Movement at a joint:

A joint is where 2 or more bones articulate (meet). Tendons attach muscles to the bones at the joint. They are inelastic so that they can transmitte nsion due to muscle contraction to the bone to effect movement. They consist of whitecollagen fibres. Ligaments attach bone to bone. They are elastic to allow movement of the bones across thejoin t. They consist of yellow elastic fibres. Energy loss at the joint is minimised by synovial fluid which is a lubricant. Articular cartilage (tyaline cartilage) cushions the bones and acts as a shock absorber at thejoint .

Antagonistic muscle pairs:

They have opposing actions i.e. when one contracts, the other relaxes. This causes movement i nopposite directions. When the muscle contracts, it causes tension that exerts a pulling force e.g. contraction ofbicep s muscle pulls the radius and ulna upwards bending the arm at the elbow. To straightenthe arm , triceps muscle contracts pulling the radius and ulna downwards. Flexor muscles bend the limb when they contract and extensor muscles straighten the armwhe n they contract.

Aerobic Respiration:
This is the splitting of glucose to release CO2as a waste product and reuniting of H2with O2witht he release of a large amount of energy. Three main stages: Stage Glycolysis Site Cytoplasm ( cytosol) Product(s) 2 ATP 2 pyruvate 2 reduced NAD 4 CO2 Krebs Cycle Mitochondrial matrix 6 reduced NAD 2 reduced FAD 2 ATP Oxidative Phosphorylation(E TC) Cristae (inner mitochondrial membranes) H2O 34 ATP

Glycolysis:
This is the metabolic pathway during which glucose is split to produce 2 pyruvate molecules(pyr uvic acid). It occurs in the cytoplasm (cytosol). First, glucose undergoes phosphorylation to become glucose-6-phosphate in a catalysedreactio n by phosphofructokinase/hexokinase. This makes glucose more reactive and prevents itfrom le aving the cell. Further phosphorylation produces fructose 1,6-bisphosphate. This is splitinto 2 tri ose phosphate (TP/GALP). Dehydrogenation produces 2 glycerate-3-phoshpate (GP) molecules, 2 reduced NAD, and 2 ATP molecules. Conversion of GP to pyruvic acid results in another 2 ATP molecules as a result ofsub strate level phosphorylation. Products of Glycolysis are; > a net of 2 ATP > 2 reduced NAD > 2 pyruvate

Metabolic pathway:
A series of enzyme-catalysed reactions that occur in small steps during which theproduct/inter mediates are substrates of the next enzyme. They are controlled by end productinhibition i.e. a ccumulation of the end product inhibits the first enzyme in the pathway e.g. ifpyruvate accumul ates, it inhibits the hexokinase.

Krebs Cycle:
This is complete oxidation of pyruvate resulting in the formation of CO2, ATP, reduced NAD andr educed FAD. It is a metabolic pathway that occurs in the mitochondrial matrix. It occurs in a series of steps with each step being controlled and catalysed by a specificintracellu lar enzyme. The reactions include; 1. Decarboxylation - catalysed by decarboxylases 2. Dehydrogenation - catalysed by dehydrogenases

Acetyl coenzyme A (CoA) (2C) from the link reaction combines with oxaloacetate (4C) to formcit rate (6C). Through a series of enzyme catalysed reactions, oxaloacetate is regenerated. 2 ATPm olecules are produced by substrate level phosphorylation.

Importance of Krebs Cycle:

1. Yields 2 ATP molecules by substrate level phosphorylation. 2. Produces reduced coenzymes whose oxidation results in ATP production by oxidativephosp horylation. Every reduced NAD produces 3 ATP molecules on oxidation and every reducedFAD p roduces 2 ATP molecules on oxidation. 3. Produces intermediate compounds for cell metabolism.

Oxidative phosphorylation:
It occurs on cristae/inner mitochondrial membranes and involves the electron transport chain(E TC). Reduced NAD/FAD carries hydrogen to the cristae. Hydrogen splits into H+and e-. Electrons are transferred along the ETC by electron carriers to O2 the final e-acceptor toform water. During the ETC, redox reactions occur catalysed by oxidoreductases such ascytochrome oxidase. During electron transfer, H+ions are pumped into the intermembrane space forming achemiosm otic gradient. Flow of protons down the gradient releases free energy for the synthesis of ATP from ADP andP i catalysed by ATPase on stalked particles.

Roles of coenzymes:
They promote the activity of dehydrogenases (hydrogen acceptors). They carry hydrogen fromg lycolysis in the cytoplasm, the link reaction and the Krebs cycle in the mitochondrial matrix tot he cristae. During aerobic respiration when they are oxidised, a lot of free energy is releasedfor oxidative phosphorylation.

