KINES 3091- Endo. Control of Metab.- Lecture #3

00:49:08
https://www.youtube.com/watch?v=wJeMYzkA0c4

الملخص

TLDRCette conférence traite de l'impact des hormones sur le métabolisme pendant l'exercice, en mettant l'accent sur les catécholamines, qui favorisent la mobilisation des combustibles comme le glycogène et les graisses. Les catécholamines augmentent la circulation sanguine vers les muscles et stimulent des enzymes comme la lipoprotéine lipase pour faciliter l'absorption des graisses. En parallèle, d'autres hormones comme le glucagon et le cortisol sont également libérées pour soutenir la production de glucose et la mobilisation des graisses. L'insuline, quant à elle, diminue pendant l'exercice pour éviter le stockage des nutriments. La conférence conclut sur l'idée que l'exercice régulier atténue la réponse hormonale au stress, rendant l'exercice moins exigeant pour le corps.

الوجبات الجاهزة

  • 💪 Les catécholamines augmentent la mobilisation des combustibles.
  • 🏃‍♂️ L'exercice stimule la libération de glucose par le foie.
  • 📉 L'insuline diminue pendant l'exercice pour favoriser la mobilisation.
  • 🔄 Le glucagon et le cortisol soutiennent la production de glucose.
  • ⚖️ L'exercice chronique réduit la réponse hormonale au stress.

الجدول الزمني

  • 00:00:00 - 00:05:00

    Cette troisième conférence aborde le contrôle endocrinien et le métabolisme pendant l'exercice, en se concentrant sur le rôle des catécholamines dans la mobilisation des combustibles. L'augmentation de la noradrénaline et de l'épinéphrine favorise la mobilisation du glycogène musculaire et hépatique, ainsi que des acides gras à partir des triglycérides intramusculaires et des tissus adipeux.

  • 00:05:00 - 00:10:00

    Après la mobilisation des graisses, l'enzyme lipoprotéine lipase (LPL) est activée dans les cellules musculaires pour permettre l'absorption des acides gras circulants. L'augmentation de la noradrénaline et de l'épinéphrine stimule l'activité de la LPL musculaire, facilitant ainsi l'accès aux graisses pour la production d'ATP.

  • 00:10:00 - 00:15:00

    La contraction musculaire peut également affecter les niveaux de glucose sanguin. Le foie joue un rôle crucial dans le maintien de la glycémie, en produisant du glucose par gluconéogenèse, surtout lorsque l'intensité de l'exercice augmente. Les catécholamines stimulent cette gluconéogenèse en favorisant l'absorption de sous-produits métaboliques par le foie.

  • 00:15:00 - 00:20:00

    Les catécholamines influencent également d'autres hormones régulatrices comme le glucagon, le cortisol et l'hormone de croissance, qui augmentent pendant l'exercice pour soutenir la mobilisation des combustibles. Le glucagon stimule la glycogénolyse et la lipolyse, tandis que le cortisol favorise la gluconéogenèse et la lipolyse.

  • 00:20:00 - 00:25:00

    L'insuline, en revanche, diminue pendant l'exercice, car elle est une hormone de stockage. La suppression de l'insuline favorise la mobilisation des combustibles, permettant aux muscles squelettiques d'accéder au glucose nécessaire à la production d'ATP.

  • 00:25:00 - 00:30:00

    L'activation de la phosphorylase dans les muscles squelettiques est également stimulée par l'augmentation du calcium intracellulaire pendant la contraction, ce qui favorise la dégradation du glycogène pour l'ATP. De plus, le calcium stimule la translocation des transporteurs GLUT4, facilitant l'absorption du glucose par les muscles en contraction.

  • 00:30:00 - 00:35:00

    Les réponses hormonales à l'exercice varient en fonction de l'intensité et de la durée. À mesure que l'intensité de l'exercice augmente, les hormones contre-régulatrices comme l'épinéphrine, la noradrénaline, le glucagon et le cortisol augmentent, tandis que l'insuline diminue.

  • 00:35:00 - 00:49:08

    L'entraînement chronique modifie la réponse hormonale à l'exercice, réduisant l'augmentation de l'activité du système nerveux sympathique et des niveaux de catécholamines. Cela signifie que l'exercice devient moins stressant pour le corps, entraînant une réponse hormonale plus atténuée et une meilleure gestion des niveaux de glucose sanguin.

اعرض المزيد

الخريطة الذهنية

فيديو أسئلة وأجوبة

  • Quel est le rôle des catécholamines pendant l'exercice ?

    Les catécholamines augmentent la mobilisation du glycogène et des triglycérides, facilitant l'accès aux combustibles par les muscles.

  • Comment l'insuline affecte-t-elle le métabolisme pendant l'exercice ?

    L'insuline diminue pendant l'exercice, ce qui favorise la mobilisation des combustibles plutôt que leur stockage.

  • Quelles hormones sont considérées comme contre-régulatrices ?

    Les hormones contre-régulatrices incluent le glucagon, le cortisol et l'hormone de croissance.

  • Comment le corps maintient-il les niveaux de glucose sanguin pendant l'exercice ?

    Le foie stimule la gluconéogenèse pour maintenir des niveaux de glucose sanguin adéquats.

  • Quel est l'effet de l'exercice chronique sur la réponse hormonale ?

    L'exercice chronique réduit la réponse du système nerveux sympathique, rendant l'exercice moins stressant.

