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physiology yr 2 > wk7 onwards > Flashcards

wk7 onwards Flashcards

1
Q

RESPIRATORY PHYSIOLOGY

A
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2
Q

upper respiratory tract

A

nose
nasal cavity
mouth
pharynx
larynx

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3
Q

laryngeal prominence

A

adam’s apple
thyroid cartilage that surrounds the larynx
protecting front and walls of larynx
is not sex specific
- larger and more visible in males due to hormonal activity during puberty

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4
Q

lower respiratory tract

A

trachea
lungs
- bronchi
- bronchioles
-> conducting (20)
-> terminal (final)
-> respiratory
alveolar ducts
alveolar sacs
-> alveolus (i)
right and left lung
- right has three lobes
- left has two lobes

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5
Q

bronchi

A

primary bronchi
- many bronchi and bronchioles
lobar bronchi
- secondary
tertiary/segmental
carina is the break between the right and left main bronchus
left main bronchus is slightly more lateral to prevent choking

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6
Q

alveoli

A

type 1 cell
- continuous lining surrounds alveolus
- main site of gas exchange
type 2 cell
- free surfaces that contain microvilli
- secrete alveolar fluid which reduces tendency for alveolus to collapse
-> called surfactant
- provides optimum conditions for gas exchange
narrow distance in terms of diffusion

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7
Q

nerves

A

phrenic nerve (c3-c5 root)
intercostal nerve (T1-T11 root)
vagus nerve (X)
glossopharyngeal nerve (IX)

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8
Q

brain

A

respiratory control centres
- pons
-> apneustic area
-> pneumotaxic area
medulla rhythmicity area
- ventral and dorsal group

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9
Q

receptors

A

chemoreceptors
- both centrally and peripherally
mechanoreceptors
- stretch receptors
irritant receptors
peripheral proprioceptors

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10
Q

chemoreceptors

A

central
- found in brain stem
peripheral
- carotid body
- aortic body

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11
Q

muscles

A

accessory muscles
diaphragm
intercostal muscles
abdominal muscles

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12
Q

Boyle’s law

A

pressure of a gas in closed container inversely proportional to volume of container at a constant temperature
p is proportional to 1/V
as volume increases the pressure decreases

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13
Q

inhalation

A

diaphragm
- contracts and flattens
external intercostals
- up and out
- elevation of ribs
increases volume and decreases alveolar pressure
air flows into the lungs
from higher pressure in atmosphere to low pressure in alveoli

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14
Q

exhalation - rest

A

passive process
- elastic recoil
elastin is structural proteins that wrap around the outside of the alveoli
-expand during inhalation due to change in volume but recoil back to original state
when elastin fails can not deal with changes in pressure
- loss of support in the airways narrows the airways and air flow limitation
hyperinflation - more air stuck in the lungs for longer periods of time as less changes in pressure

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15
Q

exhalation - exercise

A

active process
internal intercostals contract
external obliques
rectus abdominus
transverse abdominus
to force out of the lungs faster than needed at rest
still use recoil as well as active process

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16
Q

PONS (apneustic and pneumotaxic)

A

pons modifies the outputs of the medullary centres
apneustic
- prolonged and slow rate of breathing
- stimulates inspiratory neurones found in dorsal respiratory group and ventral respiratory group
- overstimulation leads to apneustic breathing
-> long gasping inspirations interrupted by short expirations
- overridden by pneumotaxic
pneumotaxic
- inhibitory impulse, limits duration
- controls inspiratory time
- increase signals increases respiration rate
- week signal prolongs and increases tidal volume

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17
Q

medulla oblongata (DRG & VRG)

A

rhythmicity
controls basic rate of breathing
dorsal respiratory group
- mainly inspiratory neurones - triggers inspiratory impulses
- located bilaterally in the medulla
- neurones extend into the VRG (ventral respiratory group)
- vagus and golossopharyngeal nerves bring sensory impulses into the DRG from the lungs and airways, the peripheral chemoreceptors and joint proprioceptors
ventral respiratory group
- do not extend into DRG
- both inspiratory and expiratory neurones
- located bilaterally in the medulla
- primarily active during exercise and stress
- can send inspiratory impulses to the laryngeal and pharyngeal muscles, diaphragm and the external intercostals
- other VRG neurones send expiratory signals to the abdominal muscles and internal intercostals
interaction between DRG and VRG inspiratory neurones gives smooth inspiration aspect, rather than gasping