Anaerobic respiration:
This is the incomplete breakdown of glucose to yield a relatively small amount of energy. Itoccu rs in the cytoplasm. Pyruvate produced by glycolysis is directly reduced to lactate. NAD isregene rated to allow glycolysis to continue yielding at least 2 ATP molecules.

The fate of lactate:

When the oxygen debt is repaid, lactate is oxidised to pyruvate. Lactate diffuses into the bloodp lasma. It is carried to the liver where oxidation occurs to pyruvate and some to glucose.Pyruvat e enters the Krebs cycle for complete oxidation to water and CO2.

The Heart, Exercise and Sport

The cardiac muscle is myogenic i.e. contracts on its own without nervous stimulation. Theelect rical excitation starts from the Sinoatrial Node (SAN) and spreads to both the atria, causingatrial systole. It spreads rapidly due to intercalated discs that act as gap junctions with lowelectrical r esistance. The excitation spreads to the Atrioventricular Node (AVN) where there is a short delay beforeth e wave of depolarization (action potential) passes into the Bundle of His which carries theexcita tion through the purkyne/purkinje tissue to the ventricles base, before spreading alongthe walls . The spread of the excitation through the heart enables the atria to contract before theventricle s and ventricular systole begins at the base so as to squeeze out most of the bloodthrough the a rteries.

The electrocardiogram (ECG)

An ECG shows the changes in the electrical excitation of the heart during the cardiac cycle.Thes e changes occur as the action potential spreads from one part of the heart to another. AnECG is used to investigate the rhythms of the heart as it is a record of the electrical activity. A normal ECG has; (a) P wave shows the spread of electrical excitation through the atria (b) QRS wave shows the spread of excitation through the ventricles (c) T wave shows the repolarisation (relaxation) of the purkyne tissue in the ventricles An ECG shows the amplitude of each wave in millivolts (mV) and the time in seconds on the x-a xis. Therefore, the heart rate can be calculated from it e.g. if it takes 0.8s from the start of oneP wave to the start of the next P wave, the heart beat is: 0.8s ----> 1 beat(60*1) / 0.8 = 75bpm 60s ----> ?

How ECGs can be used to diagnose CVDs:

The ECG is compared with the normal ECG to establish the duration of the phases and thevoltag e of each. This enables doctors to diagnose various heart diseases; Tachycardia the interval between PQRS phase is shorter. The voltage is higher.Tachycardia is the condition where the heart beats too quickly such that there isn tenough time for v entricles to empty properly. Cardiac output could decrease if therewas insufficient time to fill the ventricles between contractions. The change in cardiacoutput will depend on

whether the decrease in stroke volume is compensated by theincrease in heart rate. Ventricular fibrillation The ventricles contract weakly and erratically. The stroke volumede creases significantly and there is a fall in blood pressure. This often leads to a fatalheart attack unless there is cardiopulmonary resuscitation. Usually, a defibrillator isused to giv e the patient an electric shock. Atrial fibrillation The atria contract weakly and too fast. It is often associated with a bloodc lot (thrombus) which if pumped to the brain could starve nervous tissue of oxygenleadin g to a stroke.

The effect of exercise on ventilation:

A spirometer is used to determine the breathing rate. The subject breathes through a mouthpiece which must be sterilised or disposable. It isconnect ed to a chamber containing soda lime to absorb CO2which would otherwise cause anincrease o n the ventilation rate interfering with the investigation. As the person breaths in and out, the air tight chamber experiences a change in volume thatcau ses the lead to which a pen is attached to move up and down. This results in the pen makinga tr ace on a graph paper attached to a revolving drum. The spirometer trace (spirogram) can be used to determine different lung volumes and thefreq uency of breathing.

Tidal volume is the volume of air that is inhaled or exhaled during quiet breathing at rest.I
t is about 0.5dm3.

Inspiratory reserve volume is the volume of air that can be inhaled over and aboveno
rmal tidal volume (1.5dm3).

Expiratory reserve volume is the volume of air that can be exhaled over and abovenor
mal tidal exhalation (1.5dm3).

Vital capacity
vital capacity = tidal volume + inspiratory reserve volume + expiratory reserve volume It is the maximum volume of air that can be inhaled and exhaled by the most vigorous breathin geffort (4.5dm3).

Residual volume The volume of air that cannot be expelled remains in the lungs afterthe
strongest possible exhalation. Its about 1.5dm3. It keeps the lungs partially inflated to allowgas exchange between the breaths.

