Biology Topic 7 Flashcards

(36 cards)

1
Q

Define tendons and ligaments

A

Tendons attach muscle to bone.

Ligaments attach bone to bone.

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2
Q

Describe the structure of skeletal muscle

A

Made up of large bundles of long cells called muscle fibres.

Cell membrane of muscle fibre is the sarcolemma.

Muscle cell cytoplasm called sarcoplasm. Bits of sarcolenma fold inwards into sarcoplasm. The folds are called transverse tubules and help spread electrical impulses through the sarcoplasm.

Network of internal membranes called the sarcoplasmic reticulum runs through sarcoplasm. The sarcoplasmic reticulum stores and releases calcium ions needed for muscle contraction.

Muscle fibres have lots of mitochondria to provide ATP for contraction.

Muscle fibres have long, cylindrical organelles called myofibrils. They’re made up of actin and myosin.

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3
Q

Structure of myofibrils?

A

Thick myofilaments made of protein myosin.
Thin myofilaments made of protein actin.

Under electron microscope:

A-band: dark bands containing myosin and actin.

I-band: light bands only contain actin.

Myofibril made up of many sarcomeres. Ends of each sarcomere with z line which joins sarcomeres together.

Middle of sarcomere is M-line in the middle of the myosin filaments.

Around M-line is H-zone which only contains myosin.

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4
Q

Describe sliding filament theory

A

Myosin and actin filaments slide over one another to make sarcomeres contract. Myofilaments don’t contract themselves and stay same length.

Simultaneous contraction of many sarcomeres means myofibrils and muscle fibres contract.

Return to original length as the muscle relaxes.

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5
Q

Describe the process of muscle contraction

A
  1. Action potential triggers an influx of calcium ions.

A. Action potential from a motor neurone stimulates a muscle cell, depolarising the sarcolemma.

B. Causes the sarcoplasmic reticulum to release stored calcium ions into sarcoplasm. Calcium ions bind to troponin, causing it to change shape. This pulls the attached tropomyosin out of actin-myosin binding site on actin.

C. This exposes the myosin binding site allowing the myosin head to bind, forming an actin-myosin cross bridge.

  1. ATP provides energy needed to move myosin head.
    A. Calcium ions also activate the enzyme ATPase, which breaks down ATP to provide energy for muscle contraction.
    B. The energy released moves the myosin head, which pulls the actin filament along in kind of rowing motion.

3.
A. ATP also provides the energy to break actin-myosin cross bridge, so the myosin head detaches.

B. New cross bridge then forms. Many cross bridges form and break rapidly pulling actin filament along, shortening the sarcomere causing contraction. This repeats as long as calcium ions are bound to troponin.

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6
Q

What happens during muscle contraction when action potential stops?

A

Calcium ions unbind troponin molecules and active transported into sarcoplamic reticulum.

Troponin returns to original shape, pulling tropomyosin with them. So tropomyosin block actin-myosin binding sites again.

Sarcomere returns to relaxed length.

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7
Q

Slow twitch muscle fibres vs fast twitch muscle fibres?

A

Slow twitch:
Can work for long time without getting tired.
Energy released slowly through aerobic respiration. Lots of mitochondria and capillaries to supply muscles with oxygen.
Red colour as rich in myoglobin.

Fast twitch:
Good for short bursts

Get tired quickly

Energy released anaerobically using glycogen. Few mitochondria or blood vessels.

White colour as don’t have much myoglobin.

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8
Q

Describe step 1 of aerobic respiration, glycolysis

A

Takes place in cytoplasm

Stage 1 phosphorylation:
A. Glucose is phosphorylated by adding 2 phosphates from two molecules ATP.

B. This creates 2 molecules of triose phosphate and 2 molecules ADP.

Stage 2 oxidation:
A. Triose phosphate is oxidised, forming 2 molecules of pyruvate.

B. NAD collects the hydrogen ions, forming reduced NAD.

C. 4 ATP produced, but 2 were used up in stage one, so net gain of 2 ATP.

Net products: 2 pyruvate, 2 NADH, 2 ATP

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9
Q

describe stage 2 of aerobic respiration, the link reaction

A

Takes place in the mitochondrial matrix

  1. pyruvate is decarboxylated one carbon atom removed in form of CO2.
  2. NAD is reduced it collects hydrogen from pyruvate, converting pyruvate into acetate.
  3. Acetate is combined with coenzyme A to for acetyl CoA.

no ATP produced. Happens twice for each glucose molecule.

Net: two molecules acetyl CoA, two molecules NADH

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10
Q

describe stage 3 of aerobic respiration, the krebs cycle

A
  1. Acetyl CoA from the link reaction combines with oxaloacetate to form citrate. Coenzyme A goes back to the link reaction to be used again.
  2. the 6 carbon citrate molecule is converted to a 5 carbon intermediate. hydrogen also removed which is used to produce NADH from NAD.
  3. The 5 carbon molecule then converted to 4 carbon oxaloacetate. the hydrogen is then used to produce one FADH and two NADH. ATP is produced by transfer of phosphate from an intermediate compound to ADP- this is called substrate-level phosphorylation.
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11
Q

Products of krebs cycle and uses?

