TOPIC 7

Movement involves skeletal muscles, tendons, ligaments and joints.

Skeletal muscle is the type of muscle you use to move and they are attached to bones by tendons.

Ligaments attach bones to other bones to hold them together.

Skeletal muscles contract and relax to move bones at a joint.

For example, the bones of your lower arm are attached to the bicep muscle and a tricep muscle by tendons. The biceps and triceps work together to move your arm, as one contracts, the other relaxes.

Muscles that work together to move a bone are called antagonistic pairs.

Skeletal muscles are made up of large bundles of long cells, called muscle fibres. The cell membrane of muscle fibre cells is called the sarcolemma.

Parts of the sarcolemma fold inwards across the muscle fibre and stick into the sarcoplasm (a muscle cells cytoplasm). These folds are called transverse tubules and they help to spread electrical impulses throughout the sarcoplasm so they reach all parts of the muscle fibre.

A network of internal membranes called the sarcoplasmic reticulum runs through the sarcoplasm. This stores and releases calcium ions that are needed for muscle contraction.

Muscle fibres have lots of mitochondria to provide the ATP that's needed for contraction.

They are multinucleate which means they contain many nuclei.

Muscle fibres have lots of long, cylindrical organells called myofibrils. These are made up of proteins and are specialised for contraction.

Myofibrils contain bundles of thick and thin myofilaments that move past each other to make muscles contract.

Thick myofilaments are made of the protein myosin. Thin myofilaments are made up of the protein actin.

If you look at myofibril under an electron microscope, you'll see a pattern of dark and light bands; the dark bands contain the thick myosin filaments - these are called A-bands. Light bands contain thin actin filaments - these are called I-bands.

A myofibril is made up of many short units called sarcomeres.

The ends of each sarcomere are marked with a Z-line. Sarcomeres are joined together lengthways at their Z-lines.

In the middle of each sarcomere is an M-line. The M-line is the middle of the myosin filaments.

Around the M-line is the H-zone. This only contains myosin filaments.

Myosin and actin filaments slide over one another to make the sarcomeres contract - the myofilaments themselves don't contract and the myosin and actin molecules stay the same length.

The simultaneous contraction of lots of sarcomeres means the myofibrils and muscle fibres contract.

Sarcomeres return to their original length as the muscle relaxes.

Myosin filaments have globular heads that are hinged, so that they can move back and forth.

Each myosin head has a binding site for actin and a binding site for ATP.

Actin filaments have binding sites for myosin heads, called actin-myosin binding sites.

Two other proteins called tropomyosin and troponin are found between actin filaments. These proteins are attached to each other and they help myofilaments move past each other.

Bindings sites in resting muscles are blocked by trypomyosin, which is held in place by troponin.

This means that myofilaments can't slide past each other because the myosin heads can't bind to the actin-myosin binding site on the actin filaments.

1. An action potential from a motor neurone stimulates a muscle cell and it depolarises the sarcolemma. This spreads down to the sarcoplasmic reticulum.

2. This causes the sarcoplasmic reticulum to release stored calcium ions into the sarcoplasm. These ions bind to troponin, causing it to change shape. This then pulls the attached trypomyosin out of the actin-myosin binding site.

3. This exposes the binding site, which allows the myosin head to bind.

4. The bond formed when a myosin head binds to an actin filament is called an actin-myosin cross bridge.

5. Calcium ions activate the enzyme ATPase which breaks down ATP to provide the energy needed for muscle contraction.

6. The energy released from ATP moves the myosin head, which pulls the actin filament along in a kind of rowing action.

7. ATP also provides the energy to break the actin-myosin cross birdge so the myosin head detaches from the actin filament after it's moved.

8. The myosin head then reattaches to a different binding site further along the actin filament. A new cross birdge is formed and the cycle is repeated (attach, move, detach, reattach). The cycle will continue as long as calcium ions are present and bound to troponin.

When the muscle stops being stimulated, calcium ions leave their binding sites on the troponin molecules and are moved by active transport back into the sarcoplasmic reticulum.

This process also requires ATP.

The troponin molecules return to their original shape, pulling the attached tropomyosin molecules with them. This means the tropomyosin molecules block the actin-myosin binding sites again.

Muscles aren't contracted because no myosin heads are attached to actin filaments so there are no cross-bridges.

The actin filaments slide back to their relaxed position, which lengthens the sarcomere.

• Muscle fibres that contract slowly.
• Muscles you use for posture e.g you have a high proportion of them in your back.
• Good for endurance activities e.g maintaining posture, long-distance running.
• Can work for a long time without getting tired.
• Energy released slowly through aerobic respiration. Lots of mitochondria and blood vessels supply the muscles with oxygen.
• Reddish in colour because they're rich in myoglobin - a red coloured protein thats stores oxygen.

