[Instructor] Hi everyone.
Today's lecture is on the topic of cell signaling
and the hormonal response to exercise.
And this PowerPoint comes out of information in chapter five
of the Powers "Exercise Physiology" textbook
On our AccessPhysiotherapy website.
Please read through the following 11 objectives.
And at the end of this screencast,
come back to the slide
and be sure that you are able to
achieve all those elect objectives.
So if you are not able to, say,
graphically describe the changes in the following hormones
during graded and prolonged exercise,
go back and look at the slide or read the chapter again.
To start off with,
we've already gone over bioenergetics
and we understand the fact
that our body uses certain substances for fuel
such as glucose or fats or proteins.
And now we're gonna take a step back
and talk about how does our body know
which of these fuels to use.
How, for example,
does the body know
to release free fatty acids for lipolysis?
Well, it knows it
because of our nervous system
and our endocrine system,
and they work together closely intertwined
in the field of neuroendocrinology.
The nervous system uses neurotransmitters
to conduct messages
and to signal and stimulate cells to act,
and the endocrine system releases different hormones,
which also will then bind to different receptors
and will also stimulate different tissues to react.
The endocrine glands are where our hormones are stored,
and these endocrine glands
will release hormones directly into our blood,
which then circulates throughout our system.
And the hormones will affect
the activity of different tissues
that possess the receptor that matches that hormone.
So hormones can only bind to specific receptors
that are targeted for that specific hormone.
So you can have a lot of hormones
floating around in your body,
but they're only going to bind to a certain receptor.
There are different types of classes of hormones,
and we're gonna be going over some amino acid derivatives,
peptides or proteins, and steroids.
The effect of hormones
are determined by several different constructs.
So the first one is
how much of that hormone is floating around in our plasma.
So what's the concentration of it?
And this concentration of hormone levels in our plasma
is determined by the rate of secretion of that hormone
from the endocrine gland.
So how much or how little?
And there's some inhibitory versus facilitatory stimuli
that will determine if the endocrine gland is gonna
release a lot of hormone
or if it's gonna stop and not release anymore.
The other effect on our circulating levels of plasma hormone
is determined by the rate of metabolism
or excretion of the hormones.
So how quickly it kind of passes through our system
and is processed by our kidneys and excreted out.
And the other things that affect the concentration
and the effect of a hormone and a tissue
is determined by the quantity of the transport protein,
for example, steroid hormones,
and we'll talk about those in a bit,
and changes in our blood volume or our plasma volume.
So here's kind of an example.
So you can look here.
And so here's the pancreas.
The pancreas secretes insulin.
What tells a pancreas to secrete insulin
or to stop secreting insulin?
Well, that's determined by
levels of glucose in the blood,
levels of amino acids in the blood,
sympathetic activity of our nervous system,
or parasympathetic activity.
So you can see here if the glucose levels
or the amino acid levels in the plasma increase,
that's facilitatory
and that's gonna tell the pancreas to release insulin.
If there is some sympathetic activity,
sympathetic nervous system activity,
epinephrine is gonna be released,
which is gonna have an inhibitory effect on the pancreas,
and so insulin will not be released.
So there's different factors
that will tell a tissue or an organ to do something.
And it's this combination
of inhibitory or facilitatory signals
and whichever magnitude is the greatest
will determine the effect on the tissue
and whether or not, say, insulin will be secreted or not.
So hormones only will affect the tissue
that has its matching specific receptor.
And when a hormone does find a receptor that it binds to,
the magnitude of its effect
will depend on the concentration of the hormone
floating around in our plasma circulation,
the number of receptors on the cell,
and actually the number of receptors
can vary from 500 to 100,000 receptors on any given cell.
Receptor number isn't fixed.
It can vary.
And so the receptor number can decrease.
For example,
if it's exposed
to a chronically elevated level of a hormone,
and this is called downregulation,
this will result in a diminished response
for the same amount of hormones floating around.
So regardless of
if there's a high concentration of the hormone,
if the number of receptor sites decreases,
there will be a downregulation.
The opposite case is if there's chronic exposure
to a low concentration of a specific hormone,
which leads the body to want to have more of an effect,
so there will be an increase in a receptor number,
or upregulation,
with the tissue becoming really responsive
to the available hormone.
The way that hormones cause an effect on our body
is by modifying cellular activity,
and they do this in three different ways.
