(soft music)
-: Now we're gonna start talking about
some of the actual stimuli and adaptations
that are gonna occur as these metabolic processes
are going on within those cells.
So we're gonna focus more on the local stress
for the time being.
So, one of the biggest activators or stressors
that I can think of is gonna be that high AMP, right.
The adaptation, especially the short term one,
is gonna be that elevation in AMPK.
That AMPK is gonna multiple things
that it can stimulate both short and long term.
We're gonna look at things like the increase glucose uptake,
but also then in the long term increase glycogen uptake,
and increase glucose uptake and insulin sensitivity,
as well as adaptations to the mitochondria efficiency.
Oxidative stress, another very potent stimulus.
This one is probably what I would say is the one
that you have to be the most careful with
because there's really no downside to having AMPK activated,
but too much oxidative stress can definitely be a bad thing,
but this is one of the best stimulators
for adaptations to the mitochondria.
So if trainable, that can be a great way
to improve cellular energy production
because we can improve the number
of mitochondria we can have.
Glycogen depletion can be a stimulus itself
because if glycogen levels are low,
they're gonna influence the metabolism of the cell
to start working more on fat.
You're also gonna get AMPK to be more sensitive
when glycogen levels are low.
And then we have the calcium release
or the sarcoplasmic reticulum being stressed
by all of the calcium being released,
and that's gonna have multiple downstream things.
One of the initial ones being activating AMPK
for the short term you know,
or basically the preemptive ability to get metabolism going,
anticipating that we're gonna be
burning through a lot of fuel,
and then from a long term perspective,
there's other genes that can be turned on
when we kinda stress out that sarcoplasmic reticulum,
in terms of the ability to mobilize energy,
and to actually make the enzymes
to synthesize glycogen and stuff like that.
So volume of metabolic work can also be a factor
or also be a stimulus because it's of the amount
of total stress that we put on that sarcoplasmic reticulum,
in terms of the amount of calcium that ends up having
to shift in and out throughout a workout.
If we look at the difference between stimulating the AMPK
or lactic acid versus stimulating oxidative stress,
what we're gonna see is that the AMPK
and lactic acid stuff is gonna happen earlier
as we're approaching fatigue versus the oxidative stress
is gonna become more prevalent later.
The other thing is that this is gonna usually happen
under a higher degree of intensity
because remember the oxidative stress
just needs the mitochondria to be taxed out.
This needs us to be functioning at an intensity
higher than what the mitochondria can support, right.
So we have to be in excess of an energy demand
then what the mitochondria can provide
to really push the lactic acid up,
or to really drive that ATP down
to the point we're making lots of AMP.
Now what you will see here is
that you get to a certain point, alright.
You don't just like okay I'm going,
and then I can continue making more lactic acid, more AMP,
and continue to get that stimulus
for longer period of time under indefinite fatigue.
The reason for that being what oxidative stress do.
Well oxidative stress is going to drive down AMPK,
and it's going to stop glucose
from being delivered into the cell.
So if AMPK goes down, we start breaking down glycogen.
If we stop getting glucose coming into the cell,
we essentially between those two we have no glucose
to fuel this extra cellular energy process
that results in that lactic acid.
So if no glucose none of that,
which means that this stimulus
then is going to become less.
The dominant stimulus is gonna continue to work longer
is going to start biasing towards oxidative stress.
So there is a point in here where these things
are gonna kind of both be active and overlap.
Like I said, even when we were kinda
looking at those continuum's is that
oxidative stress is going to kick in.
So it was actually when we were talking about
lactic capacity and aerobic power.
So, this thing is about peak.
That's when we're kinda hitting lactic capacity
is where this starts to go from the peak
and start to drop off, right.
So this is being peaked lactic power,
and then where that starts to drops off,
that's when we're getting into lactic capacity.
That's where oxidative stress is going to pick up
because that's where we're really maximizing
whatever the mitochondria can do,
and that's where we're at aerobic capacity
is when we get to the point where that starts to shut off.
So aerobic power and then aerobic capacity if you will.
So, as I get into start making that oxidative stress,
some of that is going to inhibit
the ability of glucose to come in,
but I'm still driving that mitochondria
from the energy demand standpoint.
So remember a mitochondria has the two gas pedals.
