MOVESCI 340 QUESTIONS AND ANSWERS LATEST UPDATE
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endocrine system components (4)
pituitary gland, thyroid gland, adrenal gland, pancreas
amino acid derivatives
- all derived from tyrosine
- epinephrine, norepinephrine, thyroid hormones, melatonin
peptide hormones
- largest group of hormones
- ADH, oxytocin, & hormones from the hypothalamus, pituitary gland, and pancreas
(insulin & glucagon)
lipid derivatives
- mostly derived from cholesterol
- steroid hormones (testosterone, estrogen)
- released by reproductive organs & adrenal cortex
3 ways hormones are inactivated
1. diffuse to target cells & bind to receptors
2. absorbed & broken down in liver/kidney
3. broken down by enzymes in plasma or ISF
hormonal secretion under negative feedback control is based on what types of
stimuli (3):
1. humoral stimuli (changes in ECF composition)
2. hormonal stimuli (changes in circulating hormone levels)
3. neural stimuli (neural stimulation of a neuroglandular junction)
humoral stimuli (of hormone release)
- high blood glucose → stimulate pancreas to secrete insulin → promotes glucose
uptake & storage by target cells
- low blood glucose → inhibits insulin & stimulates glucagon → stimulates glycigen
breakdown in liver → increases blood glucose
hormonal stimuli (of hormone release)
anterior pituitary gland releases ACTH into the blood → in response, the adrenal cortex
secretes glucocorticoids (cortisol) → influences several target organs & helps manage
stress by increasing energy availability (glucose release)
- negative feedback: high glucocorticoid levels reduce ACTH
neural stimuli (of hormonal release)
preganglionic sympathetic nerves (from CNS) stimulate adrenal medulla → secretes
catecholamines (E & NE) into blood → "fight or flight" response → increased HR, BP, &
energy availability
hormone levels are determined by (5)
1. quantity synthesized
2. rate of catabolism
3. rate of secretion into blood
,4. quantity of transport proteins present
5. changes in plasma volume
which hormones are not lipid soluble?
epinephrine, norepinephrine, and peptide hormones
- use a receptor → effect is indirect (action is linked by G-protein)
cAMP (secondary messenger)
binding of amine-based → activates adenylate cyclase → this catalyzes ATP
degradation to cAMP → cAMP activates protein kinases → alters cellular activity
If a hormone increased intracellular cAMP, what enzyme associated with
metabolism would be activated?
AMPK (potentially a change in ATP/AMP)
receptors inside cytoplasm/nucleus
- lipid-soluble hormones (thyroid/steroid hormones) are inside the cytoplasm or nucleus
& allow for passage into membranes
- forms a hormone-receptor complex (once bound) & activates/inactivates specific
genes, altering the rate of mRNA transcription & changing the structure/function of the
cell
impacts of insulin (4)
mediates glucose metabolism, affects fat synthesis, facilitates protein synthesis,
stimulates glucose transporters
impacts of glucagon (4)
- increases blood glucose
- in liver: stimulates glycogenolysis & gluconeogenesis (& ketone synthesis) (decreases
protein breakdown & glycogen synthesis)
- in adipose tissue: increases lipolysis & decreases triacylglycerol synthesis
- produced when blood glucose levels are low/decreases (release occurs later in
exercise- a function of intensity/duration)
what secretes glucagon?
islets of langerhans
how does training impact glucagon & insulin?
it reduces their responses to exercise, indicating improvements in metabolic efficiency
- glucagon pre-training shows a steeper increase as time increases; post-training, the
response is pretty flat
- insulin pre-training shows a rapid decrease; post-training, it has a much less
pronounced effect
how do insulin & glucagon work to maintain blood glucose homeostasis?
