Topic 7 Flashcards
1
Q
What facilitates movement
A
Skeletal muscles, tendons, ligaments & joints
- skeletal muscles attached to bones by tendons
- ligaments attach bone to bone
- skeletal muscles contract/relax to move bones at a joint
- > e.g. bicep contracts -> tricep relaxes
- > pulls bone -> arm bends (flexes) at elbow
2
Q
Antagonistic Pair
A
Muscles that work together to move a bone
3
Q
Skeletal Muscles
A
ngng
4
Q
Myofibrils
A
Composed of thin & thick myofilaments
- thick = myosin (protein)
- thin = actin (protein)
Composed of many short units = Sarcomeres
5
Q
Myofibrils viewed under electron miscroscope
A
Dark band = thick myosin (and a little actin) = A band Light band = thin actin = I band End of each sarcomere marked by Z line - sarcomeres joined lengthways at Z line Middle of each sarcomere = M line - middle section (myosin only) = H zone
INSERT DIAGRAM
6
Q
Sliding Filament theory
A
Myosin + actin slide over one another (remaining the same length)
-> Sarcomeres contract
Simultaneous contraction of sarcomeres
-> myofibrils + muscle fibres -> contract
Sarcomeres return to original length as muscle relaxes
7
Q
Skeletal muscle
A
= large bundles of long cells known as muscle fibres
- composed of fast & slow twitch muscle fibres (different muscles = different proportions)
8
Q
Muscle fibres
A
Cell membrane = SARCOLEMMA
- bits of sarcolemma fold inwards across the muscle fibre & into the SARCOPLASM
= Transverse (T) Tubules -> help to spread electrical impulses across the sarcoplasm (reach all of muscle fibre)
- Sarcoplasmic reticulum stores & releases calcium ions (muscle contraction)
- lots of mitochondria (ATP)
- Multinucleated
- lots of long, cylindrical organelles = myofibrils
9
Q
Sarcoplasmic reticulum
A
Network of internal membranes in the muscle fibre, which stores and releases calcium ions
10
Q
Transverse (T) tubules
A
Bits of sarcolemma that fold inwards across the muscle fibre & into the sarcoplasm
- they help to spread electrical impulses through the whole muscle fibre (and sarcoplasm)
11
Q
Myosin filaments
A
- hinged globular heads (back & forth movement)
- binding sites for Actin & ATP
12
Q
Actin Filaments
A
- Actin-myosin binding site = binding site for myosin head
- Tropomyosin + Troponin (proteins) between filaments
- T & T are attached to one another & help myofilaments move pass one another
13
Q
Binding Sites in resting muscles
A
Blocked by Tropomyosin, which is held in place by troponin
- stops the myofilaments sliding (& myosin head entering the site)
14
Q
Muscle Contraction (process)
A
Triggered by Action Potential
- Action potential -> Influx of Calcium Ions
- ATP = energy to move myosin head
- Breaking of cross bridge
15
Q
Muscle Contraction: Action potential -> Influx of Calcium Ions
A
Action potential (from motor neurone) stimulates muscle cell
-> depolarises sarcolemma
-> spreads dow T-tubules to the sarcoplasmic reticulum
Sarcoplasmic reticulum releases stored Ca^2+ into sarcoplasm
-> Ca^2+ binds to troponin -> changes shape
-> pulls tropomyosin out of a-m binding site
Exposes site
-> myosin head binds = Actin-myosin cross bridge
16
Q
Muscle Contraction: ATP = energy to move myosin head
A
Ca^2+ activate ATPase (ATP breakdown -> energy released)
- > moves myosin head
- > pulls actin filament along (‘rowing action’)
17
Q
Muscle Contraction: Breaking of cross bridge
A
ATP = energy -> breaks a-m cross bridge -> myosin head detaches after movement Myosin head reattaches to different binding site further along -> new cross bridges -> cycle repeats Many cross bridges form + break very rapidly -> pull actin filament along -> shortens sarcomere -> muscle contracts
note: cycle continues as long as Ca^2+ is present and bound to troponin
18
Q
Excitation of motor neurone (for muscle contraction) stops
A
