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topic 7 Flashcards

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Biology 101 flashcards
1
Q

why are muscle cells multinucleate?

A

a single nucleus couldnt effectively control the metabolism of such a long cell

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2
Q

describe the structure of a muscle?

A

muscle made up of bundles of muscle fibres that are bound together by connective tissue

  • > each muscle fibre is a single muscle cell
  • > inside the muscle fibre is the cytoplasm, organelles etc.
  • > but also myofibrils composed of sarcomeres
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3
Q

sliding filament theory

A
  • nerve arrives at neuromuscular junction & calcium ions released from the sarcoplasmic reticulum.
  • diffuse through the sarcoplasm & attaches to troponin, causing it to move.
  • as a result the tropomysin on the actin filament shifts position, exposing binding sites on actin filaments.
  • myosin head binds to binding site, forming a cross bridge
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4
Q

what happens once the mysosin head has bound to the binding site on the actin filament

A

ADP + Pi are released,
myosin changes shape, nods forward & actin moves over myosin
ATP binds to the myosin head, myosin head detaches
an ATPase on the myosin head hydrolyses the ATP ( to ADP + Pi ), changed shape of head, moves to the upright position
cycle can restart

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5
Q

what happens in glycolysis?

A

starts with glucose
-> input of energy from ATP (2 phosphates are added)
splits into 2x phosphorylated 3C compounds
-> dehydrogenated ( losing 2H that are picked up by NAD)
-> substrate level phosphorylation ( creation of 4ATP from 4ADP + Pi )
2x pyruvate (3C)

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6
Q

what happens in the link reaction?

A

decarboxylated -> CO2 released as a waste product
dehydrogenated -> 2H removed and taken up by NAD
acetyl coenzyme A produced

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7
Q

What happens in the Krebs Cycle?

A 
acetyl coA combines with a 4C compound to produce a 6C compound
-> decarboxylated 
-> dehydrogenated ( NAD -> rNAD )
to produce a 5C compound
-> decarboxylated 
-> substrate level phosphorylation ( to directly synthesise 1ATP ) 
-> 2x dehydrogenated ( NAD -> rNAD )
-> dehydrogenated ( FAD -> rFAD )
to produce 4C compound
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8
Q

what happens in the ETC?

A

rNAD & rFAD carries 2H+ and 2e- to the ETC on the inner mitochondrial membrane

  • > electrons pass from one carrier to the next in a series of redox reactions (reduced when receives them, oxidised when passing them on)
  • > protons move across IMM creating high H+ concentrations in the IM space
  • > protons diffuse back into the MM down the EC gradient
  • > this allows ATP synthase to catalyse ATP synthesis
  • > electrons and H+ recombine to form hydrogen atoms which then combine with O2 to create water.
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9
Q

what happens to respiration if the supply of O2 stops

A

the ETC & ATP synthesis stops

-> O2 is the final electron acceptor

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10
Q

what part is oxidative phosphorylation?

A

synthesis of ATP in this way

  • > H+ diffusing down EC gradient through stalked particle, catalyses ATP synthesis
  • > H+ and e- recombine to form H & then combine with O2 to form water
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11
Q

what is chemiosmosis

A

all of the 4th section

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12
Q

where can fatty acids be respired?

A

through the krebs cycle

-> therefore fats can only be a fuel for aerobic respiration & cannot be used when oxygen is not available

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13
Q

what happens in anaerobic respiration?

A

pyruvate is reduced to lactate & the oxidised form of NAD is regenerated
-> the partial breakdown of glucose creates a small amount of ATP

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14
Q

in a solution, lactate forms lactic acid - what does this do?

A

as lactate accumulates, the pH of the cell falls, inhibiting the enzymes that catalyse the glycolysis reaction
-> the glycolysis reactions & the activity that depends on them cannot continue

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15
Q

what happens as the hydrogen atoms from the lactic acid accumulate in the cytoplasm?

A

they neutralise the negatively charged groups in the active site of the enzyme

  • > the attraction between charged groups on the substrate & in the active site will be affected.
  • > the substrate may no longer bind to the enzymes active site
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16
Q

what happens to lactate afterwards?

A

converted back into pyruvate
-> oxidised directly to CO2 & O2 via the Krebs cycle, releasing energy to synthesise ATP
=> O2 uptake is greater than normal in the recovery period (oxygen debt)

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17
Q

what is the immediate regeneration of ATP achieved by?