they work antagonistically
- in the pancreas: alpha cells secrete glucagon to raise blood sugar, while beta cells
secrete insulin to lower blood sugar
- in the liver: when blood sugar is high, insulin stimulates glycogen formation to lower
blood sugar, while when it is low, glucagon stimulates glycogen breakdown to raise it
- in tissue cells: insulin promotes glucose uptake to lower blood sugar
type 1 diabetes
typically occurs in younger people and is an autoimmune disease
- consists of 5-10% of all diabetes cases
- exercise has greater metabolic effects on this
, type 2 diabetes
lifestyle related & tends to occur after 40 (but recently in kids too)
- insulin resistance & impairs glucose tolerance
- often produces reduced exercise tolerance
- can be treated with exercise
- 1/3 of Americans are pre-diabetic and 84% don't know it
- T2D is releases to increased risk of CVD & cancer
normal insulin response
stimulus is a rise in blood sugar after eating → insulin is released from pancreatic beta
cells → insulin binds to muscle & adipose tissue receptors → increased glucose uptake
into cells → glucose is used for energy or stored as glycogen/fat → plasma glucose
levels return to normal
insulin-resistance response
pancreas overproduces insulin to maintain glucose levels → glucose uptake by muscle
is reduced despite high insulin
insulin-resistance risk factors
dyslipidemia, hypertension, obesity, heart disease, stroke, metabolic syndrome
type-2 diabetes insulin response
persistent insulin resistance surpasses pancreas' insulin output & blood glucose levels
remain elevated (fails to normalize glucose)
GLUT4
an insulin-sensitive glucose transporter in skeletal muscle & adipose tissue → during
muscle contraction OR when insulin binds to its receptor, GLUT4 translocates to the cell
membrane to facilitate glucose uptake from the blood into skeletal muscle
insulin-mediated GLUT4 pathway
insulin binds to insulin receptor (IR) → phosphorylates insulin receptor substrate →
activates PI3K (converts PIP2 to PIP3)→ activates PDK & Akt → translocation of
GLUT4 to cell membrane to enable glucose uptake
contraction-mediated GLUT4 pathway
physical activity stimulates AMPK, ROS, NO, and CaMK → activates AS160 →
translocation of GLUT4 to membrane
skeletal muscle: exercise training & glucose homeostasis effects
- increased blood flow → increased capillary density & improved glucose
deliver/extraction
- improved muscle quality: IIx → IIa (more efficient)
- increased biomechanical changes (increased insulin receptors, GLUT4, hexokinase,
glucose disposal enzymes, glycogen synthase activity)
pancreas: exercise training & glucose homeostasis effects
decreased hyperinsulinemia (insulin content in blood) due to improved insulin sensitivity
adipose tissue: exercise training & glucose homeostasis effects
decreased abdominal adiposity → decreased TNF-alpha (inflammatory marker),
increased GLUT4 receptor density, decreased plasma FFA
liver: exercise training & glucose homeostasis effects
- increased insulin sensitivity
- decreased gluconeogenesis
overall exercise training & glucose homeostasis effects
100% CORRECT A+ GRADED. Buy Quality Materials!
endocrine system components (4)
pituitary gland, thyroid gland, adrenal gland, pancreas
amino acid derivatives
- all derived from tyrosine
- epinephrine, norepinephrine, thyroid hormones, melatonin
peptide hormones
- largest group of hormones
- ADH, oxytocin, & hormones from the hypothalamus, pituitary gland, and pancreas
(insulin & glucagon)
lipid derivatives
- mostly derived from cholesterol
- steroid hormones (testosterone, estrogen)
- released by reproductive organs & adrenal cortex
3 ways hormones are inactivated
1. diffuse to target cells & bind to receptors
2. absorbed & broken down in liver/kidney
3. broken down by enzymes in plasma or ISF
hormonal secretion under negative feedback control is based on what types of
stimuli (3):
1. humoral stimuli (changes in ECF composition)
2. hormonal stimuli (changes in circulating hormone levels)
3. neural stimuli (neural stimulation of a neuroglandular junction)
humoral stimuli (of hormone release)
- high blood glucose → stimulate pancreas to secrete insulin → promotes glucose
uptake & storage by target cells
- low blood glucose → inhibits insulin & stimulates glucagon → stimulates glycigen
breakdown in liver → increases blood glucose
hormonal stimuli (of hormone release)
anterior pituitary gland releases ACTH into the blood → in response, the adrenal cortex
secretes glucocorticoids (cortisol) → influences several target organs & helps manage
stress by increasing energy availability (glucose release)
- negative feedback: high glucocorticoid levels reduce ACTH
neural stimuli (of hormonal release)
preganglionic sympathetic nerves (from CNS) stimulate adrenal medulla → secretes
catecholamines (E & NE) into blood → "fight or flight" response → increased HR, BP, &
energy availability
hormone levels are determined by (5)
1. quantity synthesized
2. rate of catabolism
3. rate of secretion into blood
,4. quantity of transport proteins present
5. changes in plasma volume
which hormones are not lipid soluble?
epinephrine, norepinephrine, and peptide hormones
- use a receptor → effect is indirect (action is linked by G-protein)
cAMP (secondary messenger)
binding of amine-based → activates adenylate cyclase → this catalyzes ATP
degradation to cAMP → cAMP activates protein kinases → alters cellular activity
If a hormone increased intracellular cAMP, what enzyme associated with
metabolism would be activated?