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التمرير التلقائي:
  • 00:00:00
    alright guys let's finish this lecture
  • 00:00:04
    up this is the third lecture from this
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    endocrine control and metabolism during
  • 00:00:12
    exercise material and we're gonna pick
  • 00:00:16
    up where we left off so last time we
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    left off with discussing the ways in
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    which the catecholamines contribute to
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    fuel mobilization and real broadly we
  • 00:00:28
    said that they promote it so increase in
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    norepinephrine and epinephrine
  • 00:00:37
    is going to increase the mobilization of
  • 00:00:42
    both glycogen from muscle glycogen as
  • 00:00:49
    well as from liver glycogen and increase
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    triglyceride mobilization or fatty acid
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    mobilization from intramuscular
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    triglyceride and adipose tissue
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    triglyceride so increased mobilization
  • 00:01:12
    of both of these fuels and so go back
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    and take a look at those slides we
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    talked about how the catecholamines
  • 00:01:22
    facilitate the activation of the enzymes
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    that start glycogenolysis as well as
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    lipolysis via camp second messenger
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    pathways in both cases okay so we've got
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    a pretty big lecture today or now we're
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    gonna continue on with looking at the
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    influence of the catecholamines on these
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    two factors delivery and fuel uptake and
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    mainly fuel uptake because most of the
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    the delivery influence of the
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    catecholamines is via cardiovascular
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    adaptations to either increase or
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    decrease blood flow so in the case of
  • 00:02:10
    fuel mobilization the fields been
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    released into the blood stream
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    and the influence on fuel delivery is
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    going to happen by either increasing
  • 00:02:18
    blood flow with that fuel to the
  • 00:02:20
    skeletal muscle or cut down on blood
  • 00:02:23
    flow and therefore reduce the
  • 00:02:26
    availability of that mobilize fuel to
  • 00:02:29
    the skeletal muscle which we clearly
  • 00:02:31
    don't want to do during exercise and so
  • 00:02:34
    the main emphasis will first be this
  • 00:02:37
    fuel uptake process and then I'm going
  • 00:02:42
    to talk about the other counter
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    regulatory hormones and how they
  • 00:02:48
    influence fuel use during exercise and
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    how that's coordinated by these
  • 00:02:52
    catecholamines and then we'll talk about
  • 00:02:55
    insulin and then we'll leave off with
  • 00:02:58
    some just recapping of the acute as well
  • 00:03:02
    as a brief review of the training
  • 00:03:04
    related changes that acute or occur with
  • 00:03:07
    exercies okay so we've said that and
  • 00:03:13
    again how do we how do the
  • 00:03:15
    catecholamines adjust delivery by either
  • 00:03:19
    stimulating vaso dilation via beta 2
  • 00:03:29
    receptors in the vascular endothelium or
  • 00:03:35
    vasodilation oops not visit dilation
  • 00:03:41
    that's what I just said physio
  • 00:03:44
    constriction via alpha 1 receptors right
  • 00:03:55
    ok so let's jump in and start talking
  • 00:04:00
    about this issue of uptake so we've
  • 00:04:05
    mobilized it we've delivered it through
  • 00:04:07
    phase of dilation and now let's talk
  • 00:04:10
    about uptake so if we start with looking
  • 00:04:14
    at how the skeletal muscle accesses fats
  • 00:04:19
    then we start with a increase in blood
  • 00:04:24
    flow to
  • 00:04:26
    from the fat tissue right so if we're
  • 00:04:30
    mobilizing fat out of storage in the
  • 00:04:33
    adipose tissue then it doesn't make
  • 00:04:36
    sense for us to simultaneously constrict
  • 00:04:39
    the vessels in that tissue because then
  • 00:04:41
    we mobilize it but it doesn't go
  • 00:04:43
    anywhere ray it's been released into the
  • 00:04:45
    bloodstream but if the arterioles RV's
  • 00:04:47
    are constricted then we're not sending
  • 00:04:50
    blood there so we can mobilize or get
  • 00:04:53
    that that fuel that's mobilized out of
  • 00:04:56
    that tissue and into the skeletal muscle
  • 00:05:00
    okay so we have mobilized fat or the
  • 00:05:05
    triglyceride Auto storage out of the fat
  • 00:05:08
    has been released into circulation now
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    it cannot be taken up by the skeletal
  • 00:05:15
    muscle cell automatically and instead
  • 00:05:19
    what has to happen is another enzyme
  • 00:05:21
    needs to be stimulated and that enzyme
  • 00:05:24
    is called lipoprotein lipase or LPL so
  • 00:05:29
    remember that it was HSL inside the fat
  • 00:05:33
    cell or inside the intramuscular or
  • 00:05:36
    inside the muscle cell that helped to
  • 00:05:39
    mobilize the fat out of storage but if
  • 00:05:43
    it's released into the bloodstream from
  • 00:05:45
    the adipose tissue and circulates to the
  • 00:05:47