• Muscle fibres that contract very quickly.
• Muscles you use for fast movement e.g you have a high proportion in the eyes or legs.
• Good for short bursts of speed and power, e.g eye movement, sprinting.
• Get tired very quickly.
• Energy's released quickly through anaerobic respiration using glycogen (stored glucose). There are few mitochondria or blood vessels.
• Whitish in colour because they don't have much myoglobin (so can't store much oxygen).

Aerobic respiration is the process where a large amount of energy is released by splitting glucose into CO2 and H2. It's an example of a metabolic pathway because it's made up of a series of chemical reactions.

The energy released is used to phosphorylate ADP to ATP. ATP is then used to provide energy for all the biological processes inside a cell.

There are four stages in aerobic respiration - glycolysis, the link reaction, the Krebs cycle and oxidative phosphorylation.

Glycolysis happens in the cytoplasm of the cells and the other three stages take place in the mitochondria.

Glycolysis involves splitting one molecule of glucose (6C) into two smaller molecules of pyruvate (3C). This process happens in the cytoplasm. It doesn't need oxygen to take place.

There are two stages in glycolysis - phosphorylation and oxidation.

ATOP is used to phosphorylate glucose to triose phosphate. Then triose phosphate is oxidised, releasing ATP.

• Phosphorylation: glucose is phosphorylated by adding 2 phosphates from 2 molecules of ATP. This creates 2 molecules of triose phosphate and 2 molecules of ADP.
• Oxidation: triose phosphate is oxidised (loses hydrogen), forming 2 molecules of pyruvate. NAD collects the hydrogen ions, forming 2 reduced NAD. 4 ATP are produced but 2 are used up in stage one, so there is a net gain of 2 ATP.

The two molecules of reduced NAD are used in the last stage (oxidative phosphorylation). The two pyruvate go into the matrix of the mitochondria for the link reaction.

The enzymes and coenzymes needed for the link reaction are located in the mitochondrial matrix, This means that the reduced NAD produced by the link reaction is made in the right place to be used by oxidative phosphorylation.

1. Pyruvate is deboxylated (carbon is removed) - one carbon atom is removed  from pyruvate in the form of CO2.

2. NAD is reduced - it collects hydrogen from pyruvate, changing pyruvate into acetate.

3. Acetate is combined with coenzyme A to form acetyl coenzyme A (acetyl CoA).

4. No ATP is produced in this reaction.

The Link Reaction occurs twice for every glucose molecule. For each glucose molecule: two molecules of acetyl coenzyme A go into the Krbs cycle, two CO2 molecules are released as a waste product, two molecules of reduced NAD are formed and are used in the last stage.

The Krebs Cycle involves a series of oxidation-reduction reactions. This happens in the matrix of the mitochondira. This cycle happens for every pyruvate molecule so it goes around twice for every glucose molecule.

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 6C Citrate molecule is converted to a 5C molecule (a carbon is removed). A hydrogen is removed to produce reduced NAD from NAD.

3. The 5C molecule is then converted to a 4C molecule (another carbon is removed). Decarboxylation and dehydrogenation occur to produce 1 molecule of reduced FAD and two of reduced NAD.

4. ATP is produced by the direct transfer of a phosphate group from an intermediate compound to ADP. Citrate has now been converted into oxaloacetate.

1 coenzyme A - reused in the next link reaction.

Oxaloacetate - regenerated for use in the next Krebs cycle.

2 CO2 - released as a waste product.

1 ATP - used for energy.

3 reduced NAD - used for oxidative phosphorylation.

1 reduced FAD - used for oxidative phosphorylation.

Oxidative phosphorylation is the process where the energy carried by electrons is used to make ATP. It makes ATP from the reduced coenzymes - 3 ATP are made from each reduced NAD and 2 ATP are made from each reduced FAD. Oxidative phosphorylation involves two processes - the electron transport chain and chemiosmosis.

1. Hydrogen atoms are released from reduced NAD and reduced FAD as they're oxidised to NAD and FAD. The H atom splits into protons and electrons. The electrons move down the electron transport chain losing energy at each carrier.

2. This energy is used by the electron carriers to pump protons from the mitochondrial matrix into the intermembrane space. The concentration of protons is now higher in the intermembrane space which creates an electrochemical gradient.

3. Protons move down the electrochemical gradient via ATP synthase, This movement drives the synthesis of ATP from ADP and inorganic phosphate.