Ca^2+ leaves binding site on troponin - moved by active transport back into sarcoplasmic reticulum (uses ATP) Troponin returns to original shape -> tropomyosin pulled back -> blocks a-m binding site Muscle fibres no longer contracted as: - no myosin heads attached - no cross bridges Actin filaments slide back to relaxed position -> lengthens sarcomere
19
Q
Slow twitch muscle fibres
A
- contract slowly
- muscles for posture = high proportion (e.g. back)
- endurance
- long working time before tired
- slow energy release
- -> aerobic respiration
- -> lots of mitochondria + blood vessels (good O2 supply)
- reddish colour = myoglobin rich (red coloured proteins; stores O2)
20
Q
Fast twitch muscle fibres
A
- contract quickly
- muscles for fast movement = high proportion (legs, eyes)
- short burst of speed + power
- tire very quickly
- quick energy release
- -> aerobic respiration
- -> glycogen used
- -> few mitochondria + blood vessels
- whitish colour (little myoglobin = poor O2 store)
21
Q
Aerobic Respiration
A
C6H12O6 + 6O2 -> 6CO2 + 6H2O + energy
- glucose splits into CO2 (waste) + H2 (combines with O2 -> H2O)
= metabolic pathway
- energy released is used to phosphorylate ADP
- 4 stages of AR
Coenzymes used:
- NAD + FAD transfer hydrogen from one molecule to another
- Coenzyme A transfers acetate between molecules
22
Q
Metabolic pathway
A
series of chemical reactions
23
Q
4 Stages of Aerobic Respiration
A
- Glycolysis
- Link Reaction
- Krebs Cycle
- Oxidative Phosphorylation
1 - 3 = Reaction series
4 = reaction series products used to produce ATP
24
Q
Glycolysis (process)
A
Glucose (6C) -> 2 x Pyruvate (3C) Happens in cell cytoplasm Anaerobic process (no O2) 1. Phosphorylation: - glucose phosphorylated (2 Pi from 2 ATP molecules) -> 2 ATP + 2 triose phosphate 2. Oxidation: - triose phosphate oxidised -> 2 x pyruvate - NAD collects H+ -> reduced NAD (used in 4th stage) - 4 ATP produced (net gain = 2 ATP) INSERT DIAGRAM
25
Link Reaction (process)
```
Occurs twice for every glucose molecule
Happens in mitochondrial matrix
1. Pyruvate decarboxylated
- one carbon removed
2. NAD reduced
- collects H+ from pyruvate
- pyruvate -> acetate
3. Acetate + CoEnzyme A (CoA) -> acetyl CoA
```
Note: no ATP produced
- 2 x acetyl CoA -> stage 3
- 2 x CO2 = waste
- 2 x reduced NAD -> stage 4
INSERT DIAGRAM
26
Krebs Cycle (process)
```
Cycle = once for each pyruvate
Occurs in mitochondrial matrix
Series of REDOX reactions
1. Acetyl CoA + Oxaloacetate (4C) -> Citrate (6C)
- CoA goes back to stage 2
2. Citrate -> 5C
- decarboxylation (CO2 = waste)
- dehydrogenation
--> H+ carried by reduced NAD -> stage 4
3. 5C -> Oxaloacetate
- decarboxylation (CO2 = waste)
- dehydrogenation
--> 2 x H+ carried by reduced NAD -> stage 4
--> 1 x H+ carried by reduced FAD -> stage 4
- ATP produced
--> direct Pi transfer from intermediate group = SUBSTRATE LEVEL PHOSPHORYLATION
```
INSERT DIAGRAM
27
Substrate Level Phosphorylation
Direct Pi transfer from an an intermediate group
28
Oxidative Phosphorylation
Process where energy carried by electrons from reduced CoEnzymes is used to make ATP
- occurs in/across mitochondrial membrane
- made up of two processes:
- - Electron transport Chain
- - Chemiosmosis
29
How many ATP can be produced from 1 glucose?
38
Reduced NAD = 3 ATP (energy release)
Reduced FAD = 2 ATP (energy release)
1. Glycolysis = 2 ATP + 2 reduced NAD = 8 ATP
2. Link reaction = 2 reduced NAD = 6 ATP
3. Krebs Cycle = 2 ATP + 6 reduced NAD + 2 reduced FAD = 24 ATP
Total = 38 ATP
30
Anaerobic Respiration
No O2 used
Lactate fermentation:
- glucose -> pyruvate (glycolysis)
- reduced NAD tranfers H+ to pyruvate
- > lactate + NAD produced
- NAD recycled for glycolysis
- -> glycolysis continues with no O2 allowing for small ATP production (2)
31
Lactic Acid
Lactic acid build us through Anaerobic Respiration
Broken down in two ways:
1. cell convert lactic acid -> pyruvate (re-enters into link reaction)
2. liver cells convert lactic acid -> glucose = respired or stored
32
Metabolic poisons target...