    skeletal muscle then the skeletal muscle
  • 00:05:51
    has to access it via the stimulation of
  • 00:05:53
    this other enzyme this other enzyme that
  • 00:05:56
    that breaks down lipids so it's another
  • 00:05:59
    lipase it's called lipoprotein lipase
  • 00:06:02
    and we put the M in front of it to
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    represent that this is LPL on the muscle
  • 00:06:08
    cell so if we have an increase in
  • 00:06:13
    norepinephrine and epinephrine one of
  • 00:06:22
    the things that's going to happen is
  • 00:06:23
    we're going to increase the activity of
  • 00:06:26
    muscle LPL and so that enables the
  • 00:06:30
    skeletal muscle to access any fats that
  • 00:06:33
    are floatin by in circulation this is
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    also stimulated via
  • 00:06:40
    a camp second messenger pathway and it's
  • 00:06:44
    gonna make the fat that was released by
  • 00:06:46
    the adipose tissue available to the
  • 00:06:49
    skeletal muscle cell for use for making
  • 00:06:52
    ATP right so here's our LPL enzyme and
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    here it is here and and so it kind of
  • 00:07:08
    sticks out into circulation and it grabs
  • 00:07:12
    on to these triglycerides and it breaks
  • 00:07:15
    the fatty acids and glycerol apart just
  • 00:07:17
    like hormone sensitive lipase does but
  • 00:07:20
    in this case it has or it does that
  • 00:07:24
    lipolysis for the purpose of uptake not
  • 00:07:29
    mobilization so LPL uptake that's HSL
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    mobilization fats now we have adipose
  • 00:07:56
    tissue
  • 00:07:57
    LPL as well but if adipose tissue LPL is
  • 00:08:03
    active then the fat that is in
  • 00:08:08
    circulation is going to be taken up and
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    stored so during exercise we don't want
  • 00:08:21
    to store the fats we want to keep them
  • 00:08:24
    available for the skeletal muscle tissue
  • 00:08:27
    so when norepinephrine and epinephrine
  • 00:08:31
    levels rise because exercise has begun
  • 00:08:35
    or exercise intensity is going up we're
  • 00:08:39
    going to stimulate muscle LPL but we
  • 00:08:43
    simultaneously want to inhibit or shut
  • 00:08:46
    down adipose tissue LPL and the reason
  • 00:08:50
    for that is again muscle LPL is
  • 00:08:53
    going to facilitate uptake skeletal
  • 00:08:57
    muscle uptake rate and that's going to
  • 00:09:01
    be a good thing because that's going to
  • 00:09:03
    lead to ATP synthesis for the
  • 00:09:05
    contracting skeletal muscle but in the
  • 00:09:08
    case of adipose tissue LPL that's going
  • 00:09:12
    to increase fat or adipose tissue uptake
  • 00:09:15
    and that is not going to help skeletal
  • 00:09:21
    muscle tissue make ATP instead that's
  • 00:09:23
    going to increase storage and when to
  • 00:09:29
    emphasize now exercise is not a time for
  • 00:09:41
    storage okay so because we know that
  • 00:09:54
    norepinephrine and epinephrine increase
  • 00:09:56
    during exercise their primary effect is
  • 00:09:58
    going to be on mobilizing and making
  • 00:10:00
    fuel available to skeletal muscle it is
  • 00:10:03
    simultaneously going to inhibit or
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    reduce the ability of fuel to be stored
  • 00:10:08
    in places like the liver or the adipose
  • 00:10:13
    tissue wants to get as much fuel
  • 00:10:15
    available to the contracting muscle as
  • 00:10:17
    it needs okay so I had mentioned that
  • 00:10:27
    during exercise the skeletal muscle
  • 00:10:33
    needs to access or facilitate the ATP
  • 00:10:39
    demand by mobilizing and circulating and
  • 00:10:45
    and taking up fuel but it needs to do
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    that while maintaining blood glucose
  • 00:10:52
    right and so the endocrine system is
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    trying to do meet those two demands
  • 00:11:00
    simultaneously or do those two jobs
  • 00:11:02
    simultaneously
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    so contracting skeletal muscle can work
  • 00:11:08
    to deplete blood glucose because
  • 00:11:10
    contracting skeletal muscle can access
  • 00:11:14
    glucose in the blood
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    so when skeletal muscle contracts it
  • 00:11:20
    pulls glucose out of the blood into the
  • 00:11:32
    skeletal muscle so and it uses it for
  • 00:11:37
    ATP right vehicle a colossus and so
  • 00:11:46
    contracting skeletal muscle can
  • 00:11:48
    essentially represent a threat to the
  • 00:11:51
    fairly tightly managed or regulated
  • 00:11:54
    blood glucose levels and so that is the
  • 00:11:57
    primary purpose of hepatic glucose
  • 00:12:01
    production so the livers job is or one
  • 00:12:05
    of the livers jobs is to maintain
  • 00:12:07
    acceptable blood glucose levels now it
  • 00:12:11
    needs to get glucose out of the blood if
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    it gets too high and it needs to put
  • 00:12:19
    glucose back into the blood if it gets
  • 00:12:21
    too low and I'm saying that skeletal
  • 00:12:23
    muscle can pull glucose out of the blood
  • 00:12:25
    and so during exercise the the one of
  • 00:12:29
    the tasks on the liver is to make sure
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    that blood glucose levels don't get too
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    low and so we have a pretty fairly
  • 00:12:37
    strong or significant stimulation of
  • 00:12:41
    gluconeogenesis during exercise and that
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    stimulation gets stronger as exercise
  • 00:12:48
    intensity and especially as exercise
  • 00:12:50
    duration goes up so gluconeogenesis is a
  • 00:12:54
    pretty strong or significant effect from
  • 00:13:00
    increasing exercise and one of the main
  • 00:13:05
    influences to stimulate gluconeogenesis
  • 00:13:09
    is through the influence of
  • 00:13:11
    catecholamines on the liver via this