A

using creatine phosphate

  • > stored in muscles that can be hydrolysed to create energy
  • > energy iludes to regenerate ATP from ADP + Pi ( phosphate from the creatine phosphate itself )

creatine phosphate + ADP -> creatine + ATP

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18
Q

what is aerobic capacity?

A

the ability to take in, transport and use oxygen

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19
Q

what is VO2

A

litres of O2 we consume at rest

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20
Q

what is VO2 max?

A

litres of O2 consume at maximum exercise

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21
Q

what is cardiac output

A

volume if blood pumped by the heart in min

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22
Q

when running, what is adequate O2 maintained by?

A

increasing cardiac output
faster rate of breathing
deeper breathing

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23
Q

when will someone be more suited to aerobic/ endurance type exercise?

A

if they have more efficient cardiovascular and ventilation systems

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24
Q

what does cardiac output depend on

A

the stroke volume & heart rate

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25
Q

what is stroke volume

A

volume of blood ejected from the left ventricle

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26
Q

CO = ?

A

CO = SV x heart rate

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27
Q

what is the normal stroke volume for adults at rest?

A

50-90 cm3

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28
Q

what is venous return?

A

blood returning to the heart

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29
Q

there is greater muscle contraction during exercise, what does this mean?

A

more blood returns to the heart in venous return

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30
Q

in diastole ( during exercise ) what happens? & why?

A

the heart fills with a larger volume of blood
the heart muscle is stretched to a greater extent, contracts with a greater force, so more blood is expelled
-> increases SV & CO

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31
Q

when the body id at rest, how much blood remains in the ventricles after contraction?

A

40 %

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32
Q

why may heart rates differ?

A
  • size of heart
  • body size
  • genetic factors
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33
Q

why does a larger heart have a lower resting rate?

A

expels more blood with each beat, so does bot have to beat as frequently to circulate the same volume of blood around the body.

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34
Q

the ❤️ is myogenic, what does this mean?

A

it can contract without external nervous stimulation

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35
Q

where in the ❤️ does depolarisation begin?

A

sinoatrial node (SAN)

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36
Q

what is the sinoatrial node?

A

a small area of specialised muscle fibres located in the wall of the RA, beneath the opening to the superior vena cava
-> aka pacemaker

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37
Q

what does the SAN do?

A

generates an electrical impulse, spreads across the R&L atria, causing them both to contract at the same time
-> also travels to the atrioventricular node (AVN)

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38
Q

what happens from the AVN?

A

connected to the ventricles after a delay

-> reaches the purkyne fibres

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39
Q

why is there a delay?

A

to make sure the atria have finished contracting & the ventricles have filled with blood

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40
Q

what are purkyne fibres?

A

large, specialised muscle fibres that conduct impulses rapidly to the apex of the ventricles
-> there are right and left bundles of fibres that are collectively known as tbe bundle of His

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41
Q

what do the purkyne fibres do?

A

carry the impulse to the inner cells of the ventricles and from here it spreads through the entire ventricle walls
-> wave of contraction begins starting at the apex, blood is squeezed into the pulmonary artery and the aorta

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42
Q

how can the electrical activity of the heart be detected & displayed?

A

an electrocardiogram

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43
Q

how does an ECG work?

A

electrodes are added to the chest and limbed to record the electrical currents produced during the cardiac cycle
-> when there is a change in polarisation of the cardiac muscle, a small electric current can be detected at the skin surface

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44
Q

what is a stress test?

A

ECG before, during & after exercise

-> to detect problems that only occur when the heart is working hard

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45
Q

what does the P wave show?

A

depolarisation of the atria, leading to atrial contraction

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46
Q

what is the PR interval

A

time taken for impulses to be conducted from the SAN across the atria to the ventricles, through the AVN

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47
Q

what is the QRS complex?

A

the wave of depolarisation resulting in the contraction of the ventricles

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48
Q

what is the T wave?

A

repolarisation of the ventricles during diastole

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49
Q

why does the ECG not show atrial repolarisation?

A

the signals generated are small ans are hidden by the QRS complex

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50
Q

what is bradycardia?

A

a heart rate of less than 60bpm

-> symptom of heart problems if not an athlete

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51
Q

what is tachycardia?

