Download Chapter 5 → Hormonal Responses to Exercise Objectives Objectives

Chapter 5 Î Hormonal
Responses to Exercise
Objectives
1. Describe the concept of hormone-receptor
interaction.
2. Identify the four factors influencing the
concentration of a hormone in the bld.
3. Describe the mechanism by which steroid
hormones act on cells.
4. Describe the “2nd messenger” hypothesis of
hormone action.
5. Describe the role of hypothalamus-releasing
factors in the control of hormone secretion from
the anterior pituitary gland.
Objectives
6. Describe the relationship of the hypothalamus to
the secretion of hormones from the posterior
pituitary gland.
7. Identify the site of release, stimulus for release, &
the predominant action of the following hormones:
epinephrine, norepinephrine, glucagon, insulin,
cortisol, aldosterone, thyroxine, growth hormone,
estrogen, & testosterone.
8. Discuss the use of testosterone (an anabolic
steroid) & growth hormone on muscle growth &
their potential side effects.
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Objectives
9. Contrast the role of plasma catecholamines w/
intracellular factors in the mobilization of muscle
glycogen during exercise.
10. Briefly discuss the following four mechanisms by
which bld glu homeostasis is maintained:
mobilizing glu from liver glycogen stores,
mobilizing plasma FFAs from adipose tissue,
synthesizing glu from AAs & glycerol in the liver, &
blocking glu entry into cells.
Objectives
11. Describe the Δs in the hormones insulin,
glucagon, cortisol, growth hormone, epinephrine,
& norepinephrine during graded & prolonged
exercise & discuss how those Δs influence the
four
ou mechanisms
ec a s s used to maintain
a ta the
t e [b
[bld
d glu].
g u]
12. Describe the effect of changing hormone &
substrate levels in the bld on the mobilization of
FFAs from adipose tissue.
Neuroendocrinology
Neuroendocrinology
• Neuroendocrine system
• Endocrine glands
• Hormones
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Neuroendocrinology
[Bld Hormone]
Neuroendocrinology
Factors That Influence the Secretion
of Hormones
Figure 5.1
Neuroendocrinology
Hormone-Receptor Interactions
3
Neuroendocrinology
Mechanisms of Hormone Action
Neuroendocrinology
Mechanism of
Steroid
Hormone
Action
Figure 5.2
Neuroendocrinology
Cyclic AMP “2nd Messenger” Mechanism
Figure 5.3
4
Neuroendocrinology
Calcium & Phospholipase C 2nd
Messenger Mechanisms
Figure 5.4
Neuroendocrinology
Insulin Receptor
Figure 5.5
Neuroendocrinology
In Summary
ƒ The hormone-receptor interaction triggers events at the
cell; changing the concentration of the hormone, the
number of receptors on the cell, or the affinity of the
receptor for the hormone will all influence the magnitude
of the effect.
ƒ Hormones bring about their effects by modifying mb
transport, activating/suppressing genes to alter pro
synthesis, & activating 2nd messengers (cyclic AMP,
Ca++, inositol triphosphate, & diacylglycerol).
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Hormones: Regulation & Action
Hypothalamus & Pituitary Gland
• Hypothalamus
– Controls secretions from pituitary gland
• Anterior Pituitary Gland
– Adrenocorticotropic hormone (ACTH)
– Follicle-stimulating
Follicle stimulating hormone (FSH)
– Luteinizing hormone (LH)
– Melanocyte-stimulating hormone (MSH)
– Thyroid-stimulating hormone (TSH)
– Growth hormone (GH)
– Prolactin
• Posterior Pituitary Gland
– Oxytocin
– Antidiuretic hormone (ADH)
Hypothalamus
• Stimulates release of hormones from anterior
pituitary gland
– Releasing hormones or factors
p
• Provides hormones for release from posterior
pituitary gland
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Anterior Pituitary Gland
• Adrenocorticotropic hormone (ACTH)
– Stimulates cortisol release form adrenal glands
• Follicle-stimulating hormone (FSH)
• Luteinizing hormone (LH)
– Stimulates production of testosterone & estrogen
• Melanocyte-stimulating hormone (MSH)
• Thyroid-stimulating hormone (TSH)
– Controls thyroid hormone release from thyroid gland
• Prolactin
• Growth hormone (GH)
Growth Hormone
Influences on Growth Hormone Release
Figure 5.6
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A Closer Look 5.1
Growth Hormone & Performance
In Summary
ƒ The hypothalamus controls the activity of both the
anterior pituitary & posterior pituitary glands.