One is the incoming fuel and the other is the incoming ADP
because we've burnt through a bunch of energy.
So that pull, the second gas pedal,
all of the used energy is gonna continue
to drive this process even though the oxidative stress
maybe slowing down some of the fuel delivery,
so we won't be getting as much glucose in the cell.
The mitochondria is still gonna try and take up energy
if that electron transport chain is pulling on it,
if there is anything to use.
So it's not until we get a significant amount
of oxidative stress then that's gonna dump off.
So we look at those in terms of time to fatigue,
the oxidative stress happens when we are
at a longer state of fatigue.
So if I wanted to focus on oxidative in general,
I would do longer sets than if I was
focusing on AMPK or lactic acid.
In this case, I would need higher intensity.
This could be lower intensity but longer,
but not so low that it's below the threshold
for creating oxidative stress.
If we look at all the things
that are being stressed or taxed
within a lactic or AMPK driven workout,
we're gonna see things like well one,
lactic acid system is better be
the thing that's getting stressed.
We're gonna see a lot of glycogen depletion
because what's our fuel source?
If we are working at high intensity
and we are creating lactic acid,
we know we're burning through a lot of glucose.
That has to be the case.
So we're gonna see glycogen depletion,
especially if we're not getting a lot of carbohydrates
in the workout or post training.
So you may want glycogen depletion in the workout
and then refilling afterwards.
You may want to try and limit depletion.
You may want to have depletion during and after.
It all depends on what the whole purpose
of you doing this type of workout is for.
There's different contexts that we would use that,
in terms of what are goal was for a person.
We look at electrolytes because we're doing a lot of,
a lot of metabolic work.
We are gonna see, you know, just the alkalinity being taxed.
There is gonna be some oxidative stress,
but not a tremendous amount.
So, oxidative stress a little bit.
I don't know how good the colors show up on here,
but it should show up pretty good.
So the more red, the more stress.
The more green, the less stress.
So mechanical damage should be very little.
If I stop at stimulating AMPK
and lactic acid, if I stop there,
I should get minimal information,
but that's because oxidative stress
is staying under control.
What you will find is that that will change
when we look at oxidative stress.
The neurotransmitters because as long
as they're not overdoing the volume,
I should not be really taxing my neurotransmitters,
especially from a muscular perspective.
Now, if I'm in a position where this type
of thing is messing with my gut,
which when we get into like some of the advanced modules,
we'll talk about how gut health
with certain types of training,
there can be some bad interactions.
I could potentially tax my nervous system
and things like that just because I wasn't,
the system wasn't trainable but from a health perspective,
not that my muscles weren't ready for that.
So the big thing to take is lactic acid
and glycogen depletion are the two things
that are going to be fairly taxed,
but inflammation, mechanical damage,
neurotransmitters should basically,
essentially be getting a de-load
Inflammation will start to go up
as we add oxidative stress to it.
Electrolytes and oxidation are going
to not necessarily get de-loaded,
but they're not being overly taxed.
So if I have very healthy mitochondria,
that little bit of oxidation,
that might be even less significant.
If I have really good cellular health
from a nutritional perspective,
that's also gonna minimize that,
and then if I have been conditioned,
my ability to make my own antioxidants will be good,
so I will be able to deal with that
without it adding much stress to my body,
without it digging into my recover-ability, okay.
If I were to add mechanical damage,
or add inflammation, or add a bunch of neurological stress,
that would drastically add to the recovery
that I needed making this less trainable
because it's gonna dig into my recover-ability.
If we're looking at oxidative work, alright,
there's still gonna be some lactic acid
'cause we're gonna kinda probably a little bit of that
on the way to the oxidative level of fatigue.
Still gonna have some electrolytes going on there
in terms of like needing to rebalance that alkalinity.
Mechanical damage should be limited,
but that does not mean there will be tissue trauma,
because oxidative stress remember can damage tissues.
So because oxidative stress alone will damage tissue,
we will get inflammation.
That is not necessarily a bad thing
if our goal was to stimulate the things
that are stimulated with oxidative stress.
So when we are doing oxidative stress,
we can be doing it for a metabolic goal.
There's also the context of using oxidative stress
as a stimulator for hypertrophy
because of this inflammatory signaling.
