Exam 2 Review Slides Flashcards
upregulation
increase in receptor number in response to low concentration of hormone increases sensitivity
ex) stress hormone concentration was low after a period of no exercise many receptors are causing very high BP and HR in response to exercise
downregulation
decrease in receptor number in response to high concentration of hormone
ex) high cortisol in bloodstream leads to a decrease in cortisol receptors to prevent cortisol from attacking proteins and breaking down tissue
the magnitude of hormone effect is dependent on (3)
- concentration of hormone (blood volume)
- number of receptors on cell
- affinity of the receptor for the hormone
Endocrine glands
- release hormones directly into bloodstream
- ductless
Hormones & their divisions
- bind to protein receptors to exert specific effect
- divided into: amino acid derivatives, peptides, steroids
mechanisms of hormone action: activation of genes genes to alter protein synthesis levels
steroid hormones
mechanisms of hormone action: second messengers in the cell via G protein
cyclin AMP (cAMP)
CA++
Inositol triphosphate
Diacylglycerol (DAG)
Hypothalamus
- most initial signals for hormone secretion comes from here
- stimulates release of hormones from anterior pituitary gland by releasing hormones or factors
- provides hormones for release from posterior pituitary gland
Anterior pituitary gland (7)
-most hormones from here are stimulating/releasing, their job is to move down and affect other glands that produce hormones with biological effect
- adrenocortizotropic hormone (ACTH)
- follicle-stimulating hormone (FSH)
- Lutenizing hormone (LH)
- Melanocyte-stimulating hormone (MSH)
- Thyroid-stimulating hormone (TSH)
- Prolactin
- Growth hormone (GH)
Posterior pituitary gland
- oxytocin
- antidiuretic hormone (ADH),, acts on kidneys to reduce water loss to maintain plasma volume
Thyroid gland
- stimulated by TSH
- releases calcitonin, regulates plasma Ca++ BLOCKS release from bone when Ca++ concentration is high
Parathyroid gland
- parathyroid hormone, primary regulator of plasma Ca++, STIMULATES Ca++ release from bone when concentration is low, STIMULATES reabsorption of Ca++ by kidneys
Adrenal medula
- above (inside) kidney
- secrete catecholamines: epinephrine and norepinephrine
Epinephrine and norepinephrine
- fast-acting hormones, part of “fight or flight”
- bind to adrenergic receptors, alpha and beta
adrenal cortex
- outside portion of gland above kidney
- secretes steroid hormones, aldosterone, cortisol, sex steroids
renin and aldosterone
hormones for blood pressure control, water balance, control of Na+ reabsorption and K+ secretion
pancreas
- both exocrine and endocrine functions
- releases insulin, glucagon, somatostatin, and digestive enzymes and bicarbonate
glycogenolysis is related to
exercise intensity
high intensity exercise results in greater and more rapid glycogen depletion (around 75% VO2 max)
Plasma epinephrine
- stimulates glycogenolysis
- high intensity exercise results in more plasma epinephrine
faster glycogen depletion in high intensity rages is mediated by epinephrine
control of muscle glycogen breakdown
- under dual control
- predominant mechanism: epinephrine-cyclic AMP (second messenger), via beta-androgenic receptors, E binds to B-receptor which uses cyclic-AMP which leads to glycogenolysis
- backup mechanism: Ca++ calmodulin
4 processes that maintain plasma glucose
- mobilizing glucose from liver glycogen stores
- mobilizing FFA from adipose tissue to spare blood glucose
- gluconeogenesis from amino acids lactic acid and glycerol
- blocking entry of glucose into cells, forces use of FFA
Effectors from control for plasma glucose
- slow acting: thyroxine, cortisol, growth hormone
- fast acting: epinephrine, norepinephrine, insulin and glucagon
Insulin vs glucagon roles
- insulin uptake and storage of glucose and FFA, decrease during exercise and following training
- glucagon released by pancreas to mobilized glucose and FFA during exercise, decreased following training
2 adjustments of blood flow during exercise
- increased cardiac output
- redistribution of blood flow from inactive organs to active skeletal muscle
pulmonary circuit
- right side of heart
- pumps deoxygenated blood to lungs via pulmonary arteries
- returns oxygenated blood to left side of heart via pulmonary veins
systemic circuit
- left side of heart
- pumps oxygenated blood to body via arteries
- returns deoxygenated blood to the right side of the heart via veins
layers of the heart
- epicardium
-myocardium (contracts) - endocardium
cardiac vs skeletal muscles
Both: striated, contain contractile proteins and actin and myosin
- cardiac muscles are shorter and branched
- cardiac muscles are connected by incercalated discs
- cardiac muscles are aerobic and have many mitochondria gut only one nucleus
- skeletal muscle fibers have satellite cells
phases of the cardiac cycle, how exercise impacts them
- systole: contraction
- diastole: relaxation
- during exercise diastole gets significantly shorter
Factors that influence arterial blood pressure
- blood volume increase, HR increase, SV, blood viscosity, and peripheral resistance increase all cause an increase in arterial blood pressure
mean arterial pressure (MAP), equation, regulation
average pressure in arteries
- cardiac output * total vascular resistance
MAP=DBP + 0.33(SBP-DBP)
- Short term regulation: SNS and baroreceptors (increase in SNS activity = decrease in BP)
- long term regualation: kidneys via control of blood volume, reduce blood volume -> decrease SV -> reduce cardiac output-> decrease in MAP
(similar to diuretics medication)
pacemaker for heart
SA node (sinoatrial node)
- in right atria, initiates depolarization
AV node (atrioventricular node)
- passes depolarization to ventricles
bundle branches
connect atria to left and right ventricle
purkinje fivers
spread wave of depolarization throughout the ventricle
electrocardiogram (ECG)
records electrical activity of the heart
- P wave, atrial depolarization
- QRS complex, ventricular depolarization and atrial repolarization
- T wave, ventricular repolarization
cardiac output (Q)
Q= HR * SV
Heart rate regulation
- PNS via vagus nerve, slows HR by inhibiting SA and AV node
- SNS via cardiac accelerator nerves, increases HR by stimulating SA and AV node
3 effectors of stroke volume
- Average aortic blood pressure, afterload
- strength of ventricular contraction, contractility
- end-diastolic volume (EDV), preload
Average aortic blood pressure, afterload
- pressure the heart must pump against to eject blood (MAP)
strength of ventricular contraction, contractility
- enhanced by circulating E and NE and direct sympathetic stimulation of the heart
end-diastolic volume (EDV), preload
- volume of blood in ventricles at the end of diastole
fick equation
VO2 = Q x a-vO2 difference
HRmax=208-(0.7*age)