So they can alter the activity of our DNA
to modify protein synthesis
to actually make our bodies produce more protein.
They can activate secondary messengers
or they can change the membrane transport capability.
So for example,
in the first one,
the stimulation of DNA to modify protein,
steroids are able to diffuse easily through cell membranes
and they then bind to a protein receptor
in the cytoplasm of the cell.
This specific binding steroid receptor complex
will enter the nucleus
and it will carry instruction codes for protein synthesis
and it will initiate the steps
leading to the synthesis of a specific messenger RNA
that carries the codes from the nucleus to the cytoplasm
where the specific protein is then synthesized.
Secondary messengers or second messengers
address hormones that are not like steroids.
So steroid hormones, as I said,
they can easily move and diffuse through cell membrane
and modify the protein synthesis.
This process, actually I did neglect to say,
this process of stimulating protein synthesis
takes a long time to activate.
So it's a slow process.
But once the proteins are made,
it has a long lasting effect.
Other hormones, however,
because of their size or their structure
can't easily cross the cell membrane,
so these hormones will bind to a receptor
that is on the surface of the cell membrane
and they won't really pass through
and they'll activate proteins within the cell.
So they'll activate a G protein,
which will then create a reaction inside the cell.
And the G protein,
it may open an ion channel
to allow calcium to enter the cell,
or it may activate an enzyme in the membrane,
and so it will activate other structures in the cell.
And so these are then second messengers.
So for example, cyclic AMP, calcium,
and these are involved in,
say, for example,
cyclic AMP,
it will activate proteins
that directly alter cellular activity.
They do this, for example,
in converting glycogen to glucose in the muscle
and triglycerides to free fatty acids.
Cyclic AMP is inactivated by phosphodiesterase,
which is an enzyme that converts cyclic AMP to 5 AMP.
So an interesting fact
with this cyclic AMP and phosphodiesterase
is that caffeine interferes with phosphodiesterase activity.
And so that's going to facilitate cyclic AMP
to continue to exert its effect for longer period of time.
So caffeine will exert this effect on adipose tissue,
causing free fatty acids
to continue to be mobilized at a faster rate.
If the G protein activates calcium ion channel,
then the calcium is gonna enter the cell
and bind to and activate different proteins
to influence cellular activity,
kind of in the same way that cyclic AMP does.
So these are hormones then activating second messengers
to cause a reaction.
Lastly, hormones can work
to help substances move in and out of cells,
so crossing the cell membrane.
So they can bind to a receptor on the membrane
and activate carrier molecules
in or near the membrane surface
to increase the movement of substrates or ions
from outside to inside the cell.
For example,
insulin is gonna bind to receptors
on the surface of the cell,
which will mobilize glucose transporters
located in the membrane.
And so these transporters are gonna link up with glucose
that's circulating outside the cell.
And if the glucose, blood glucose levels are high,
this hormone action will act to transport glucose
to diffuse into the cell where it's needed.
If the individual doesn't have enough adequate insulin,
for example, in somebody with uncontrolled diabetes,
the glucose accumulates within the plasma
because the glucose transmitters or transporters
are not activated.
So here's an example of
a hormone passing through the plasma membrane here
and then binding with the receptors
inside a target cell,
so then it can go in,
and this is where it's gonna stimulate protein synthesis.
So it's affecting the DNA and the messenger RNA,
creating a protein synthesis right here.
Hormones are secreted from our endocrine glands.
And the main glands are the pituitary gland,
which is located at the base of the brain
and attached to our hypothalamus.
The gland, it has two lobes,
an anterior lobe and a posterior lobe.
And then we have our thyroid and parathyroid glands,
adrenal glands,
our pancreas, which we've talked a little bit about already,
that releases insulin,
and testes and ovaries.
The hypothalamus is gonna stimulate the release of hormones
from the anterior pituitary gland,
which then provides hormones
for release from the posterior pituitary gland.
The anterior pituitary gland hormones
include adrenocorticotropic hormone, or ACTH,
follicle-stimulating hormone, FSH,
luteinizing hormone,
melanocyte-stimulating hormone, or MSH,
thyroid-stimulating hormone,
growth hormone, and prolactin.
And as I noted,
most or many of the hormones
released from the anterior pituitary gland
are going to stimulate other endocrine glands,
with the exception of prolactin,
which will affect,
effectively target the breast to produce milk.
