7 Flashcards

(113 cards)

1
Q

muscles and tendons and ligaments

A

tendons are muscle to Bone and ligaments are bone to bone- connnecting tissues- interact to enable movement
muscles can only ever get smaller- flexing require muscles pairs

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2
Q

agonist and antagonist

A

muscle pairs there is is an agonist (flexer) muscle doing work to create an action and antagonist relaxes (extensor)

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3
Q

muscle cells

A

very long tubular cells that stack together to create a whole mucle- tubule called muscle fibres
Muscles exist in bundles within bundles, muscle cells exist in fibres fibres are split into sarcomere units cell membrane of fibres is called sarcolemmacell cytoplasm is called sarcoplasm sarcoplasmic reticulum is endoplasmic reticulum of muscle cells multinicleatedmyofibrils of actin and myosin

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4
Q

filaments

A

actinthinon the outside myosinthick middleslide over each other changing muscle length
broken up into sarcomeres

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5
Q

joints and movements

A

muscles bring about movement ta a joint- produced by the coordinated action of several muscles- muscles shorten, pulling the bone and so moving the joint

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6
Q

antagonist

A

muscle cannot push-only. pull- can only contract
a pair of muscles that work together
a muscle that contracts to causes extension of a joint is called an extensor; corresponding flexor muscle contracts to reverse thee movement
flexor- active msucel-actively contracting
extensor- relaxing muscle- stretching out to allow a movement

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7
Q

joint structure

A

hip, knee and ankle joints synovial joints- bones that move in joints are operated by a cavity filled with synovial fluid, which enables them to move freely
bones held together by ligaments that control and restrict the amount of movement of the joint
tendons attacj muscles to the bones, enabling the muscles to power joint movement- cartilage protects bones within joints

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8
Q

muscles

A

muscles made up of bundles of muscle fibres, each a single muscle cell- can be several cm in length- multinucleate cells- single nuclei could not effectively control the metabolism of such long cells- muscle cells stripped
bundles of muscle fibres bound together by connective tissue, continuous with the tendons
inside the muscle fibre is the cytoplasm containing mitochondria and other organelles- within each muscle fibre there are numerous myofibrils; each is composed of repeated contractile units called sarcomeres

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9
Q

sarcomere

A

muscle exist in bundles within bundles muscle cells exit in fibres
fibres split into sarcomere
made up of thin proteins actin and thicker proteins myosin- contractions r brought about be co-ordinated sliding of these protein filaments within sacromeres
proteins overlap and give muscle fibre its striped appearance- where actin filaments occur in their own their are light bands on the sacromere- both actin and myosin=dark bands- only myosin intermediate bands
when the muscle contracts the actin moves between myosin- shorterns length of sacromere hence shortening length of muscle
I band=length of actin
H= length of myosin on its own- variable on contraction
A= overall length of myosin
separated of sarcomere by z lines

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10
Q

how sarcomeres shorten

A

actin molecules associated with 3 other protein molecules- troponin and tropomyosin. Myosin molecules have a golf club shpae; club shafts lie together as a bundle with the heads protruding along their length
in a contraction when the muscle shortens the change in orientation of the myosin head brings about the movement of actin- myosin heads attach ti the actin and dip forward, sliding the actin over the mysoin

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11
Q

slidning filament theorey

A

when a nerve impulse arrives at a neuromuscular junction, calcium ions are released from the sarcoplasmic reticulum- specialised type of endoplaasmic reticulum- calcium ions diffuse through the sarcoplasm initiating mvoement of protein filamentsaction potential from nerve depolarises sarcolemma and reacher sarcoplasmic reticulumdepolarisation of SR triggers release sore of ca into sarcoplasmca2+ attaches to the troponin molecules, causing it to moveas a result the tropomyosin on the actin filaments shifts its position exposing myosin binding sites in the actin filamentsmyosin heads bind with myosin binding sites on the actin filaments forming cross bridgesshortens sarcomere cases contractionwhen myosin head binds to actin, ADP and Pi on the myosin head are releasedmyosin changes shape causing myosin head to nod forward- results in the relative movement of the filaments; the attched actin moves over the myosinAn ATP molecule binds to the myosin head- causes myosin head to detach from the actinan ATPase on the myosin head hydrolyses the ATP forming ADP and Pihydrolysis causes a change in the shape of the myosin head- returns to upright position, enables a repeat of the cyclecollective bending of many myosin heads combine to move the actin filaments relative to the myosin filament- muscle contraction
ca return to sarcoplasmic reticulum by diffusion