A

a heart rate greater than 100bpm

-> symptom of CVD, heart failure etc

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52
Q

what is ischaemia?

A

the heart muscle does not receive blood due to atherosclerosis causing a blockage of the coronary arteries.
-> the normal electrical activity and rhythm of the heart are disrupted & arrhythmias can affect a larger area of heart muscle

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53
Q

what are arrhythmias?

A

irregular bearings caused by electrical disturbances

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54
Q

what is heart rate controlled by?

A

the cardiovascular control centre in the medulla oblongata

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55
Q

what NS is involved in the system between the ❤️ and ccc?

A

autonomic

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56
Q

what does the sympathetic nerve do?

A

increases HR

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57
Q

what does the parasympathetic nerve do? ( vagus nerve )

A

decrease HR

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58
Q

what do both nerves send impulses to ?

A

the SAN

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59
Q

what can the ccc detect?

A
  • accumulated CO2 in blood
  • accumulated lactate in blood
  • reduction of O2
  • increased temp
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60
Q

what happens at the sound of a start pistol?

A
  • skeletal muscles contract
  • stretch receptors in the muscles and tendons are stimulated
  • send impulses to the ccc
  • raised heart rate via the sympathetic nerve
  • increase in venous return
  • rise in the SV
  • increased HR & SV = higher CO
  • oxygen and fuel to muscles faster
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61
Q

to prevent BP rising too high, what happens?

A

pressure receptors on the aorta and carotid artery send nerve impulses back to the ccc
-> inhibitory nerve impulses are then sent to the SAN

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62
Q

what is the affect of sympathetic/parasympathetic nerves on intercostal muscles?

A 
sympathetic = increased breathing rate 
parasympathetic = decreases breathing rate
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63
Q

what is the affect of sympathetic/parasympathetic nerves on heart?

A 
sympathetic = increases heart rate and stroke volume 
parasympathetic = decreases heart rate and stroke volume
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64
Q

what is the affect of sympathetic/parasympathetic nerves on the gut?

A 
sympathetic = inhibits peristalsis 
parasympathetic = stimulates peristalsis

peristalsis = muscle contractions in the gut wall that moves food through the gut

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65
Q

what affects does adrenaline have?

A
  • directly affects the SAN , increasing the heart rate to prepare the body for the likely physical demands
  • dilation of arterioles supplying skeletal muscles & constricts those going to the digestive system & other non essential organs, maximising blood flow to the active muscles
66
Q

what is tidal volume?

A

volume of air we breathe in and out at each breath

67
Q

what is vital capacity?

A

the max volume if air we can inhale and exhale

68
Q

how can we determine the rate of O2 consumption using a spirometer trace?

A
  • decrease in volume between two points on the trace, gives volume of oxygen in a given time
  • divided by the times for the fall

value in cm3s-1

69
Q

what is the minute ventilation?

A

volume if air taken into the lungs in one min

70
Q

how is minute ventilation calculated?

A

tidal volume x breathing rate

avg volume x breaths per min

71
Q

what controls breathing ?

A

the ventilation centre in the medulla oblongata

72
Q

where does the ventilation centre send impulses?

A

to external intercostal muscles and diaphragm muscles every 2-3 seconds

73
Q

what muscles are stimulated during deep inhalation?

A

external intercostals
diaphragm
neck
upper chest

74
Q

as the lungs inflate, stretch receptors in the bronchioles are stimulated - the stretch receptors send inhibitory impulses back to the ventilation centre
, what does this mean?

A

impulses to the muscles stop
the muscles relax
inhalation stops
exhalation allowed

75
Q

what causes exhalation?

A

elastic recoil of the lungs & gravity (helping to lower the ribs)
-> not all the air is exhaled with each breath, the residual air mixes with the inhaled air

76
Q

when do the internal intercostal muscles contract?

A

only during deep exhalation

77
Q

at rest, what is the most important stimulus controlling breathing rate & breathing depth?

A

concentration of dissolved CO2 in arterial blood, via its effect on pH
-> a small increase in CO2 concentration causes a large increase in ventilation

78
Q

how does carbonic acid impact breathing?