A

1 Coenzyme A: reused in link reaction.

Oxaloacetate: used in next krebs cycle.

2 CO2: waste product

1 ATP: use for energy

3 NADH: in oxidative phosphorylation.

1 FADH: in oxidative phosphorylation.

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12
Q

Describe stage 4 of aerobic respiration, oxidative phosphorylation

A

takes place in the crista.

Hydrogen atoms released from FADH and NADH. They split into protons and electrons.

Electrons move along the electron transport chain, losing energy as they do. This energy is used to pump protons from mitochondrial matrix into intermembrane space.

This forms a proton gradient as more protons in intermembrane space than mitochondrial matrix.

Protons move back into mitochondrial matrix via ATPase. this movement drives synthesis of ATP from ADP and Pi. This process is known as chemiosmosis.

At the end of the chain, protons, electrons and oxygen form water. Oxygen is said to be the final electron acceptor.

38 ATP molecules produced from one glucose.

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13
Q

Describe how you would carry out experiment to measure respiration

A

set up respirometer

set up two tubes containing potassium hydroxide, which absorbs CO2.

place organism on gauze in one and glass beads in the other as a control.

Syringe sets manometer to known level.

Leave for set amount of time. During that time there will be decrease in air in tube due to oxygen consumption by organism. All CO2 absorbed by potassium hydroxide.

Decrease in air volume lowers pressure in tube, causing coloured liquid in manometer to move towards test tube.

Distance moved by liquid in a given tie is measured.

control other variables like temperature and potassium hydroxide volume

Repeat and calc mean volume O2 to increase precision.

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14
Q

why do human muscle cells sometimes convert pyruvate to lactate?

A

Cells convert pyruvate to lactate when they respirate anaerobically.

So that NADH can be converted to NAD. For use in glycolysis so that it can continue without oxygen.

So ATP can be provided when oxygen is unavailable

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15
Q

Why does lactic acid need to be broken down?

A

builds up after period of anaerobic respiration

it can be broken down in 2 ways:
1. Cells can convert the lactic acid back to pyruvate.

  1. Liver cells can convert the lactic acid back to glucose which is then respired or stored.
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16
Q

How does cardiac muscle control regular beating of the heart?

A

Cardiac muscle is myogenic- which can contract and relax without signals from neurones.

  1. Process starts at the sino-atrial node (SAN) in wall of right atrium. SAN sends wave of electrical activity over atrial walls. This causes atria to contract.
  2. Band of non conducting tissue stops electrical activity reaching ventricles from atria directly. Instead electrical activity transferred to atrio-ventricular node (AVN).
  3. The AVN then passes the electrical wave over the bundle of his/purkyne fibres.
  4. purkyne fibres carry electrical wave to ventricular walls, causing the ventricles to contract.
17
Q

How can ECGs be used to diagnose heart problems?

A

Too fast = tachycardia about 120 bpm.

Too slow = bradycardia about 60 bpm.

Early contraction of atria or ventricle = ectopic heartbeat.

Really irregular heartbeat = fibrillation.

18
Q

How does the medulla oblongata control breathing rate?

A
  1. inspiratory centre of the medulla oblongata sends impulses to intercostal and diaphragm muscles to make them contract.
  2. This increases the volume of the of the lungs, decreasing the pressure in the lungs.
  3. Air enters the lungs due to pressure difference between the lungs and air outside.
  4. As lungs inflate, stretch receptors in the lungs are stimulated. The stretch receptors send nerve impulses back to the medulla oblongata. This inhibits the action of the inspiratory centre.
  5. The expiratory centre then sends nerve impulses to intercostal and diaphragm muscles to make them relax. This causes the lungs to inflate, expelling air. As the lungs deflate, stretch receptors become inactive. The inspiratory centre is no longer inhibited ad the cycle starts again.
19
Q

How does exercise trigger an increase in breathing rate?

A

1.During exercise, CO2 levels in blood increase. This dissolves in blood to form carbonic acid, lowering blood pH.

  1. Chemoreceptors are present in medulla oblongata, aortic bodies and carotid arteries that are sensitive to pH changes.
  2. If they sense pH decrease, they send nerve impulses to the medulla oblongata. This sends more frequent nerve impulses to intercostal and diaphragm muscles to increase rate and depth of breathing.
  3. This speeds up gaseous exchange. CO2 drops and and extra O2 supplied to muscles. pH returns to normal and breathing rate decreases.
20
Q

What happens when blood pressure is high?

A

Baroreceptors in aortic and carotid detect high blood pressure.

impulses are sent to the cardiovascular control centre in medulla oblongata, which send impulses along parasympathetic neurones. These secrete acetylcholine, which binds to receptors on the SAN.