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12
Q

releasing energy- how ATP is formed

A

in a solution phosphate ions are hydrated- in order to create ATP phosphate must be seperated from these water molecules- requires energy- ATP in water higher in energy than ADP and phosphate ions in water- a lot of energy is released as bonds form between water and phosphate, used to supply energy requiring reactions- hydrolysied ATP to occur- small amount of energy required to break bonds between ADP and pi

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13
Q

carbohydrate oxidation

A

in aerobic respiration the hydrogen stored in glucose is brought together with 02 to form water- bonds between carbon and hydrogen in glucose not as strong as bonds between hydrogen and oxygen so the input of energy needed to break bonds in glucose and oxygen is not as great as energy released when bonds in c02 and h20 are formed- release of energy used to generate ATP
glucose and 02 not brought together directly as influx of energy could damage cell- glucose split in a series of steps controlled by intracellular enzymes
C6H12O6+6O2->6CO2+6H2O+energy transferred

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14
Q

glycolysis

A

in cytoplasm
oxidationstores of glycogen in muscle or liver cells first converted into glucose- glcuose quite stable and unreavtive so first reaction needs an input of energy from ATP2 phosphate groups r added to the glucose from 2 ATP molecules increasing the reactivity of gluscoesplit into two 3 carbon molecules- phosphorylatedeach intermediate 3C sugar is oxidised producing a 3 carbon compound pyruvate2 hydrogen atoms are removed during the reaction and taken up by coenzyme NAD- non protein organic molecules- produces reduced coenzyme- 2 reduced NADglucose is on a higher energy level than pyruvate so on conversion some energy becomes available for direct creation of ATP- substrate level phosphorylation - 2 ATP made from for each pyruvate- 4ATP in total
Alternative pathway: pyruvate is converted into lactate and oxidises RNAD to NADNAD is regenerated and so can repeat glycolysis cycle instead of continuing to Krebs cycle produces ATP on its ownRNAD: 2 ATP: 2

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15
Q

link reaction

A

pyruvate passes into the mitochondrial matrix- where it is completely oxidised forming carbon dioxide and waterpyruvate is decarboxylated- co2 released as a waste producydehydrogenated- 2 hydrogen are removed and taken up by coenzyme NAD- produces reduced NADresulting 2 carbon molecule acetate which combines with coenzyme A to from acetyl coenzyme AA- coenzyme A carries the 2C acetyl group to the Krebs cycleRNAd:4 ATP:2

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16
Q

Krebs cycle

A

each 2 carbon acetyl CoA combines with a 4 carbon compound to create a six compound- in a circular pathway of reactions the go 4 carbon compound recreatedeach 2 carbon molecule entering the kerb cycle results in production of 2 molecules of co2 through decarboxylation and one ATP by substrate level phosphorylation and 4 pairs of hydrogen atoms (dehydrogenation)- taken up by hydrogen acceptors- coenzyme NAD and FAD- hydrogen atoms are subsequently evolved in ATP production via electron transport chainacetate separated from acetyl CoAacetate enter kerb cycle and combines with oxalocetate (4C) to give citrate 6Ccitrate in decarboxylated releasing CO2 and RNADformation of 5C compound and further decarboxylation resulting in release of co24c undergoes further reactions relating, ATP,RNAD and RFAD2x RNAD- 4HATP1xRFAD- 2Hrearrangement with isomerase produces oxaloacetate to restart cycle and release RNADRNAd: 10 RFAD:2 ATP:4