A

-CO2 dissolves in the blood plasma, making carbonic acid
- carbonic acid dissociates into hydrogen ions and hydrocarbonate ions, lowering the pH
( CO2 + H2O -> H2CO3 -> H+ + HCO3- )
-chemoreceptors sensitive to hydrogen ions are located in the ventilation centre, they detect the raise in H ion concentration
-impulses sent to other parts of the ventilation centre
- impulses are sent from the ventilation centre to stimulate the muscles involved in breathing.

79
Q

what fled increasing CO2 and the associated fall in pH lead to?

A

increase in rate and depth if breathing through more frequent and stronger contraction of the appropriate muscles

80
Q

what do more frequent, deeper breaths maintain?

A

a steel concentration gradient of CO2 between the alveolar air and the blood
-> ensures efficient removal of CO2 from the blood & uptake of O2 into the blood

81
Q

what does a decrease in CO2 mean?

A

pH rises

decreased depth & rate

82
Q

what does the motor cortex control?

A

movement

83
Q

as soon as exercise begins, what do impulses from the motor cortex do?

A

have a direct effect on the ventilation centre in the medulla oblongata, increasing ventilation sharply

84
Q

what is aerobic capacity dependent on?

A
  • uptake / transport of O2 to the muscles

- efficiency of O2 use in muscle cells

85
Q

slow twitch muscle fibres

A
86
Q

fast twitch fibres

A
87
Q

define homeostasis

A

maintenance of a stable internal environment

88
Q

what does each condition that is controlled have?

A

a norm value/ set point, usually the optimum, that the homeostatic control mechanisms are trying to maintain.
-> receptors are used to detect deviations from the norm, they are connected to a control centre, which turns on/off effectors

89
Q

what is the deviation from the norm resulting in a change in the opposite direction, back to the norm known as?

A

negative feedback

90
Q

how is glycolysis an example of negative feedback?

A

when the level of ATP in the cell rises, it inhibits one of the enzymes catalysing an early step in the pathway. ATP production falls, maintaining a steady concentration of ATP in the cell.
-> ATP binds to phosphofructokinase, it doesn’t bind to the active site, but to another site, so the shape of the enzyme & its active site change, preventing an enzyme substrate complex from forming

91
Q

how is testosterone an example of negative feedback?

A

change in testosterone levels is detected by the hypothalamus.

  • > a decrease causes gonadotrophin-releasing hormone to be produced by the hypothalamus
  • > stimulates the pituitary gland to release hormones that stimulate the testes to synthesise testosterone.
92
Q

how is birth an example of positive feedback?

A
  • the pressure of the baby on the uterus is detected
  • nerve messages to the hypothalamus causes the hormone oxytocin to be released
  • contractions of the uterus speed up and become more intense
  • the increase in contractions makes the pressure of the baby on the uterus wall increase
  • more oxytocin released
  • increased contraction until the baby is born
93
Q

what is positive feedback?

A

the output from the control centre moves the condition further from the set point

94
Q

what is thermoregulation?

A

the control of body temperature

95
Q

what is human body temp?

A

37.5°

96
Q

what does the heat loss centre stimulate?

A

swear glands to produce sweat

97
Q

what does the heat loss centre inhibit?

A

contraction of arterioles ( dilates capillaries )
hair erector muscles ( lie flat )
liver ( reduces metabolic rate )
skeletal muscles ( relax - no shivering )

98
Q

what does the heat gain centre stimulate?

A
  • arterioles in skin to constrict
  • hair erector muscles contract
  • liver raises metabolic rate
  • skeletal muscles contract in shivering
99
Q

what does the heat gain centre inhibit?

A

sweat glands

100
Q

what does shivering do?

A

transfers energy to muscle tissue, which hells maintain body temp

101
Q

what does sweat do?

A

released on the skin via the sweat duct evaporates, taking heat energy from the skin

102
Q

why are hairs raised in cold weather?

A

contractions of the erector muscles

-> aim is to trap a layer of air that insulates the body

103
Q

in cold weather, what happens to arterioles?

A

arterioles constricts -reduces blood flow to the surface capillaries
shunt vessel dilates
-> less energy is lost
-> vasoconstriction

104
Q

what happens to arterioles in warm conditions?

A

shunt vessel constricts
arterioles dilate, blood flows closer to the skin, more energy is lost
-> vasodilation

105
Q

what is radiation?

A

energy can be radiated from one object to another through air

106
Q

what happens in conduction?