ƒ GH is released from the anterior pituitary gland & is
essential for normal growth.
ƒ GH ↑s during exercise to mobilize FFAs from adipose
tissue & to aid in the maintenance of bld glu.
Posterior Pituitary Gland
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Δ in Plasma [ADH] during Exercise
Figure 5.7
Thyroid Gland
• Stimulated by TSH
• Triiodothyronine (T3) & thyroxine (T4)
– Establishment of metabolic rate
– Permissive hormones
ƒ Permit full effect of other hormones
• Calcitonin
– Regulation of plasma Ca+2
ƒ Blocks release from bone, stimulates excretion by kidneys
• Parathyroid Hormone
– 1° hormone in plasma Ca+2 regulation
ƒ Stimulates release from bone, stimulates reabsorption by
kidneys
In Summary
ƒ Thyroid hormones T3 & T4 are important for maintaining
the metabolic rate & allowing other hormones to bring
about their full effect.
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Parathyroid Gland
• Parathyroid hormone
– 1° hormone in plasma Ca+2 regulation
– Stimulates Ca+2 release from bone
– Stimulates reabsorption of Ca+2 by kidneys
– Converts vitamin D3 into a hormone that ↑ Ca+2
absorption from GI tract
Adrenal Medulla
Effects of E &N
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In Summary
ƒ The adrenal medulla secretes the catecholamines
epinephrine (E) & norepinephrine (NE). E is the adrenal
medulla’s 1° secretion (80%), while NE is primarily
secreted from the adrenergic neurons of the sympathetic
nervous system.
t
ƒ Epinephrine & norepinephrine bind to α- &
β-adrenergic receptors &bring about Δs in cellular activity
(e.g., ↑d HR, mobilization of FAs from adipose tissue) via
2nd messengers.
Adrenal Cortex
• Secretes steroid hormones
– Derived from cholesterol
• Mineralcorticoids
– Aldosterone
– Maintenance of plasma Na+ &K+
• Glucocorticoids
– Cortisol
– Regulation of plasma glu
• Sex steroids
– Androgens & estrogens
– Support prepubescent growth
Aldosterone
• Control of Na+ reabsorption & K+ secretion
– Na+/H2O balance
• Regulation of bld volume &bld pressure
– Part of renin
renin-angiotensin-aldosterone
angiotensin aldosterone system
– All three hormones ↑ during exercise
• Stimulated by:
– ↑d [K+]
– ↓d plasma volume
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Δ in Renin, Angiotensin II, &Aldosterone
during Exercise
Figure 5.8
Cortisol
Control of
Cortisol Secretion
Figure 5.9
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In Summary
ƒ The adrenal cortex secretes aldosterone
(mineralcorticoid), cortisol (glucocorticoid), &estrogens
&androgens (sex steroids).
ƒ Aldosterone regulates Na+ &K+ balance. Aldosterone
secretion ↑s w/ strenuous exercise, driven by the reninangiotensin system.
ƒ Cortisol responds to a variety of stressors, including
exercise, to ensure that fuel (glu &FFAs) is available, &to
make AAs available for tissue repair.
A Closer Look 5.2
Adipose Tissue Is an Endocrine Organ
Pancreas
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In Summary
ƒ Insulin is secreted by the β cells of the islets of
Langerhans in the pancreas &promotes the storage of
glu, AAs, &fats.