4. The movement of H+ ions across a membrane, which generates ATP is called chemiosmosis.

5. At the end of the transport chain the protons, electrons and O2 from the blood combine to form water. Oxygen is the last electron acceptor.

Some metabolic poisons target the electron carriers, preventing them from passing on electrons. This can be fatal for the organism.

Cardiac muscle is myogenic meaning it can contract and relax without receiving signals from neurones. It controls the regular beating of the heart.

1. The process starts in the sino-atrial node, which is in the wall of the right atrium. It is like a pacemaker and sets the rhythm of the heartbeat by sending out regular waves of electrical activity. This means the right and left atria to contract at the same time.

2. A band of non-conducting collagen tissue prevents the waves of electrical activity from being passed directly from the atria to the ventricles.

3. The waves of electrical energy are transferred from the SAN to the atrioventricular node. This is responsible for passing the waves of electricity to the bundle of His but there is a slight delay to make sure the ventricles contract after the atria have emptied.

4. The bundle of His is responsible for conducting the waves of electrical activity to the finer muscle fibres called the purkyne fibres. These carry waves of electrical activity into the muscular walls of the right and left ventricles, causing them to contract simultaneously from the bottom up.

A doctor can use an electrocardiograph to check someone's heart function, it records the electrical activity of the heart. The heart muscle depolarises (loses electrical charge) when it contracts and repolarises (regains charge) when it relaxes.

1. The P wave is caused by contraction (depolarisation) of the atria.

2. The main peak of the heartbeat with the dips at either side is called the QRS complex and is caused by contraction (depolarisation) of the ventricles.

3. The T wave is due to relaxation (repolarisation) of the ventricles.

The height of the wave indicates how much electrical charge is passing through the heart. A bigger wave means more electrical charge and a stronger contraction.

Doctors compare their patients' ECGs with a normal trace. This helps them to diagnose any problems in the hearts rhythm, which may indicate cardiovascular disease or other heart conditions.

Heartbeats that are too fast are known as tachycardia. This is good during exercise but at rest it means the heart is not pumping blood efficiently. A heartbeat can also be too slow, this is called bradycardia.

An ectopic heartbeat is an extra heartbeat. This is caused by an early contraction of the atria compared to previous heartbeats. It can be caused by early contraction of the ventricles too.

Fibrillation is an extremely irregular heartbeat. The atria and ventricles completely lose their rhythm and stop contracting properly. This is very serious and can lead to death.

Breathing rate and heart rate increase when you exercise.

When you exercise your muscles contract more frequently, which means they use more energy. To replace this energy your body needs to do more aerobic respiration, so it needs to take in more oxygen and breathe out more carbon dioxide.

The body does this by:

•  increasing breathing rate and depth to obtain more oxygen and to get rid of more carbon dioxide.
• increasing heart rate to deliver oxygen and glucose to the muscles faster and remove extra carbon dioxide produced by the increased rate of respiration in muscle cells.

The medulla oblongata (a part of the brain) has areas called ventilation centers. There are two ventilation centers - the inspiratory centre and the expiratory centre. They control the rate of breathing.

1. The inspiratory centre in the medulla oblongata sends nerve impulses to the intercostal and diaphragm muscles to make them contract. This increases the volume of the lungs which lowers the pressure.

2. The inspiratory centre also sends nerve impulses to the expiratory centre. These impulses inhibit the action of the expiratory centre.

3. Air enters the lungs due to the pressure difference between the lungs and the air outside. Stretch receptors are stimulated in the lungs back to the medulla oblongata. These impulses inhibit the action of the inspiratory centre.

4. The expiratory centre then sends nerve impulses to the diaphragm and intercostal muscles to relax which causes the lungs to deflate. The stretch receptors become inactive and the inspiratory centre is no longer inhibited and the cycle starts again.

Exercise triggers an increase in breathing rate by decreasing blood pH.

During exercise, the level of carbon dioxide in the blood increases, which decreases the pH of the blood.

There are chemoreceptors (receptors that sense chemicals) in the medulla oblongata, aortic bodies (clusters of cells in the aorta) and carotid bodies (clusters of cells in the carotid arteries) that are sensitive to changes in blood pH.

If the chemoreceptors detect a decrease in blood pH, they send nerve impulses to the medulla oblongata which sends more frequent nerve impulses to the intercostal muscles and diaphragm. This increases the rate and depth of breathing.

This causes gaseous exchange to speed up. The CO2 level drops and extra O2 is supplied for the muscles - the pH returns to normal and breathing rate decreases.

Ventilation rate also increases with exercise. Ventilation rate is the volume of air breathed in or out in a period of time.

