Topic 7 Flashcards
What facilitates movement
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
Antagonistic Pair
Muscles that work together to move a bone
Skeletal Muscles
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Myofibrils
Composed of thin & thick myofilaments
- thick = myosin (protein)
- thin = actin (protein)
Composed of many short units = Sarcomeres
Myofibrils viewed under electron miscroscope
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
Sliding Filament theory
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
Skeletal muscle
= large bundles of long cells known as muscle fibres
- composed of fast & slow twitch muscle fibres (different muscles = different proportions)
Muscle fibres
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
Sarcoplasmic reticulum
Network of internal membranes in the muscle fibre, which stores and releases calcium ions
Transverse (T) tubules
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)
Myosin filaments
- hinged globular heads (back & forth movement)
- binding sites for Actin & ATP
Actin Filaments
- 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
Binding Sites in resting muscles
Blocked by Tropomyosin, which is held in place by troponin
- stops the myofilaments sliding (& myosin head entering the site)
Muscle Contraction (process)
Triggered by Action Potential
- Action potential -> Influx of Calcium Ions
- ATP = energy to move myosin head
- Breaking of cross bridge
Muscle Contraction: Action potential -> Influx of Calcium Ions
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
Muscle Contraction: ATP = energy to move myosin head
Ca^2+ activate ATPase (ATP breakdown -> energy released)
- > moves myosin head
- > pulls actin filament along (‘rowing action’)
Muscle Contraction: Breaking of cross bridge
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
Excitation of motor neurone (for muscle contraction) stops
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
Slow twitch muscle fibres
- 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)
Fast twitch muscle fibres
- 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)
Aerobic Respiration
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
Metabolic pathway
series of chemical reactions
4 Stages of Aerobic Respiration
- Glycolysis
- Link Reaction
- Krebs Cycle
- Oxidative Phosphorylation
1 - 3 = Reaction series
4 = reaction series products used to produce ATP
Glycolysis (process)
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
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
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
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Substrate Level Phosphorylation
Direct Pi transfer from an an intermediate group
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
How many ATP can be produced from 1 glucose?
38
Reduced NAD = 3 ATP (energy release)
Reduced FAD = 2 ATP (energy release)
- Glycolysis = 2 ATP + 2 reduced NAD = 8 ATP
- Link reaction = 2 reduced NAD = 6 ATP
- Krebs Cycle = 2 ATP + 6 reduced NAD + 2 reduced FAD = 24 ATP
Total = 38 ATP
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)
Lactic Acid
Lactic acid build us through Anaerobic Respiration
Broken down in two ways:
- cell convert lactic acid -> pyruvate (re-enters into link reaction)
- liver cells convert lactic acid -> glucose = respired or stored
Metabolic poisons target…
Electron carriers
- stop electron & chemiosmosis
- stops reduced NAD + FAD oxidation
- -> stops regeneration
- -> stops Krebs cycle
- ATP synthesis falls -> fatal
Oxidative Phosphorylation (process)
- H atoms released from reduced NAD + FAD (-> oxidised back)
- H -> H+ + e- - Electrons move down electron transport chain (ETC)
- lose energy at each carrier - Energy used by electron carriers
-> pumps protons (H+) from the mitochondrial matix -> intermembrane space - Concentration of protons = higher in intermembrane than matrix
-> electrochemical gradient - protons move down gradient into matrix
- via ATP synthase
-> drives synthesis of ATP (Pi + ADP -> ATP) - Movement of H+ across membrane generates ATP
= Chemiosmosis - End of ETC finishes int the mitochondrial matrix
- H+ + e- + O2 -> H2O
- oxygen = final electron acceptor
INSERT DIAGRAM
Chemiosmosis
The movement of ions via diffusion across a semi-permeable membrane
Cardiac muscle
Is Myogenic
- 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 - Band of non-conducting collagen tissue prevents impulse from passing to ventricles
- Impulse transferred from SAN to AVN
- AVN = Atrioventricular node - AVN leaves a slight delay before passing on impulse to Bundle of HIS
- slight delay allows atria to fully contract & empty - Bundle of HIS = muscle fibre group
- conducts impulse to Purkyne Fibres - Purkyne fibres carry impulse
- cause ventricles to simultaneously contract from the bottom u[
Myogenic
Contracts & relaxes without requiring a neurone signal
Electrocardiograph
Records electrical activity of the heart
- electrodes placed on chest
- trace produced = ECG (electrocardiogram)
Electrocardiogram
- P wave = contractions of atria (first peak)
- QRS complex = contraction of the ventricles (main peaks + troughs either side)
- T wave = relaxation of ventricles; repolarisation (last peak)
- Height = amount of electrical charge
- bigger wave = more
- (higher) P + R = stronger contractions
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
