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Exercise Physiology > Exam 2 Review Slides > Flashcards

Exam 2 Review Slides Flashcards

1
Q

upregulation

A

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

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2
Q

downregulation

A

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

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3
Q

the magnitude of hormone effect is dependent on (3)

A
  1. concentration of hormone (blood volume)
  2. number of receptors on cell
  3. affinity of the receptor for the hormone
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4
Q

Endocrine glands

A
  • release hormones directly into bloodstream
  • ductless
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5
Q

Hormones & their divisions

A
  • bind to protein receptors to exert specific effect
  • divided into: amino acid derivatives, peptides, steroids
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6
Q

mechanisms of hormone action: activation of genes genes to alter protein synthesis levels

A

steroid hormones

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7
Q

mechanisms of hormone action: second messengers in the cell via G protein

A

cyclin AMP (cAMP)
CA++
Inositol triphosphate
Diacylglycerol (DAG)

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8
Q

Hypothalamus

A
  • 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
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9
Q

Anterior pituitary gland (7)

A

-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)

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10
Q

Posterior pituitary gland

A
  • oxytocin
  • antidiuretic hormone (ADH),, acts on kidneys to reduce water loss to maintain plasma volume
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11
Q

Thyroid gland

A
  • stimulated by TSH
  • releases calcitonin, regulates plasma Ca++ BLOCKS release from bone when Ca++ concentration is high
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12
Q

Parathyroid gland

A
  • parathyroid hormone, primary regulator of plasma Ca++, STIMULATES Ca++ release from bone when concentration is low, STIMULATES reabsorption of Ca++ by kidneys
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13
Q

Adrenal medula

A
  • above (inside) kidney
  • secrete catecholamines: epinephrine and norepinephrine
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14
Q

Epinephrine and norepinephrine

A
  • fast-acting hormones, part of “fight or flight”
  • bind to adrenergic receptors, alpha and beta
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15
Q

adrenal cortex

A
  • outside portion of gland above kidney
  • secretes steroid hormones, aldosterone, cortisol, sex steroids
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16
Q

renin and aldosterone

A

hormones for blood pressure control, water balance, control of Na+ reabsorption and K+ secretion

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17
Q

pancreas

A
  • both exocrine and endocrine functions
  • releases insulin, glucagon, somatostatin, and digestive enzymes and bicarbonate
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18
Q

glycogenolysis is related to

A

exercise intensity
high intensity exercise results in greater and more rapid glycogen depletion (around 75% VO2 max)

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19
Q

Plasma epinephrine

A
  • stimulates glycogenolysis
  • high intensity exercise results in more plasma epinephrine
    faster glycogen depletion in high intensity rages is mediated by epinephrine
20
Q

control of muscle glycogen breakdown

A
  • 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
21
Q

4 processes that maintain plasma glucose

A
  • 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
22
Q

Effectors from control for plasma glucose

A
  • slow acting: thyroxine, cortisol, growth hormone
  • fast acting: epinephrine, norepinephrine, insulin and glucagon
23
Q

Insulin vs glucagon roles

A
  • 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
24
Q

2 adjustments of blood flow during exercise

A
  • increased cardiac output
  • redistribution of blood flow from inactive organs to active skeletal muscle
25
Q

pulmonary circuit

A
  • right side of heart
  • pumps deoxygenated blood to lungs via pulmonary arteries
  • returns oxygenated blood to left side of heart via pulmonary veins
26
Q

systemic circuit

A
  • left side of heart
  • pumps oxygenated blood to body via arteries
  • returns deoxygenated blood to the right side of the heart via veins
27
Q

layers of the heart

A
  • epicardium
    -myocardium (contracts)
  • endocardium
28
Q

cardiac vs skeletal muscles

A

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

29
Q

phases of the cardiac cycle, how exercise impacts them

A
  • systole: contraction
  • diastole: relaxation
  • during exercise diastole gets significantly shorter
30
Q

Factors that influence arterial blood pressure

A
  • blood volume increase, HR increase, SV, blood viscosity, and peripheral resistance increase all cause an increase in arterial blood pressure
31
Q

mean arterial pressure (MAP), equation, regulation

A

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)

32
Q

pacemaker for heart

A

SA node (sinoatrial node)
- in right atria, initiates depolarization

33
Q

AV node (atrioventricular node)

A
  • passes depolarization to ventricles
34
Q

bundle branches

A

connect atria to left and right ventricle

35
Q

purkinje fivers

A

spread wave of depolarization throughout the ventricle

36
Q

electrocardiogram (ECG)

A

records electrical activity of the heart
- P wave, atrial depolarization
- QRS complex, ventricular depolarization and atrial repolarization
- T wave, ventricular repolarization

37
Q

cardiac output (Q)

A

Q= HR * SV

38
Q

Heart rate regulation

A
  • 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
39
Q

3 effectors of stroke volume

A
  • Average aortic blood pressure, afterload
  • strength of ventricular contraction, contractility
  • end-diastolic volume (EDV), preload
40
Q

Average aortic blood pressure, afterload

A
  • pressure the heart must pump against to eject blood (MAP)
41
Q

strength of ventricular contraction, contractility

A
  • enhanced by circulating E and NE and direct sympathetic stimulation of the heart
42
Q

end-diastolic volume (EDV), preload

A
  • volume of blood in ventricles at the end of diastole
43
Q

fick equation

A

VO2 = Q x a-vO2 difference

44
Q

HRmax=208-(0.7*age)

A
45
Q
A
45
Q
A

Exercise Physiology (5 decks)

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