Topic 7: Run for your Life Flashcards

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1
Q

7.1 The ——– membrane secretes ——– fluid in a ——– joint. What does this fluid enable?

What is the role of the cartilage?

A

The synovial membrane secretes synovial fluid, which allows the bones of a synovial joint to move freely. The synovial fluid acts as a lubricant, reducing the friction between the cartilage of the joints during movement, and thereby minimizing wear and tear.
The cartilage protects bones within joints, by absorbing synovial fluid and acting as a shock absorber.

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2
Q

7.1 What is the role of ligaments? Which properties allow them to be effective?

A

Ligaments attach bones to other bones, controlling and restricting the movement in a joint. They are therefore strong and flexible (or elastic).

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3
Q

7.1 What is the role of tendons? Which properties allow them to be effective?

A

(Skeletal) muscles are attached to bones by tendons, which tend to be inelastic.

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4
Q

7.1 What is the role of skeletal muscles? What are antagonistic muscle pairs?

A

Skeletal muscle is the type of muscle used for movement. These muscles contract and relax to move bones at a joint. Muscles that work together to move a bone are called antagonistic pairs. Muscles can only pull through contraction - they can not push. Therefore two muscles are required, creating opposite forces, to move a bone.

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5
Q

7.1 How do extensors and flexors interact to enable movement?

A

A muscle that contracts to cause extension of a joint (so that it straightens) is called an extensor, while the corresponding relaxing muscle will be a flexor. A muscle that contracts to cause a joint to bend is called a flexor, with the corresponding relaxing muscle an extensor. So when an extensor contracts, the flexor will relax and the joint will straighten. When a flexor contracts, the extensor will relax and so the joint will bend.

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6
Q

7.2 Explain the structure of a sarcomere.

A

Within each muscle fibre, there are myofibrils. A myofibril is made up of many short contractile units called sarcomeres. The sarcomere is made up of two protein molecules: a thick myofilament, called myosin, and a thin myofilament called actin. Under an electron microscope, the myofibril exhibits a striped appearance. Dark bands contain the thick myosin filaments, and some overlapping thin actin filament (A-bands). Light bands contain thin actin filaments alone (I-bands) and intermediate-coloured bands contain thick myosin filaments alone (H-zone). In the middle of each sarcomere, and the middle of the myosin filaments, is the M-line. The ends of each sarcomere are marked with a Z-line. Sarcomeres are joined together lengthways at their Z-lines.

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7
Q

7.2 Give an overview of how muscle contraction works.

A

Myosin and actin filaments slide over one another to make the sarcomeres contract - this is the sliding filament theory. The myofilaments themselves don’t contract, remaining the same length. This simultaneous contraction of many sarcomeres results in a contraction of myofibrils and muscle fibres.

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8
Q

7.2 Explain the structure of actin and myosin.

A

Two other proteins called tropomyosin and troponin are attached to each other, found between actin filaments. Actin filaments have binding sited for myosin heads, called actin-myosin binding sites. Myosin filaments have globular heads that are hinged, enabling them to move back and forth. Each myosin head has a binding site for actin and a binding site for ATP.

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9
Q

7.2 In a resting muscle, what prevents it from contracting?

A

In an unstimulated muscle, the actin-myosin binding site is blocked by tropomyosin, which is held in place by troponin. So filaments can’t slide past each other because myosin heads can’t bind to the actin-myosin binding site on the actin filament.

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10
Q

7.2 Explain how an influx of calcium ions is triggered in a muscle cell.

A

When an action potential from a motor neurone arrives at the neuromuscular junction, it stimulates the muscle cell, depolarising the sarcolemma (the membrane of the muscle fibre). Depolarisation spreads down the tranverse (T) tubules (where the sarcolemma folds, spreading electrical impulses to all parts of the muscle fibre) to the sarcoplasmic reticulum - this releases stored calcium ions into the sarcoplasm (the cytoplasm of a muscle cell).