The medulla oblongata controls heart rate and is controlled unconciously by the cardiovascular control centre in the medulla oblongata. This control centre controls the rate at which the SAN fires.

Chemical receptors and pressure receptors detect stimuli in the blood. There are pressure receptors called baroreceptors in the aortic and carotid bodies. They're stimulated by high and low blood pressure.

Electical impulses from these receptors are sent to the medulla oblongata along sensory neurones.

The cardiovascular control centre processes the information and sends impulses to the SAN along sympathetic or parasympathetic neurones - these release different chemicals onto the SAN which determines whether it speeds up or slows down the heart rate.

Cardiac output is the total volume of blood pumped by a ventricle every minute.

The equation for working out cardiac output is:

                                              heart rate (beats per minute) x stroke volume

Stroke volume is the volume of blood pumped by one ventricle each time it contracts.

Cardiac output increases during exercise because heart rate and stroke volume increase.

You can rearrange the equation to find stroke volume or heart rate:

                                              cardiac output / heart rate

You could be asked to use these equations in the exam.

Tidal volume is the volume of air in a normal breath.

Breathing rate is how many breaths are taken, usually in a minute.

Oxygen consumption is the volume of oxygen used by the body, often expressed as a rate.

Respiratory minute ventilation is the volume of gas breathed in or out in a minute.

                   respiratory minute ventilation: tidal volume x breathing rate

A spirometer is a machine that can give readings of tidal volume and allow measurement of a person's breathing rate, oxygen consumption and respiratory minute ventilation.

1. A spirometer has an oxygen-filled chamber with a movable lid.

2. A person breathes through a tube connected to the oxygen chamber. As the person breathes in the lid of the chamber moves down. When they breathe out it moves up.

3. These movements are recorded by a pen attached to the lid of the chamber, this writes on a rotating drum which creates a spirometer trace.

4. The total volume of gas in the chamber decreases over time. This is because the air that's breathed out is a mixture of oxygen and carbon dioxide but the carbon dioxide is absorbed by soda lime in the tube. This means there's only oxygen in the chamber which the person inhales from.

5. As this oxygen gets used up by respiration, the total volume decreases.

Exercises causes an increase in breathing rate and tidal volume, as well as an increase in oxygen consumption and respiratory minute ventilation. A spirometer can be used to investigate the effect that exercise has on these things.

1. A person breathes into a spirometer for one minute at rest and recordings are taken.

2. The person then exercises for two minutes. While the person is exercising, the spirometer chamber is refilled with oxygen.

3. Immediately after the person stops exercising, they breathe into the spirometer again and recordings are taken for another minute.

4. The recordings taken before and after exercise are then compared.

Your external environment and what you're doing can affect your internal environment - the blood and tissue fluid that surrounds your cells.

Homeostasis involves control systems that keep your internal environment within narrow limits - your internal environment is kept in a state of dynamic equilibirum (fluctuating around a normal level).

Keeping your internal environment constant is vital for cells to function normally and to stop them being damaged. If body temperature is too high enzymes may become denatured.

Cells need a constant energy supply to work so blood glucose concentration must be carefully controlled and it's monitored by cells in the pancreas.

Water is essential to keep the body functioning so the amount of water in the blood needs to be kept constant. Water is lost during the removal of waste products from the body. The kidneys regulate the water content.

Homeostatic systems use negative feedback to reverse a change. These systems involve receptors, a communication system and effectors.

Receptors detect when a level is too high or too low and this information is communicated via the the nervous system or the hormonal system to effectors.

The effectors respond to counteract the change which brings the level back to normal. The mechanism that restores the level to normal is called a negative feedback mechanism.

Negative feedback keeps things around the normal level e.g body temperature is usually kept within 0.5 degrees above or below 37 degrees.

Negative feedback only works within certain limits - if the change is too big then the effectors may not be able to counteract it.

Some changes trigger a positive feedback mechanism, which amplifies the change.

The effectors respond to further increase the level away from the normal level.

Positive feedback is useful to rapidly activate somethings e.g blood clots after injury.

Positive feedback can also happen when a homeostatic system breaks down e.g if you're cold for too long (hypothermia).

Positive feedback isn't involved in homeostasis because it doesn't keep your internal environment stable.

Many mechanisms are used to change body temperature.

Mechanisms to reduce body temperature:

• Sweating - more sweat is secreted when the body is too hot.
• Hairs lie flat - erector pilli muscles relax so hairs lie flat and less air is trapped so the skin is less insulated.
• Vasodilation - arterioles near the surface of the skin dilate, more heat is lost from the skin.

