonged exposure to oxidative stress
from creating that training stimulus
could not be a good idea because what you're going to do
is you're going to expend an extended amount of time
doing things that are inhibiting
nutrient uptake into those cells.
Now in a healthy cell as we correct this oxidative balance,
do we then have the potential to reverse these?
Yes.
So if you train and you create some oxidative stress,
does that mean now you're not going to recover from that?
Well if you have the appropriate nutrition
and you have the cellular health to be able to rebalance
from that, to create antioxidants to rebalance that,
and then start opening the doors back up,
then yes you can do that.
But it's all dependent on what a person has
in terms of their nutritional reserves
and their cellular health.
Now so being able to decide from a training program
do I want to trick, do I want to work
in a metabolic phase to the point where I'm getting
a lot of oxidative stress,
or is that going to do more harm than good?
In which case I need to focus more on getting AMPK up
and not creating as much oxidative stress.
And so there is going to be ways
that we can design programs that are going to either focus
on one or the other or some combination of both.
And those are all going to fit in with the person
depending on their nutrition,
depending on their cellular health,
and depending on what they've been training
at different periods of time in terms
of can they adapt to it, will they be trainable,
can they recover form that stress and actually
make improvements from that stress.
So it's very important to know these things.
Overall, big thing is that oxidative stress
is going to ultimately slow this down
so you can see that there will be a performance drop off
because if I am slowing down energy being shuttled
into the mitochondria, slowing down ATP production,
there's going to be a sharp reduction in performance.
If you also look at this in the context
of what's going on in training,
if I'm doing a set and I'm creating oxidative stress
it is going to take me longer to recover
from an energy perspective before the next set
because I have all this stuff that's inhibiting
my ability to rebalance that energy.
So it takes longer to recover from metabolic work
when I extend it to the point where
it becomes highly oxidative.
Much harder than it is if I'm focusing solely on lactic.
And those are going to be two different things.
There can be overlap, but they're going two different
things when we get into program design
and actually writing these.
So we look at oxidative stress,
we're just summarizing those mechanisms.
We've got the electron transport chain
when that's under high stress,
when that gas pedal is pushed down all the way,
any sort of issues in that citric acid cycle
where the electron transport chain are going
to create that electron link.
That's what creates those oxidative stresses.
So most important thing is understanding
that these two things need to be healthy
in order for you to be able to train
under high metabolic demand with minimal oxidative stress.
So the poorer your mitochondrial health,
the faster you will start making oxidants
when you do a little bit of metabolic work,
which is why a certain rep range
for one person may be totally different
than the other because they will start
making oxidative stress at different points.
Same thing with the lactic acid.
Different level of health with the mitochondria
and the energy production and the nutrient transport,
you take two people and you put both of them on ten reps,
for one person they might have really good
mitochondrial health and it's not
even metabolically demanding,
for another person it might be extremely lactic
or extremely oxidative for them
because their energy production is so poor
because of some nutritional deficiencies
or poor programming and periodization.
When we look at what is ultimately going to lead to this,
it's the time spent near fatigue in training
that is going to be the thing
that puts oxidative stress up the most
when we actually want it.
So we we're trying to stimulate oxidative stress
with training, it's how much time
we're working in fatigue.
So if you're doing a set of ten
and you actually fail on ten, guess what,
the first few reps you're not going
to be making significant oxidative stress
because you likely haven't depleted enough energy
or got into enough fatigue that the mitochondria
is like running at its red line.
It's not full to the floor.
We're not running the citric acid cycle
and the electron transport chain at their full speed.
So the amount of free oxidants,
the amount of electrons leaking there
is going to be minimal.
However, when we do stuff where we do super sets
and drop sets and tri sets or we do very very high reps
and things like that where we're actually spending
a lot of time where we are in somewhat
of an exhausted state from a metabolic energy perspective,
that's where we're going to make the most oxidants,
the most free radicals.
It's when we have taxed the energy system
in a state of fatigue.
When I say energy system I really mean the mitochondria.
When we have taxed the mitochondria
to a point where it's been working at max capacity
for an extended period of time,
because we're going to be accumulating oxidants
the entire time it's working at max capacity.