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11
Q

7.2 Explain the process of contraction of skeletal muscle in terms of the sliding filament theory.

A

When the calcium ions are released, they attach to the troponin, causing it to change shape and move. As a result, the attached tropomyosin also moves, exposing the actin-myosin binding sites and enabling the myosin head to bind - actin-myosin cross bridges are formed. When the myosin head binds to the actin (with ADP and Pi still attached), stored energy (from a previous hydrolysis of ATP into ADP and Pi) is released and the myosin head changes shape - it moves forwards, pulling the actin filament to the center of the sarcomere. The ADP and Pi molecules are also released from the myosin head, allowing it to change shape for an ATP molecule to attach. The ATP molecule causes it to change shape once again, releasing it from the actin-myosin binding site. Calcium ions also activate the enzyme ATPase, which breaks down the ATP into ADP and Pi (attaching them to the myosin head), releasing energy. The hydrolysis causes a change in shape in the myosin head, returning it to its upright position (with stored energy). The myosin head will reattach to a different binding site, and so the cycle will continue as long as calcium ions are present.

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12
Q

7.3 i) Explain the overall reaction of aerobic respiration?

A

C6H12O6 + 6O2 -> 6CO2 + 6H2O
In aerobic respiration, a respiratory substrate (such as glucose) is split, releasing carbon dioxide as a waste product and reuniting hydrogen with atmospheric oxygen, resulting in a large release of energy.
[During photosynthesis, water is split to form oxygen and hydrogen - the hydrogen is stored in a carbohydrate (such as glucose), but is brought together with oxygen to form water during aerobic respiration]

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13
Q

7.3 ii) What is respiration?

A

Respiration: a many-stepped process with each step controlled and catalysed by a specific intracellular enzyme.

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14
Q

7.4 Explain the role of glycolysis in aerobic respiration.

A

Glycolysis (the first stage in both aerobic and anaerobic respiration) happens in the cytoplasm of cells [stores of glycogen must first be converted to glucose - the main respiratory substrate].
1. Glucose is phosphorylated: 2 phosphates are removed from 2 ATP molecules, and added to the glucose - this results in 2 ADP molecules, and 2 molecules of triose phosphate (an intermediate phosphorylated 3C compound).
2. The 2 molecules of triose phosphate are oxidised, forming 2 molecules of the 3C pyruvate. The coenzyme NAD collects 2 hydrogens, forming 2 reduced NAD molecules.4 inorganic phosphates are removed from the triose phosphates, reacting with 4 ADP molecules to form 4 ATP molecules {in substrate-level phosphorylation}.
Glycolysis results in a net gain of 2 ATP molecules, and 2 reduced NAD molecules.

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15
Q

7.5 Explain the role of the link reaction in aerobic respiration.

A

The link reaction takes place in the mitochondrial matrix (because the required enzymes and coenzymes are there, and the reduced NAD produced by the link reaction are in the right place for oxidative phosphorylation, which occurs across the inner mitochondrial membrane). Each molecule of 3C pyruvate is decarboxylated (releasing 1 molecule of CO2) and dehydrogenated (releasing two hydrogen atoms, and therefore reducing 1 NAD coenzyme). The resulting 2C acetyl compound then combines with coenzyme A to form acetyl coenzyme A (acetyl CoA). So 2 pyruvate molecules produce 2 CO2 molecule, 2 reduced NAD molecules, and 2 molecules of acetyl CoA (so there are 2 link reaction per glucose molecule).

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16
Q

7.5 Explain the role of the Krebs cycle in aerobic respiration.

A

The Krebs cycle is controlled by a specific intracellular enzyme, which is found in the matrix of the mitochondria (so this is where the Krebs cycle takes place).
- Each 2C acetyl CoA molecule from the link reaction combines with a 4C compound to form a 6C compound.
- This 6C compound is decarboxylated (releasing 1 molecule of CO2) and dehydrogenated (releasing two hydrogen atoms, and therefore reducing 1 NAD coenzyme), forming a 5C compound.
- The 5C compound is then decarboxylated (releasing 1 molecule of CO2), and dehydrogenated 3 times (releasing 6 hydrogens, which form 2 reduced NAD molecules and 1 reduced FAD molecule). One molecules of ATP is also produced (by substrate-level phosphorylation). This regenerates the 4C compound.
So each acetyl CoA molecule produces 2 CO2 molecules, 3 reduced NAD molecules, 1 reduced FAD molecule, and 1 ATP molecule.
The Krebs cycle happens once per acetyl CoA molecule, or once per pyruvate molecule (so 2 Krebs cycles take place per glucose molecule).

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17
Q

7.5 What is substrate-level phosphorylation?

A

When a phosphate group is directly transferred from one molecule to another it’s called substrate-level phosphorylation: the energy for the formation of ATP comes from the substrates.