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    cyclic A&P second messenger path
  • 00:13:16
    and the main effect of the
  • 00:13:20
    catecholamines is going to be this
  • 00:13:24
    uptake of these byproducts of metabolism
  • 00:13:29
    for example lactate or the glycerol from
  • 00:13:32
    the triglycerides pyruvate from slow
  • 00:13:34
    glycolysis lactate from fast glycolysis
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    even amino acids if you're breaking down
  • 00:13:39
    proteins can be taken up by the liver
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    and used to synthesize new glucose that
  • 00:13:46
    new glucose then is released into
  • 00:13:48
    circulation bringing blood glucose
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    levels back up to acceptable limits or
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    ranges okay now I had mentioned that one
  • 00:14:04
    of the ways in which the catecholamines
  • 00:14:06
    influence fuel metabolism during
  • 00:14:09
    exercise is indirectly through their
  • 00:14:12
    influence on these other counter
  • 00:14:14
    regulatory hormones and so those other
  • 00:14:17
    counter regulatory hormones include the
  • 00:14:20
    hormone glucagon cortisol and growth
  • 00:14:24
    hormone and so you can see that when
  • 00:14:27
    catecholamine levels rise again increase
  • 00:14:30
    in norepinephrine and epinephrine
  • 00:14:33
    they're going to cause all those changes
  • 00:14:35
    that we've talked about already directly
  • 00:14:39
    but they will simultaneously influence
  • 00:14:42
    the endocrine organs that increase the
  • 00:14:44
    production of glucagon increase the
  • 00:14:46
    production of cortisol and increase in
  • 00:14:48
    production of growth hormone so
  • 00:14:50
    norepinephrine and epinephrine will
  • 00:14:52
    stimulate the pancreatic alpha cells to
  • 00:14:57
    produce and release glucagon so as
  • 00:15:01
    exercise intensity goes up we're gonna
  • 00:15:04
    see a stronger and stronger increase in
  • 00:15:07
    sympathetic nervous system activity
  • 00:15:08
    which is going to result in more and
  • 00:15:11
    more norepinephrine epinephrine being
  • 00:15:13
    released from the adrenal medulla into
  • 00:15:15
    circulation among other places that
  • 00:15:19
    norepinephrine and epinephrine is going
  • 00:15:21
    to bind to receptors on the pancreas and
  • 00:15:23
    stimulate those pancreatic alpha cells
  • 00:15:26
    to release glucagon
  • 00:15:27
    now as glucagon
  • 00:15:30
    levels go up in the bloodstream they are
  • 00:15:33
    going to promote glycogenolysis and
  • 00:15:36
    lipolysis in the exact same way that we
  • 00:15:41
    saw the catecholamines promote
  • 00:15:43
    glycogenolysis and lipolysis and i'll
  • 00:15:47
    remind you of what those are here in an
  • 00:15:50
    upcoming slide so glucagon promotes
  • 00:15:54
    mobilization of glucose and lipid out of
  • 00:15:58
    storage
  • 00:15:59
    just like norepinephrine and epinephrine
  • 00:16:01
    do the norepinephrine and epinephrine is
  • 00:16:05
    also going to bind to receptors on the
  • 00:16:10
    adrenal cortex so this is the outer
  • 00:16:13
    portion of the adrenal gland and it's
  • 00:16:17
    going to stimulate the adrenal cortex to
  • 00:16:20
    produce and release cortisol into
  • 00:16:23
    circulation
  • 00:16:24
    now as cortisol levels go up the primary
  • 00:16:28
    effect is to promote gluconeogenesis and
  • 00:16:34
    lipolysis okay so gluconeogenesis is
  • 00:16:38
    going to restore blood glucose levels
  • 00:16:44
    and the promotion of lipolysis is going
  • 00:16:52
    to increase availability of fats in lieu
  • 00:16:56
    of glucose so if there's a greater
  • 00:17:01
    availability of fats then the skeletal
  • 00:17:08
    muscle might be able to use the fat
  • 00:17:10
    instead of using the glucose and if it's
  • 00:17:13
    not using the glucose then it's not
  • 00:17:16
    threatening blood glucose levels as much
  • 00:17:19
    and so the overall focus or primary
  • 00:17:22
    purpose of cortisol is really to
  • 00:17:26
    maintain or manage blood glucose levels
  • 00:17:29
    and it does that in these two ways to
  • 00:17:31
    promote gluconeogenesis production of
  • 00:17:33
    glucose by the liver as well as the use
  • 00:17:37
    of fats rather than glucose by the
  • 00:17:39
    skeletal muscle by making more fat
  • 00:17:41
    available through lipolysis
  • 00:17:43
    now we have a similar goal or influenced
  • 00:17:48
    by the hormone growth hormone and growth
  • 00:17:53
    hormone is going to increase in response
  • 00:17:55
    to the catecholamines binding to
  • 00:17:57
    receptors on the pituitary gland and as
  • 00:18:01
    growth hormone levels increase they're
  • 00:18:05
    also going to help promote the use of
  • 00:18:09
    fats over glow glucose and in doing so
  • 00:18:13
    help preserve or restore blood glucose
  • 00:18:17
    levels so that that variable is is where
  • 00:18:22
    it should be and is not you're not
  • 00:18:25
    struggling with hypoglycemia so cortisol
  • 00:18:30
    helps preserve blood glucose through
  • 00:18:32
    both gluconeogenesis and lipolysis
  • 00:18:35
    growth hormone helps preserve leg
  • 00:18:38
    glucose by promoting lipolysis and then
  • 00:18:41
    glucagon is gonna mobilize fuel in
  • 00:18:44
    general just increase the mobilization
  • 00:18:48
    of glucose out glycogen in the
  • 00:18:50
    mobilization of fatty acids out of
  • 00:18:53
    adipose tissue now there is another
  • 00:18:58
    major effect of the catecholamines on
  • 00:19:01
    the regulatory hormone insulin and so
  • 00:19:06
    we've seen that the counter regulatory
  • 00:19:09
    hormones they're all going to go up so
  • 00:19:11
    norepinephrine epi go up and in turn
  • 00:19:14
    glucagon cortisol and growth hormone
  • 00:19:16
    levels are going to increase also but
  • 00:19:20
    insulin is going to decrease we want to
  • 00:19:24
    suppress insulin levels and so the
  • 00:19:30
    amount of insulin in the blood is
  • 00:19:32
    actually going to decrease as exercise
  • 00:19:35