Electron carriers
- stop electron & chemiosmosis
- stops reduced NAD + FAD oxidation
- -> stops regeneration
- -> stops Krebs cycle
- ATP synthesis falls -> fatal
33
Oxidative Phosphorylation (process)
1. H atoms released from reduced NAD + FAD (-> oxidised back)
- H -> H+ + e-
2. Electrons move down electron transport chain (ETC)
- lose energy at each carrier
3. Energy used by electron carriers
-> pumps protons (H+) from the mitochondrial matix -> intermembrane space
4. Concentration of protons = higher in intermembrane than matrix
-> electrochemical gradient
5. protons move down gradient into matrix
- via ATP synthase
-> drives synthesis of ATP (Pi + ADP -> ATP)
6. Movement of H+ across membrane generates ATP
= Chemiosmosis
7. End of ETC finishes int the mitochondrial matrix
- H+ + e- + O2 -> H2O
- oxygen = final electron acceptor
INSERT DIAGRAM
34
Chemiosmosis
The movement of ions via diffusion across a semi-permeable membrane
35
Cardiac muscle
Is Myogenic
1. SAN = Sino-atrial node
- In wall of right atrium
= pacemaker
- sets rhythm by sending out impulses to atrial walls
-> cause right + left atria to contract simultaneously
2. Band of non-conducting collagen tissue prevents impulse from passing to ventricles
3. Impulse transferred from SAN to AVN
- AVN = Atrioventricular node
4. AVN leaves a slight delay before passing on impulse to Bundle of HIS
- slight delay allows atria to fully contract & empty
5. Bundle of HIS = muscle fibre group
- conducts impulse to Purkyne Fibres
6. Purkyne fibres carry impulse
- cause ventricles to simultaneously contract from the bottom u[
36
Myogenic
Contracts & relaxes without requiring a neurone signal
37
Electrocardiograph
Records electrical activity of the heart
- electrodes placed on chest
- trace produced = ECG (electrocardiogram)
38
Electrocardiogram
1. P wave = contractions of atria (first peak)
2. QRS complex = contraction of the ventricles (main peaks + troughs either side)
3. T wave = relaxation of ventricles; repolarisation (last peak)
4. Height = amount of electrical charge
- bigger wave = more
- (higher) P + R = stronger contractions
39
Using ECG's
Can be compared to normal trace -> diagnose health issues
- too fast = tachycardia
- too slow = bradycardia
- ecotopic heartbeat = 'extra' heartbeat
- Fibrilation = v. irregular
40
Tachycardia
Too fast heart beat (above 100 bpm)
41
Bradycardia
Too slow heart beat (less than 60 bpm)
42
Ecotopic heartbeat
Extra heartbeat
- earlier contraction of atria (P wave)
- Can be caused by ventricles
- if occasionally present (in a healthy individual) = not an issue
43
Fibrilation (ECG)
Very irregular
- atria or ventricles completely lose their rhythm
- stop contracting properly
- > chest pain, fainting, lack of pulse, death
44
Exercise ->
- more frequent muscle contractions
- more energy recquired
- more aerobic respiration
- -> increased breathing rate + depth (better gas exhange)
- -> increased heart rate (delivery/removal)
45
Medulla Oblongata
MO controls breathing rate via two ventilation centres
- inspiratory
- expiratory
46
Medulla Oblongata effect on breathing rate
1. Inspiratory centre sends nerve impulses to the intercostal + diaphram muscles -> contract
2. Increases lung volume -> lowers the pressure
- signal also sent to expiratory centre to inhibit
3. Air enters lungs due to pressure difference
4. Lungs inflate
- stretch receptors stimulated
- nerve impulses sent to MO to inhibit Inspiratory centre
5. Expiratory centre sends nerve impulse to diaphram and intercostal muscles -> relax
- lungs deflate -> air expelled
- stretch receptors become inactive
- Inspiratory centre no longer inhibited -> cycle restarts
47
Exercise -> decreased blood pH ->
Increased breathing rate
- exercise -> increased CO2 in blood -> decreased pH
- chemoreceptors in medulla oblongata:
- - aortic bodies + carotid bodies
- -- sensitive to changes in blood pH
- Change detected -> nerve impulse to MO
- > more frequent impulses to intercostal muscle and diaphram
- > increases rate + depth of breathing
- > gaseous exchange speeds up
- > CO2 reduced, extra O2 supplied -> blood pH balances
48
Carotid bodies
Clusters of receptor cells in the carotid arteries
49
Aortic bodies
Clusters of receptor cells in the aorta
50