A

direct contact between objects & a direct energy transfer between them

107
Q

what happens in convection?

A

air lying next to the skin is warmed by the body, as the air expands and rises, it is moved away by air currents & replaced by cooler air
-> energy loss by bulk movement of air

108
Q

what is evaporation?

A

energy required ( latent heat of evaporation ) to convert water from liquid to vapour
-> energy required to evaporate sweat is drawn from the body, cooling it
( only cools when the water evaporates)

109
Q

at 37.5°, the body is warmer than the environment, so energy is transferred to the environment - what happens in cold environments?& what does the body do?

A

excessive cooling, body can lose thermal balance - core body temp begins to fall
the hypothalamus detects this & increases metabolic rate & slows energy loss

110
Q

what does moderate exercise do ?

A
  • increase in natural killer cells ( lymphocyte ) that provide non specific immunity
  • > release perforin (protein), makes pores in the target cell membrane, allow other molecules to enter and cause apoptosis
111
Q

what does vigorous exercise do?

A

number & activity of …. falls

  • natural killer cells
  • phagocytes
  • B cells
  • T helper cells

-> specific immune system js temporarily depressed

112
Q

what does the decrease of t helpers mean?

A

reduces amount of cytokines available to activate lymphocytes
-> reduces quantity of antibody produces

113
Q

why does vigorous exercise trigger an inflammatory response?

A

occurs in muscles as a response due to damage in muscle fibres due to heavy exercise

114
Q

what hormones, released during vigorous exercise, suppress the immune system?

A

adrenaline and cortisol

115
Q

what wear and fear injuries particularly affect the knee?

A
  • wearing away of articular cartilage that covers the surfaces of bones
  • patellar tendinitis ( kneecap does not glide smoothly across the femur due to damage to the femur )
  • the bursae (fluid sacs that cushion the points of contact between bones) can swell with extra fluid
  • sudden twisting / abrupt movements of the knee
116
Q

what is keyhole surgery on joints known as?

A

arthroscopy

117
Q

why is keyhole surgery good

A
  • fast recovery
  • less bleeding
  • less pain
  • less risk of infection
118
Q

what do ligaments do?

A

join bone to bone, control joint movement& prevent it from being overstretched

119
Q

what does the posterior cruciate ligament do?

A

prevents the knee from being bent too far back

damaged by : falling on a bent knee

120
Q

what does the anterior cruciate ligament do?

A

prevents the knee from bending too far forward

damaged by: sudden turning/ pivoting/ cutting manoeuvres

121
Q

what does repeated damage to a joint mean?

A

affects cartilage & shortens athletes career

122
Q

what is a prosthesis?

A

artificial body part that helps them to regain some degree of normal function or appearance

123
Q

when else can prosthetics be used?

A

to replace damaged or diseased joints that have bit responded to medical or other therapy

124
Q

what are advantages of physical activity?

A
  • increases arterial vasodilation & lowers blood pressure
  • increases levels of HDLs and lowers LDLs
  • balanced energy input/output maintains a healthy weight
  • increased sensitivity to insulin
  • increased bone density & reduces its loss during old age
  • reduces risk of some cancers
  • improves mental well being
125
Q

who is considered obese ?

A

someone who’s bmi is over 30

bmi = mass/height2

126
Q

what does obesity lead to?

A

high bp & high blood LDL levels

-> risk of coronary heart disease and stroke

127
Q

what are some examples of prohibited drugs for athletes?

A

human growth hormone, insulin & epo

-> even though they are steroid hormones

128
Q

what does growth hormone do & where is it produced?

A

stimulates growth

pituitary gland

129
Q

what does follicle-stimulating hormone do & where is it produced?

A

controls testes & ovaries

pituitary gland

130
Q

what does anti diuretic hormone do & where is it produced?

A

causes reabsorption of water in the kidneys

pituitary gland

131
Q

what does thyroxine do & where is it produced?

A

raises basal metabolic rate

thyroid gland

132
Q

what does adrenaline do & where is it produced?

A

raises basal metabolic rate, dilates blood vessels, prepares body for action
adrenal gland

133
Q

what does insulin do & where is it produced?

A

lowers blood glucose concentration

pancreas

134
Q

what does oestrogen do & where is it produced?