So when you look at why in the context
in which you would take somebody
and do an oxidative stress based workout,
you have to figure out okay what are we doing
to mitigate that inflammation or are we trying to,
or what are we gonna do in terms of the volume of work,
because this is gonna be correlated to not just the amount,
but also the volume of work of oxidative stress that you do,
and if we're just going metabolic,
likely there's gonna be a lot lower volume of this type
of stimulus then if we were doing it for hypertrophy,
and our goal was to get a lot of that inflammatory response.
If we look at glycogen we're gonna get some depletion there,
but likely not as much as the lactic protocol,
which is really running off of glucose for a fuel source.
Again, the neurotransmitters should not
be negatively impacted unless this becomes excessive
'cause stress and inflammation are gonna hurt
everything across the board, right.
They're gonna take away our recover-ability period.
So, if you do this system I would say
of all the training stimulus's,
the one it's easiest to overdo the volume is gonna be
the oxidative stress because the oxidative stress
has so many consequences with it
that if you are not able to train,
or if you're not trainable, not able to recover from them,
could potentially actually decrease the recovery
and decrease what your output is from workout to workout.
You get all that inflammation,
which is all flow massive energy sap
and can affect nutrient transport,
and can dysregulate systemic hormones.
So this is one of those stimulus's where
if you overdo the volume or you do that phase too long,
you can start working backwards relatively fast,
which is a shame because a lot of people,
because this is associated with hard work,
because it takes you deep into fatigue,
a lot of people like to hit this button all the time,
and so they're stressing out their system,
and that's why you see a lot of people
develop chronic fatigue and gut issues,
and brain issues and stuff like that,
because they're constantly checking off these boxes
in their program and they're not ever de-loading
from those stressors or from those stimulus's.
If we look at the AMP.
If we look at what that's gonna give for us,
we already talked about the AMPK.
That's the main.
That's the main beneficiary there is getting that.
We need the high rate.
I can't emphasize that enough.
High rate of ATP consumption.
It's not the amount, so it's not the volume of work.
It's not like how long you've fatigued.
So it's like doing longer sets
doesn't necessarily get you there efficiently.
It's doing high rate of fatigue.
So sometimes for advanced people
that means you need to be creative.
You need to do something where you're gonna have
like super sets or drop sets or something
to be able to maintain higher intensity over time,
so that you're depleting energy faster, right,
just 'cause if you pick a weight
that you can do for 20 versus doing a set of 10,
dropping and then doing another set of 10,
overall you use more weight on the 10 10
because you'll be able to use more weight for the first 10
because it doesn't need to be weight
that you can do an extra 10.
So, because you can use more load,
you can work at a higher rate of energy consumption,
so when we're focusing on this,
it's not because it's metabolic.
It's not necessarily just high rep.
It also has to be a certain intensity.
So it's a high intensity in relative to metabolic work.
Not high intensity in terms of neurological work.
It meets lactic acid threshold
when the glucose is available.
So, you can activate AMP,
or make AMP, and activate AMPK without glucose.
You can do that.
So, you don't need lactic acid to be able to create AMP.
However, lactic acid is an important systemic stimulator,
but in terms of locally, it helps us correlate
that we're on the right path in terms of our training
'cause if we're at a high rate of ATP consumption,
and glucose is available to use,
we will also make a lot of lactic acid.
So sometimes it's really hard to assess what's going on
in the cell when somebody's doing a set of leg extensions.
Like, you don't have a little barometer that says,
oh they have this much AMP right now,
so it's like okay two more and then we're done,
but lactic acid gives us a really valuable marker
for the fact that this is the stimulus that we're getting.
So from a local perspective lactic acid correlates
to the fact that we're using AMP as the stimulus for AMPK.
When we don't have glucose available,
then it becomes much harder to know what we're doing.
The other thing is when we don't have glucose available,
we're much more likely to jump over to oxidative stress
because we're not able to fuel that high intensity work.
We're not able to fuel that high energy demand,
and because there's not glucose available,
the mitochondria's gonna be more taxed to try and get
that energy from fatty acids and stuff like that
so it's coordination of fuel becomes more difficult
'cause it's only got one fuel source to run off of,
and that fuel source doesn't come in as fast as glucose
or as readily so that mitochondria gets stressed more.