18
Q
  1. 6 What is oxidative-level phosphorylation?
A

Oxidative-level phosphorylation is the process where the energy carried by electrons, from reduced coenzymes, is used to make ATP: it involved the electron transport chain and chemiosmosis.

19
Q

7.6 How is ATP synthesised by oxidative-level phosphorylation?

A

The reduced coenzymes carry hydrogen atoms to the mitochondrial matrix, where the hydrogen atoms split into protons (H+) and electrons (e-). The electrons move down the electron transport chain (in the inner mitochondrial membrane), going from one electron carrier to another in a series of redox reactions, releasing energy. This energy is used by the electron carriers to pump protons from the mitochondrial matrix into the the intermembrane space. This creates a steep electrochemical gradient across the inner membrane. Protons move down the electrochemical gradient, back into the mitochondrial matrix, via the enzyme ATP synthase: this synthesises ATP from ADP and Pi (this process is known as chemiosmosis). Within the mitochondrial matrix, the protons, electrons and oxygen combine to form water (1/2 O2 + 2e- + 2H+ → H2O). The oxygen is said to be the final electron acceptor.

20
Q

7.7 Outline what happens after a period of anaerobic respiration in animals.

A

In anaerobic respiration, glycolysis takes place to produce 2 pyruvate molecules, 2 reduced NAD molecules and 2 ATP molecules (per one glucose molecule). The 2 reduced NAD molcules then transfer their hydrogens to the 2 pyruvate molecules: the pyruvate is reduced into lactate, and the oxidised NAD is formed.
Lactate builds up in the muscles, and forms lactic acid in solution. This decreases the pH of the cells, and inhibits the enzymes that catalyses the glycolysis reaction (the hydrogen ions from the lactic acid neutralise the negatively charged groups in the active site, affecting the attraction between the substrate and the enzyme).
The lactate can be converted back into pyruvate, which is oxidised directly to CO2 and H2O via the Krebs cycle (in aerobic respiration), thus releasing energy to synthesis ATP. As a result, oxygen uptake is greater than normal in the recovery period after exercise (i.e. the oxygen debt). Some lactate can be converted into glucose, which is stored in the liver as glycogen.

21
Q

7.8 i) Outline the myogenic nature of cardiac muscles.

A

The heart is myogenic: it can contract without external nervous stimulation.

22
Q

7.8 ii) Explain how the normal electrical activity of the heart coordinates the heart beat.

A

Contraction of the cardiac muscles is initiated by a change in polarity, which spreads like a wave of depolarisation from cell to cell.

1) Depolarisation begins at the sinoatrial node (SAN), also known as the pacemaker, in the wall of the right atrium.
2) The SAN generates an electrical impulse, which travels to the right and left atria, causing them to contract simultaneously.
3) A band of non-conducting collagen tissue in the walls prevents the wave of deploarisation from being passed directly from the atria to the ventricles.
4) Instead, the impulse is passed from the SAN to the atrioventricular node (AVN). There is a slight delay, ensuring that the atria have finished contracting and that the ventricles have filled with blood before they contract.
5) The electrical impulse travels from the AVN to the bundle of His (a group of large, specialised muscle fibres), which is then conducted along the (finer) Purkyne fibres to the right and left ventricle walls.
6) The first ventricular cells to be depolarised are in the apex of the heart, so that the wave of contraction travels upwards, allowing the blood is pushed into the aorta and the pulmonary artery.

23
Q

7.8 iii) How can electrocardiograms (ECGs) be used to aid the diagnosis of cardiovascular disease (CVD) and other heart conditions?

A

An electrocardiograph records changes in polarisation using electrodes placed on the chest and limbs. During the cardiac cycle, the heart muscle depolarises when it contracts, and repolarises when it relaxes. This produces an electrocardiogram:
1) P wave: depolarisation of the atria, leading to contraction of the atria (atrial systole).
2) PR interval: the time taken for the impulse to be conducted from the SAN across the atria to the ventricles, through the AVN.
3) QRS complex: the wave of depolarisation resulting int the contraction of the ventricles (ventricular systole).
4) T wave: repolarisation (relaxation) of the ventricles (diastole).
The ECG does not show atrial repolarisation because the signals generated are small and hidden by the QRS complex.
Doctors compare their patients’ ECGs with a normal trace, allowing them to diagnose any problems with the heart’s rhythm.