Total lung capacity

Total lung capacity = vital capacity + residual volume It is the maximum value of air that the lungs can hold (6dm3).

Ventilation rate:
Ventilation rate = tidal volume * frequency of inspiration (breathing rate) units:dm3min-1 During exercise, the ventilation rate increases e.g.: At rest, the frequency of inspiration is 1.5 breaths per minute and the tidal volume is 0.5dm3.Duri ng exercise, the volume of each breath (tidal volume) rises to 3dm3and the breathing rate is45bp m. Determine the % increase in the ventilation rate and account for this increase. ventilation rate at rest : 0.5 * 15 = 7.5dm3min-1 ventilation rate during exercise : 3* 45 = 135dm3min-1 135 - 7.5 = 127.5 (127.5 / 7.5) * 100 = 1700 % This ensures quick supply of O2to respiring skeletal muscle tissues and rapidremoval of CO2fro m the tissues.

Regulation of the ventilation rate

It is effected by the respiratory centre (ventilation centre) in the medulla oblongata in the hindbra in. It has an inspiratory and expiratory centre. Nerve impulses from these centres are conducted to intercostal musckes by intercostal nerves an ddiaphragm muscles by the phrenic nerve. During exercise, CO2concentation in the blood increases. This is detected by chemoreceptors int he medulla, carotid and aortic bodies. Impulses are then transmitted to intercostal and diaphragm muscles from the respiratory centre. They stimulate more frequent and stronger contractions ofth e effectors. This increases the ventlation rate to reduce theCO2concentation and to increasetheO2 supply to respiring tissues.

The effect of exercise on cardiac output:

cardiac output = heart rate * stroke volume (dm3min-1) (bpm) (dm3)

During exercise, cardiac output increases as more oxygen has to be transported quickly torespirin g muscles while waste products such as CO2and lactic acid has to be removed from themuscles. The increase in cardiac output is as result of the increasein the heart rate and the cardiac volume. Trained individuals have greater cardiac volumes as their heart muscles are stronger. Their heartr ate is slightly less than that of untrained individuals.

Regulation of cardiac output:

Although myogenic, the rate at which cardiac muscle contracts is controlled by thecardiovascular centre in the medulla. This control centre sends nerve impulses to the SAN through the sympathertic nerve and thepara sympathetic nerve (vagus nerve). The sympathetic nerve increases the heart rate while theparasy mpathetic nerve decreases the heart rate. The variation in the heart rate is brought about by stimuli that include; 1.The concentration CO2in the blood - During exercise, the CO2concentration increases due tores piration. Chemoreceptors in aortic and carotid bodies detect the increase and conductimpulse s to the cardiovascular centre of the brain. Impulses are conducted to the SANthrough the sy mpathetic nerve. This increases the frequency of electrical excitation/impulsesfrom the SAN. As a result, the heart rate increases. 2.Pressure changes - As the atria fill with blood, stretch receptors in their walls send impulses tot he cardiovascular control centre. This results in more impulses along the sympathetic nervet o the SAN resulting in an increase in the heart rate and stroke volume. As blood pressureincr eases, baroreceptors in the carotid artery are stimulated. Nerve impulses to thecardiovascular centre result in parasympathetic stimulation of the SAN. This decreases thefrequency of ner ve impulses in the pacemaker and hence decreaes the heart rate. Arteriesdilate leading to a dr op in blood pressure. 3.The hormone adrenaline - At the start of exercise, adrenaline causes thecardiovascular centreto conduct nerve impulses through the sympathetic nerve to the SAN. This causes an increasin t he heart rate and blood pressure. The consequence is increased supply of O2and glucoseto sk eletal muscle tissue.

Homeostasis
This is the maintenace of a constant internal environment in dynamic equilibrium. Homeostasis mechanisms include; 1. Receptors - detect a deviation of a factor from the set point (normal/optimum level) e.g.therm oreceptors in the hypothalamus 2. Co-ordinator (regulator) - endocrine/nervous system that controls correctiveprocesses 3. Effectors - carry out corrective processes to cancel out the deviation 4. Negative feedback - a self regulating mechanism in which a deviation is detected andcorrecti ve processes cancel out the deviation by returning the factor back to the set point.