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17
Q

electron transport chain

A

hydrogen atoms released during glycolysis, link reaction and Krebs cycle are taken up by coenzymes- NAD and FADwhen a coenzyme accepts a pair of hydrogens with their electrons, the coenzyme is reduced becoming reduced NAD or reduced FAD- the reduced coenzyme shuttles the hydrogen atoms to the elctron transport chain on the mitochondrial inner embraceeach hydrogen tom’s electron and proton then separate with electron passing along a chin of electron carriers in the inner itochondriaal membranereduced coenaaayme carries 2H+ and electron to electron transport chain on inner mitochondrial membranehydrogen splits into 2 electrons and 2 H+electrons pass from one electron carrier to the next in a series of redox reactions- lose energy- absorbed by H+protons move across the inner mitochondrial membrane from the mitochondrial matrix creating high H+ conc in the intermemebrane spaceh+ diffuse back into the mitochondrial matrix down the electrochemical gradient- high to lowh+ diffusion down ATP synthase to catalyse ATP synthesiselectrons and H+ ions recombine to form hydrogen atoms with then combine with oxygen to form water- supply of o2 stops electron transport chain and ATP synthesis stops
movement called chemiosmosis
RNAD=10 RFAD=2 ATP=4
10x3=30- as RNAD carry 3 hydrogens
2x2=4- as RFAD carry 2 hydrogens
+4
total ATP= 38 per glucose

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18
Q

adaptations of sarcomeres

A

parts of sarcolemma fold inward giving T tubules which conduct elec to entire fibre and all movement of ca2+
sarcoplasmic reticulum specialed to sorare and release ca2+ necessary for contraction
have many mitochondria for continued aerobic respiration

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19
Q

tertiary structure of myosin

A

Globular head which is flexible and able to fold straight bundled part R groups arranged to bind to ATP

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20
Q

reduced NAD
reduced FAD

A

can produce up to 3 ATP
can produced 2 ATP

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21
Q

why ATP is broken down in glycolysis

A

donates phosphates to glucose- phosphorylated
produces 3 carbon compound
supplies energy to break the bonds

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22
Q

lactate breakdown

A

wate product of anerobic respiration= lactic acid
glucos- pyruvate - lactate to lactic acid- process stops at glycolysis
conversion from glucose to lactate

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23
Q

chemiosmosis

A

energy released as electrons pass down the electron transport channel - energy used to move hydrogen ions from the matrix, across the inner mitochondrial membrane and into the intermembrane space - creates a steep electrochemical gradient across the inner membrane - there is a large diff in conc of H+ across the membrane ad a large elec diff, making the intermembrane space more pos than the matrix
the hydrgen ions diffuse down this electrochem gardient through hollow protein channels situated within ATP synthase embedded and protruding from, the inner memebrane. As the hyrodgen pass through the channels ATP synthesis is catalysed by the ATP synthase- hydrogen ions cause a change in shape of the of the enzymes active site enabling ADP and phosphate ions to bind to the site
within the matrix the H+ and electron recombine to form hydrogen atoms - combine with oxtgne to form water - the oxygen acting as a final carrier in the electron transport chain is thus reduced - oxidative phosphorylation

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24
Q

measuring rate of respiration

A

Control variables: age, mass, species of maggots Can be used to compare respiration at different temperatures by measuring distance traveled by coloured liquid Method: Set up respirometer as shown: pipette and coloured bead of liquid with attached scale or markings showing distance; alternatively mark start point of coloured bead place 5g of maggots over guaze and soda lime open 3 way tap and adjust start point of coloured dye, note as start point Close 3 way tap and start the stopwatch - measure distance every 30s and note distance moved by dye calculate volume used by using distance x π x r2Oxygen consumption rate given by distance over time