So in essence, if this is your stimulus,
it's best done with glucose in the diet,
or better yet glycogen already stored in those cells.
Our others that are activators.
We already walked through these,
but we got glycogen depletion, calcium.
Both of those are gonna be other,
but not as potent activators as AMPK.
The thing is is that you stack all this stuff together.
So we got good contractions.
We got high rated demand and we deplete
glycogen during training.
That's gonna be my maximum total stimulus,
which is gonna be really good if my goal is
to get tons and tons adaptations from AMPK,
which is gonna be things like increase glucose uptake,
increase insulin sensitivity, increase glycogen synthesis,
and improve mitochondrial efficiency.
Local adaptations, right.
I guess I just said most of these, right.
So we get all these things.
We also get increased fatty acid metabolism,
especially short term.
So when we stimulate AMPK because it's going
to stimulate the replacement of glycogen,
the glucose that comes in post training
is gonna be less likely to be used for fuel
and more likely to be used for stored glycogen
and then fat will be being burned to fuel that process.
So we'll actually be burning fat for the cell
to do whatever its recovery processes are,
while the incoming carbohydrates are used
to replenish glycogen levels and that's very important
because if we look at trying to recover,
we can turn on a lot of recovery genes
when energy is rebalanced.
So if we can do dual purpose we can be
fueling the cell right now with fat,
and all the carbs are being stored
to replenish those glycogen levels,
versus the carbs are coming in.
Some of them are being used for energy,
and then what's left is stored.
That's a much less sufficient way of getting fully covered
then being able to use both fuel sources simultaneously.
So we're also going to increase fatty acid metabolism,
especially short term to fill up those glycogen levels.
Once those are full, if I get enough stimulus,
and I keep hitting this button often enough,
I will train my body to get really good
at using fat for fuel at rest.
So I'll get these mitochondria adaptations
to be more efficient at using fat for fuel,
which is really good because what it does
is it decreases the amount of glycogen
that you're gonna go through between workouts,
doing essentially nothing or just like your daily activities
so it helps you conserve more glycogen
for high intensity exercise because you can perform
higher low intensity exercise
with fat alone or with mostly fat.
You need to dip into the glycogen less often
because you're able to make more ATP from fat
because you're better at fatty acid metabolism.
Another huge benefit is you get the activation
of longevity genes like sirtuin genes
that can help actually extend the life of the cell.
It can help protect.
They turn on genes to help prepare the DNA and stuff
because when we create these highly metabolic environments,
one of the things that our cells anticipates it happens
is that we had a little bit of this like metabolic damage
from the free radicals and stuff that were created.
So, these genes are basically programmed
to make sure we maintain and repair things.
So this type of training helps keep the active enzymes
and proteins that are there for cell maintenance and repair,
which can improve longevity.
Would also improve my tolerance
to volume per muscle per training.
So we're gonna spend a lot of time talking about
how one particular phase of training,
or one particular stimulus and adaptation
could potentiate the recovery
or the performance in a different stimulus,
or for a different adaptation.
So when we look at being able to improve fat metabolism
and improve glucose transport,
and improve energy efficiency,
what that's gonna do is it's gonna make it
so that I can handle a higher volume of work
within a workout because one will have
more glycogen just period.
So having more glycogen to do more high intensity work.
I'll be better at getting glucose in that
to fuel more high intensity workout,
so I'll be better at pulling it in from the blood.
I'll also have just a better recovery
between sets that can be fueled with fat
because I'll be better at fatty acid metabolism.
So all of that combined means that
I can handle more volume in a workout,
which is important if I'm becoming advanced as a trainee
and now I need a higher volume of work
to say stimulate hypertrophy,
'cause if the thing that's keeping me
from being able to progress in my hypertrophy training
is simply an energy perspective,
my metabolic performance is the thing
that's affecting my ability to get the stimulus
that I need for hypertrophy, well it doesn't matter
how well designed my hypertrophy workout is
because I'm not gonna be able to hit the threshold needed
for those hypertrophy adaptations
because simply I need to be better.
I either needed incoming glycogen.
I needed a better glucose transport.
I needed a better fatty acid metabolism.
From low any of those things, stress hormones are gonna
have to go up to help with the fuel delivery,
which ultimately gonna take away
from the hypertrophy stimulus.