If we look at the other thing
that's going to slow this down,
it's simply just going to be the rebalancing of the energy.
So as ATP levels, so as high ATP and low AMP,
the opposite of what stimulates AMPK,
is going to decrease AMPK.
So if this was up here when I was demanding energy,
as my body starts to recup that energy,
it's going to slow that back down.
So if I were to take plenty of time between sets,
or as soon as I'm done training my body
is going to shift into this.
Which is why I can take up the most nutrients
at a cellular level immediately post training
if as long as there's not oxidative stress inhibiting that.
So this is just simple rebalance.
My body is saying hey we've rebalanced the energy,
we don't need any more incoming fuel
and we don't need to be sending fuel to the mitochondria
to be burned because we don't have any ADP
to be converted over into ATP.
We don't have any creatine to recycle at this point in time
so we can go to our maintenance level metabolic rate,
to which case we would like in healthy cells
to see less glucose and actually more fat
being burned in that particular state.
So let's recap with this, with the very first concept
which was this concept of energy systems.
So with energy systems and training
we tend not to look at the same thing
as what we saw in the first part.
It's like okay ATP, creatine,
it's like what the creatine said.
In programming the language tends to be along this line
of we have alactic power, alactic capacity,
lactic power, lactic capacity,
aerobic power, aerobic capacity.
And to summarize what the concepts of these are
it's like alright this would be peak power.
So this would be how much power can I use,
or how much intensity can I produce
and be using mainly my ATP and creatine reserves.
So this would be maximal intensity
and this would kind of be how long can
I run at that peak power.
So this is like when do I get to the point
where I can no longer use those creatine reserves
and everything else below.
So that's the most important thing
is that if we look at this,
this system, if I'm training this system,
it's using everything else below.
When I switch to here, it's using everything else below it.
And it's going to continue like that as I go down with this.
So this is where that stacking thing is.
So if I'm using this, and this runs off the creatine system,
and the ATP that's stored,
well once I use that what has to fuel that?
Well okay glucose is going to have to replenish that,
right and if I have enough time then also some fatty acids
and stuff are also all working all the time
to replenish this.
When you start getting into fatigue
what you'll see is not that any of these get checked off,
it's that these are now at a point
where they're at submaximal capacity.
So at any given time,
so when I'm at rest I'm using fat.
I'm not using fat to maximum capacity yet,
but if I start being a little active I might start using
fat at it's maximal capacity.
But once I exceed that,
we'll have to start dipping into some glucose.
Once I've reached the point where it's like
okay I'm using energy faster than what the mitochondria
can give it back, now I have to dip into my buffers
and I have to start using my creatine
or I have to start using my adenylyl kinase
and start actually breaking down and cannibalizing ATP
to meet that higher energy demand.
So as I go up certain things are now
all running at capacity.
And other things may simply be limited.
So this alactic power is alright what is the maximal amount,
what is my peak power alactic capacity.
How long can I run before I am now below peak power?
When I get to these, now we're looking
at actually what I can fuel that first part
of glycolysis with that's not in the mitochondria,
so the part is pushing to lactate,
how fast can that run?
What is the peak power that I can have
when essentially the creatine system is exhausted
and so the fastest source of energy that I have
is that first step of glycolysis.
Keeping in mind everything underneath is still supplying it.
So it's this plus everything below.
So it's how much peak power can I get if that's what I have.
And then how long can I function at that
before performance is then going to drop off.
So remember in that aspect,
so with the lactic acid generation we're using that,
we're converting pyruvate to lactic acid
as a way to be able to continue recycling that NAD
and keep doing that first part of glycolysis
at a faster RPM than what the
mitochondria is actually running at.
But I can only do that at a certain rate
because I have to be able to one, reverse engineer that,
two, I have to be able to get that lactic acid out
because it kind of functions on a concentration.
So if I have this much pyruvate
and this much lactic acid,
they can kind of inter-convert back and forth.
They are essentially interchangeable.
They can convert back and forth.
As pyruvate builds up,
my body says well lets start making more lactate
to balance that out.
As I keep running this,
what's going to happen in order to get that more NAD
is I'm going to be making more and more lactate.