Mechanisms to increase body temperature:

• Shivering - the muscles contract in spasm and more heat is produced from increased respiration.
• Much less sweat - less sweat is released which reduces the amount of heat loss.
• Hairs stand up - erector pilli muscles contract when ot's cold which traps more air to prevent heat loss.
• Vasoconstriction - arterioles constrict, reduces heat loss.
• Hormones - the body releases adrenaline and thyroxine, these increase metabolism.

The hypothalamus controls body temperature and is maintained at a constant level.

The hypothalamus receives information about temperature from thermoreceptors (temperature receptors).

Thermoreceptors send impulses along sensory neurones to the hypothalamus, which sends impulses along motor neurones to effectors (muscles and glands) which triggers mechanisms dependent on the temperature.

The effectors respond to restore the body temperature back to normal.

The control of body temperature is called thermoregulation.

Hormones can affect transcription factors.

In a cell there are proteins called transcription factors that control the transcription of genes.

Factors that increase the rate are called activators and those that decrease the rate are repressors. Hormones can affect the activity of transcription factors.

Some hormones can cross the cell membrane, enter the nucleus and bind to transcription factors to alter gene transcription.

At normal body temperature, the thyroid membrane receptor (a transcription factor) binds to DNA at the start of the DNA.

This decreases the transcription of a gene coding for a protein that increases metabolic rate.

At cold temperatures thyroxine is released, which binds to the thyroid hormone receptor, causing it to act as an activator.

The transcription rate increases, producing more protein. The protein increases the metabolic rate, causing an increase in body temperature.

Some hormones can't cross the cell membrane but can still affect the activity of transcription factors.

They bind to receptors in the cell membrane, which activate messenger molecules in the cytoplasm of the cell.

These messenger molecules activate enzymes called protein kinases, which trigger a chain of reactions (a cascade) inside the cell.

During the cascade, transcription factors can be activated - these affect the transcription of genes in the cell nucleus.

Keyhole surgery is a way of doing surgery without making a large cut in the skin. Surgeons make a smaller cut in the patient and insert a video camera and specialised medical instruments through the incision.

There are many advantages to this such as: the patient loses less blood and have less scarring of the skin, patients are in less pain after their operation and they recover more quickly, this makes it easier for the patient to return to normal activities.

Damaged cruciate ligaments can be fixed by keyhole surgery.

Cruciate ligaments are the ligaments found in the middle of your knee. connecting your thigh bone to your lower leg bone.

Damaged cruciate ligaments can be removed and replaced with a graft.

Proteses can replace damaged body parts. Sometimes it is possible to replace damaged or missing body parts with an artificial device called a prosthesis.

Protheses can be used to replace whole limbs or parts of limbs. Some protheses include electronic devices that operate the prosthesis by picking up information sent by the nervous system.

Prostheses make is possible for people with some disabilities to participate in sport and make it possible for people who have certain injuries to play sport again.

Damaged knee joints can be replaced by prosthetic joints.

A metal device is inserted into the knee to replace damaged cartilage and bone. The knee joint and the ends of the leg bones are replaced to provide a smooth knee joint. Cushioning in the new joint helps to reduce the impact on the knee.

A knee joint replacement allows people with serious knee problems to move around and participate in low-impact sports.

When involved in a very competitive sport, some people choose to take performance-enhancing drugs (drugs which improve a persons performance).

There are various kinds of performance-enhancing drugs that have different effects on the body, for example:

• Anabolic steroids - these drugs increase strength, speed and stamina by increasing muscle size and allowing athletes to train harder.
• Stimulants - these drugs speed up reactions, reduce fatigue and increase aggression.
• Narcotic analgesics - these drugs reduce pain, so injuries don't affect performance.

Performance-enhancing drugs are banned in most sports. Athletes can be tested for drugs at any time and if they're caught they can be banned from competing.

Some people think that performance-enhancing drugs should be banned from all sports and think the use of drugs is morally wrong and that they should never be used. Other people think that the use of these drugs can be justified in certain circumstances.

Against using performance enhancing drugs:

• Some performance-enhancing drugs are illegal.
• Competitions become unfair if some people take drugs - people gain an advantage by taking drugs, not through training or hard work.
• There are some serious health risks associated with the drugs used.
• Athletes may not be fully informed of the health risks of the drugs they take.

For using performance enhancing drugs:

• It's up to each individual - athletes have the right to make their own decision.
• Drug free sport isn't really fair anyway - different athletes have access to different training facilities.
• Athletes that want to compete at a higher level may only be able to by using performance-enhancing drugs.