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18
Q

central chemoreceptors

A

respond to increases in hydrogen ions
during exercise increase in co2 production -> increase in H+

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19
Q

peripheral chemoreceptors

A

found within the carotid and aortic bodies
glomus cell is an example
contain K+ channels so K+ leaks out of the cell
low oxygen level e.g. during exercise
- potassium channels close
- build up of K+ inside of the glomus cell
- membrane depolarises
- open calcium channels and calcium floods into the cell
exocytosis of dopamine across and out of the cell
glomus cell can respond to increases in PCO2 and decreases in PO2

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20
Q

ventilatory threshold

A

point at which pulmonary ventilation increases disproportionately with oxygen consumption during graded exercise

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21
Q

assessing diaphragm fatigue

A

two small slightly inflated balloons down throat
- one measures esophageal pressure
-gastric pressure
one above where diaphragm is and one below
can take EMG measurements
stimulation diaphragm with phrenic stimulation
- allows to twitch the diaphragm
- look at pressure difference and assess diaphragm fatigue

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22
Q

Babcock et al., 2002
- respiratory muscle unloading

A

assisted ventilation during 8-13 mins of exhaustive exercise
those assisted with ventilation lowered cost of breathing
VO 2 was a lot lower
looked at twitch pressures after stimulating diaphragm
following exercise in normal group pressure differences have dropped instigating diaphragm fatigue
assisted ventilation much higher pressure difference following exercise

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23
Q

CARDIOVASCULAR PHYSIOLOGY

A
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24
Q

cardiovascular system

A

two circuits - one low pressure, one high pressure
pump = heart
high pressure circuit = arteries
exchange vessels = capillaries
low pressure = veins

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25
Q

cardiovascular system function

A

delivery of o2 and other nutrients
removal of co2 and other waste products
support thermoregulation and control body fluid balance
hormone transport
regulation of immune function

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26
Q

system parts and function

A

heart - pressure creation
arteries and arterioles - carry blood away from heart
capillaries - exchange
veins and venules - carry blood towards the heart

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27
Q

heart blood flow

A

2 pumps
-right heart
-> receives blood returning from throughout the body
-> pumps deoxygenated blood to the lungs
- left heart
-> receives oxygenated blood from the lungs
-> pumps oxygenated blood to all other tissues in the body

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28
Q

valves

A

atrioventricular valves separate the atriums from the ventricles
- tricuspid - one way blood flow from the right atrium to the right ventricle
- bicuspid - one way blood flow from the left atrium to the left ventricle
semilunar valves
- pulmonary prevents backflow from the arteries to the ventricle
- aortic separates left ventricle from opening of aorta

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29
Q

sinoatrial node

A

superior part of right atrium
spontaneously depolarises and repolarises to provide innate stimulus for the heart to actually contract
natural pacemaker of the heart
electrical impulses spread from SA via tracks into AV node and also into left atrium

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30
Q

electrical impulse route

A

SA node
AV node
Bundle of His
Bundel branches

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31
Q

atrioventricular node

A

located in right atrium in inferior part of chamber
conduct electrical impulse from atrium to ventricles
delay in signal as less gap junctions
smaller diameter of fibres
spreads into the AV bundle/ Bundle of His

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32
Q

AV bundle/ Bundle of His

A

transmits impulse rapidly throughout ventricles through Purkinje system

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33
Q

AV bundle branches

A

formed from AV bundle
penetrate both right and left ventricles

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34
Q

P wave

A

first appears on ECG trace
represents atrial depolarisation
occurs when impulse travels from the SA node through the atria until it reaches AV node

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35
Q

QRS complex

A

ventricular depolarisation
impulse travels from the AV bundle to the purkinje fibres and though the ventricles
atrial repolarisation happening at same time but bc of lower amplitude dont see it on QRS complex