24
Q

7.9 i) Explain how to calculate cardiac output.

A

cardiac output (cm3 min-1) = heart beat (beats per minute) x stroke volume (cm3)
Cardiac output is the total volume of blood pumped by the heart in one minute.
Stroke volume is the volume of blood pumped by one ventricle each time it contracts.

25
Q

7.9 ii) Explain how the ventilation is controlled.

A

The ventilation center in the medulla oblongata controls ventilation:
The ventilation centre sends nerve impulses to the intercostal and diaphragm muscles, making them contract: this increases the volume of the lungs, which lowers the pressure in the lungs and forces air in (inhalation). As the lungs inflate, stretch receptors in the lungs are stimulated. The stretch receptors send nerve impulses back to the medulla oblongata, which inhibits the impulses to the intercostal and diaphragm muscles, forcing them to relax. The elastic recoil of the lungs causes them to deflate and expel air (exhalation). As the lungs deflate, the stretch receptors become inactive, and the impulses from the ventilation centre are no longer inhibited.

26
Q

7.9 ii) Explain changes in ventilation during exercise.

A

When you exercise, your muscles contract more frequently, which means that they use more energy from aerobic respiration: so variations in ventilation (i.e. an increased breathing rate and an increased depth) enable rapid delivery of oxygen to the tissues, and the removal of carbon dioxide from them. Here’s how it happens:
1) During exercise, the level of carbon dioxide increases, which dissolves in the blood to form carbonic acid. This decreases the pH of the blood.
2) Chemoreceptors in the medulla oblongata, aorta and carotid artery sensitive to changes in blood pH detect this decrease, and send nerve impulses to the medulla oblongata.
3) The medulla oblongata sends more frequent nerve impulses to the intercostal and diaphragm muscles, causing an increase in ventilation rate (i.e. the volume of air breathed in or out in a period of tine).
4) This causes gas exchange to speed up: the CO2 levels decrease and the more O2 is supplied to the muscles (so the pH returns to normal, and the breathing rate decreases).
The opposite response occurs when CO2 decreases, causing the pH o rise and therefore a decrease in rate and depth of breathing.

27
Q

7.9 ii) Explain how the heart rate is controlled.

A

The heart rate is controlled by the cardiovascular centre in the medulla oblongata. Internal stimuli (in the blood) is detected by chemoreceptors and pressure receptors (baroreceptors), which send electrical impulses to the medulla oblongata along sensory neurones. The cardiovascular centre then sends impulses to the SAN along nerves forming part of the autonomic nervous system (which then release certain neurotransmitters to change the heart rate) :

  • The sympathetic nervous system (more specifically the sympathetic nerve) increases the heart rate.
  • The parasympathetic nervous system (more specifically the vagus nerve) decreases the heart rate.
28
Q

7.9 ii) Explain changes in heart rate as a result of changes in blood pressure.

A

Baroreceptors detect high blood pressure (i.e. the stimulus), and send impulses to the cardiovascular centre via sensory neurones. These in turn send impulses along parasympathetic neurones, which secrete neurotransmitters that bind to receptors on the SAN: the SAN fires impulses less frequently, causing heart rate to slow, thereby reducing blood pressure.
Baroreceptors detect low blood pressure (i.e. the stimulus), and send impulses to the cardiovascular centre via sensory neurones. These in turn send impulses along sympathetic neurones, which secrete neurotransmitters that bind to receptors on the SAN: the SAN fires impulses more frequently, causing heart rate to speed up, thereby increasing blood pressure.

29
Q

7.9 ii) Explain changes in heart rate during exercise (and

A

During exercise:
Chemoreceptors in the medulla oblongata, aorta and carotid artery detect changes in the blood (i.e. low O2, high CO2, or low pH levels), and send impulses to the cardiovascular centre via sensory neurones. These in turn send impulses along sympathetic neurones, which secrete neurotransmitters that bind to receptors on the SAN: the SAN fires impulses more frequently, causing heart rate to speed up, thus returning O2, CO2 and pH levels back to normal.
And vice versa:
Chemoreceptors in the medulla oblongata, aorta and carotid artery detect changes in the blood (i.e. high O2, low CO2, or high pH levels), and send impulses to the cardiovascular centre via sensory neurones. These in turn send impulses along parasympathetic neurones, which secrete neurotransmitters that bind to receptors on the SAN: the SAN fires impulses less frequently, causing heart rate to slow down, thus returning O2, CO2 and pH levels back to normal.