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25
anaerobic respiration
Alternative glycolysis pathway (anaerobic): glucose -> pyruvate ->reduced -> lactate -> lactic acid conversion from glucose to lactate regenerated NAD allowing ATP to be produced anaerobically through glycolysis cycle lactic acid breakdown: oxidation to pyruvate first Reused in Krebs recycled to glucose in liver for use or further conversion to glycogenoxidation of lactate to pyruvate requires oxygen, leaving organisms in an oxygen debt after
26
effect of lactate build up
enzymes function efficently over a narrow pH range - as hydrogen ions from the lactic acid accumulate in the cytoplasm, they neutralise the neg charged groups in the active site of the enzyme- the attaraction between the charged groups on the substrate and in the active site will be affected- the substrate may no longer be able to bind to the active site
27
getting rid of lactate
after a period of anaerobic respiration most of the lactae is converted back into pyruvate it is oxidised directly to carbon dioxide and water via the kreb cycle thus releasing enrgy to synthesise ATP As a result oxygen uptake is greater than normal in the recovery period after exercise excess oxygen requirement called oxygen debt
28
supply instant energy
immediate regeneration of ATP achieved through use of creatine phosphate- stored in muscles and hydrolysed to release energy- used t regenerate ATP from ADP and phosphate (from CP)- does not require energy and requires short intense enrgy
29
results of anerobic repsiration
No link reaction as triose phosphate is not produced No dehydrogenation to reduce NAD/FAD in Krebs cycle No regeneration of NAD/FAD from oxidative phosphorylation so electron transport chain does to occur Overall no final ATP synthesis in oxidative phosphorylation
30
aerobic capacity
ability to take in, transport and use o2
31
cardiac output
CO= stroke vole (blood ejected from the LV) x heart rate during exercise their is greater muscle action so more blood returns to heart- venous return
32
how is cardiac muscle myogenic
no need for electrical impulse from brain to beat - can contract without external nervous stimulus nodes control contraction of cardiac muscle
33
components in heart beat
SAN: sinoatrial node, pacemaker, induces contraction of atria AVN: atrioventricular node, induces contraction of ventricles Bundle of His: collection of muscle cells specialised for conduction to Purkyne fibres Purkyne fibres: finer muscle fibres in ventricle walls allowing simultaneous contraction of L/R
34
how contraction occurs
SAN acts as a pacemaker and depolarises regularly. Generates an electrical impusle Causes contraction of atria After a time gap the impulse reaches the AVN - delay ensures that atria hace finished contracting and ventricles have filled with blood before ventrical contraction AVN causes contraction of ventricles upwards through bundle of His and Purkyne fibres Purkyne fibres large, specialised muscle fibres that conduct impulses rapidly to the apex of the ventricles- right and left bundles collectively callded bundle of His fibres continue around each ventricle and divide into smaller branches that penetrate the ventricle muscle- carry the impulse to the inner cells of the ventricles where it spreads through the entire ventricle wall 1st ventricular cells to depolarise are at apex of heart , begins there and travels upwards
35
ECG
graphic record of the electrical activity during the cardiac cycle P wave: atria contraction/depolarisation PR interval: time taken for an impulse to be conducted from the SAN across the atria to the ventricles, through the AVN QRS complex: contraction of ventricles T wave: relaxation and repolarisation of ventriclesIrregularities can be seen as different time intervals between beats - suggests CVD tachycardia: too fast ectopic heartbeat: extra contraction fibrillation: irregular heartbeat does not show atrial repolarisation becuase the signals generated are small and hidden by the QRS complex 1 square= 0.04 seconds, one large square=0.2 seconds heart= no. or large squares between QRS complex x 0.2- one beat in seconds- /60
36
cardiac output and ventilation control
Changes in ventilation and cardiac output allow rapid delivery of oxygen/removal of carbon dioxide increase with exercise to meet oxygen demands for aerobic respiration move blood to muscles to provide oxygen and remove carbon dioxide steepens diffusion gradient between capillaries and muscle cells, allowing efficient gas exchange
37
nervous control of heart rate
under control of cardiovascular control centre in medulla oblongata CO is controlled by changes in blood pressure from use of muscles Baroreceptors detect changes in pressure and signal this to the medulla oblongata and cardiac control centre Changes in pressure are detected in medulla oblongata and carotid/aortic bodies Activate either parasympathetic or sympathetic pathways to signal change in AVN AVN depolarises more/less depending on needs, changing CO- CO= Stroke volume x heart rate Changes can also be brought about by pH changes in blood and ultimately follow the same activation pathway