Tachycardia
Too fast heart beat (above 100 bpm)
Bradycardia
Too slow heart beat (less than 60 bpm)
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
Fibrilation (ECG)
Very irregular
- atria or ventricles completely lose their rhythm
- stop contracting properly
- > chest pain, fainting, lack of pulse, death
Exercise ->
- more frequent muscle contractions
- more energy recquired
- more aerobic respiration
- -> increased breathing rate + depth (better gas exhange)
- -> increased heart rate (delivery/removal)
Medulla Oblongata
MO controls breathing rate via two ventilation centres
- inspiratory
- expiratory
Medulla Oblongata effect on breathing rate
- Inspiratory centre sends nerve impulses to the intercostal + diaphram muscles -> contract
- Increases lung volume -> lowers the pressure
- signal also sent to expiratory centre to inhibit - Air enters lungs due to pressure difference
- Lungs inflate
- stretch receptors stimulated
- nerve impulses sent to MO to inhibit Inspiratory centre - 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
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
Carotid bodies
Clusters of receptor cells in the carotid arteries
Aortic bodies
Clusters of receptor cells in the aorta
Ventilation rate + exercise =
An increase in ventilation rate due to increased breathing rate + depth
Ventilation rate
Volume of air breathed in & out in a period of time
Medulla Oblongata’s effect on Heart Rate
MO unconsciously controls HR via the Cardiovascular Control Centre (CCC) in the MO
- CCC controls the rate the SAN fires at (heart beat rythm)
- Animals alter HR to respond to internal stimuli
- 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) - Receptors send electrical impulses along sensory neurones to the MO
- CCC processes information & sends impulses to SAN via sympathetic/parasympathetic neurones
- release different neurotransmitters onto SAN
- > sympathetic = increase
- > parasympathetic = decrease
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
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
Cardiac Output (CO)
Total volume of blood pumped by a ventricle each minute
Stroke Volume (SV)
Volume of blood pumped by one ventricle each time it contracts
Cardiac Output equation
CO (cm^3min^-1) = HR (bpm) x SV (cm^3)
note: CO increases during exercise -> HR + SV increase
Inverse Cardiac output equation
SV = CO/HR
Purkyne Fibres
Finer muscle fibres in r/l ventricle walls
SAN
Sino-atrial node
- in wall of right atrium
= pacemaker
AVN
Atrioventricular node
Cardiac Muscle diagram
INSERT DIAGRAM
Tidal Volume
Volume of air in a normal breath
- around 0.4 dm^3
Breathing rate
How many breaths taken (per minute)
Oxygen consumption
Volume of oxygen used by the body (expressed as a rate)
Respiratory minute ventilation
Volume of gas breathed in/out in a minute
- also known as respiration rate
Respiratory minute ventilation equation
RMV = tidal volume x breathing rate (breaths per min)
Spirometers
Measures Ventilation
- oxygen filled chamber with movable lid
- Person breathes through tube connected to chamber
- Breathes in -> chamber lid moves down
- breathes out -> chamber lid moves up - Movement recorded by a pen attached to the lid
- > writes on rotating drum = spirometer trace - 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
Using Spirometers to investigate the effect of exercise
- person breathes into spirometer for 1 minute at rest
- recordings taken - Person exercises for 2 minutes
- spirometer chamber refilled with O2 - immedietly after exercise stops -> breathe into Spirometer again -> recordings taken for a minute
- recordings taken before + after compared
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)
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
Homeostasic blood glucose content
usually = 90mg per 100 cm^3 of blood
- monitored by pancreatic cells
- essential for constant energy
Homeostatic Systems
= receptors, communication system + effectors
- effectors counteract change ( to normal)
= negative feedback mechanism
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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)
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
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)
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
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
Hypothalamus
Control body temperature = thermoregulation
- receives info from thermoreceptors
- thermoreceptors send impulses along sensory neurones -> hypothalamus -> motor neurones -> effectors
- effectors respond -> counteract to norm
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)
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)
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
Knee Joint Diagram
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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
Anabolic steriods
Increased strength, speed + stamina -> increased muscle size
- allows for harder training
- side effect: increased aggression
Stimulants
Speed up reactions & reduce fatigue
- increase aggression
Narcotic Analgesics
Reduce pain
- injuries reduce performance impact
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
Transcription Factors
Proteins that control gene transcription within cells
- bind to DNA sites near the start of a gene
- > increase/decrease transcription rate