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36
Q

T wave

A

ventricles repolarising

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37
Q

ECG - abnormal
- bradycardia
- tachycardia

A

lead to irregular heart rhythms known as arrhythmias
most common are bradycardia - resting heart rate is lower than 60 bpm
tachycardia - resting heart rate higher than 100 bpm

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38
Q

Henry’s law

A

‘mixture of gas is in contact with a liquid each gas dissolves in the liquid in proportion to it’s partial pressure and solubility until equilibrium is achieved and the gas partial pressure are equal in both locations’
solubility is constant
pressure gradient is critical
- gases diffuse from high pressure areas to low pressure areas

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39
Q

blood pressure

A

pressure exerted by blood on vessel walls
- usually refers to arterial blood pressure
systolic blood pressure
- ventricular systole
diastolic blood pressure
- ventricular diastole
mean arterial pressure
=2/3 DBP + 1/3 SBP

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40
Q

cardiac output

A

total volume of blood pumped by the ventricle per minute (Q)
Q (L) = HR x SV
SV (ml) = EDV -ESV
= end diastolic volume - end systolic volume
Q = HR x (EDV-ESV)

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41
Q

stroke volume

A

volume of blood pumped during one beat
- EDV - end diastolic volume = 100 ml normal
- ESV - end systolic volume = 40 ml normal

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42
Q

heart rate variability

A

variation in time interval between heartbeats aka beat to beat interval
RR variability
high HRV is associated with positive outcomes
- good emotional regulation
- well being
- information processing
low HRV is associated with negative outcomes
- depression, anxiety, poor emotional regulation
- IBS
- ageing
- cardiac mortality
RR variability - between QRS of one beat and another beat

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43
Q

autonomic control (sympathetic / parasympathetic)

A

inotropic action = increase beat strength
- more calcium and more cross bridges formed
chronotropic = increase in time
sympathetic (fight or flight)
- increase heart rate and inotropism
parasympathetic (relaxation)
- decrease heart rate and inotropism

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44
Q

oxygen consumption

A

vo2 is the difference between volume of gas inhaled and volume of gas exhaled per unit of time

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45
Q

determinants of O2 - The Fick equation

A

cardiac output (Q)
blood flow and oxygen extraction
The Fick equation
= Q* (CaO2 - CvO2)

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46
Q

maximal oxygen uptake

A

assess ‘ the integrated functioning of the pulmonary, cardiovascular and muscle systems to uptake, transport and utilise 02 …’
maximum rate at which an individual can take up and utilise oxygen while breathing at sea level
maximum rate of ATP resynthesis
generally in two people with same VO2 max, one with a higher lactate threshold will perform better in endurance events

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47
Q

cardiac output and exercise

A

in response to exercise
increase in cardiac output
increase in HR
increase in SV
increasing chronotropic effect
- decreasing beat to beat interval
inotropic effect
- stronger contraction
Frank Starling mechanism
- greater end diastolic volume stretches myocardial muscle and thus can result in more forceful contraction

48
Q

blood pressure and exercise

A

systolic blood pressure increases with intensity
- stroke volume and heart rate have increased the cardiac output
- amount of blood pumped in each ventricular systole is higher
- pressure exerted on the walls is higher
mean diastolic pressure is going to maintain or may decrease
- to create more space for amount of blood that has increased, arteries dilate
- decreases diastolic pressure
both blood pressure higher for arms than legs
- due to higher muscular mass in upper body
- leads to higher increase in both systolic and diastolic pressures

49
Q

blood lactate

A

lactate threshold - increase in lactate above the baseline value
lactate turnpoint - sudden and sustained breakpoint in lactate
two people with same VO2 max
- one with higher lactate threshold will perform better in endurance events

50
Q

haemoglobin 02 affinity affected by

A

acidity
pco2
2,3 - BPG (2,3- DPG)
temperature

51
Q

02 extraction and exrecise

A

increased extraction of o2 from the blood
due to oxyhaemoglobin disassociation curve
- s shaped curve
- higher pO2 = higher saturation

