1
Q
satellite cells
A
- undifferentiated cells that increase the number of nuclei in muscles which promotes growth and strengthening
- training activated
2
Q
synaptic cleft
A
the gap between the motor neuron and the muscle cell that the AP crosses
3
Q
ACh
A
acetylcholine
- neurotransmitter released to be diffused across synaptic cleft
4
Q
neuromuscular junction (NMJ)
A
- when the nerve impulse reaches the endo f the motor nerve it comes to the synaptic cleft
- ACh in released and diffused across the cleft to bind to the recptor site on the mtor and plate
- opens sodium channels on the sarcolemma allowing sodium to diffuse into the muscle fiber
-results in depolarization called the end-plate potential (EPP)
-this is the signal to begin the contractile process
5
Q
sliding filament thoery
A
- ATP binds to myosin head
- ATP causes cross bridges to “cock”
- cross bridges attach to myosin head
- bind to actin
- power stoke and slide
6
Q
force regulations
A
- type and number of motor units recruited
- initial muscle length (length-tension relationship)
- nature of the neural stimulation (simple twitch, summation, tetanus)
- contractile history
7
Q
size principle name
A
Henneman’s principle
8
Q
Henneman’s size principle
A
MUs recruit from smallest to largest based on the force required
- first recruited is last to de-recruit
9
Q
tetanus
A
sustained muscle contraction
10
Q
what happens if previous activity is non-fatiguing
A
force production enhanced
- more sensitive to Ca
- phosphoralation of myosin light chain
11
Q
skeletal muscle fibre types
A
- slow oxidative (type I)
- fast oxidative glycolytic (type IIa)
- fast glycolytic (type IIx)
12
Q
influences of force type distribution
A
- genetics
-training - hormone concentration
13
Q
biochemical properties of muscle fibres
A
- oxidative capacity (# of cappilaries, mitochondria, amount of myoglobin)
- speed of ATP degragation
- absence of contractile proteins
14
Q
contractile properties of muscle fibres
A
- maximal force produced
- speed of contraction
- maximum power output
- muscle fibre efficiency
15
Q
immunohistochemical staining
A
straining of a muscle biopsy in order to see the amount of fast vs slow twitch fibres in the muscle
16
Q
immunohistochemical staining colours
A
- blue = type I fibres
- green = IIa fibres
- Black IIx fibres
- red = dystrophin (protein in sarcolemma)
17
Q
causes of fatigue
A
- CV system (O2)
- energy supply system (inadequate ATP)
- neuromuscular system
- thermoregulation
- biochemical (stresses in other systems)
- psychology
-central governor model (prevent catastrophic failure by homeostasis)
18
Q
central causes of fatigue
A
- motor cortex (pain)
- spinal cord (impaired recruitment of MN and firing frequency)
19
Q
peripheral causes of fatigue
A
- NMJ (impaired neuromuscular transmission)
- impaired conduction of action potentials
- Ca2+ (impaired release
- imparied cross bridge cycling (myosin and actin
- low force/power output
20
Q
two hypothesis of peripheral fatigue
A
- accumulation hypothesis (lactic acid, H+, Ca, Pi, etc)
- depletion hypothesis (ACh, glycogen, BG, O2, etc)
21
Q
accumulation of too much potassium (K)
A
- can block nerve transmission to T-tubules
22
Q
purpose of cardiovascular system
A
- transport O2
- removal of CO2
- regulation of temp
23
Q
two major adjustments of the CV system during exercise
A
- increased cardiac output
- redistribution
24
Q
cardiac output equation
A
Q = HR x SV
25
blood flow equation
change in pressure / resistance
26
resting heart rate (RHR)
- normal (60-8b5pm)
- elite (28-40 bpm)
27
typical heart rate timing
distole - 0.5 sec
systole - 0.3 sec
28
elite heart rate timing
distole - 0.13 sec
systole - 0.2 sec
29
why does heart rate increase with exercise
initially increases abruptly with the withdrawal of PNS
- SNS kicks in and HR continues to rise
30
max heart rate equations
220 - age
or
208 - (0.7 x age)
31
heart rate variability
wide variety of HRV is considered healthy
32
stroke volume
(end dystolic volume - end systolic volume
33
stroke volume is determined by
- end -diastolic volume
- vascular resistance
- contractibility
34
frank-starling law
the heart adjusts its stroke colume and cardiac output in response to changes in venous return and end diastolic volume
35
veinous return
amount of blood returned to the heart
36
three principles of EDV
- venoconstriction
-muscle pump
- respiratory pump
37
vascular resistance