And if I can't get that out of the cell,
the lactate builds up in relationship to the pyruvate,
in which case those enzymes,
because they can go either direction,
so pyruvate can be converted to lactate,
lactate back into pyruvate,
so if it's start getting so that the ratio
is there's a ton of lactate and very little pyruvate,
what'll happen is the enzyme will start working in reverse
and I'll essentially lose performance at that point.
So that's where my capacity will drop off.
And then we get into the aerobic power
and the aerobic capacity portion
and essentially this is where we get into
some real gray area in terms
of what is really fatiguing in these.
Because now I'm going to be getting
into a point like at this barrier
where lactic capacity can kind of meets aerobic power,
likely the thing that's going to be shutting things off
is going to be actually oxidative stress.
So in that instance that's going to be the thing
that's going to start cutting off your performance.
When you get to this for now we're usually functioning
at something that is going to be below
the oxidative mechanism or that oxidative stress
is going to take a lot of time to build up
because the intensity now is so low.
But when we're here that intensity
and energy demand is high that when I'm kind of
at this level I've red lined the mitochondria.
So the mitochondria if I'm training here
is red lined during the set.
But it may not be red lined the entire work out.
So obviously if I'm working here I need long rest periods.
So the mitochondria is maybe going to work hard
for a very very short period of time.
So I will burn through some ATP, some creatine,
the mitochondria will rev really fast
and replace that and then it will calm back down.
As I get further down this chain
usually what happens is that my work to rest ratio increases
so I'm spending more time with
that mitochondria maximally revved.
And when I get to lactic capacity,
that's usually where here's now where I'm starting
to see some oxidative stress become prevalent.
And when I get into aerobic power,
that's really where I'm kind of like now the whole thing,
like aerobic power is essentially this,
like what is the peak if I'm running the mitochondria
at it's maximum capacity what is the peak power
I can produce when the mitochondria is fully taxed.
Aerobic capacity then would be how,
basically what can I continue to do
when I'm below the oxidative threshold.
When I'm working the mitochondria
but not at a rate where there's
significant oxidative stress.
That's how I would kind of separate those.
So hopefully that gives you guys an idea
of what's actually supposed to be happening
when you train these systems.
So knowing what we talked about in terms
of how the mitochondria functions
and all of the things that are going to affect
the ability to restore energy
and the mitochondrial health being a huge factor
and when we actually fatigue
and when we actually start to make lactic acid
or make oxidative stress,
you can see that if we set rules for these,
where it's like okay alactic power is this,
and alactic capacity is this,
and okay these are the set set work to rep ratios
and these are the set intensities,
that's not going to be the same.
This whole continuum needs to be individualized
because the more healthy a person's energy system
and mitochondria well then obviously some of these things
like their work to rest ratios are going to change.
The less healthy, so if somebody is not healthy,
from an energy perspective they're going
to work this way on the continuum.
So things that should,
things that should be not very taxing,
or taxing to the lactic system,
will become taxing to the lactic system
if your energy system is poor
or if your mitochondrial health is poor
or your ability to take up nutrients is poor.
If you have poor mitochondrial function,
or if you have dysregulated glucose metabolism
or whatever it may be,
oxidative stress is going to kick in sooner.
So these things are going to get tapped out earlier.
So remember it works this way, whatever is at the top,
that's the thing that's being stressed.
And everything else is supporting it.
But what's below is not taxed.
It's not maxed out, it's just supporting the top thing.
As I move down, now this is the thing that's
maximally taxed, everything else below is supporting it.
As I move down, this is the thing that's taxed,
everything else below is supporting it.
And it works down.
So the only thing that's working to fatigue
should be whatever is at the top.
And a person jumps up that in correlation
to a set rep to work ratio if their energy systems,
if their mitochondrial health is optimal as it should be.
Last one here, what's going to go on,
what's going to determine the metabolic stimulus.
What fuel is available will be huge.
How much of that fuel is available.
So do we have glycogen?
And if we have glycogen, how much?
Because that's going to be huge.
Because it can't create lactic acid without glucose.
The best source of glucose is going to glycogen.
What about AMPK?
The more glycogen, well okay the AMPK is going
to come on a little slower a little less aggressively
if it senses that we have a big storage of glucose.