52
Q

2,3- biphosphoglycerate

A

BPG is formed during glycolysis
- helps to unload o2 by binding with Hb
higher affinity for BPG so haemoglobin offloads the oxygen

53
Q

pco2

A

pCo2 rises
- affinity of Hb decrease
harder tissue is working more o2 is released

54
Q

oxygen utilisation

A

increased extraction of o2 from the blood
dilation of peripheral vascular beds
increased Q
increase in pulmonary blood flow
increase in ventilation

55
Q

NEURONE PHYSIOLOGY

A
56
Q

anatomy of a neuron

A

dendrites (little trees)
soma
- cell body
axon hillock
- initiation of axon potentials
axon
- no protein synthesis
axon terminal
-> synapses
- synaptic cleft is space between neurons and what attaching to

57
Q

axoplasmic transport

A

microtubules within axon
- made of tubulin
anterograde transport
- protein kinesin
- transport to axon tip
retrograde transport
-protein dynein
- transport to cell body

58
Q

action potentials

A

resting membrane potential
sufficient stimulus above threshold (- 55mV) action potential generated
depolarisation of the cell
Na VG gates open and Na in
repolarisation at approx + 30 mV
Na close and VG K open and K out
delayed closing of VG K channels so undershoot past resting potential

59
Q

resting membrane potential

A

extracellularly have sodium and chloride
within cytosol have potassium, inorganic phosphate and amino acids
membrane permeability differs for sodium and potassium
inwards flow of sodium ions does not match outward flow of potassium ions
Na/K pump actively transports 3 Na out of the cells whilst pumping 2 K into the cells
- costs ATP

60
Q

action potential propagation

A

continuous conduction
depolarisation and repolarisation occurs and the spreads to the adjacent membrane and down the axon

61
Q

synapses

A

electrical synapses
- found in heart
chemical synapses
- found in muscle

62
Q

electrical synapses

A

gap junctions
- bidirectional
- ions and small molecules
connexins
- six connexins form a connexon
- two, one from each gap junction then bind together
desmasones
- keep everything held together
electrical transmissions very close together

63
Q

chemical synapses

A

synaptic vesicles pass neurotransmitters across the synpatic cleft
neurons
muscle fibres
CNS
- axondendritic
-> synapse between one axon of one neuron to another dendrite
- axosomatic
-> nerve between a cell body and the axon of another
- axoaxonic
->between two axons

64
Q

neuromuscular junction

A

1.action potential is arriving at the neuromuscular junction
2. VG calcium ion channels
- influx of calcium to the synaptic end bulb
3. acetylcholine in vesicles is expelled via exocytosis into the synaptic cleft
4. efflux potassium restores the resting potential in synaptic bulb
- allows further action potentials to arrive
5. acetylcholine diffuses across the synaptic cleft and binding to receptors
6. influx of Na and generates action potential
7. acetylcholine esterase breaks down the receptor bound acetylcholine into acetate and choline
8. choline then taken back into synaptic end bulb for the re-synthesis of acetylcholine

65
Q

exocytosis

A

snare proteins - calcium activates snare proteins that are outside vesicles and also within the cell membrane
- V-snare (vesicles)
-> synaptotagmin
-> synaptobrevin
- T-Snare (found on the cell membrane)
-> Snap - 25
-> syntaxin

66
Q

muscle contraction

A
  1. nerve impulse arrives at terminal of motor neuron, ACh leaves neuron via exocytosis
  2. ACh diffuses across synaptic cleft and triggers action potential
  3. muscle AP travels along transverse tubule opening Ca2+ release channels in SR, allowing calcium ions into sarcoplasm
  4. Ca2+ bins to troponin, exposing binding sites for myosin
  5. myosin heads bind to actin and initiate power stroke
  6. Ca2+ release channels in SR close and Ca2+ active transport pumps use ATP to restore low level of Ca2+ in sarcoplasm
67
Q

neurotransmitters

A

most are either
- amino acids
- amines (derived from amino acids)
- peptides (constructed from amino acids)
- major exception is ACh