aortic pressure
38
ejection fraction
portion of blood pumped out of LV each beat
39
stroke volume during exercise
increase linearly and levels out at 40-60% VO2max
- doesnt always level out in elite athletes
40
cardiac output
- measured in L/min
- reflects the functional capacity of the CV system
41
2 factors that drive the relaxation of capillary sphincters
1. driving force of increased local BP
2. local metabolites
42
aortic blood pressure
systolic / diastolic (120/80)
43
pulse pressure
systolic - diastolic
120-80
= 40
44
mean arterial pressure (MAP)
average pressure during a cardiac cycle
45
MAP equation
DBP + 0.33 (SBP-DBP)
- does not work for exercise
46
Acute BP regulation
short term
- SNS
- baroreceptors (pressure sensory)
increase BP = decreased Q and TVP)
47
chronic BP regulation
blood volume controlled by kidneys
48
3 important components of CV system
- heart
-vascular network
- blood
49
blood O2 carrying capacity
- 15g/100ml
- each g binds 1.34ml O2
50
redistribution of blood flow
1. pump more blood
2. re-direct blood
51
double production or rate-pressure product
HR x SBP
- indicates the work of the heart
52
central command thoery
changes at onset of exercise is due to centrally generated CH motor sugnals
- set general patterns of the CV response
53
CV control during exercise
- initial drive (central command theory - anticipates ex)
- fine tuned by feedback
54
pulmonary ventilation
breathing air through mouth or nose to the lungs
55
external respiration
O2 from the lungs to the blood and CO2 from blood to lungs
56
internal respiration
O2 from blood to cells and CO2 from cells to blood
57
cellular respiration
O2 from cells to mitochondria and CO2 from mitochondria to O2
58
respiratory zone
300 million alveoli
- rapid gas exchange
59
boyles law
- pressure of gas is inversely proportional to the volume of the container
- increased volume = decrease pressure
60
air flow
P1 - P2 / resistance
61
pulmonary ventilation
amount of air moved into the lungs in a minute
- (V)
62
tidal volume
(Vt)
- amount of air moved per breath
63
breathing frequency
(f)
- number of breaths per minute
64
pulmonary ventilations =
Vt x f
or
Va + Vd
65
alveolar ventilation
(Va)
- volume of air that reaches the respiratory zone
66
dead-space ventilation
(Vd)
- volume of air that remains in conducting airways
67
minute ventilation
(Ve)
- air flow eahc minute
- hoe muvh air per breath and how many breaths per minute
Ve = Vt x f
68
alveolar ventilation
(Va)
- "fresh" air per minute
Va = (Vt -Vd) x f
69
ERV (expiratory reserve volume)
maximum volume of air expired after a normal expiration
70
IRV (inspiratory reserve volume)
max air inspired after a normal breath
71
RV
air left in lungs after MAXIMAL exhalation
72
forced vital capacity (FVC)
max stroke volume of the lungs
73
dynamic breathing depends on:
- max stroke volume
- speed of breathing rate
74
forced expiratory volume (FEV o.1)
FEV0.1 / FVC
- indicates pulmonary airflow capacity
75
ssex differences
decreased:
- lung capacity
-airway diameter
-diffusion surface
- static and dynamic function measures
76
daltons law
each gas contributes to hte toal pressure in proportion to its number of molecules
77
partial pressure
= total pressure x fraction of gas
78
henrys law of gas exchange
each gas will dissolve in the liquid in proportion to its partial pressure
79
partial pressure added inside alveoli
Ph2O = 47mmHg
80
factors effecting gas exchange
1. partial pressure
2. solubility of the gas
3. surface area and thickness
81
ficks law of diffusion
Vgas = Q x a-vO2 difference
82
ventilation -perfusion ratio
rate of alveolar ventilation to pulmonary BF
(high value = too much VE, too low = too much BF)
83
O2 content of blood
97% Hgb saturation
84
normal oxygen %
15g% - men
13g% - women
85
pH shift
increase in pH = shift left
decrease in pH = shift right
- increase in H+ weakens O2 and Hgb bonds
86
temperature shift
increase temp weakens O2 and Hgb bonds
- shift right
87
2,3 DPG shift
added = shift right
none= shift left
- can bind to Hgb and reduce its affinity to O2
88
myoglobin
facilitates O2 transfer to mitochondria
89
arteriovenous O2 difference
describes the difference between he O2 content of arterial blood and mixed venous blood
- average = 4-5 ml O2/100ml
90
CO2 transports in blood
- bicarbonate (70%)
- dissolved in plasma (10%)
- bound to Hb (20%)
91
research methods
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