38
sympathtic nerve
action- Increase SAN depolarisation- increases heart rate associated neurotransmitter- Adrenaline stimaluetd by- Low O2, high CO2 (heart not working hard enough), Low BP, High pH
39
parasympathtic nerve
action- Decrease SAN depolarisation associated neurotransmitter- Acetylcholine stimuated by- High O2, low CO2 (heart working too hard), High BP, Low pH
40
hormonal effects on heart rate
adrenaline has a direct effect on the SAN increasing the heart rate as well as causing dilation of arterioles supplying skeletal muscles and consctriction of arterioles going to digestuve system and other non essential muscles
41
control of ventilation
Affected by changes in stretch receptors in intercostal muscles/diaphragm and medulla oblongata and changes in CO2/O2 levels Inspiratory centres in medulla oblongata send nerve impulses to intercostal muscles to make them contract - stimulates inspiratory centres volume of lung increases, decreasing pressure also inhibits expiratory centres air enters the lungs due to pressure differences, stimulating stretch receptors to send impulsesimpulses reach medulla oblongata, which signals inhibition of inspiratory centre (muscles relax) and stimulates expiratory centre diaphragm and intercostal muscles relax, lungs deflate, and stretch receptors are no longer stimulated cycle restarts
42
control of breathing rate and depth
conc of dissolved co2 in arterial blood- increase in conc causes a large increase in ventilationcarbon dioxide dissolves in blood plasma making carbonuc aciddissociates into H+ and hydrogencarbonate ions- lowers pHchemoreceptors sensitive to H+ are located in ventilation centre of medulla oblongata- detect rise in H+ conc impulses are sent to other parts of vemtilation centre impulses sent from ventilation centre to stimulate muscles involved in breathing
43
slow twitch fibres v fast twitch fibres
Slow twitch- Slow contraction, endurance + Mitochondria for aerobic respiration (ATP),high conc of respitory enzymes, Lots of capillaries for efficient exchange , Myoglobin with oxygen stores giving red colour- releases o2 when conc low Fast twitch - Fast contraction, instant power, Less mitochondria , Less capillaries , Less myoglobin, reliant on anerobic respiration
44
negative feedback loop
a response which maintains homeostatic balance, reversing a change in the body to return to normal limits homeostatic control mechanisms such as receptors are used to detect deviations to the norm, connected to a control centre which turns on or off effectors to bring condtion back to norm val
45
positive feedback
a response which exaggerates and amplifies a response in the body to enhance the effect eg inflammatory response
46
examples of neg feedback
glycolysis - when ATP levels on cell raises, it inhibits one of the ezymes involved in early stage - ATP binds to phosphofructokinase which catalyses early stages og glycolysis- chnages active site
47
thermoregulation
control of body temperture to ensure enzymes in body working at an optimum rate
48
temp control receptors and detectors
chnages in blood temp detected by receptors in the hypothalamus thermoreceptors in the skin detect temp changes- skin warm impulses sent to hypothalamus initiating the heat loss responses and inhibiting heat gain responses
49
body response if hot
more sweat produced and evaporated to remove heat from skin vasodilation of cells at skin surface allow heat loss via radiation erector Pili muscles lie flat radiate heat
50
body response if cold
Shiver to produce heat from respiration (exothermic) sweat glands not activated erector Pili muscles contract to trap air for insulation vessels near skin vasoconstrict release of Adrenalin and thyroxine to increase metabolism (exothermic)
51
how sweat reduces heat loss
evaporates taking heat energy away from skin- sweat glands stimulated by nerves from hypothalamus
52
raising of hairs
trap layer of air that insulates the body
53
blood flow thermoregulation
in colder conditions the muscles in the arteriole walls contract causing the arterioles to constrict, reducing blood supply to surface if cappilaries - diverted through shunt vessels which dilates- blood flows further from skin si less energy is lost- vasoconstricton - opposite in warmer- vasodilation
54
energy loss
radiation conduction- energy transfer between objects convection- cool air surrounds body, heats from body, expands/rises/moved away- will be replaced by cool air evaporation
55
effects of exercise on immunity
moderateincreases the no. and activity of natural killer cells- non specfic immunity against infected cells- release protein perforin which makes pores in memebrane allowing other molecuules to enter to cause apoptosis vigorousfall in many cells involved in immune response