68
Q

neurotransmitter groups

A

cholinergic neurons
catecholaminergic neurons
serotonergic neurons
amino acidergic neurons

69
Q

cholinergic neurons

A

acetylcholine (ACh)
all motor neurons in spinal cord and brain stem
requires specific enzyme to synthesise
- choline acetyltransferase
Acetyl- CoA + choline -> acetylcholine
acetylcholine esterase breaks it back down

70
Q

catecholaminergic neurones

A

dopamine, norepinephrine, epinephrine
-the precursor is tyrosine
dopamine is pleasure neurotransmitter - addiction
epinephrine (adrenaline) - fight or flight neurotransmitter
norepinephrine (noradrenaline)

71
Q

serotonergic neurons

A

use serotonin
serotonin (5-hydroxytryptamine( 5-HT))
tryptophan precursor
serotonin is mood neurotransmitter contributing to good wellbeing and happiness e.g. help with sleep and digestive system regulation
serotonin affected by exercise and exposure to light
seems to inhibit dopamine production
low levels of serotonin can lead to an overproduction of dopamine which tends to lead to impulsive behaviours

72
Q

amino acidergic neurons

A

glutamate
- memory neurotransmitter
- highly toxic
glycine
GABA
- gammaminobutyric acid
- calming neurotransmitter
- inhibitory in nature formed from glutamate
- lots of anti-anxiety medication based around

73
Q

cocaine

A

dopamine released via exocytosis across the synaptic cleft and binds to receptor on the post-synaptic membrane
released and reuptake in end bulb and broken down by this MAO (monamineoxidase) allowing reformation of dopamine
cocaine stops the re uptake of dopamine from the synaptic cleft

74
Q

Botox

A

essentially paralysing the muscle
Botulinum toxin cleaves SNARE proteins and stops the vesicles from binding to the membrane
no acetylcholine binding to the membrane, there’s no muscle contraction

75
Q

scopolamine

A

devil’s breath
zombie drug
anti anticholinergic neurone

76
Q

measurement tools

A

dynamometer
magnetic stimulation
electrical stimulation
electromyography

77
Q

dynamometer

A

measuring force, strength
- newtons or newton meters
absolute values
- total newtons
relative values
- newtons per bodyweight

78
Q

electromyography

A

recording changes in electrical potential of a muscle
- surface
- intramuscular

79
Q

magnetic stimulation

A

areas of central control
- arms greater fine motor movement
- legs smaller area

80
Q

electrical stimulation

A

common example
- femoral stimulation
-> femoral nerve
-> gluteal fold
stimulation intensity
- 130% of M-max or maximal twitch
zap someone small amount and then increase until don’t see any change in twitch response of the muscle
- multiple by 130 % and that would be value that use to stimulate someone

81
Q

motor evoked potential (MEP)

A

elicit the stimulation from the motor cortex
magnetic stimulation
electrical stimulation

82
Q

MWAVE

A

elicited from the nerve or directly from the muscle
responding to electrical stimulation
compound muscle action potential (CMAP)
summation of muscle action potential

83
Q

measurements

A

excitability
- M- wave amplitude (M wave measure from electrical stimulation at the muscle)
- M- wave area
contractility
- twitch force
- time to peak twitch
- half relaxation time
- electromechanical delay
voluntary activation
- takes into account how much someone is pushing to begin with
- ask someone to maximally contract (superimposed)
- stimulate on top of that contraction (potentiator twitch)
- if no increase, shows that they are 100% activated
VA= (1-(superimposed twitch / potentiated twitch))*100

84
Q

AGEING

A
85
Q

decline in strength - ageing

A

decrease in strength clear after the age of 60 yrs of eccentric, isometric or concentric contraction
power max and normalised power max both by body mass and leg length significantly decline with age in both men and women
unloading shortening velocity has no significant difference
when normalised to leg length also no significant difference
steady declines of ~ 1-2% per year
at 70-80 yrs, 20-40% lower on tests of isometric strength than young adults
very old show even greater (~50%) reduction
decrease in force, decrease in power but no real decrease in velocity

86
Q

ageing

A

increasing age there is a decrease in force-generating capacity but no changes in maximum shortening velocity of muscles that control leg multi-joint movements
an ageing-related decline in muscular power performance has much larger effects on the force than on the shortening velocity of muscles
finding suggests that decrease in muscle force-generating capacity and power with ageing may primarily lead to loss of mobility
inactive so lose strength ?
or lose strength so inactive?