30
Q

7.10 i) Outline the structure of a muscle fibre.

A

The cell membrane of a muscle cell/fibre is called the sarcolemma, and the muscle cell’s cytoplasm is called the sarcoplasm.
Some parts of the sarcolemma fold inwards across the muscle fibre and stick to the sarcoplasm, forming transverse (T) tubules - these help to spread electrical impulses throughout the sarcoplasm so that they reach all parts of the muscle fibre.
A network of internal membranes called the sarcoplasmic reticulum runs throughout the sarcoplasm - this stores and releases calcium ions that are needed for muscle contraction.
Muscle fibres have lots of mitochondria to provide ATP needed for muscle contraction. They also contain many nuclei.
Muscle fibres have lots of long, cylindrical organelles called myofibrils.

31
Q

7.10 ii) Outline the structural and physiological differences between fast and slow twitch muscle fibres.

A

Slow twitch muscles are specialised for slower, sustained contraction and can cope with long periods of exercises. They are fatigue-resistant, and a large amount of aerobic respiration is carried out. They therefore have a lot of mitochondria, a high concentrations of respiratory enzymes, and a numerous capillaries. They also contain large amounts of the dark red pigment myoglobin (oxygen store).
Fast twitch muscles are specialised for rapid, intense contraction and can cope with short bursts of speed and power. They fatigue quickly, and ATP is produced almost entirely from anaerobic glycolysis - (so they have a high glycogen content). They therefore contain few mitochondria, a low concentration of respiratory enzymes, and a small number of capillaries. They also have very little myoglobin.

32
Q

7.11 ii) Explain the principles of negative feedback in maintaining systems within narrow limits.

A

The maintenance of a stable internal environment is called homeostasis. Each condition has a norm value or set point (usually the optimum for that condition). Receptors detect deviations from the norm, and send information to control centers (via the nervous system or the hormonal system), which in turn send signals (i.e. nerve impulses or hormones) to effectors. The effectors responds to counteract the change, bringing the condition back to normal. This process is known as negative feedback: a deviation from the norm results in a change in the opposite direction, restoring the condition back to normal. This means that conditions controlled by homeostasis fluctuate around the norm value, i.e. within narrow limits, so that the environment is kept in a state of dynamic equilibrium. If a change exceeds the narrow limits, then homeostatic control and negative feedback won’t work to restore it back to normal.

33
Q

7.11 i) Explain what is meant by positive feedback control.

A

Positive feedback is the enhancing or amplification of an effect by its own influence on the process which gives rise to it, i.e. the output from the control centre moves the condition further from the set point. Positive feedback isn’t involved in homeostasis because it doesn’t keep your internal environment stable.

34
Q

7.12 Outline the importance of homeostasis in maintaining a constant temperature, including the role of the hypothalamus.

A

The control of body temperature is called thermoregulation. The hypothalamus (in the brain) maintains body temperature at a constant level through the process of negative feedback. Thermoreceptors detect a deviation from the normal temperature, and send impulses along sensory neurones to the hypothalamus. This in turn sends impulses along motor neurones to effectors, which respond to restore the body temperature back to normal.
Maintaining a constant temperature is important for the action of enzymes: at lower temperatures, the rate of reaction would be too slow for the body to remain active, and at higher temperatures, the enzymes would denature. So when exercising, for example, the temperature rises but homeostasis restores it so that the body is in a state of dynamic equilibrium.

35
Q

7.12 Outline the mechanisms of thermoregulation in reducing body temperature.

A

Mechanisms of thermoregulation to reduce body temperature:

1) The hypothalamus stimulates sweat glands to secrete sweat. As the water in sweat evaporates, it takes heat away from the skin.
2) The hypothalamus inhibits the erector pili muscles, so that they relax and the hair lie flat. Less air is trapped by the flatten hair, and the skin is less insulated, so heat can be lost more easily.
3) The hypothalamus inhibits the contraction of the arterioles near the surface of the skin, allowing them to dilate (vasodilation). More blood flows through the capillaries in the surface layers of the dermis. Thus more heat is lost from the skin by radiation, and the temperature is lowered.
4) The hypothalamus inhibit the skeletal muscles from contracting, so that they relax to reduce shivering.
5) The hypothalamus inhibits the production of some hormones (e.g. adrenaline and thyroxine). This decreases the rate of metabolism and so less heat is produced.