If it doesn't sense it, it's going to reach out
to the body and say hey I need glucose sooner.
Lets think back to the systemic regulation.
If I have cells that are panicking
and reaching out for glucose right away
under a lower intensity exercise,
what demand does that then put
on my body to support blood sugar.
Well it's going to be more
because the muscles are going
to be taking sugar out of the blood
sooner and at a greater rate which means
now okay in order to support that blood glucose
I'm going to need more stress hormones.
I'm going to need more cortisol, or more catecholamines,
which are going to be working on what?
Well they're going to be working on my liver.
So now my liver has got to work hard.
Well what if it's glycogen levels are lower?
Well not it has to work harder.
What's that do to the stress hormones?
Now they've got to go up even further.
So do you think that, alright what fuel sources
do I have available and where are going to affect
how a particular set and rep scheme
or any particular program stimulus
is going to affect me?
Absolutely.
So what's available, and then what's being burned.
How do I, obviously it has to be available to be burned,
but the other thing that's going to affect
what's being burned is the intensity of the exercise
and that work to rest ratio.
So basically how much does the energy system get to recover.
How much ATP do I get to replenish between sets
because if my work to rest ratio is high,
I'm doing a lot of work and I'm resting very little,
I don't have that much time to recover
so I have to use faster sources of fuel
to recover between sets which means glucose
becomes more of a dominant fuel source
regardless of how long the actual set was.
So I could do sets of three,
but if I rest less between sets of three
it becomes more glucose dominant than
if I take longer rests between sets of three.
I could do sets of 20, same thing would still apply.
Proportionally it would be more glucose demanding
if I had less rest between until it gets to a point
where I've worked it so low of an intensity.
So if my work to rest ratio or my set length
gets to a point where my intensity becomes so low
that I can do most of that work just by metabolizing fat
because it's just the energy demand is not that high,
then it would drop back off and become less glucose.
So that's where we get into lower intensity exercises.
So it is kind of a bell shaped curve,
but for a majority of the stuff we would do
in a weight room training setting,
then we're looking at okay work to rest ratio
is in general is usually going
to increase carbohydrate demand.
As long as we don't get to a significantly low intensity.
And that's going to have to be,
from an intensity perspective,
you're looking at where when you can maintain
an activity for three four minutes plus
that's probably now an intensity level
where it's going to switch over to becoming
now fat can actually start becoming
a greater portion of that equation.
Especially as you do it for a longer period of time.
The rate at which that fuel is being burned,
not only because do I need faster fuels
to do certain things, but as I'm burning that fuel fast
I turn on certain signals.
So the faster I burn fuel, the faster I deplete ATP,
the more likely I'm going to activate AMPK
because I'm going to make AMP from burning
through all the energy fast.
I'm going to have to break down the ADP,
cannibalize that and make some AMP,
which is going to drastically increase
the amount of incoming glucose
and the amount of fuel that I'm burning,
especially glucose being driven down that pathway
and through the beginning stage of glycolysis
exaggerated there going into the lactic phase if needed.
The duration work to rest ratio,
kind of already hit that,
and then the systemic demand is also
going to be a part of that.
So we kind of talked about this in the context of a cell.
So that cell functioning on it's own.
But when we look at getting to the point where
the cells are then reaching to the body for nutrition,
so they're reaching to the blood for glucose
to keep fueling this process,
well the more muscles I have working
the more things that are asking for glucose,
which means that glucose demand is higher,
which means the stress hormone then is,
stress hormones are higher,
the more tissues I have that are releasing lactic acid,
means the more lactic acid going into the liver,
so the systemic stimulus that I get is going
to be affected not just by what mechanism
I choose to train an individual muscle with,
or the individual cell within that muscle with,
but the size of that muscle or the amount
of tissue just in general,
so all of the muscles together collectively
that I'm taxing is going to affect the systemic adaptations
that I get in terms of stress response,
growth hormone response, lactic acid recycling,
and that whole energy deficit that I'll create
by having to recycle a lot of lactic acid.
Those things are going to be dependent
on not just all of the above,
but then the amount of tissue that
is being affected by all of the above.