    intensity goes up now if you remember
  • 00:19:38
    insulin is a horrid hormone
  • 00:19:55
    and when did I say on the last slide
  • 00:19:57
    exercise is not a time for storage and
  • 00:20:02
    so it should make some intuitive sense
  • 00:20:04
    that if we don't want to store we want
  • 00:20:06
    to mobilize fuel then we should suppress
  • 00:20:09
    or inhibit a hormone that stops
  • 00:20:13
    mobilization and promote storage and
  • 00:20:15
    that's exactly what happens when
  • 00:20:18
    norepinephrine and epinephrine stimulate
  • 00:20:20
    the pancreatic beta-cells
  • 00:20:23
    to stop secreting insulin and so over
  • 00:20:28
    time insulin levels are going to
  • 00:20:31
    decrease and so that helps promote
  • 00:20:35
    mobilization over storage and it also
  • 00:20:41
    preserves glucose for uptake by the
  • 00:20:46
    skeletal muscle rather than other
  • 00:20:49
    tissues that aren't really essential
  • 00:20:52
    during exercise so remember that at rest
  • 00:20:56
    or if we're talking about other tissues
  • 00:20:59
    other than skeletal muscle that those
  • 00:21:03
    many of those tissues need insulin in
  • 00:21:07
    order to get to the glucose that's in
  • 00:21:10
    circulation so resting skeletal muscle
  • 00:21:13
    is the same at rest if we want to get
  • 00:21:17
    glucose out of the blood because it's
  • 00:21:19
    too high we like to send it into
  • 00:21:22
    skeletal muscle tissue and for us to be
  • 00:21:24
    able to do that at rest we need insulin
  • 00:21:27
    levels to climb insulin will bind to its
  • 00:21:30
    membrane receptor on the skeletal muscle
  • 00:21:32
    cell and stimulate the glute for glucose
  • 00:21:36
    transport mechanism which will move to
  • 00:21:39
    the surface of the skeletal muscle cell
  • 00:21:41
    and essentially facilitate the diffusion
  • 00:21:45
    of glucose from the bloodstream into the
  • 00:21:48
    interior of the skeletal muscle cell
  • 00:21:50
    however we don't want that happening in
  • 00:21:56
    non-essential or essentially non
  • 00:21:58
    skeletal muscle cell tissues the reason
  • 00:22:01
    for that is again because skeletal
  • 00:22:03
    muscle is contracting it has a very high
  • 00:22:05
    ATP demand so as much as possible we
  • 00:22:08
    want to
  • 00:22:08
    serve glucose for the skeletal muscle
  • 00:22:12
    tissue because it has such a high demand
  • 00:22:16
    for ATP synthesis so if it's not staying
  • 00:22:19
    in the blood to maintain blood glucose
  • 00:22:22
    levels we would like to see it going
  • 00:22:25
    into the skeletal muscle cells for ATP
  • 00:22:30
    synthesis and so suppressing insulin is
  • 00:22:34
    going to help prevent those
  • 00:22:36
    non-essential tissues from taking up any
  • 00:22:39
    of the glucose that's in the blood and
  • 00:22:43
    therefore preserving it either to
  • 00:22:45
    maintain blood glucose levels or to help
  • 00:22:48
    meet that demands for ATP synthesis and
  • 00:22:51
    the working skill muscle and I'll talk a
  • 00:22:55
    little bit more about how that happens
  • 00:22:57
    in another slide coming up but I just
  • 00:23:00
    want to remind you I said early on in
  • 00:23:02
    that last slide that glucagon
  • 00:23:05
    essentially promotes mobilization just
  • 00:23:08
    like epinephrine and norepinephrine do
  • 00:23:10
    so if you remember these figures we
  • 00:23:13
    talked about these when we looked at how
  • 00:23:15
    epinephrine stimulates glycogenolysis
  • 00:23:21
    all right so this one is glycogenolysis
  • 00:23:24
    and this was adipose tissue lipolysis
  • 00:23:31
    and the enzyme for glycogenolysis is
  • 00:23:38
    that phosphorylase a and the enzyme for
  • 00:23:42
    lipolysis is that hormone sensitive
  • 00:23:44
    lipase and if you back up and you see at
  • 00:23:47
    the top of both of these figures
  • 00:23:49
    glucagon does the exact same thing that
  • 00:23:53
    happened nephron did except it it does
  • 00:23:57
    it in the skeletal muscle or excuse me
  • 00:23:59
    it does it in the liver tissue
  • 00:24:02
    specifically glucagon can bind with
  • 00:24:06
    receptors on adipose tissue just like
  • 00:24:09
    epinephrine can and promote lipolysis
  • 00:24:11
    just like epinephrine so same camp
  • 00:24:15
    mediated second messenger pathways
  • 00:24:19
    and that's why we say that glucagon and
  • 00:24:23
    the catecholamines are essentially
  • 00:24:24
    redundant because they're both strong
  • 00:24:28
    promoters of fuel mobilization out of
  • 00:24:32
    storage there we go
  • 00:24:38
    and I've also said already repeatedly
  • 00:24:42
    that insulin is a storage hormone and we
  • 00:24:44
    don't want to store during exercise so
  • 00:24:47
    what I'd like you to do is zoom in on
  • 00:24:49
    this figure and look and see how insulin
  • 00:24:53
    is functioning so if you remember this
  • 00:24:56
    was fat tissue lipolysis so fat
  • 00:25:01
    so like pollicis and we were exploring
  • 00:25:11
    with this figure how both glucagon and
  • 00:25:14
    epinephrine can cause this increase in
  • 00:25:19
    cyclic ANP which will stimulate hormone
  • 00:25:23
    sensitive lipase which will mobilize
  • 00:25:26
    glycerol and fatty acid out of storage
  • 00:25:29
    and release them into those into
  • 00:25:31
    circulation if you look at how insulin
  • 00:25:35
    affects lipolysis we can see that when
  • 00:25:41
    insulin binds to its receptor same cell
  • 00:25:45
    still the fat cell except in this case
  • 00:25:48
    we're looking at what happens with
  • 00:25:50
    insulin binding to the insulin receptor
  • 00:25:53
    insulin is going to work through oh look
  • 00:25:56
    you should recognize this second
  • 00:25:59
    messenger pathway
  • 00:26:01
    we've got insulin binding to its
  • 00:26:02
    receptor it's gonna stimulate this
  • 00:26:06
    phospho tool inositol to be broken down
  • 00:26:10
    into ip3 and dag the ip3
  • 00:26:14
    in turn will activate or eventually
  • 00:26:18
    stimulate the activation of this enzyme
  • 00:26:22
    phosphodiesterase what does
  • 00:26:24
    phosphodiesterase do it shuts down camp