Ventilation rate + exercise =
An increase in ventilation rate due to increased breathing rate + depth
51
Ventilation rate
Volume of air breathed in & out in a period of time
52
Medulla Oblongata's effect on Heart Rate
MO unconsciously controls HR via the Cardiovascular Control Centre (CCC) in the MO
1. CCC controls the rate the SAN fires at (heart beat rythm)
2. Animals alter HR to respond to internal stimuli
3. Chemical + pressure receptors detect stimuli in the blood:
- baroreceptors (aortic + carotid bodies) = high + low blood pressure
- chemoreceptors (aortic + carotid bodies +& MO) = blood O2 levels; CO2 + pH (secondary indicators)
4. Receptors send electrical impulses along sensory neurones to the MO
5. CCC processes information & sends impulses to SAN via sympathetic/parasympathetic neurones
- release different neurotransmitters onto SAN
- > sympathetic = increase
- > parasympathetic = decrease
53
Baroreceptors
High Blood pressure:
- Impulse to CCC -> impulse along parasympathetic neurones
- > secrete acetylcholine -> binds to SAN
- > decreased SAN firing -> lowers BP
Low Blood pressure:
- Impulse to CCC -> impulse along sympathetic neurones
- > secrete noradrenaline -> binds to SAN
- > increased SAN firing -> raises BP
54
Chemoreceptors
High blood O2/Low CO2/High pH:
- Impulse to CCC -> impulse along parasympathetic neurones
- > secrete acetylcholine -> binds to SAN
- > decreased SAN firing -> lowers HR
Low blood O2/High CO2/Low pH:
- Impulse to CCC -> impulse along sympathetic neurones
- > secrete noradrenaline-> binds to SAN
- > increased SAN firing -> raises HR
55
Cardiac Output (CO)
Total volume of blood pumped by a ventricle each minute
56
Stroke Volume (SV)
Volume of blood pumped by one ventricle each time it contracts
57
Cardiac Output equation
CO (cm^3min^-1) = HR (bpm) x SV (cm^3)
note: CO increases during exercise -> HR + SV increase
58
Inverse Cardiac output equation
SV = CO/HR
59
Purkyne Fibres
Finer muscle fibres in r/l ventricle walls
60
SAN
Sino-atrial node
- in wall of right atrium
= pacemaker
61
AVN
Atrioventricular node
62
Cardiac Muscle diagram
INSERT DIAGRAM
63
Tidal Volume
Volume of air in a normal breath
| - around 0.4 dm^3
64
Breathing rate
How many breaths taken (per minute)
65
Oxygen consumption
Volume of oxygen used by the body (expressed as a rate)
66
Respiratory minute ventilation
Volume of gas breathed in/out in a minute
| - also known as respiration rate
67
Respiratory minute ventilation equation
RMV = tidal volume x breathing rate (breaths per min)
68
Spirometers
Measures Ventilation
1. oxygen filled chamber with movable lid
2. Person breathes through tube connected to chamber
3. Breathes in -> chamber lid moves down
- breathes out -> chamber lid moves up
4. Movement recorded by a pen attached to the lid
- > writes on rotating drum = spirometer trace
5. Total volume of gas in chamber decreases over time -> air breathed out = O2 + CO2 mixture
- CO2 absorbed by soda lime in tube
- only O2 in inhalation chamber -> used by respiration -> chamber vol decreases
INSERT DIAGRAM
69
Using Spirometers to investigate the effect of exercise
1. person breathes into spirometer for 1 minute at rest
- recordings taken
2. Person exercises for 2 minutes
- spirometer chamber refilled with O2
3. immedietly after exercise stops -> breathe into Spirometer again -> recordings taken for a minute
4. recordings taken before + after compared
70
Spirometer trace
```
Breathing rate (per min) = number of peaks in trace in a minute
Tidal volume = average difference in the volume of gas between each each peak & trough on the trace
Oxygen consumption = the change in volume of gas in spirometer (read values from troughs)
```
71
Homeostasis
Maintenance of a stable internal environment
- counteracts impacts of external environment + activity
- control systems (kept within narrow limits)
- internal environment = state of dynamic equilibrium
72
Homeostasic blood glucose content
usually = 90mg per 100 cm^3 of blood
- monitored by pancreatic cells
- essential for constant energy
73
Homeostatic Systems
= receptors, communication system + effectors
- effectors counteract change ( to normal)
= negative feedback mechanism
INSERT DIAGRAM
74
Negative Feedback Mechanism