So here's a list of the hormones
that I just rattled off earlier.
And our ACTH will stimulate cortisol
to be released from the adrenal glands.
Our luteinizing hormone
will stimulate production of testosterone and estrogen.
Thyroid-stimulating hormone will control
the thyroid hormone release from our thyroid gland.
Growth hormone stimulates the release
of insulin-like growth factors.
And this is responsible for our muscle growth.
In addition to working to facilitate muscle hypertrophy,
growth hormone also has important effects
on other substrates such as protein, fat,
and carbohydrate metabolism.
The growth hormone,
it's secreted from the anterior pituitary gland
and it really affects many,
the growth of all tissues
through the release of insulin-like growth factors.
Production of growth hormone increases with exercise
to help maintain our plasma glucose concentration.
So you can see that
when we have growth hormone
and insulin-like growth factors circulating
and with increased production of them,
there'll be an increase
in the synthesis of new glucose in the liver,
so gluconeogenesis,
and there'll be an increase
in the mobilization of fatty acids from adipose tissue,
and so,
which is what we want when you're exercising.
So it's kind of sparing the plasma glucose,
which as opposed to the insulin reaction in the pancreas.
So the pancreas is gonna sense
excessive blood concentrations of glucose
and will act to produce insulin
to move the glucose into cell.
So again, it really depends what the body needs
and there's this really fine balance
to keep us all working and moving.
Growth hormone, as noted on the other slide,
it's gonna facilitate protein synthesis,
so it's gonna help with muscle hypertrophy
and it's gonna facilitate bone growth,
our long bone growth,
so femur, humerus, tibia.
It has been used to treat childhood dwarfism.
Some athletes use this to try to build up their muscles,
and there are some issues with that.
There are more adverse effects than there are benefits.
So some of the adverse effects
is that although growth hormone will increase
the protein synthesis of muscle,
it actually is a connective tissue protein.
So it facilitates collagen production
more than a contractile element.
So what you see consistent with this
is the fact that you will have some strength gains,
but they're not gonna match gains in muscle size.
So you're not gonna get that hypertrophy that you would get
with just doing normal resistance training alone.
The other issue is that
there's definitely side effects of overuse.
So chronic use of growth hormone can lead to diabetes,
because of the fact that it's gonna
keep that plasma glucose levels high,
hyperlipidemia, arthritis,
enlarged heart or cardiomegaly,
it's been associated with carpal tunnel syndrome.
So it's not advocated to take
if you don't need it for some type of medical reason.
The posterior pituitary gland,
which is also under the control of the hypothalamus.
So just to reiterate,
the hypothalamus controls the activity of
both the anterior pituitary
and the posterior pituitary glands.
Posterior pituitary gland
releases oxytocin and antidiuretic hormone.
And so oxytocin will stimulate smooth muscle
during childbirth and milk production,
so in the pregnant woman.
And the antidiuretic hormone
reduces water loss from the body,
so it's antidiuretic,
to maintain our plasma volume.
It favors resorption of water
from the kidney tubules to blood capillaries.
This antidiuretic hormone is released
when stimulated.
And high plasma osmolarity
and low plasma volume will stimulate this.
So when we're sweating without water replacement,
our plasma is gonna become really concentrated,
and so the antidiuretic hormone
will then be stimulated to produce,
to kind of reduce our water loss.
This ADH increases obviously during exercise
at greater than 50% of our VO2,
which is more that moderate to vigorous exercise.
And this is to maintain our plasma volume.
And so you can see here,
here's our percent of VO2 max for exercising.
So the exercise intensity.
So low intensity down here,
kind of starting to be moderate,
and then when we're getting above 60,
we're getting into that vigorous level.
And you can see the ADH, the plasma levels of ADH,
are pretty much zero at this low-intensity.
And then as our intensity starts to increase,
the plasma ADH levels are gonna increase.
Our thyroid gland releases our thyroid hormones.
And the thyroid hormones are
the kind of key to establishing our overall metabolic rates.
The thyroid gland produces two hormones, T3 and T4,
or triiodothyronine and thyroxine.
And the thyroid-stimulating hormone
is what stimulates the thyroid gland
to produce these two hormones.
They have like what's called a latent period
between the time that T3 and T4 are elevated
and the time when their effects are observed.
So it's not an immediate response.
The latent period is like six to 12 hours for T3
and two to three days for T4.