  • 00:26:28
    if camp levels aren't coming up HSL
  • 00:26:31
    isn't coming
  • 00:26:32
    if HSL isn't active we're not mobilizing
  • 00:26:36
    and we're keeping fuel in storage so
  • 00:26:41
    again insulin is a storage hormone it
  • 00:26:44
    works against the hormones that mobilize
  • 00:26:48
    fuel out of storage
  • 00:26:50
    so if exercise is not a time for storage
  • 00:26:55
    not only do we want to promote
  • 00:26:59
    mobilization through the effects of
  • 00:27:04
    glucagon and epinephrine
  • 00:27:07
    we also simultaneously want to shut down
  • 00:27:12
    any insulin inhibition of those
  • 00:27:16
    mobilization efforts and so we're gonna
  • 00:27:22
    reduce the insulin influence we're going
  • 00:27:26
    to prevent the secretion of insulin by
  • 00:27:31
    the pancreas and that will stop it from
  • 00:27:35
    inhibiting the mobilization efforts of
  • 00:27:38
    the counter regulatory hormones whoops
  • 00:27:48
    we see a similar effect of insulin on
  • 00:27:52
    glycogenolysis so I'd say this is
  • 00:28:11
    right and we we said hey look
  • 00:28:14
    epinephrine and glucagon will stimulate
  • 00:28:18
    either skeletal muscle or in the case of
  • 00:28:21
    glucagon hepatic glycogen Allah says it
  • 00:28:25
    again is a camp second messenger pathway
  • 00:28:29
    that will ultimately activate this
  • 00:28:33
    glycogen phosphorylase enzyme and that
  • 00:28:37
    will pull glucose out of glycogen and
  • 00:28:40
    that glucose can be either released into
  • 00:28:43
    circulation from the liver or used by a
  • 00:28:46
    glycolysis within the skeletal muscle
  • 00:28:49
    cell right but in the case of if we look
  • 00:28:55
    at how insulin influences this pathway
  • 00:28:58
    insulin again promotes storage in doing
  • 00:29:02
    that it's going to inhibit mobilization
  • 00:29:05
    and so just like we saw it inhibiting
  • 00:29:08
    the activation of hormone sensitive
  • 00:29:11
    lipase insulin will also inhibit the
  • 00:29:15
    activation of phosphorylase and it does
  • 00:29:19
    this in a couple different ways one way
  • 00:29:22
    is again through that PDE producing that
  • 00:29:27
    phosphodiesterase it's going to shut
  • 00:29:29
    down camp and if we need a camp to
  • 00:29:34
    stimulate the activation of
  • 00:29:35
    phosphorylase then insulin will in turn
  • 00:29:38
    shut down the that process that
  • 00:29:42
    activation of a phosphorylase but we
  • 00:29:46
    also can see that insulin will stimulate
  • 00:29:48
    a different enzyme called phosphatase
  • 00:29:52
    and phosphatase will also shut down the
  • 00:29:57
    activation of phosphorylase it just does
  • 00:30:00
    it at a different point in the second
  • 00:30:04
    messenger pathway by which epinephrine
  • 00:30:06
    or glucagon stimulates phosphorylase so
  • 00:30:10
    phosphatase will directly turn activated
  • 00:30:15
    phosphorylase off whereas this PDE route
  • 00:30:20
    in impairs the activation of
  • 00:30:23
    phosphorylase
  • 00:30:24
    by shutting camp down way upstream and
  • 00:30:29
    then thirdly insulin will actually
  • 00:30:31
    promote the activation of this enzyme
  • 00:30:35
    glycogen synthase and glycogen synthase
  • 00:30:39
    as its name suggests is the enzyme
  • 00:30:42
    that's going to synthesize glycogen so
  • 00:30:52
    if we turn off phosphorylase and we turn
  • 00:30:54
    on synthase that those three mechanisms
  • 00:30:58
    are certainly promoting storage putting
  • 00:31:02
    glucose molecules together into making
  • 00:31:05
    glycogen rather than breaking down
  • 00:31:08
    glycogen and using it to provide glucose
  • 00:31:12
    for either blood glucose regulation or
  • 00:31:16
    for used by the skeletal muscle cell for
  • 00:31:18
    ATP synthesis okay I had said in a
  • 00:31:28
    previous slide that skeletal muscle is
  • 00:31:32
    pretty amazing because it can feed
  • 00:31:33
    itself and if you remember what I had
  • 00:31:36
    talked about was the fact that
  • 00:31:38
    contraction mediated increases in
  • 00:31:41
    intracellular calcium can not only
  • 00:31:45
    facilitate contraction but will also
  • 00:31:48
    increase the activation of phosphorylase
  • 00:31:52
    and therefore start breaking down
  • 00:31:55
    intramuscular glycogen stores and start
  • 00:31:59
    feeding and the skeletal muscle with
  • 00:32:02
    glucose for glycolysis so increase in
  • 00:32:05
    skeletal muscle contraction is brought
  • 00:32:09
    about by an increase in intracellular
  • 00:32:11
    calcium levels inside that skeletal
  • 00:32:14
    muscle cell and that can lead to
  • 00:32:16
    contraction but it can also stimulate
  • 00:32:20
    glycogen phosphorylase
  • 00:32:33
    which is going to stimulate
  • 00:32:36
    glycogenolysis for ATP production now we
  • 00:32:43
    see a similar effect of not breaking
  • 00:32:48
    down glycogen but also the increase in
  • 00:32:53
    intracellular calcium leading to the
  • 00:32:58
    activation of those gluts for transport
  • 00:33:02
    proteins and glute for transport
  • 00:33:10
    proteins are going to increase glucose
  • 00:33:12
    uptake by the skeletal muscle cell so
  • 00:33:20
    contraction itself will lead to the
  • 00:33:24
    breakdown of skeletal muscle glycogen
  • 00:33:25
    for ATP synthesis it will also lead to
  • 00:33:29
    the uptake of available glucose from the
  • 00:33:31
    blood for ATP synthesis during
  • 00:33:35
    contraction and just like we saw with
  • 00:33:38
    the activation of the phosphorylase
  • 00:33:41
    enzyme this is mediated through that
  • 00:33:44
    increase in calcium leading to an
  • 00:33:48
    activation of calmodulin and so this
  • 00:33:51
    next slide I'll just zoom in on this
  • 00:33:53
    figure so we can look at it in a little
  • 00:33:55
    bit more detail so we have said that at
  • 00:34:00
    rest so resting skeletal muscle cells or
  • 00:34:05
    other non skeletal muscle tissue
  • 00:34:17
    insulin is required for the cell to
  • 00:34:21
    access the glucose in the blood and this
  • 00:34:24
    has a lot of detail that you don't need
  • 00:34:26
    to know but again the insulin binds to