Negative feedback in thermoregulation

During exercise, metabolic reaction generate heat. Respiration in the muscles increases heatprod uction leading to high body temperature. Thermoreceptors in the hypothalamus detect the rise in the core temperature of the body.Nervei mpulses are conducted from the heat loss centre by motor neurons to the skin. The followingcorr ective processes promote heat loss and reduce heat production: Sweating increases Sweat glands increase sweat production. As the water in the sweat evaporates, latent heatofvapor ization is absorbed from the body causing cooling effect. Vasodilation occurs The shunt vessel is closed and more blood flows to capillaries close to the skin surface. This isbe cause the sphincter muscles around the superficial arterioles relax. As more blood flowsthrough s uperficial capillaries, heat loss by conduction and radiation increases. Hair lies flat Erector pili muscles (hair) relax, hair lies flat. No air is trapped therefore, there is no insulationca using increased heat loss by radiation and conduction. No shivering No heat generation causing involuntary muscle contraction. These corrective processes reduce the body temperature to the set point. This is importantbecaus e very high temperatures can denature enzymes that regulate metabolic processes. If it rises above critical temperature, positive feedback occurs. The metabolic rate increases andr eaction rates double for every 100c rise in temperature. This would lead to more heat beinggener ated causing further rise in temperature culminating in death at420c.

When the body temperature drops below the optimum, cold receptors in the hypothalamus andth e skin detect the fall. Nerve impulses promote the following corrective processes in theeffectors: Vasoconstriction The shunt vessel dilates, sphincter muscles around superficial arterioles contract. Less bloodflow s through superficial capillaries. This reduces heat loss by conduction and radiation. Hair stands upright The erector pili muscles contract; hair stands up. It traps a layer of air which provides insulation. Air is a poor conductor of heat. Shivering This is rapid and involuntary contractions of skeletal muscles that generate heat. Metabolic reactions Metabolic reactions in the liver increase. This generates more heat to raise the body temperatureb ack to optimum levels.

Gene Expression:
A gene is a length of DNA with base sequences that code for the sequence of amino acids in apol ypeptide chain. Gene expression involves protein synthesis i.e. transcription followed by translation. For transcription to occur, DNA transcription factors such as hormones are required. A hormone is a chemical secreted by ductless (endocrine) glands into the blood to be transported to a specific target organ where it affects activity. Hormones are peptides or steroids. They affect particular target organs because they bind tospeci fic receptors on the cell surface membrane. The 3-D shape of the hormone and that of therecepto r is complementary. Hormones act as transcription factors by causing release of a second messenger or by enteringthe nucleus and activating genes. Two modes of action; 1. Steroid hormones - They enter the cytoplasm where they bind to receptors on the cell surface membrane. The hormone receptor complex enters the cell because steroids are lipid soluble. The hormone then acts as a transcription factor by binding onto the DNA and switching on specificge nes. The receptor moves to the cell surface membrane and fuses with it as it is fluid. Theprotein s ynthesized as a result could be fibrous resulting in stronger muscles. This is effected byanabolic s teroids used as performance enhancing drugs by sprinters and weigt lifters. Steroidhormones hav e slow but long-lasting effects.

2. Peptide hormones -e.g. erythropoietin. They do not enter the target cell as they are not lipidso luble. When the peptide hormone binds to the receptors on the cell surface membrane, a secondm essenger,cyclic adenosine monophosphate (CAMP), is released into the cytoplasm. It triggersa ca scade of events that cause activation of transcription factors. This includes activation ofenzymes that lead to activation of genes. Erythropoietin leads to synthesis and activation ofenzymes that p romote synthesis of erythrocytes/red blood cells.

Performance enhancing drugs

Drugs taken for athletic performance enhancement are of two types; 1. Unbanned substances - these include nutritional supplements e.g. creatine containingsupplem ents which increase levels of phosphocreatine in the muscles. PCr+ ADP ---> ATP This is required to phosphorylate ADP to release ATP for high intensity short duration events e.g .weightlifting and sprints using fast twitch muscle fibres. Side effects include: hypertension;kidn ey damage 2. Banned substances - are drugs including anabolic steroids, erythroproietin and diuretics. (a) Anabolic steroids e.g. nadrolone - mimic testosterone and are used as musclebuilders. Theyen hance short bursts of high intensity activity. This is because they increase the number of fasttwitc h muscle fibres for events like sprint races and weight lifting. Side effects include:hypertension; i nfertility, low sperm count and even impotence in males; disruption of themenstrual cycle; increa sed aggression especially in young athletics. (b) Erythropoietin - hormone that increases production of erythrocytes. This leads to increasedO2 and hence aerobic respiration, the high ATP production has been shown to enhance aerobicperfor mance by 10%. Side effects include: stroke; CHDs (CVDs).

