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Hormones

Berry College - Dept. of Kinesiology
by

David Elmer

on 21 April 2015

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Transcript of Hormones

Hormones
released by endocrine organs into the blood
circulate to tissues elsewhere in the body
one of the primary ways that the body maintains homeostasis
binding to receptors allow hormones to only take effect in certain tissues
usually only present in microgram, nanogram, or picogram amounts
4 factors governing hormone concentration:
Rate of secretion
from endocrine gland
Rate of removal
by metabolism or excretion
Amount of
(for certain hormones)
Plasma volume
depends on input to endocrine organ
stimulatory or inhibitory
most are influenced by multiple inputs
ex.
insulin secretion
-from pancreas
influenced by:
plasma glucose and amino acids
plasma epinephrine
parasympathetic neurons
sympathetic neurons
other hormones
or
metabolism primarily accomplished by the
deactivation
removal
can metabolize and excrete hormones
liver
kidneys
blood flow to liver and kidneys is reduced during exercise, which reduces the rate of hormone metabolism and excretion
measuring hormones in urine can give insight to hormone levels in the body
hormone must be "free" (not bound to a receptor) to exert an affect
transport protein
amount of free hormones depends on...
quantity
capacity
affinity
...of transport protein
-how much
-max amount of hormone that can bind
-tendency of transport protein to bind hormone
changes in plasma volume affect concentration independently of rate of secretion and rate of removal
decrease amount of plasma
=
increase hormone concentration
must correct for plasma change to assess endocrine gland activity
hormone-receptor interaction
up-regulation
down-regulation
chronic low exposure to a hormone results in increases in the number of receptors
increased response when hormone is present
chronic high exposure to hormone can decrease the number of receptors
diminished response to the presence of the hormone
when all the receptors are bound, the system is
saturated
since receptors bind hormones based on "shape", anything that looks similar can and will compete for receptor sites
drugs can block receptors to limit a hormones actions
mechanisms of action
alter membrane transport
alter DNA activity
activate special proteins by "second messengers"
increase or decrease the transport of a particular substance into or out of the cell
example:
insulin
-binds receptors on cell surface
results in glucose transporters being localized in cell membrane
glucose transporter bind glucose and bring it into the cell
activates or suppresses genes that leads to specific mRNA synthesis
DNA
mRNA
protein
translated into
transcribed to
some hormones are too big to fit into cell
bind to membrane receptors that activate a
G protein
-link between hormone-receptor interaction and activities within the cell
cyclic AMP
Ca++ ion channel
phospholipase C
Regulation and Action
OR
ovary
pituitary
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hypothalamus
pituitary
pituitary
anterior
posterior
thyroid
parathyroid
adrenal
pancreas
testes ovaries
cortex
adrenal
medulla
releasing hormones
neural input
ACTH
adrenocorticotrophic hormone
FSH
follicle stimulating hormone
LH
luteinizing hormone
MSH
melanocyte stimulating hormone
TSH
thyroid stimulating hormone
GH
growth hormone
prolactin
directly stimulates the breast to produce milk
controls rate of thyroid hormone formation and secretion from thyroid gland
stimulates production and secretion of cortisol in the adrenal cortex
stimulates production of testosterone in the testes
OR
stimulates production of estrogen in the ovaries
stimulates production of melanin
may increase sexual arousal in brain
stimulates sperm production in seminiferous tubules
converts androgen to estrogen in ovaries
stimulates release of insulin-like growth factors (IGF-1) in the liver & other tissues
although this can be produced by other means as well
spares blood glucose
hormones formed in hypothalamus, passed down to posterior pituitary via nerves, and released in blood stream
oxytocin
smooth muscle stimulator, especially during childbirth
responsible for milk "let-down" to release milk from the breast
ADH
anti-diuretic hormone
reduces water loss from the body
stimulates reabsorption of water from kidney tubules back into bloodstream
2 major stimuli:
1. high plasma osmolality
potentially caused by heavy sweating without fluid replacement
2. low plasma volume
loss of blood or inadequate hydration
osmoreceptors
in hypothalamus detect this
stretch receptors
in left atrium of heart detect this
/ parathyroid gland
T
T
3
4
triiodothyronine
thyroxine
more potent than T4
released in larger quantities, but it is mostly converted to T3
help establish overall metabolic rate
hypothyroidism could result in obesity (although this is rarely the case)
permissive hormones - allow other hormones to exert full effect
slow to take effect, but long lasting
6-12 hours for T3
2-3 days for T4
during exercise, increase in free hormones resulting in faster uptake
increased uptake results in increased secretion
also influenced by cortisol and prolactin increase during exercise
calcitonin
regulates plasma calcium content
blocks calcium release from bone
stimulates calcium excretion at kidneys
lowers plasma calcium
not increased during exercise
parathyroid
responds to low plasma calcium levels
hormone
stimulates bone to release calcium
increases renal absorption of calcium
stimulates kidney to convert vitamin D into a hormone that increases calcium absorption in GI tract
increased during intense or prolonged exercise
due to reduced calcium, and increased H+ ions and chatecholamines
opposing effects
epinephrine
norepinephrine
catecholamines
(adrenaline)
(noradrenaline)
affects:
cardiovascular system
respiratory system
gastrointestinal (GI) tract
liver
other endocrine glands
muscle
adipose tissue
involved in maintenance of blood pressure
regulate plasma glucose concentration
respond to emotional stimuli
bind to receptors on target tissues
adrenergic