  • 00:34:29
    its receptor mechanism it's going to
  • 00:34:32
    function via this ip3 pathway and lead
  • 00:34:39
    to the stimulation of or the activation
  • 00:34:44
    of glute 4 which is gonna migrate over
  • 00:34:54
    here and imbed itself in the membrane of
  • 00:34:59
    the cell and allow for glucose to be
  • 00:35:04
    brought from the outside to the inside
  • 00:35:05
    and so at rest we need insulin for the
  • 00:35:10
    skeletal muscle cell to be able to
  • 00:35:12
    access that glucose why does it want
  • 00:35:14
    glucose well a couple reasons it can use
  • 00:35:18
    that glucose that it just brought in to
  • 00:35:20
    make glycogen for future use or it can
  • 00:35:24
    use it for resting ATP demand and
  • 00:35:27
    perhaps more importantly it represents a
  • 00:35:32
    way in which the body can get the
  • 00:35:34
    glucose out of the bloodstream which is
  • 00:35:36
    super important for maintaining the
  • 00:35:39
    health of the blood vessels we can't
  • 00:35:41
    have real high blood glucose levels
  • 00:35:43
    during contraction though we don't need
  • 00:35:47
    insulin to be able to access glucose and
  • 00:35:50
    get it into the skeletal muscle cell and
  • 00:35:53
    thank goodness because what happens to
  • 00:35:55
    insulin levels during exercise insulin
  • 00:35:58
    goes down right we've talked already
  • 00:36:00
    about the fact that as exercise
  • 00:36:03
    increases we're gonna have a suppression
  • 00:36:06
    of insulin now if we needed insulin to
  • 00:36:13
    be able to access glucose then that
  • 00:36:16
    would be counterproductive right we're
  • 00:36:19
    suppressing the insulin so how the heck
  • 00:36:22
    do we get to the glucose and circulation
  • 00:36:24
    well fortunately again during
  • 00:36:27
    contraction when part of contraction is
  • 00:36:30
    an
  • 00:36:30
    increase in intracellular calcium levels
  • 00:36:33
    some of that calcium is going to bind to
  • 00:36:35
    troponin and enable actin and myosin
  • 00:36:38
    cross bridge formation and force
  • 00:36:40
    production but some of that calcium is
  • 00:36:43
    actually going to stimulate calmodulin
  • 00:36:49
    and that calmodulin will come down and
  • 00:36:55
    stimulate that glute 4 and cause it just
  • 00:37:02
    like we saw with insulin to translocate
  • 00:37:04
    and get over here and embed itself in
  • 00:37:06
    the membrane of the cell and again allow
  • 00:37:10
    for the diffusion of the glucose that's
  • 00:37:13
    in circulation across that cell membrane
  • 00:37:15
    into the skeletal muscle cell now
  • 00:37:17
    because this is a contracting cell what
  • 00:37:20
    is that glucose going to be used for ATP
  • 00:37:24
    synthesis it will not be used synthesis
  • 00:37:31
    for it will not be used for glycogen
  • 00:37:35
    synthesis right because this is
  • 00:37:37
    contracting we're not going to store
  • 00:37:39
    fuel while we're contracting we're going
  • 00:37:42
    to use it up well we're contracted
  • 00:37:50
    alright let's finish up these last
  • 00:37:52
    slides and just look at some trends in
  • 00:37:56
    how our regulatory and counter
  • 00:37:58
    regulatory hormones respond to exercise
  • 00:38:01
    let's first look at how they respond to
  • 00:38:05
    increases in exercise intensity and so
  • 00:38:07
    across the x-axis we've got percent of
  • 00:38:11
    vo2 max as our means of measuring
  • 00:38:15
    intensity so obviously maximal intensity
  • 00:38:18
    is down here on the right and rest is
  • 00:38:21
    down here on the left and then we have
  • 00:38:24
    the change in plasma hormone
  • 00:38:27
    concentration remember that collectively
  • 00:38:30
    epinephrine norepinephrine growth
  • 00:38:32
    hormone cortisol and glucagon are
  • 00:38:34
    together referred to as our counter
  • 00:38:37
    regulatory hormones
  • 00:38:46
    and insulin is our standalone regulatory
  • 00:38:53
    hormone and just like you would expect
  • 00:38:58
    based on what we've been talking about
  • 00:39:01
    as exercise intensity goes up we're
  • 00:39:05
    going to see a progressive increase in
  • 00:39:07
    all of those counter regulatory hormones
  • 00:39:10
    now differently as exercise intensity
  • 00:39:14
    goes down we're gonna see a progressive
  • 00:39:16
    decrease in that regulatory hormone
  • 00:39:20
    insulin now some interesting data has
  • 00:39:24
    shown that at very high exercise
  • 00:39:27
    intensities well we can actually
  • 00:39:29
    sometimes see this blip back upward in
  • 00:39:33
    insulin and this does this isn't shown
  • 00:39:37
    always or demonstrated in all data but
  • 00:39:42
    the reason why we might see a actual
  • 00:39:47
    reduction in the the decrease right and
  • 00:39:50
    and maybe even a slight increase in
  • 00:39:52
    insulin at very high exercise
  • 00:39:54
    intensities is because at those same
  • 00:39:58
    exercise intensities the counter
  • 00:40:01
    regulatory hormones have so strongly
  • 00:40:05
    stimulated hepatic glucose production
  • 00:40:08
    and that the body sometimes experiences
  • 00:40:15
    hyperglycemia
  • 00:40:24
    and again blood-glucose is a very
  • 00:40:28
    tightly regulated variable and so if
  • 00:40:31
    that is the case at those very high
  • 00:40:33
    exercise intensities if the hepatic
  • 00:40:35
    glucose production the release of
  • 00:40:37
    glucose into circulation by the liver is
  • 00:40:40
    so high then we actually may need to
  • 00:40:44
    start stimulating non contractile
  • 00:40:47
    tissues to help get some of that glucose
  • 00:40:50
    back out of the blood and try and keep
  • 00:40:52
    blood glucose levels within acceptable
  • 00:40:55
    regions but you know for the most part
  • 00:40:59
    we're gonna see insulin goes down and
  • 00:41:02
    everything else goes up as exercise
  • 00:41:04
    intensity goes up we see a similar
  • 00:41:09
    pattern in response to increases in
  • 00:41:14
    exercise duration so exercise duration
  • 00:41:17
    is down here across the x-axis and again
  • 00:41:20
    plasma hormone concentration of the
  • 00:41:24