So that's like if you're have a hypothyroid problem
and you're taking thyroid replacement,
you don't see an immediate effect
when you first start taking this medication.
There's evidence that during exercise
there's an increase in secretion of these T3 and T4
high thyroid hormones,
but it doesn't appear to have any change
in release of these hormones with resistance training.
The thyroid also releases calcitonin,
which is involved in a minor way
in the regulation of plasma calcium levels.
Calcium is a crucial ion
for normal muscle and nerve function.
As our plasma concentration of calcium increases,
calcitonin is released,
that's increased.
And this calcitonin will block
the release of calcium from the bone.
So if you have high levels of calcium
already in your bloodstream,
you don't wanna be taking it out from your bone.
And if you have high levels in your bloodstream,
you wanna excrete it.
So calcitonin will block
the release of calcium from the bone
and it will stimulate the excretion of calcium
from the kidneys
to lower the plasma concentration levels.
As the calcium concentration is brought back to normal,
the rate of calcitonin secretion is reduced.
So from the prior slide, we just talked about calcitonin
and the minor role it plays
in regulating calcium levels in the plasma.
And we talk specifically about high levels.
The parathyroid hormone, on the flip side,
is the primary hormone in regulating plasma calcium levels.
The parathyroid gland will release parathyroid hormone
in response to a low plasma calcium concentration.
So this hormone will stimulate bone
to release calcium into the plasma
and simultaneously increase the renal absorption of calcium.
So you're not excreting it.
So the parathyroid hormone will do everything it can
to boost the plasma levels of calcium,
kind of the total opposite of the calcitonin.
The parathyroid hormone also stimulates the kidney
to convert a form of vitamin D into a hormone
that increases the absorption of calcium from the GI tract.
And exercise will increase
the concentration of our parathyroid hormone in our plasma.
The adrenal medulla is part of our
sympathetic nervous system.
And 80% of this gland's production is epinephrine.
It also produces norepinephrine,
but 80% is epinephrine.
Again, part of the sympathetic nervous system.
These are really fast-acting hormones,
part of our fight-or-flight system.
They affect receptors in our cardiovascular
and respiratory systems,
in our stomach, our GI tract,
muscle, our fat adipose tissue.
They're involved in the maintenance of our blood pressure
and our plasma glucose concentration.
They bind to adrenergic receptors,
which are divided into two major categories.
So the alpha receptor and the beta receptor.
The effects of this hormone
depend on which is used and the receptor type,
and they can be both excitatory or inhibitory.
For example,
the alpha and the beta receptors have different effects.
So if epinephrine or norepinephrine
is attaching to a beta receptor,
heart rate's gonna increase,
pulse is gonna increase,
bronchodilation is gonna increase.
Conversely,
if the epinephrine or norepinephrine
is attaching to an alpha cell,
we're gonna have vasoconstriction.
So it's gonna kind of oppose the action
of the beta cells
where they're gonna be causing a vasodilation,
a bronchodilation.
And so here's the table
depicting what I was just talking about.
So here are our beta cells, our beta receptors,
and if we stop right here,
it's gonna have all of these effects
on the different tissues.
So increased heart rate,
lipolysis, bronchodilation, vasodilation.
And then the alpha receptors,
there's gonna be more a vasoconstriction,
an increase in the phosphodiesterase enzymatic activity.
And now let's talk a little bit about the adrenal cortex.
The adrenal cortex stimulates a variety of,
or the release of a variety of different steroid hormones
that can be categorized in three ways.
So there's the mineralocorticoids,
the glucocorticoids,
and the sex steroids.
And the mineralocorticoids are aldosterone,
which is gonna maintain
our plasma levels of sodium and potassium,
our glucocorticoids,
which is gonna regulate cortisol
and regulation of our plasma glucose,
and then our sex steroids,
which is estrogens, androgens,
support of, kind of starting up puberty.
So aldosterone is one of the mineralocorticoids.
And as we talked about on the prior slide,
it's going to work to ensure the sodium potassium balance.
So it will control sodium resorption and potassium secretion
to help regulate and maintain that homeostasis.
So aldosterone is directly involved
in maintaining plasma volume and blood pressure.
'Cause if our plasma volume drops,
our blood pressure is going to drop.
And there's two things
that will control the aldosterone secretion.
So aldosterone will be released from the adrenal cortex
if there's an increase in the potassium concentration.