(2nd messenger system)
type of adrenergic receptor determines action
80%
20%
mineralocorticoids
glucocorticoids
sex steroids
aldosterone
cortisol
androgens
estrogens
maintain Na+ and K+ concentrations in plasma
involved in plasma glucose regulation
support prepubescent growth
associated with postpubescent sex drive in women
regulates Na+ reabsorption and K+ secretion in the kidney
involved in regulating plasma volume and blood pressure
increased K+ concentration increases aldosterone secretion, stimulating kidneys to excrete K+ and pump Na+ back into bloodstream
low blood pressure results in release of renin from kidneys
2 mechanisms
1.
2.
angiotensinogen
renin
angiotensin I
angiotensin II
ACE
stimulates aldosterone release, which increases Na+ reabsorption
powerful vasoconstrictor
increases plasma volume
helps maintain plasma glucose during exercise and long-term fasting (starvation)
promote tissue breakdown to form amino acids, which are used by liver for gluconeogenesis
stimulate mobilization of free fatty acids from adipose tissue
stimulate liver enzymes involved in gluconeogenesis
block entry of glucose into tissues
forces tissues to use more fats as fuel
responds to a variety of stresses in the body
opposing effects
insulin
glucagon
somatostatin
stimulates tissues to take up nutrients and store them
glucose
glycogen
amino acids
proteins
fats
stimulation of glucose uptake is most known role
no insulin (or insulin insensitivity) = limited glucose uptake and glucose accumulation in the blood
kidney reabsorption of glucose is overwhelmed
glucose lost in urine, taking large volumes of water with it
diabetes mellitus
secretion is increased by:
increased plasma glucose concentration
increased plasma amino acid concentration
decreased sympathetic stimulation
increased parasympathetic stimulation
decreased epinephrine and norepinephrine
stimulates mobilization of glucose from stores in liver and free fatty acids from adipose tissue
spares blood glucose as a fuel
stimulates gluconeogenesis in the liver
secretion is increased by low plasma glucose and sympathetic stimulation
modifies activity of GI tract to control rate of entry into circulation
may help regulate insulin secretion
testosterone
estrogens
(LH)
or
anabolic
- tissue building
androgenic
- promotes masculine characteristics
stimulates protein synthesis
acutely increased during exercise
(returns to normal within 2 hours)
chronically decreased due to exercise
(still within normal range)
both aerobic and resistance trained men
estradiol
estrone
estriol
stimulates breast development, female fat deposition, and secondary sex characteristics
progesterone
follicular phase:
LH stimulates production of androgens
FSH converts androgens to estrogens
luteal phase:
estrogens and progesterone produced by corpus luteum
exercise results in small increases estradiol and progesterone by decreasing the rate of removal
not affected by cycle phase
exercise and the menstrual cycle:
anaerobic performance not affected
no clear results for aerobic performance
glucose mobilization is lower during luteal phase
can be offset by glucose feeding
no effect on fat utilization
increased protein catabolism due to progesterone during luteal phase
amenorrhea
primary
absence of menstrual cycle in girls who have not menstruated by age 15
secondary
onset of amenorrhea after menarche
increased prevalence in young women with low body weight that are involved in:
aesthetic sports
endurance sports
weight-class sports
... with high training volumes
college runners:
range of incidence from 3-60% when volume increased from 16 km/week to 113 km/week and body weight decreased from 60 kg to 50 kg
amenorrhea
osteoporosis
could also lead to
in young women
endorphins
block pain by acting on opiate receptors in brain
stimulated by exposure to stress, such as exercise
fuel usage:
intensity
duration
controlled by hormones
muscle-glycogen utilization
controlled via second messenger system
epinephrine stimulates cyclic AMP
intracellular calcium simulates calmodulin
blood glucose homeostasis (sparing)
4 processes:
mobilize glucose from liver glycogen stores
mobilize plasma FFA from adipose tissue to spare plasma glucose
increase gluconeogenesis in liver from amino acids, lactate, and glycerol
block glucose entry into cells to force cells to use FFA
1.
2.
3.
4.
permissive / slow acting hormones
fast acting hormones
T
3
and
T
4
influence the number of receptors on the surface of a cell
e.g.
without T3, epinephrine has very little effect on mobilizing FFA
exercise results in greater free T3, but also increased rate of removal
anterior pituitary makes up for this by secreting more TSH
cortisol
stimulates FFA mobilization from adipose tissue
breaks down protein to make glucose from resulting amino acids in liver
decreases rate of glucose utilization in cells
no immediately noticeable effects on metabolism (slow acting)
increase due to exercise may be related to tissue repair
increased rate of removal
increased rate of secretion, despite increased rate of removal
growth hormone
supports the actions of cortisol
decreases glucose uptake by tissue
increases FFA mobilization
enhances gluconeogenesis in liver
increased during exercise
spares plasma glucose
epinephrine and norepinephrine
mobilizes glucose from liver
mobilizes FFA from adipose tissue
interferes with glucose uptake by tissues
increases glycogenolysis
stimulated by low plasma glucose
can adapt to exercise training
increases during exercise
reduced secretion during fixed workload
increased capacity under stressful situation
insulin
glucagon
vs.
responsible for uptake and storage or glucose and FFA
responsible for mobilization of stored glucose and FFA
during exercise:
blood glucose is maintained by decreased insulin and increased glucagon
trained people:
increased glucagon sensitivity
decreased glucose uptake
increased fat utilization
how does exercise increase glucose uptake?
increased blood flow to muscles - delivers more glucose & insulin
exercise-induced increases in glucose transporters on cell surface
increased insulin sensitivity with exercise (acute and chronic)
Full transcript