    counter regulatory hormones and then our
  • 00:41:26
    regulatory hormone insulin here on the y
  • 00:41:30
    axis and again know that is the arrival
  • 00:41:35
    of the mailman Sofie can't stand the
  • 00:41:39
    mailman okay so again as exercise
  • 00:41:43
    duration this time increases we see a
  • 00:41:47
    progressive ink Lea increase in our
  • 00:41:50
    counter regulatory hormones and a
  • 00:41:52
    progressive decrease in our regulatory
  • 00:41:54
    hormone insulin now the last concept I
  • 00:42:02
    want to leave you with is this idea that
  • 00:42:06
    one of the main effects of chronic
  • 00:42:10
    exercise training is that exercise
  • 00:42:17
    becomes less of a stressor now remember
  • 00:42:29
    the sympathetic nervous system responds
  • 00:42:33
    to stress
  • 00:42:34
    right increase stress increase SNS
  • 00:42:40
    activity
  • 00:42:41
    it's fight-or-flight and stress is
  • 00:42:43
    stress it's not going to be able to
  • 00:42:45
    differentiate between holy crap I've got
  • 00:42:47
    four midterms today and oh I'm going out
  • 00:42:51
    for an exercise or a jog or or run up a
  • 00:42:57
    hill or something right stress is stress
  • 00:42:58
    so when exercise intensity or duration
  • 00:43:02
    goes up we see an increase in
  • 00:43:06
    sympathetic nervous system activity
  • 00:43:08
    however as you do more exercise this
  • 00:43:14
    increase becomes attenuated or lessened
  • 00:43:19
    so that instead of looking like that
  • 00:43:23
    we've got an increase in exercise
  • 00:43:25
    instead of SNS coming up dramatically we
  • 00:43:29
    might see a small increase in
  • 00:43:31
    sympathetic nervous system activity and
  • 00:43:33
    so this is pre-training
  • 00:43:39
    and this is post training and I you know
  • 00:43:47
    I joke sometimes but it's true if you
  • 00:43:50
    take somebody who's been habitually
  • 00:43:52
    sedentary or sedentary for a fairly
  • 00:43:54
    prolonged period of time and they
  • 00:43:56
    undertake an exercise session the body
  • 00:43:59
    will literally respond in the same way
  • 00:44:03
    that it would respond to any other
  • 00:44:05
    life-threatening stressor and exercise
  • 00:44:10
    can be interpreted as a life-threatening
  • 00:44:13
    experience especially if it if it's not
  • 00:44:16
    something that the person ever does but
  • 00:44:19
    if they keep exercising adaptations to
  • 00:44:23
    training will dampen or attenuate that
  • 00:44:28
    flight or flight response and that's
  • 00:44:30
    reflected in a an overall reduction I
  • 00:44:35
    got a cough hold on
  • 00:44:38
    sorry a small with me not lower a
  • 00:44:42
    smaller increase in epi and nor epi okay
  • 00:44:56
    so remember that a lot of the influence
  • 00:45:01
    of exercise on our counter regulatory
  • 00:45:03
    hormones was facilitated by the increase
  • 00:45:08
    in epi and norepi so if you don't
  • 00:45:12
    produce as much epi and nor epi because
  • 00:45:15
    you are trained then in turn you're not
  • 00:45:20
    gonna produce as much of the counter
  • 00:45:23
    regulatory hormones and you're not gonna
  • 00:45:26
    suppress the regulatory hormone as much
  • 00:45:29
    and so that's what we're seeing on these
  • 00:45:32
    figures so before training in an
  • 00:45:36
    untrained person exercise starts
  • 00:45:42
    increase in sympathetic nervous system
  • 00:45:46
    activity is going to increase norepi
  • 00:45:50
    and epi and what's that going to do
  • 00:45:54
    that's going to cause counter regulatory
  • 00:45:57
    glucagon to also increase dramatically
  • 00:46:00
    right but following training
  • 00:46:10
    exercise starts and you've got a smaller
  • 00:46:14
    increase in SNS activity you've got a
  • 00:46:18
    smaller increase in norepinephrine and
  • 00:46:22
    epinephrine and look the the effect
  • 00:46:25
    downstream on the pancreatic alpha cells
  • 00:46:30
    is a very flatlined response to plasma
  • 00:46:35
    glucagon remember that glucagon is
  • 00:46:37
    redundant in its effects on mobilizing
  • 00:46:42
    fuel and so maybe this is just
  • 00:46:44
    reflective that you know the influence
  • 00:46:47
    the increase in norepinephrine and
  • 00:46:48
    epinephrine are doing just fine on their
  • 00:46:51
    own mobilizing fuel and we really don't
  • 00:46:53
    need to see a big change in in glucagon
  • 00:46:57
    levels okay and so just like we see a
  • 00:47:01
    smaller increase in glucagon we're gonna
  • 00:47:07
    see a smaller decrease in insulin so
  • 00:47:11
    again in the untrained state we're gonna
  • 00:47:13
    see a stronger decrease in insulin as
  • 00:47:15
    exercise progresses and in a trained
  • 00:47:19
    state you don't have to reduce insulin
  • 00:47:22
    so much to meet the demands of exercise
  • 00:47:29
    and sure enough just like I suggested in
  • 00:47:34
    that previous slide these are this is
  • 00:47:36
    looking at the effects of training on
  • 00:47:42
    exercise induced changes in
  • 00:47:44
    norepinephrine and epinephrine and so
  • 00:47:46
    certainly in the first few weeks of
  • 00:47:51
    exercise training we see that when
  • 00:47:54
    exercise starts both epi and norepi
  • 00:47:57
    levels rise significantly and that keeps
  • 00:48:01
    happening for several weeks and then
  • 00:48:04
    over time as the body goes ooh hoo
  • 00:48:06
    she's just exercising again it's not
  • 00:48:09
    literally life or death situation I'm
  • 00:48:12
    not actually needing to fight or flee I
  • 00:48:15
    am just exercising and so as a result
  • 00:48:18
    there is a much smaller chain
  • 00:48:22
    in norepinephrine and epinephrine
  • 00:48:24
    following training and that collectively
  • 00:48:27
    reflects a reduced overall sympathetic
  • 00:48:31
    nervous system response to exercise why
  • 00:48:38
    is that exercise is less of a stressor
  • 00:48:49
    when you were trained alright folks
  • 00:49:01
    that's it
  • 00:49:03
    you made it congratulations
الوسوم
  • catécholamines
  • métabolisme
  • exercice
  • hormones
  • insuline
  • glucagon
  • cortisol
  • mobilisation
  • glycogène
  • lipides