So this increase in potassium concentration
will stimulate aldosterone secretion,
which is gonna stimulate the kidneys' transport mechanisms
to secrete those potassium ions.
Aldosterone secretion is also controlled
by changes in our plasma volume
or a fall in the blood pressure of our kidneys
or an increase in sympathetic nerve activity to the kidney.
So these changes will stimulate the kidney
to secrete enzymes.
And so these enzymes will enter the plasma
and convert into angiotensin I,
which is then converted into angiotensin II.
And these are powerful,
really, really powerful vasoconstrictors.
So if you have high blood pressure,
you don't want that vasoconstriction,
and these people might be prescribed ACE inhibitors.
And an ACE inhibitor is an angiotensin converting enzyme.
So that produces angiotensin II,
which is the vasoconstrictor.
So then you get prescribed this ACE inhibitor,
so it doesn't produce that enzyme,
which will effectively decrease the vasoconstriction.
So exercise will affect the changes in renin.
Renin is that enzyme in the kidney
that I talked about earlier.
And this renin is what will convert
to angiotensin I and angiotensin II.
And you can see again with moderate to vigorous exercise
the activity of aldosterone
and these subsequent hormones will increase.
And that's you're exercising,
you do not want kind of vasodilation,
you want vasoconstriction,
you want your blood to be pumped fast and efficiently
to your working muscles and organs.
Cortisol is a glucocorticoid
and it is secreted by the adrenal cortex as well.
And cortisol contributes
to the maintenance of our plasma glucose
during long-term fasting
and also during exercise through a variety of mechanisms.
So it's gonna promote protein breakdown for gluconeogenesis.
If we're exercising and we don't have enough glucose,
it will stimulate free fatty acid mobilization
from adipose tissue.
It stimulates glucose synthesis
and it blocks the uptake of glucose into the cells
to promote the use of free fatty acids as fuel.
And so cortisol, it's stimulated by exercise,
but is also stimulated by stress.
So cortisol will be stimulated by stress
via the activity of the adrenocorticotropic hormone,
which comes from the anterior pituitary gland,
which we talked about earlier.
And so this is,
it could be good stress
or it could be not good stress,
and it's part of
something called a general adaptation syndrome, or GAS.
And this is looking at the kind of pathologic,
physiologic effects of chronic stress.
So you can look here,
here's our immune system's adaptive response.
And so here's kind of baseline level.
And if something happens, some stressful activity,
your body's alarm system is gonna go off,
you may go in shock,
which is going to totally deplete your response,
but then it's gonna quickly revert
more towards a resistance phase.
But you can't maintain,
your body can't maintain this resistance phase forever.
So it might get to the point where you enter this fatigue,
exhaustion, kind of overuse phase.
We'll talk about this a little bit more
in one of our other lectures
when we're looking at exercise and fatigue
and kind of over-training.
So there's a perfect amount,
it's like Goldilocks, the just right amount.
Too little isn't enough to stimulate a change,
and too much, it has adverse effects on our body.
So our adipose tissue is also actually an endocrine organ,
and our adipose tissue produces a hormone called leptin.
And the primary function of the hormone leptin
is the regulation of our adipose tissue mass
through mediation of effects on the hypothalamus.
And so leptin will act on the hypothalamus,
which affects our perception of hunger, food use,
physical activity and exercise and energy balance.
So our appetite is influenced by our production of leptin.
Some people have a decreased sensitivity to leptin.
And so this can lead to obesity
where people don't feel full.
So in spite of high leptin levels,
they never feel full.
And so they'll keep eating
even in spite of the fact that they have high energy stores
and high levels of leptin.
So we talked about the pancreas earlier,
and the pancreas has exocrine and endocrine functions.
It does secrete insulin from the beta cells
and it works to promote the storage of glucose,
amino acids and fats.
If you're not producing insulin,
this leads to diabetes mellitus.
The pancreas also produces glucagon from the alpha cells.
Remember we talked about the alpha and beta cells earlier.
Actually, we talked about alpha and beta receptors earlier
for norepinephrine and epinephrine.
But glucagon is gonna promote
the mobilization of fatty acids and glucose.
It also produces somatostatin.
And this controls the rate of entry of nutrients
into our circulation.
And the pancreas also secretes digestive enzymes and bicarb
into the small intestine.
So it is effective in helping our acid-base balance.