Ethics of performance enhancing drugs

Ethical reasons:
> we can no longer compare athletes fairly > these drugs are illegal > some managers can make athletes to use the drug without their decision (un-informed) > there are health risks with a possibility of death

Unethical reasons:
> an individual has a right to make their own decision > drug free sport is not fair anyway due to differences in training resources > athletes are subjected to immense pressure from their sponsors, managers and fans > financial rewards outweigh possible risks

Changes in muscle strength with time

Muscle strength has increased over the years. This could be as a result of; (a) use of anabolic steroids that promote muscle development (b) use of higher and stronger doses (c) use of more effective training equipment and regime However, muscle strength reaches a maximum. Reasons for this include; (a) genetic maximum (b) weigtlifters choosing not to use the drugs because of awareness of the side effects and as ares ult of more effective screening methods

Athleticism
Phenotype is as a result of the interaction between the genotype and the environment. Althoughm uscle development can be improved by diet, drugs or training, the extent of muscledevelopment i s influenced by a person's genetic makeup (genotype). It depends on the inheritedproportion of fa st and slow twitch muscle fibres. Athleticism is polygenic inheritance which shows normal distribution i.e. continuous variation.T herefore, athletic performance is a product of many genes and environmental factors such astrain ing diet and drugs.

Effects of too little exercise

Obesity
If energy intake exceeds expenditure, the excess is stored as adipose tissue resulting in excessive body mass with a BMI of above 30. Research has shown a gradual increase in the prevalance of obesity amongst adults in the UK.Thi s significant increase in obesity can be attributed to; (a) junk foods with high energy content (b) low levels of physical activity associated with sedentary lifestyles

The incidence is higher in women than men because of hormonal differences. Testosteroneprom otes skeletal muscle develoment whereas oestrogen promotes increased fat deposition.Generally, men engage in more physical activities than women. There is a slight correlation between obesity and decreased levels of exercise. This is becauselac k of exercise results in excess energy being stored as adipose (fat) tissue. This is not a causal relationship because; 1. Low levels of exercise is not directly responsible for obesity 2. There are other factors such as diet and genetic make up which contribute to beingoverweight

Type II diabetes
It is associated with obesity. This is due to lack of insulin receptors in the body. About 10% ofthe UK population that is over 65 years have the condition. The slight positive correlation between lack of adequate exercise and type II diabetes is in people who are at a risk because of being overweight. Therefore, it can be considered to be a weakcausa l link although other factors such as diet and body mass have to be taken into consideration. An increase in exercise levels in overweight individuals reduces the risk of type II diabetes.

CHDs
Low levels of exercise increases the risk of CHDs because of increased blood cholesterol levelsa nd hypertension especially in overweight individuals.

Dangers of too much exercise

Respiratory tract infections
Research has established a causla link between excessive exercise and respiratory tract infections .This is because excessive exercise decreases T killer, T helper and B cell counts. The depressedi mmune system makes athletes susceptible to infections. This is aggravated by the hormonescorti sol and adrenaline which supress inflammation and reduce the activity of B cells duringstress.

Damage to ligaments
These have elastic fibres to allow movement of bones at joints. Their damage will restrict themo vements.

Damage to tendons
These have non-elastic fibres so that when the muscle contracts, they can transmit the tension top ull the bones. If damaged due to steenous activity, the pulling force is not transmitted to thebones .

Articular cartilage
This is a smooth skeletal tissue that allows friction free movement at the joints and acts as ashoc k absorber. Its damage contributes to osteoarthritis. Joints swell rendering movement verypainful .

How medical technology enables those with injury toparti cipate in sports:
Sports expose athletes to injuries especially at the joints (damage of ligaments, tendons,andcartill age). Bones can also be fractured to extents where healing is very difficult ortakes a verylong tim

e. However, medical technologies have enabled proper diagnosis ofthe injuries andhence more ef fective interventions.

Keyhole surgery
MRI gives a precise image of the damage so that the damaged part can be removed throughkeyh ole surgery. A fibre optic with a small camera and light is used to observe the inside of thejoint. Using small surgical instruments, the damaged tissue can be removed. As the cuts are verysmall, recovery takes short duration. This has been used to replace torn ligaments and tendonswith dona ted tissues.

Using prosthetics
These are artificial limbs and joints used to replace damaged ones, especially knee joints. Those with artificial joints can participate in moderate sports but not those that may involve twists andt urns or falling because they can lead to damage of other joints. The artificial joint consists ofmet al and plastic which can be worn out leading to inflammation. There is a debate that lead toIAFF banning the use of prosthetic limbs in competition.