36
Q

7.12 Outline the mechanisms of thermoregulation in increasing body temperature.

A

Mechanisms of thermoregulation to increase body temperature:

1) The hypothalamus inhibits the sweat glands so that less sweat is secreted, reducing the amount of heat loss via evaporation.
2) The hypothalamus stimulated the erector pili muscles to contract, which makes the hair stand up. This layer of hair traps air and provides insulation, thereby preventing heat loss.
3) The hypothalamus stimulates the arterioles near the surface of the skin to constrict (vasodilation), so that less blood flows through the capillaries in the surface layer of the dermis. Thus less heat is lost from the skin by radiation, preventing heat loss.
4) The hypothalamus stimulates the skeletal muscles to contract in spasms, which makes the body shiver. Thus more heat is produced from increased respiration.
5) The hypothalamus stimulates the production of some hormones (e.g. adrenaline and thyroxine). These increase the rate of metabolism and so more heat is produced.

37
Q

7.13 Outline the possible disadvantages of exercising too much and exercising too little.

A

The possible disadvantages of exercising too much include wear and tear on joints, and the suppression of the immune system. The possible disadvantages of exercising too little include an increased risk of diabetes, CVD and diabetes.

38
Q

7.14 Explain how keyhole surgery can enable those with injuries and disabilities to participate in sports.

A

In keyhole surgery, a small incision is made in the skin, and using either fibre optics or a minute video cameras, as well as specialised medical equipment, it is possible to repair damaged joints. These operations are non-invasive, so patients lose less blood and have less scarring of the skin. Patients are usually in less pain after their operation and they recover more quickly, because less damage is done to the body. This makes it easier for the patient to return to normal activities and their hospital stay is shorter.

39
Q

7.14 Explain how prostheses can enable those with injuries and disabilities to participate in sports.

A

A prosthesis is an artificial body part used by someone with a disability to enable them to regain some degree of normal function or appearance. Prostheses can be used to replace whole limbs or parts of limbs.

40
Q

7.15 Discuss different ethical positions relating to whether the use of performance-enhancing substances by athletes is acceptable.

A

Absolutists think that performance-enhancing drugs should be banned from all sports:
1) Some performance-enhancing drugs are illegal.
2) Competition becomes unfair if some people gain an advantage through taking drugs, rather than hard work or training.
3) There can be some serious health risks and side effects associated with the drugs used.
4) Athletes may not be fully informed of the health risks of the drugs they take.
Rationalists think that the use of these drugs can be justified in certain circumstances:
1) It’s up to each individual, i.e. athletes have the right to make their own decision about taking drugs and whether they’re worth the risk or not.
2) Drug-free sport isn’t really fair anyway: different athletes have access to different training facilities, coaches, equipment, etc. The use of performance-enhancing drugs might overcome these inequalities.
3) Athletes that want to compete at a higher level may only be able to do so by using performance enhancing drugs.

41
Q

7.16 Explain how genes can be switched on and off by DNA transcription factors, including hormones.

A

Hormones are chemical messengers that affect specific target cells, modifying their activity - they are released directly into the blood from endocrine glands.

1) Peptide (protein) hormones can’t easily pass across the cell membrane (because they’re charged and lipid-insoluble). They therefore bind to receptors on the cell surface membrane, which activate a messenger molecules in the cytoplasm of the cell, called a secondary messenger. These messenger molecules activate enzymes called protein kinases, which trigger a cascade (a chain of reactions) inside the cell. During the cascade, transcription factors can be activated (which affect the transcription of genes within the nucleus).
2) Steroid (lipid) hormones pass through the cell membrane and bind directly to a receptor molecules within the cytoplasm. Once activated, the hormone-receptor complex functions as a transcription factor, and can therefore affect the transcription of genes within the nucleus.
- Transcription of a gene only takes place when a transcription initiation complex (i.e. RNA polymerase and transcription factors) bind to the promoter region on DNA. The gene remains switched off until all the required transcription factors are present in their active forms. Transcription of a gene can be prevented by a protein repressor molecule attaching to either the DNA of the promoter region or the transcription factors themselves, preventing the formation of the transcription initiation complex. Other repressor molecules be may inactive transcription factors.