Testosterone and estrogen and progesterone
are the primary sex steroids
that are secreted by our testes and our ovaries.
The testosterone is released from the testes.
It promotes tissue muscle building
and enhance performance during athletic events.
It also promotes the typical masculine characteristics
such as like a deep voice,
the high muscle mass to fat mass ratio in men
as compared to women,
where estrogen and progesterone,
progesterone are release from the ovaries
and work to maintain our reproductive function.
Testosterone is both an anabolic and androgenic steroid,
which causes size changes,
increases lean body mass, muscle mass and strength.
And so scientists have developed synthetic steroids
to promote tissue growth
in patients who experience atrophy
as a result of prolonged bedrest.
And so people think that they're effective
in helping the average person
increase their muscle mass.
For athletes,
the anabolic steroids do improve lean body mass
and muscle mass and strength,
particularly in combination with resistance training.
But there's lots of negative side effects
of taking these anabolic steroids.
So now we're gonna talk about muscle
and its effect on hormone production.
Skeletal muscle produces myokines when the muscle contracts.
And myokines are small proteins or proteoglycan peptides.
And these small proteins
are produced and released by the muscle cells
in response to muscle contraction.
And these myokines have endocrine type effects.
They can stimulate glucose uptake and fatty acid oxidation.
They can promote blood vessel growth within muscles,
so to increase the circulation and capillary density.
They can promote liver glucose production,
so gluconeogenesis,
and triglyceride breakdown,
so breaking down the free fatty acids.
Interleukin 6 or IL-6 is an anti-inflammatory myokine,
so skeletal muscle produces myokines,
and this is a specific type of myokine.
And it will help give an anti-inflammatory effect
while suppressing other pro-inflammatory hormones.
So preventing inflammation.
The important thing to know
is that regular exercise
will promote this anti-inflammatory environment,
which is great to remember
and talk about with our clients and our patients
that exercise can have a aid
and promote reduction in chronic inflammation
and reduce risk of heart disease,
type two diabetes, and certain types of cancers.
So looking at our muscle glycogen utilization,
glycogenolysis or the process of glycogen breakdown
is related to our exercise intensity.
And high-intensity exercise
will result in greater and more rapid glycogen depletion.
That makes sense.
Plasma epinephrine, our hormone,
is a powerful stimulator of this glycogenolysis.
And so high-intensity exercise results in greater increases
in our plasma epinephrine levels.
So you can see here on this y-axis
the epinephrine levels in nanomoles up to zero to nine,
and then the time for exercise
and the percent of our VO2 max.
Our blood glucose balance during exercise
is maintained through different processes.
So we do need that constant turnover
or that we need supplies of glucose
to maintain our exercise and activity levels.
And we have enough stored for about two hours of activity.
Our plasma glucose is maintained
through four different processes.
So mobilization of glucose from liver glycogen stores,
mobilization of free fatty acid from adipose tissue,
which will spare the blood glucose
and maintain the blood glucose levels,
gluconeogenesis from amino acids, lactic acid and glycerol,
which occurs in the liver,
blocking the entry of glucose into the cells,
which will force the use of free fatty acid as a fuel.
So all ways to control and maintain a plasma glucose level,
which is controlled by hormones.
So the slow-acting hormones are gonna be our thyroxine,
which is a thyroid hormone,
cortisol, and growth hormone.
And remember our fast-acting hormones
are the epinephrine, norepinephrine, insulin, and glucagon.
So the thyroid hormones will allow other hormones
to exert the full effect.
Our T3 will enhance the effect of epinephrine
to mobilize free fatty acids from adipose tissue.
And there isn't a real significant change during exercise.
Cortisol, which is a slow-acting hormone,
will stimulate free fatty acid mobilization
from our adipose tissue.
It will enhance the production of glucose in the liver
or gluconeogenesis.
It will decrease the rate of glucose
being used by the cells.
And exercise will,
exercise will affect cortisol levels in different ways.
So during high-intensity exercise,
there's gonna be a linear increase with cortisol levels.
So when we're at moderate to vigorous levels,
the cortisol level is gonna increase.
When we're doing low-intensity exercise,
the cortisol level is actually gonna decrease.
This is because of the fact that
during light exercise,
cortisol is removed faster
than the adrenal cortex can secrete it.
And during intense exercise,
the increase in plasma cortisol
was due to a high rate of secretion
that more than doubled the rate of removal.