87
Q

why decline in strength as get older

A

muscle- fibre loss of motor units begins near the age of 50-60
muscle size begins to decrease at ~30 yrs, decreasing 10% by 50 yrs and parallels reduced fibre size
muscle area declines markedly due to the decrease in total number of fibres that receive stimulation

88
Q

arms vs legs - ageing

A

leg strength deteriorates quicker than arm strength
reduction in physical activity primarily associated with decreased use of lower body muscles
sedentary lifestyle more likely to bring about atrophy in those muscles

89
Q

counteract the effect - ageing

A

metabolic rate decreases 5% each decade after 40
- decreased muscle mass
REx increases our muscle mass
- increased metabolic rate
- increased resting metabolic rate
- decreased body fat
resistance training used to do this
increase in muscle cross-sectional area leads to increase in strength
muscle strength is a product of the neural drive to the muscle

90
Q

why counteract the effect - ageing

A

muscle hypertrophy - increase in muscle sizes
type 1 and type 2 - increase in both types so ratio doesn’t change between type 1 and type 2
proportion didn’t change

91
Q

neural function and ageing

A

muscle strength is coming from the size of the muscle and neural drive to that muscle
40% decline in spinal cord axons
10% decline in nerve conduction velocity (Laroche 2007)
reduction in the pathway but also slowing of that pathway

92
Q

nerve conduction velocity - ageing

A

nerve conduction velocity decrease
- structural changes in myelinated neurons -> increased internal distances between nodes of ranvier = longer to process
- preferential loss of fastest conducting axons
- decrease in soma size
-> less ability to produce proteins
-> less ability to produce acetylcholine for transfer

93
Q

nerve conduction velocity and training - ageing

A

increasing movement tends to increase nerve conduction velocity
diabetes
- a reduction in Na/K AtPase activity
- increased Na+, K+, sortibol, fructose = increase osmosis
- accumulated water compresses nerves = decrease the nerve conduction velocity (NCV)
training alters this
- yoga lead to an increase in NCV
-> less compression of nerves due to increased action of Na/K pump

94
Q

deterioration in lung function with ageing

A

lung function gradually deteriorates with advancing age and appears to be a natural process (even in the absence of substances capable of promoting lung irritation and inflammation)
aerobic training or training can bring about changes
older functional demonstrate better capacities than sedentary subjects
reduction in muscle mass
- ability for bodies to uptake oxygen and utilise oxygen converting into energy why vo2 max decreases

95
Q

cardiovascular function with ageing

A

decline in aerobic capacity
appears that Vo2 max declines at approximately 1% per year
will occur twice as fast if sedentary compared to physically active individuals
blood flow and ability for body to pump blood round the heart over time slows

96
Q

sprint power with ageing

A

running velocity declined from ~ 5-7% per decade
main factors
- reduced stride length
- increase in contact time of foot with ground
-> reduction in tendon compliance

97
Q

heart rate and cardiac output with ageing

A

heart rate max decreases with age
as reduction in electrical activity of the synoatrial node
heart is pumping less, cardiac output is going to be less
recoil within artery walls and contraction does not function as well
lower leg blood flow
arterial wall properties change due to inability of internal diameter to expand and recoil - aspects of vasodilation and vaso constriction is restricted
more problems with blood pressure
more risk of heart disease
reduction in peripheral blood flow associated with age related decline in muscle mass
reduction in cerebral blood flow = less blood to the brain = less oxygen supplied to brain = increase dimentia risk
- cerebral vaso constriction

98
Q

body composition changing with age

A

after 18 years of age can gain body weight and fat until about 50/60
after start to see decrease in body mass but still increasing body fat
decrease in fat free mass