AMPK (potentially a change in ATP/AMP)
receptors inside cytoplasm/nucleus
- lipid-soluble hormones (thyroid/steroid hormones) are inside the cytoplasm or nucleus
& allow for passage into membranes
- forms a hormone-receptor complex (once bound) & activates/inactivates specific
genes, altering the rate of mRNA transcription & changing the structure/function of the
cell
impacts of insulin (4)
mediates glucose metabolism, affects fat synthesis, facilitates protein synthesis,
stimulates glucose transporters
impacts of glucagon (4)
- increases blood glucose
- in liver: stimulates glycogenolysis & gluconeogenesis (& ketone synthesis) (decreases
protein breakdown & glycogen synthesis)
- in adipose tissue: increases lipolysis & decreases triacylglycerol synthesis
- produced when blood glucose levels are low/decreases (release occurs later in
exercise- a function of intensity/duration)
what secretes glucagon?
islets of langerhans
how does training impact glucagon & insulin?
it reduces their responses to exercise, indicating improvements in metabolic efficiency
- glucagon pre-training shows a steeper increase as time increases; post-training, the
response is pretty flat
- insulin pre-training shows a rapid decrease; post-training, it has a much less
pronounced effect
how do insulin & glucagon work to maintain blood glucose homeostasis?
they work antagonistically
- in the pancreas: alpha cells secrete glucagon to raise blood sugar, while beta cells
secrete insulin to lower blood sugar
- in the liver: when blood sugar is high, insulin stimulates glycogen formation to lower
blood sugar, while when it is low, glucagon stimulates glycogen breakdown to raise it
- in tissue cells: insulin promotes glucose uptake to lower blood sugar
type 1 diabetes
typically occurs in younger people and is an autoimmune disease
- consists of 5-10% of all diabetes cases
- exercise has greater metabolic effects on this
, type 2 diabetes
lifestyle related & tends to occur after 40 (but recently in kids too)
- insulin resistance & impairs glucose tolerance
- often produces reduced exercise tolerance
- can be treated with exercise
- 1/3 of Americans are pre-diabetic and 84% don't know it
- T2D is releases to increased risk of CVD & cancer
normal insulin response
stimulus is a rise in blood sugar after eating → insulin is released from pancreatic beta
cells → insulin binds to muscle & adipose tissue receptors → increased glucose uptake
into cells → glucose is used for energy or stored as glycogen/fat → plasma glucose
levels return to normal
insulin-resistance response
pancreas overproduces insulin to maintain glucose levels → glucose uptake by muscle
is reduced despite high insulin
insulin-resistance risk factors
dyslipidemia, hypertension, obesity, heart disease, stroke, metabolic syndrome
type-2 diabetes insulin response
persistent insulin resistance surpasses pancreas' insulin output & blood glucose levels
remain elevated (fails to normalize glucose)
GLUT4
an insulin-sensitive glucose transporter in skeletal muscle & adipose tissue → during
muscle contraction OR when insulin binds to its receptor, GLUT4 translocates to the cell
membrane to facilitate glucose uptake from the blood into skeletal muscle
insulin-mediated GLUT4 pathway
insulin binds to insulin receptor (IR) → phosphorylates insulin receptor substrate →
activates PI3K (converts PIP2 to PIP3)→ activates PDK & Akt → translocation of
GLUT4 to cell membrane to enable glucose uptake
contraction-mediated GLUT4 pathway
physical activity stimulates AMPK, ROS, NO, and CaMK → activates AS160 →
translocation of GLUT4 to membrane
skeletal muscle: exercise training & glucose homeostasis effects
- increased blood flow → increased capillary density & improved glucose
deliver/extraction
- improved muscle quality: IIx → IIa (more efficient)
- increased biomechanical changes (increased insulin receptors, GLUT4, hexokinase,
glucose disposal enzymes, glycogen synthase activity)
pancreas: exercise training & glucose homeostasis effects
decreased hyperinsulinemia (insulin content in blood) due to improved insulin sensitivity
adipose tissue: exercise training & glucose homeostasis effects
decreased abdominal adiposity → decreased TNF-alpha (inflammatory marker),
increased GLUT4 receptor density, decreased plasma FFA
liver: exercise training & glucose homeostasis effects
- increased insulin sensitivity
- decreased gluconeogenesis
overall exercise training & glucose homeostasis effects