So that's why there's a linear increase.
Growth hormone during exercise.
Recall that growth hormone plays a major role
in the synthesis of protein tissues,
acting through kind of enhanced secretion of
insulin growth hormone factors from the liver.
But growth hormone can also influence
our fat and carbohydrate metabolism.
The growth hormone will also support the action of cortisol
and it will decrease the glucose uptake by the tissues.
It will increase free fatty acid mobilization.
It will enhance gluconeogenesis in the liver.
So again, other ways to produce fuel.
So the exercise effect of growth hormone.
Exercise will cause an increase in plasma growth hormone
with increased exercise intensities.
This is just a schematic showing that.
So plasma growth hormone,
again, as the intensity of exercise increases,
the plasma levels of growth hormone will also increase.
Looking at the difference
between control groups and runners,
runners will see a significant increase
in plasma growth hormone
as compared to other people.
Epinephrine and norepinephrine,
we talked earlier, they're fast-acting hormones.
They will help us maintain our blood glucose levels
during exercise.
They will facilitate muscle glycogen mobilization,
increase liver glucose mobilization,
increase free fatty acid mobilization,
and interfere with glucose uptake.
So the net effect
is to ensure our blood plasma glucose levels
remain stable.
Our plasma epinephrine and norepinephrine
increase during our exercise,
and this is, we talked about this earlier,
which helps us to keep exercising,
increasing our heart rate, increasing our blood pressure
through the vasoconstriction action.
And we need less of this with training.
So the more we train,
the less our body is gonna need
to produce the levels of epinephrine and norepinephrine.
It'll take less of it to create...
This can happen as quickly as
within three weeks of training.
So here's plasma catecholamines response
to exercise following training.
And here's our norepinephrine and our epinephrine.
And here's our three-week mark.
Initially when we first start off,
when we exercise,
we're producing higher levels
of both norepinephrine and epinephrine.
But as we train,
we don't need to produce as much to get our body to respond.
So looking at insulin and glucagon,
they have opposite effects,
they're both fast-acting hormones.
And recall that insulin
works to address the blood glucose
or the plasma glucose level.
So if there's too much glucose in the blood,
insulin will be released
to promote absorption of the glucose into the cell.
So during exercise and activity,
you don't want that to happen.
So you want the muscles to be able to use
that free floating glucose.
You don't want it to be taken up by the tissues.
So during exercise,
the plasma concentration of insulin will decrease
during exercise.
And there's decreased insulin response with training.
Conversely,
with glucagon,
the plasma concentration
is going to increase during exercise.
And also there's a decreased response following trainings.
So this insulin and glucagon secretion
are influenced by our catecholamines.
So here's the drop in the insulin,
and you can see the difference between an untrained person
and a trained person.
So over time,
with exercise,
the production of insulin is going to decrease,
where conversely,
glucagon is going to increase during exercise.
And so this is showing the effect of the catecholamines,
the epinephrine and norepinephrine
on insulin and glucagon secretion.
So epinephrine, norepinephrine
will decrease the production of insulin,
whereas the epinephrine and norepinephrine
will increase the production of glucagon.
Effect of the sympathetic nervous system
on substrate mobilization.
So during submaximal exercise,
again just another schematic showing,
when the sympathetic nervous system is activated,
epinephrine and norepinephrine are going to be released,
the production of insulin will drop,
because we don't want the blood glucose levels to drop.
The glucagon levels will increase.
The adipose cells will be stimulated
to release free fatty acids.
And so the plasma levels of free fatty acid will increase.
The liver is going to be producing glycogen, glucose,
and the blood levels of glucose will be maintained.
So looking at the hormonal response to exercise,
notice that with increasing intensities of exercise,
these hormones, epinephrine, norepinephrine,
growth hormone, cortisol, glucagon,
their levels will increase.
The production and synthesis of those hormones
will increase.
And you can see the plasma concentration of those hormones
is increased with increasing intensities.
So this is blood or plasma concentration
taken in response to graded exercise.
And then this is a plasma hormone concentration
with prolonged exercise.
So here's now time.
So you see the same type of response
that as our time increases,
you're gonna see an increase
in the plasma concentrations of these hormones.
That is it. The end.
So go back to the first slide or the objective slide,
and see if you have any questions.
Again, look in chapter five at the Powers book
and let me know if you have any questions.
Talk to you soon.