56
medical tech
Keyhole surgery: small incision made to reach desired area with camera, light source and special toolsBenefits: faster recovery, less invasive, less risk of infectionProstheses: artficial replacment of limbs/parts of limbsMay have electronic devices connected to nervous system to allow movementcan be used to replace knee joints to increase cushioningQuicker recovery times allow athletes to return to sport Prostheses give athletes opportunity to perform in sports previously not possible
57
how a knees susceptible to wear and tear injuries
articular cartilage covering the surface of the bones wears away so that the bones may actually grind on each other causing damage that can lead to inflammation and a form of arthritispatellar tendonitis occurs when kneecap does not glide smoothly across the femur due to damage of th articular cartilage on the femur the bursae that cushion the points of contact between bones, tendons and ligaments can swell up withe extra fluid - may push against other tissues in joints causin inflammation and tenderness sudden twisting or adrupt movement of the knee joint often reuslts in damage to ligaments
58
advantages of physical actvity
increase arterial vasodilation lowers blood pressure- reduces risk of conary heart diseaseincreases level of HDLs and reduces LDLs balance between energy output and input helps maintain healthy weightincreased sensitvity of muscle cells to inslin improves blodd glucose regulation and reduces likelihood of developing type 2 diabetesphysical actvity increases bone density and reduces its loss during old agereduces risk of some cancersimproves mentak wellbeing
59
chnages in exercis with graphical evidnece
Result of over exercising - wear and tear on joints, immune system suppression leading to increased risk of infection Result of under exercising - increased obesity risk, CVD, diabetes
60
for performance enhancing drugs
Autonomy, individual choice Competition isn’t fair anyways, think access/funding Enables some athletes to reach a higher level
61
against performance enhancing drugs
Some PEDs are illegal Serious health risks associated Cannot ensure users will be fully informed
62
hormones
chem messangers released from endocrine glandspituitary gland- growth hormone, folicle stimulating hormone (controls testes and ovaries) , antidiuretic hormone ( causes reabsorption of water in kidenys) thyroid- thyroxine- raises basal metabolic rateadrenal- adrenaline- raises basal metabolic rate. dilates blood vessels, prep bod 4 actionovary- oestrogentestis- testostrone
63
how hormones affect target cells
peptide hormones such as insulin are unable to pass through cell membrane easily, charged, bind to receptors on membrane activating secondary messenger in cytoplasm- brings chem changes in the cell which directly or indirectly affects gene transcription
64
transcription factors
Activating tissue: chemical signal binds to receptors in some tissues causing epigenetic changes, regulates transcription factor, TF or repressor binds to promoter region Activation from cell membrane: bind to receptors in CSM, activate messenger molecules in cytoplasm, activation of kinases triggering cascade for synthesis of TF Transcription factors: prevent repressor binding to promoter region, RNA polymerase is able to bind, transcription occurs steriods pass through cell membrane and binnd to receptors in cytoplasm- hormone-receptor complexes bring abut characteristic repsonse - act as transcription factors switiching enzyme synthesis on or off
65
how transcription factors work
RNA polymerase and cluster of transcription factors bind to DNA- transcritption initation complex- binds to promoter region'- trancription proceeds most created in an inactive foorm and activated by action hormones , growth factors or regulatory molecules - genes switched off until all required transcription factors are present in their active form prevented by protein repressor moleules attaching to promoter region- blocks attachment of transcription factors preventing devlopment of transcritpion initation complex- repressors may be inactive transcription factors- activator molecules in the cell stimulate bidning of transcription initation coplex
66
erythropoietin
peptide hormone produced by kidneys stimulates the formation of new RBC in bone marrow - low o2 in blood detcted by kidney which releases erythropoietin too high= too many RBC increasing risk of thrombosis
67
testosterone
steriod hormone produced in testes- androgens causes devlopment of male sexual organs- causes development of secondary sex characteristics binds to andrgen receptors and modify gene expression to later development if cell- increase muscle devlopment through protein synthesis anabolic steriods devloped to replciate testosterone effects effects on cholesterolincreases production of LDLs and increases breakdown of HDLshigh cholesterol associated with risk of athersclorsis- CVD - as HDLs take cholesterol to licvver to breakdown whilst LDLs accumulate in blood