ƒ Glucagon is secreted by the α cells of the islets of
Langerhans in the pancreas &promotes the mobilization
of glu &fats.
Testes &Ovaries
• Testosterone
– Released from testes
– Anabolic steroid
ƒ Promotes tissue (muscle) building
ƒ Performance
P f
enhancement
h
t
– Androgenic steroid
ƒ Promotes masculine characteristics
• Estrogen &Progesterone
– Released from ovaries
– Establish &maintain reproductive function
– Levels vary throughout the menstrual cycle
Control of Testosterone Secretion
Figure 5.10
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Control of Estrogen Secretion
Figure 5.11
Δ in FSH, LH, Progesterone, & Estradiol
during Exercise
Figure 5.12
A Closer Look 5.3
Anabolic Steroids &Performance
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In Summary
ƒ Testosterone & estrogen establish &maintain
reproductive function & determine secondary sex
characteristics.
ƒ Chronic exercise (training) can ↓ testosterone levels in
males & estrogen levels in females. The latter adaptation
has potentially negative consequences related to
osteoporosis.
Hormonal Control of Substrate Mobilization During Exercise
Muscle Glycogen Utilization
Glycogen Depletion during Exercise
Figure 5.13
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Plasma [EPI] during Exercise
Figure 5.14
Hormonal Control of Substrate Mobilization During Exercise
Control of Muscle Glycogen Utilization
Δs in Muscle Glycogen Before & After
Propranolol Administration
Figure 5.15
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Control of Glycogenolysis
Figure 5.16
In Summary
ƒ Glycogen breakdown to glu in muscle is under the dual
control of epinephrine-cyclic AMP &Ca+2-calmodulin. The
latter’s role is enhanced during exercise due to the ↑ in
Ca+2 from the sarcoplasmic reticulum. In this way, the
d li
delivery
off ffuell ((glu)
l ) parallels
ll l th
the activation
ti ti off
contraction.
Hormonal Control of Substrate Mobilization During Exercise
Bld Glu Homeostasis during Exercise
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Hormonal Control of Substrate Mobilization During Exercise
Thyroid Hormones
Hormonal Control of Substrate Mobilization During Exercise
Cortisol
Hormonal Control of Substrate Mobilization During Exercise
Role of Cortisol in the Maintenance of
bld glu
Figure 5.17
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Hormonal Control of Substrate Mobilization During Exercise
Δs in Plasma Cortisol
during Exercise
Figure 5.18
Hormonal Control of Substrate Mobilization During Exercise
Growth Hormone
Hormonal Control of Substrate Mobilization During Exercise
Role of Growth Hormone in the
Maintenance of Plasma glu
Figure 5.19
20
Hormonal Control of Substrate Mobilization During Exercise
Δs in Plasma Growth Hormone during
Exercise
Figure 5.20
Hormonal Control of Substrate Mobilization During Exercise
In Summary
ƒ The hormones thyroxine, cortisol, & growth hormone act
in a permissive manner to support the actions of other
hormones during exercise.
ƒ Growth hormone & cortisol also provide a “slow-acting”
effect on CHO & fat metabolism during exercise.
