NEUROENDOCRINOLOGY Flashcards
hormones
chem messengers
- reg macronutrient stores
- fight/flight
- adaptive response (training adaptations)
neuroendocrinology
hormones plus nervous system/NT communiction
systematic control of systems
hormone classes
based on chem makeup
- steroids: from lipids, slow acting
- a.a. derivatives
- peptides/proteins: fast acting, acute response
how do hormones enter cell
steroidal hormones bind to albumin protein bcs are hydrophobic
- can cross fatty cell memb
non-steroidal activate receptors on cell memb, don’t enter
what impacts blood hormones concentration
- rate of secretion: how much hormone
- rate of metabolism/excretion: if bind to receptor, are activated and not in blood
- numb of trans proteins: specific to steroid hormones, if able to move into cell or stay in blood
- changes in plasma vol: dec plasma vol i.e. sweat, increases hormone conc
downregulation and upregulation
upreg: inc receptor number bcs low hormone conc
downreg: dec receptor numb bcs high hormone conc
3 steps of how hormones work
- alter DNA activity to modify protein synthesis:
- steroid hormones release off transporter to cross cell memb
- non-steroid ones don’t need transport thru blood
- in cytosol, binds to transport to nucleus
- in nucleus, create mRNA as blueprint for protein
- mRNA leaves and causes protein synthesis - activating 2nd messengers via G protein
- cyclic AMP/cAMP: hormone binds to protein complex, initiates cascade of events….occurs in blood, hormone doesn’t enter cell
- adenylate cyclase turns ATP to cAMP…this makes protein kinase become active, which initiates cellular resp
- phospholipase C: breaks down pip2, which can do diff functions
- altering memb transport
- i.e. insulin via tyrosine kinase
- insulin binds to receptor n cell, then phosphorylate self to cause response…activates glucose synthase
- activates glucose to become glycogen
major endocrine glands
- thyroid
- parathyroid
- PANCREAS: insulin, glucagon
- testes/ovaries
- adipose: makes adipocytes
- hypothalamus - ant/post pituitary
- muscle: myokines
- ADRENAL GLAND: adrenal medulla epi and NE
estrogen and progesterone
estrogen stims breast dev, fat deposition, secondary sex characters
- inc reliance on FAT AS FUEL in exercise
progesterone imp reproduction
both fluctuate w menstruation
testosterone
anabolic: tissue building
androgenic: promotes masc traits
high musc to fat ratio
can stim protein synthetic resp w training bcs is RELEASED DURING EXERCISE
growth hormone
effects ALL tissue growth
- amino acid uptake and protein synthesis
- secreted by hypothalamus
increases release of IGF/insulin like growth factor
- aids w tissue growth
adipose tissue
stores TGs and secretes hormones
leptin: influences appetite thru hypothalamus…feel full
- inc insulin sensitivity and FFA oxidation
adiponectin: inc insulin sensitivity and FA oxidation
muscle
produces myokines when contracts
inc glucose uptake
inc BV growth
inc liver glucose production
redunant control
substrate utilization under control of multiple mechanism
peptide hormones involved w exercise
nonsteroidal
from pancreas: slow acting
- insulin: inc nutrient uptake, dec breakdown
- glucagon: inc nutrient release, and inc storage breakdown
from adrenal medulla: fast acting
- epi: inc lipolysis, inc musc glucogenolysis
- NE: inc liplysis, cariorespiratory function
plasma epinephrine
main driver of glycogen brekdown initiated by 2nd messenger
activates protein kinase
propranolol
drug that blocks adrenergic receptors
blocks glycolysis thru NE and E, but OTHER mechanisms involved in glycogen depeltion
- dual control continues glycolysis
dual control of glycogen depletion
epi-camp via adrenergic receptors
ca-calmodulin: inc during exercise bcs ca release from SR
- not impacted by adrenergic receptor blocking drugs
how is blood glucose maintained during exercise
- mobilization of glucose from liver glycogen stores:
- liver glycogen becomes glucose in blood - mobilization of FFA from adipose tissue
- if cam use fat instead of liver stores, will
- don’t waste stores - gluconogenesis: from a.a., lactic acid, glycerol
- blocking entry of glucose into cells:
- by slow acting hormones/cortisol, growth hormone, thyroxine
- by fast acting hormones i.e. NE, E, insulin, glucagon
role of coritsol
stims fat and protein breakdown
- glucose production from non-glucose stores
decreases in low intensity, inc during high
stimulated by exercise and stress
role of growth hormone
inc FFA oxiation, inc non-glucose derivatives to glucose
supports cortisol
inc w exercise intensity
somatostatin
released by pancreas
regs rate of entry of nutrients into circulation
training effects on insulin and glucagon
trained ppl have LESS change in plasma glucagon
after training, glucose conc maintained via small changes in insulin and glucagon
FFA mobilization during exercise
FFA mobilization dec during heavy exercise reardless of hormonal stim for mibilization
bcs:
- high lvls lactic acid promotes resynth of TGs
- elevated H lvls inhibits HSL
- inadequate blood flow to adipose tissue
- insufficient albumin to move FFA