This causes the SAN to fire impulses less frequently to slow heart rate and reduce blood pressure to normal.

21
Q

What happens when blood pressure is too low?

A

Baroreceptors in aortic and carotid bodies detect low pressure in the blood.

Impulses sent to cardiovascular control centre in the medulla oblongata, which sends impulses along sympathetic neurones. These secrete noradrenaline which binds to receptors on SAN.

SAN fires more frequent impulses to increase heart rate and increase blood pressure back to normal.

22
Q

What happens when low CO2 levels cause high blood pH levels?

A

Chemoreceptors in the aortic and carotid bodies and medulla detect high pH.

Impulses sent to cardio vascular control centre in the medulla oblongata, which sends impulses along parasympathetic neurones. They secrete acetylcholine which binds to SAN.

SAN fires less frequent impulses to decrease heart rate and return O2, CO2 and pH levels to normal.

23
Q

What happens if high CO2 levels cause low blood pH?

A

Chemoreceptors in carotid and aortic bodies and medulla detect low pH.

They send impulses to the cardiovascular control centre, which sends impulses along sympathetic neurones. these secrete noradrenaline, which binds to receptor on SAN.

This causes the SAN to send more frequent impulses to increase heart rate and increase O2 levels to decrease CO2 levels to return pH level in blood to normal.

24
Q

Cardiac output equation?

A

Cardiac output (cm³ min -¹) = heart rate (bpm) × stroke volume (cm³)

25
Respiratory minute ventilation equation?
Respiratory minute ventilation = tidal volume × breathing rate ( breaths per minute)
26
Mechanisms to reduce body temperature?
1. Sweating- more sweat secreted from sweat glands. Water in sweat evaporates from surface of the skin and takes heat away from body. 2. Piloerector muscles relax so less air is trapped so skin less insulated and heat can be lost more easily. 3. vasodilation- arterioles near surface of skin. More blood flows through capillaries in surface layer of the dermis. More heat lost by radiation.
27
Mechanisms to increase body temperature?
1. Shivering- muscles contract in spasms making body shiver, and more heat produced by increased respiration. 2. Much less sweat secreted from sweat glands. 3. piloerector muscles contract, trapping air and reducing heat loss. 4. Vasoconstriction: arterioles near surface of skin constrict, so less blood flows near surface layer of dermis. Reducing heat loss. 5. Hormones- body releases adrenaline and thyroxine. Increasing metabolism, producing more heat.
28
What happens when body temperature exceeds normal?
Thermoreceptors detect temperature is too high. They send impulses to hypothalamus, which sends signals along motor neurones to effectors. effectors respond to return temperature to normal, e.g. vasodilation, sweating, piloerector muscles relax.
29
What happens when body temperature too low?
Thermoreceptors detect temperature is too low. They send impulses to hypothalamus, which sends signals along motor neurones to effectors. effectors respond to return temperature to normal, e.g. vasoconstriction, releasing adrenaline and thyroxine, piloerector muscles contract.
30
Example of how peptide/steroid hormones work? thyroxine
1. At normal body temperature, the thyroid hormone receptor (a transcription factor) binds to DNA at start of gene. 2. This decreases the transcription of a gene coding for a protein that increases metabolic rate. 3. At cold temperatures thyroxine is released, which binds to the thyroid hormone receptor, causing it to act as an activator. 4. Transcription rate increases, producing more protein. The protein increases the metabolic rate, causing an increase in body temperature.
31
Describe how protein hormones operate from the cell membrane.
Some hormones cant cross membrane, but can still affect activity of transcription factors. They bind to receptors on the cell membrane, which activate messenger molecules in the cytoplasm. These messenger molecules activate enzymes called protein kinases, which trigger a cascade inside the cell. During the cascade, transcription factors can be activated- these then affect expression of genes in the nucleus.
32
keyhole surgery advantages?
Operations dont involve opening up the patient as much, so lose less blood and less scarring. Less damage so patients in less pain and recover more quickly. so shorter hospital stay. e.g. damaged cruciate ligaments can be fixed by keyhole surgery.
33
Prostheses?
Used to replace whole limbs or parts of limbs. e.g. prosthetics can fix broken joints using prosthetic joints.
34
Describe types of PEDs?
Anabolic steroids- increase strength, speed and stamina by increasing muscle and allowing people to train harder. Increases aggression. Stimulants- speed up reactions, reduce fatigue and increase aggression. Narcotic analgesics- reduce pain, so injuries dont affect perfomance.
35
Arguments against PEDs?
Some PEDs are illegal competitions become unfair if some people take drugs health risks e.g. heart problems and high bp. Athletes may not be informed of health risks of drugs they take
36
Arguments for PEDs?
Up to the individual drug free sport isnt fair anyway as some athletes have better access to training facilities. Athletes that want to compete at a higher level may only be able by using PEDs.