68
problems with anabolic steriods
high BP liver damages changes in menstral cycle decrease sperm prodcution kidney failure heart duisease
69
ceratine
amnio acid- derived compunds- absorbed unchanged and acrried in the blood to tissues and skeletal muscles increase amounts of ceratine phosphate in muscles- helps hsort term high intensity exercise diarrohea nausea vomiting high bp kidney damage muscle cramps
70
why the outer mitochondrial matrix is not permeable to hydorgen ions
this means that hydrogen ions cannot leave the mitochondria reaulting in the accumulating in the intermemebrane sapce in order for mitchondria to move down electrochemical gradient by chemiosomis to synthsise ATP
71
role of ETC
recieves hydrogen from reduced NAD/FAD , oxidsed, this breaks the hydrogen into protons and eletcrons - electrons transported through a series of redox reactions, energy used to pump protons into intermembrane spaxe
72
where is carbon dioxide removed from during krebs
c5 or c6
73
calcium ions during SFT
electrical impulse depolarise neuromuscular junction, this cuases calcium ion channels on the sacroplasmic reticulum to open, releasing calcium ions from within the SR into the sarcoplasm, these calcium ions bind onto the troponin on the myofibrils casuing it to change shape, which inturn moves the tropomyosin filament, exposing the myosin binding site. taken back into SR by AT
74
how extensors and flexors work together
both tendons that connect muscle to bone, atognistic apirs that work togwther to bring about a movemnt
75
how mucsle fibres adapted
sarcolemma contains volatge gated channels to allow depolarisation of muscle fibres, many mitochonfria, presence of myobfibrils wich interact to allow a muscle contraction to occur
76
myosin structure and fucntion
part straigth to form a bundle with other mysoin, part folded into a gobular structure head that can form bonds withc acti, part contians an area that can bond with ATP
77
hoe adrenaline acts in heart beat
is acrried in the blood and acts on SAN increases the frequency of impulses produced by SAN which spread across the heart increases rate at which heart contracts
78
control variables for spirometre experiment
level of fitnessexposure to smae evironemtal conditionsbody mass
79
how exercise auses an increase in breathing rate
exercise initates imuslses form motor cotrex/strech receptors in muscles which are sent to the medulla olongata leading to increased implses to intercostal muscles/diaghrpam
80
effect if exercise on changes of oxygen consumption
exercise will increase oxygen consumptionthis is due to increased aerobic respirationbecause more ATP is needed by muscles oxygen debt- oxygen is required to convert lacate to pyruvate in liverxygen consumption starts to decrease follwoing exercise
81
respitary miunte ventiliation
tidal volume x ventilation/breathing ratefind differences in peak to trough volume to give tidal volume
82
how oxygen consumption is calculated from spirmeter
difference in vol of one peak/trough comapred to a subsquent one - divide time by two and multiply by 60
83
how heart rate is decreased follwing exercise
chemoreceptors detect a change in CO2 the CV control centre recives impulses from chemoreceptors and sends impulses to heart via the parasympathetic nerve pathway, these are sent to the SAN which thereby depolarises less often reducing heart rate
84
gene doping
non medical use of cells, genes or gene expression to enhance performance
85
stimulants
makes athletes more alert and masks fatigue heart failure, addiction
86
anabolic agents-n steroids
helps athletes train harder increases aggression + kidney failure
87
diuretics
remove fluids from body- used to make the wright- severe dehydration
88
narcotic analgesics
mask pain caused by injury or fatigue which makes injury worse- addcotve
89
peptides and hormones
Erythropoietin- RBCs give more energy- risk of stroke or heart problems- stimulates production of more RBC carrying more o2 to muscles HGH-builds muscle- abnormal growth, heart disease, diabetes, arthoritisis
90
effects of body mass and surface area on thermoregulation and sweating
Smaller organisms or people with higher SA:V lose heat faster. Larger organisms or people with lower SA:V retain heat better. Higher body mass = more metabolic heat production. But also a lower SA:V, meaning slower heat loss. Larger individuals tend to retain heat more effectively → may need to sweat more during exercise to cool down.
91
process of thermoregulation
thermoreceptors in hypothalamus or skin detect changes in heat theremoregulatory centre in hypothalamus stimulated which sends impulses to sweat glands increases blood flow to surface by vasodilation/contriction of shunt vessels decrease metabolic rate
92
effects of over exercising