A

promotes developement of ovaries and female secondary sexual characteristics
ovaries

135
Q

what does testosterone do & where is it produced?

A

promotes the development of male secondary sexual characteristics

136
Q

why can’t peptide hormones pass through cell membranes easily & what do they do instead?

A

the are charged

  • > hormone binds to a receptor on the CM, this activates another molecule in the cytoplasm ( 2nd messenger )
  • > the functional second messenger activates enzymes or transcription factors, brings about chemical changes within the cell, directly or indirectly by affecting gene transcription
137
Q

examples of peptide hormones

A

EPO
human growth hormone
insulin

138
Q

how do steroid hormones work?

A

pass through the CM & binds directly to a receptor molecule within the cytoplasm.
-> the hormone-receptor complex functions as a transcription factor, switching enzymes on or off

139
Q

what is the ‘transcription initiation complex’ ?

A

RNA polymerase & a cluster of associated protein groups binding to the DNA

140
Q

what is the promoter region?

A

a section of DNA adjacent to the gene to be transcribed

141
Q

when does transcription proceed?

A

when the transcription initiation complex has formed and is correctly attached to the DNA

142
Q

are transcription factors present in all cells?

A

some cells

-> others are synthesised only in a particular cell type or at a particular stage of development

143
Q

in what form are most transcription factors created?

A

inactive,

then converted to the active form by the action of hormones etc

144
Q

when is the gene switched on?

A

when all required transcription factors are present in their active forms
-> the transcription initiation complex can then form and attach to the promotor region successfully

145
Q

how can transcription be prevented?

A

protein repressor molecule attaching to the promotor region, blocking the binding site for transcription factors, preventing the formation of a transcription initiation complex

146
Q

where else can protein repressor molecules attach?

A

to the transcription factors themselves, preventing the formation of the transcription initiation complex

147
Q

what do activator molecules do ?

A

stimulate the binding of the transcription initiation complex

148
Q

the control of transcription initiation is an important mechanism in determining what?

A

whether or not a gene is expressed

149
Q

what is EPO?

A

erythropoietin

  • > a peptide hormone produced naturally by the kidneys
  • > it stimulates the formation of new red blood cells in bone marrow
150
Q

what happens if blood O2 concentration falls?

A
  • the kidney detects low blood O2 concentration
  • releases erythropoietin into the blood
  • stimulates bone marrow
  • bone marrow produces more RBCs
  • increased no. of RBCs increases O2 carrying capacity
  • blood O2 concentration rises
151
Q

what happens if EPO levels are too high?

A

the body will produce too many RBCs, increasing the risk of thrombosis, possibly leading to heart attack and stroke

152
Q

what does testosterone do?

A

binds to androgen receptors ( male hormone receptors) , which are numerous on cells in target tissues

  • > they modify gene expression to alter the development of the cell
    ie. they increase anabolic reactions, such as protein synthesis in muscle cells, increasing the size and strength of the muscle
153
Q

why aren’t testosterone injections very effective?

A

testosterone is quickly broken down

-> synthetic anabolic steroids have been manufactured by chemical modification of testosterone

154
Q

what are negatives of anabolic steroids?

A 
cause:
high blood pressure 
liver damage
changes in menstrual cycle
reduced sperm count/ impotence
kidney failure 
heart disease
155
Q

what are anabolic steroids classes as in the UK?

A

prescription only

156
Q

how can anabolic steroid ( and their by-products ) be easily detected ?

A

in urine samples

157
Q

what testosterone: epitestoterone ratio is considered doping?

A

above 4:1

158
Q

what is creatine?

A

a performance enhancing substance that is not banned

  • > increase the amount of creatine phosphate in the muscles
  • > should increase performance during repeated, short-duration, high intensity activity
159
Q

what are adverse affects of using creatine supplements?

A 
diarrhoea 
nausea 
vomiting 
high bp 
kidney damage 
muscle cramps
160
Q

why is there a ban on performance enhancing drugs?

A

to protect the health of athletes & ensure there is fair competition

161
Q

why do people think the use of drugs is ethically acceptable?

A

athletes have a right to decide themselves if the risk outweighs the benefit
already inequality of competition due to differences in training time and resources

162
Q

why do people think drugs should be banned?

A

athletes cannot make a properly informed decision

they come under pressure to take illegal drugs

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