Hormonal Control of Substrate Mobilization During Exercise
Epinephrine & Norepinephrine
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Hormonal Control of Substrate Mobilization During Exercise
Role of Catecholamines in Substrate
Mobilization
Figure 5.21
Hormonal Control of Substrate Mobilization During Exercise
Δ in Plasma E & NE during Exercise
Figure 5.22
Hormonal Control of Substrate Mobilization During Exercise
Plasma Catecholamines Responses to
Exercise following Training
Figure 5.23
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Hormonal Control of Substrate Mobilization During Exercise
Fast-Acting Hormones
Hormonal Control of Substrate Mobilization During Exercise
Effects of Insulin & Glucagon
Figure 5.24
Hormonal Control of Substrate Mobilization During Exercise
Δs in Plasma Insulin
during Exercise
Figure 5.25
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Hormonal Control of Substrate Mobilization During Exercise
Δs in Plasma Glucagon
during Exercise
Figure 5.26
Hormonal Control of Substrate Mobilization During Exercise
Effect of E & N on Insulin & Glucagon
Secretion
Figure 5.27
Hormonal Control of Substrate Mobilization During Exercise
Effect of the SNS on Substrate
Mobilization
Figure 5.28
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Hormonal Control of Substrate Mobilization During Exercise
Summary of the Hormonal Responses
to Exercise
Figure 5.29
Hormonal Control of Substrate Mobilization During Exercise
In Summary
ƒ Plasma glu is maintained during exercise by ↑ng liver
glycogen mobilization, using more plasma FFA, ↑ng
gluconeogenesis, & ↓ng glu uptake by tissues. The ↓ in
plasma insulin & the ↑ in plasma E, NE, GH, glucagon, &
cortisol
ti l d
during
i exercise
i control
t l th
these mechanisms
h i
tto
maintain the [glu].
Hormonal Control of Substrate Mobilization During Exercise
In Summary
ƒ glu is taken up 7-to 20-times faster during exercise than
at rest—even w/ the ↓ in plasma insulin. The ↑s in
intracellular Ca+2 & other factors are associated w/ an ↑
in the number of glu transporters that ↑ the mb transport
of g
o
glu.
u
ƒ Training causes a reduction in E, NE, glucagon, & insulin
responses to exercise.
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Hormonal Control of Substrate Mobilization During Exercise
Hormone-Substrate Interaction
Hormonal Control of Substrate Mobilization During Exercise
Δs in Plasma FFA Due to
Lactic Acid
Figure 5.30
Hormonal Control of Substrate Mobilization During Exercise
Effect of Lactic Acid on FFA Mobilization
Figure 5.30
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Hormonal Control of Substrate Mobilization During Exercise
In Summary
ƒ The plasma [FFA] ↓s during heavy exercise even though
the adipose cell is stimulated by a variety of hormones to
↑ triglyceride breakdown to FFA & glycerol. This may be
due to: (a) the higher [H+] inhibiting hormone
sensitive
se
s e lipase,
pase, (b) the
e high
g levels
e es o
of lactate
ac a e du
during
g
heavy exercise promoting the resynthesis of
triglycerides, (c) an inadequate bld flow to adipose
tissue, or (d) insufficient albumin needed to transport the
FFA in the plasma.
Study Questions
1.
Draw & label a diagram of a negative feedback mechanism
for hormonal control using cortisol as an example.
2.
List the factors that can influence the [bld] of a hormone.
3.
Discuss the use of testosterone & growth hormone as aids
to ↑ muscle size &strength, &discuss the potential long-term
consequences of such use.
4.
List each endocrine gland, the hormones(s) secreted from
that gland, & its (their) action(s).
5.
Describe the two mechanisms by which muscle glycogen is
broken down to glu (glycogenolysis) for use in glycolysis.
Which one is activated at the same time as muscle
contraction?
Study Questions
6.
Identify the four mechanisms involved in maintaining the bld
[glu].
7.
Draw a summary graph of the Δs in the following hormones
w/ exercise of increasing intensity or duration: epinephrine,
norepinephrine cortisol growth hormone,
norepinephrine,
hormone insulin,
insulin &
glucagon.
8.
What is the effect of training on the responses of
epinephrine, norepinephrine, & glucagon to the same
exercise task?
9.
Briefly explain how glu can be taken into the muscle at a
high rate during exercise when plasma insulin is reduced.
Include the role of glu transporters.
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Study Questions
10. Explain how FFA mobilization from the adipose cell ↓s
during maximal work in spite of the cell being stimulated by
all the hormones to break down triglycerides.
11. Discuss the effect of glu ingestion on the mobilization of
FFAs during exercise
exercise.
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