results in wear and tare injuries of joints/cartilage/tendons/ligaments- therefore leading to joint damage suppresses immune system- reduces T cell numbers and therby anti body production increased risk of infection
93
why it takes Time for blood to heat from external environment
time for heat to warm blood because of the ;ayer of insulation in the skin takes time for blood to circulate around the body
94
how a single gene can result in multiple different primary structures
pre mrna splicing/psot-trasncriptional modfication exons can be joined together in different sequences - producing different sequence of amino acids
95
how some genes can be expressed in some tissues but not others
hormones/chem signals bind to receptors only found in certain tissues regulATING transcription factors and repressor proteins these bind to promoter region of the gene therefore site on or off the gene- depending on whether they allow or prevent RNA polymerase from binding
96
how transcription factors turn on a gene
TF interact with promoter region on gene by forming a transcription imitating complex that binds to promoter region allowing RNA polymerase to bind and transcribe the gene
97
Explain how the pH of the blood of a sprinter is returned to its original level after a race
low pH is due to acid in the blood- carbon dioxide as waste from anaerobic respiration as well as lactic acid from lactate produced in anaerobic respiration lactate taken to liver where in is converted back into pyruvate- body in an oxygen debt, as oxygen required for the conversion of lactate- with production of reduced NAD / eq ; {lactate / pyruvate} converted to glucose / glycogen ;pyruvate into mitochondria ; idea of chemoreceptors detecting change in pH ; idea of response e.g. increased { nerve impulse rate from medulla / breathing rate / heart rate} ; .(dissolved) CO2 from blood (diffuses) into alveoli / eq
98
tidal volume
volume of air passing in and out of the lungs in a resting breath- volume of air from a trough to a peak
99
inspiratory reserve volume
inhaling as much as you can oppodite= expiratory reserve volume
100
vital capacity
the maximum amount of air we can inhale and exhale
101
how spirometer changes after exercise
more peaks/troughs in same amount of time more distance between peaks and troughs
102
variables to control with spirometer
age, body index (BMI), gender, lifestyle, fitness level, health status
103
how the SAN works (mark scheme)
imitates impulses in atria - causes atria to contract forcing oxygenated blood into the ventricle- electrical activity received by AVN which sends impulses down bundle of HIS and pyrukne fibres
104
what is measured on x and y axis of electrochariogram
x: time y:PD
105
what are transcription factors
Proteins that control the transcription of specific genes-They bind to specific DNA sequences (usually in promoter regions) to:Activate (as activators) Or repress (as repressors) the transcription of target genes They help RNA polymerase know when and where to transcribe a gene.
106
effect of hormones as transcription factors
Lipid-soluble → pass through the cell membrane. Bind to intracellular receptors (in the cytoplasm or nucleus). The hormone-receptor complex acts as a transcription factor: Enters the nucleus Binds to specific DNA sequences (hormone response elements) Activates or represses transcription of target genes
107
Non-Steroid Hormones & Drugs (e.g., Adrenaline, Caffeine, Other Molecules): TF
Not lipid-soluble → bind to receptors on the cell membrane. Trigger second messenger systems (e.g., cAMP pathway). These second messengers activate transcription factors inside the cell. Leads to indirect activation of gene transcription.
108
why slow twitch causes less fatigue
person B has more slow twitch fibres than person A (1) slow twitch are more efficient at aerobic respiration because they have more mitochondria (1) slow twitch have many capillaries to give good oxygen supply (1) slow twitch have lots of myoglobin to store oxygen (1) therefore less likely to build up lactate
109
why muscles occur in antagonistic pairs
muscles can only work in one direction (1) therefore a need to create opposite forces (1) so must have extensors and flexors
110
transcription factor mark scheme
a protein that controls {the activation / transcription} of genes
111
how and why ATP is used
contains {phosphate / P-O-P} bonds (1) that when hydrolysed {releases / provides supplies} energy (1) description of how energy is used (1) ATP {immediate source of energy /releases energy rapidly} (1)
112
what is metabolic rate
the rate of energy expenditure in an organism.
113
hibernation
lowered body temperature and reduced ATP production- lower metabolic rates reduce oxygen demand and cellular respiration. metabolic suppression prevents oxidative stress and energy depletion. MP6: Link reduced metabolic rate to the conservation of stored energy reserves (fat/glycogen).