99
Q

ALTITUDE

A
100
Q

what is altitude

A

height of an object or point in relation to sea level or ground level
medicine defines altitude at 1500m above sea level

101
Q

hypoxia

A

inadequate supply of oxygen to respiring tissue (Kent 1999)
become hypoxic when exercising to a certain level
can become hypoxic in any environment

102
Q

altitude and hypoxia

A

altitude provides exposure to a hypoxic environment
high altitude
- decreased ambient temperature
- increased solar radiation
- decreased barometric pressure (why experience hypoxic environment)

103
Q

change in barometric pressure

A

’ the pressure is less the higher one goes as there is less mass of pushing down on top’ - Blaise Pascal 1648
the lower down the more stuff on top so the higher pressure
always 21% oxygen wherever

104
Q

dalton’s law

A

the total pressure exerted is equal to the sum of the partial pressures of the individual gases
atmospheric pressure
- decreases at higher altitude
- if atmospheric pressure drops partial pressure will drop

105
Q

ambient air

A

o2 = 20.93% co2 = 0.03% N2 = 79.04%
barometric pressure (Sea level) = 760 mmHg
partial pressure = fractional concentration x total gas pressure
- oxygen - 159 mmHg (0.2093 * 760 = 159)
- Co2 - 0.2 mmHg
- N2 - 600 mmHg
at different altitudes the percentages stay the same but pressure changes and thus partial pressures change

106
Q

hypo, hyper and norm

A

hypoxia: low oxygen pressure (PO2) (altitude)
- hypobaric hypoxic (low pressure, low oxygen) <- up mountain
- normobaric hypoxia (normal pressure, low oxygen) <- altitude chamber (reduces partial pressure of oxygen)
normoxia: normal oxygen pressure (PO2) (sea level) <- walking around normally
hyperoxia: high oxygen pressure (PO2)

107
Q

oxygen cascade

A

fall in PO2 reduces the driving pressure for gas exchange in the lungs and in turn produces a cascade of effects to the level of the mitochondria, the final destination of the O2

108
Q

oxygen saturation

A

o2 saturation falls as altitude increases due to decrease in cascade of oxygen pressure

109
Q

why athletes faster at shorter distance at moderate altitude

A

less friction for the runner
less stuff in the air

110
Q

maximal oxygen uptake and altitude

A

Vo2 decreases with increasing altitude
decrease 1% for every 100m above 1500m altitude

111
Q

hypobaric vs normobaric hypoxia

A

during exercise minute ventilation was lower in HH compared with NH after 8 hours
sympathetic nervous system activity increased with exposure to high altitudes

112
Q

altitude sickness

A

mild altitude sickness (AMS)
high altitude pulmonary oedema (HAPE)
high altitude cerebral oedema (HACE)

113
Q

AMS

A

symptoms
- headache
-nausea
-fatigue
causes
- ascending faster than 500m/d
- exercise vigorously
can take tablets

114
Q

HAPE

A

develops after 2-3 days at altitude >2500m
can be fatal within hours
accumulation of fluid in the lungs that prevents the air spaces from opening up and filling with fresh air with each breath
symptoms (>2500m)
- excess fluid in the lungs
- breathlessness
- fever
- coughing frothy spit
causes
- ascending faster than 500m/d
- exercise vigorously

115
Q

HACE

A

an increase in blood flow to thebrain is a normal response to low oxygen levels as body needs to maintain constant supply of oxygen to the brain
if blood vessels in brain are damaged fluid may leak out and result in HACE
1% of people above 3000m get HACE
symptoms
- severe headaches
- vomiting, confusion, drowsiness
- coma
causes
- ascending faster than 500m/d
- exercising vigorously

116
Q

immediate response at altitude

A

hyperventilation
increase in blood flow during rest and sub-maximal exercise
- resting systemic BP increases
- increase in sub maximal blood flow compensates for arterial desaturation

117
Q

longer term responses - acclimitisation

A

increased blood O2 carrying capacity
- initial decrease in plasma volume
- increase in RBC concentration and Hb synthesis

physiology yr 2 (3 decks)

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