Maintains normal levels by counteracting change
- e.g. temp= 0.5 +/- 37 C
- only works within certain limits (too large and it cannot counteract)
75
Positive Feedback mechanism
Amplifies a change from the normal level
- effectors respond to further increase
- useful to rapidly activate
- can happen when homeostatic systems break down (hypothermia)
- not part of homeostasis as it does not provide a stable internal environment
76
Platelets & Positive Feedback
Platelets activate:
- > chemical released
- > triggers more platelets to be activated
- > quickly form blood clot at injury site
- > ends with negative feedback (blood clot detected)
77
Reducing body temperature
Sweating:
- more secreted -> water evaporates from skin surface -> heat lost -> skin cooled
Hairs lying flat (mammals):
- erector pilli muscles relax -> hair lies flat -> less air trapped -> heat lossed
- layer of hair insulates by trapping air = poor conductor
Vasodilation:
- aterioles near skin surface dilate -> more blood flows via the capillaries to the skins surface -> heat lost via radiation
78
Increasing body temperature
Shivering:
- muscles contract in spasms -> shiver -> heat from increased respiration
Reduced sweat:
- reduced secretion
Hairs stand up:
- erector pili muscles contract -> hairs stand up -> more air trapped
Vasoconstriction:
- arterioles near the skin surface constrict -> less blood flows to surface layer of dermis
Hormones:
- adrenaline + thyroxine -> increased metabolism -> more heat produced
79
Hypothalamus
Control body temperature = thermoregulation
- receives info from thermoreceptors
- thermoreceptors send impulses along sensory neurones -> hypothalamus -> motor neurones -> effectors
- effectors respond -> counteract to norm
80
Hormones affect on Transcription Factors (inside cells)
= Steroid + thyroid hormones
Cross cell membrane -> bind to nucleus -> bind to transcription factors
E.g. normal body temp:
- thyroid hormone receptor (transcription factor) binds to DNA at start of gene
- > decreases transcription of gene coding for protein that increases metabolic rate
Cold body temp -> thyroxine released
- binds to thyroid hormone receptor -> acts as an activator
- transcription rate increased -> produces more protein -> increases metabolic rate (& temp)
81
Keyhole Surgery
Small incision where a tiny video camera and specialised instruments are inserted
- less blood lost
- less pain
- quicker recovery time
- less scaring
- shorter hospital stay -> quicker return to normal activities
e. g. cruciate ligaments
- damaged one removed
- replaced with graft (likely from leg tendon)
82
Prostheses
Replaces whole or part of a limb
Can include electronic devices that operate the prosthesis by picking up information sent by the nervous system
e. g. Knee joints -> prosthetic
1. Metal device replaces damaged cartilage + bone
2. Joint + end of bones replaced to provide a smooth joint
- cushioning helps to reduce impact
3. Allows people to move around & participate in low impact sport
83
Knee Joint Diagram
ngng
84
Performance Enhancing Drugs (For/Against)
Absolutionist argument:
- illegal
- unfair competition
- serious health risks (high bp + heart problems)
- > may not be dully informed
Rationalist argument:
- have the right to make their own decisions
- situation dependent
- overcome inequalities in training, coaches, equipment etc
- may be necessary to compete at a higher level
85
Anabolic steriods
Increased strength, speed + stamina -> increased muscle size
- allows for harder training
- side effect: increased aggression
86
Stimulants
Speed up reactions & reduce fatigue
| - increase aggression
87
Narcotic Analgesics
Reduce pain
| - injuries reduce performance impact
88
Hormones affect on Transcription Factors (working at cell membrane)
= protein hormones
Cannot cross the cell membrane
Bind to receptor in membrane -> activate messenger molecules in cytoplasm of cell
- messenger molecules activate protein kinase (enzyme) -> trigger cascade in cell
- during cascade transcription factors can be activated
-> then affect transcription of genes in cell nucleus
89
Transcription Factors
Proteins that control gene transcription within cells
- bind to DNA sites near the start of a gene
- > increase/decrease transcription rate
