PE A&P AS.txt

Support, protect, movement, blood cell production, mineral store

• Skull
• Thoracic girdle
• Vertebrae column

• Shoulder girdle & upper limbs
• Pelvic girdle & lower limbs

Bony framework upon which rest of body is built. Provides attachments for muscular system & carries & protects cardio & respiratory systems.

Attaches to & moves skeleton. Has obvious stripes on it caused by long muscle fibres of which it's composed. Only type of muscle under conscious control.

The place on body where two or more bones meet.

Bones of upper & lower limbs and their girdles that join to the axial skeleton.

Forms the long axis of the body and includes the bones of the skull, spine & rib cage.

Tough band of fibrous tissue, slightly elastic connective tissue that attaches one bone to another. Binds ends of bones to avoid dislocation.

Very strong connective tissue attaches skeletal muscle to bone.

Longer than it is wide, consists of a shaft (diaphysis) and 2 ends (epiphysis). Ends are covered by articular cartilage to absorb shock & prevent friction. Large cavity in diaphysis & small cavities in each epiphysis.

Between diaphysis & epiphysis. Responsible for promoting longitudinal bone growth until physical maturity.

Found in bones, contain bone marrow which generates new blood cells & stores fat.

Main component of bone, fibrous protein with great strength.

Mineral that keeps bones hard & strong. 99% of bodies calcium found in bones.

No movement, most stable found between bones in skull & between fused bones of sacrum & coccyx.

Little movement, stable, found between bodies of adjacent vertebrae in cervical, thoracic & part of lumbar spine.

Free movement, least stable found between bones of arms & legs.

Thin layer of glassey smooth cartilage, quite spongy, covers ends of bones. Absorbs shock, prevents friction.

Ligament, articular cartilage, joint capsule, synovial fluid

Slippery fluid in joint cavity reduce friction between articular cartilage & joint.

Tough fibrous tissue, two layers fibrous capsule lies outside synovial membrane. Fibrous capsule strengthens joint & synovial membrane lines joint & secretes synovial fluid.

Space within synovial joint contains synovial fluid.

Flattened fibrous sac lines with synovial fluid contains thin film of synovial fluid. Prevents friction of sites in the body where ligaments, muscles, tendons or bones may rub together.

Wedge of white fibrocartilage, improves fit between adjacent bone ends, making joint more stable & reducing wear & tear on joint surfaces.

Fatty pad provides cushioning between fibrous capsule & bone or muscle.

Upright standing position head, shoulders, chest, palms, hips, knees & toes facing forward.

Shoulder, hip. Ball shaped head of 1 bone articulates with cup like shape of other. Movement can occur in 3 planes. Allows greatest range of movement.

Elbow, knee, ankle. Cylindrical protusion of one bone articulates with trough shaped depression of other. Movement restricted to 1 plane joint allows bending & straightening only.

Radio ular, spine (atlas/axis) rounded/pointed structure of 1 bone articulates with ring shaped structure of adjacent bone. Movement restricted to one plane. Allows rotation about its longitudinal axis only.

Wrist. Similar to ball & socket but much flatter articulating surfaces forming much shallower joint. Movement can occur in 2 planes allows second greatest range of movement.

Spine ( between vertebrae in cervical, thoracic & parts of lumbar) articulating surfaces almost flat & similar size. Allows movement in 3 planes but severely limited.

Towards front of body.

Towards back of body

Towards head or upper part of body.

Towards feet or lower part of body.

Towards middle of body

Towards outside of body.

Makes body part move in forward direction from anatomical position.

Makes body part move in backwards direction from anatomical position.

Knee joint.

When shoulder is already flexed with arm parallel to ground & shoulder joint moves towards body.

When shoulder joint with arm parallel to ground moves away from middle of body.

Body part moves away from mid line of body.

Body part moves towards mid line of body.

When a body part moves about its long axis. E.g screwdriver is rotation at the shoulder.

Body part performing circumduction stays still while furthest end of body part moves in a circle

Makes palm face down

Makes palm face upwards.

Bending the spine sideways.

When the foot moves towards the shin.

When the foot moves away from the shin.

• Agonist muscle- wrist flexors
• Antagonist muscle- wrist extensors
• Location- anterior forearm

• Agonist muscle- wrist extensors
• Antagonist muscle- wrist flexors
• Location- posterior forearm

• Agonist- pronator teres
• Antagonistic- supinator
• Location- superior anterior forearm

• Agonist- supinator
• Antagonist- pronator teres
• Location- lateral anterior forearm

• Agonist- biceps brachii
• Antagonist- triceps brachii
• Location- anterior upper arm

• Agnostic- triceps brachii
• Antagonistic- biceps brachii
• Location- posterior upper arm

• Agonist- anterior deltoid
• Antagonist- posterior deltoid
• Location- covers shoulder joint

• Agonist- posterior deltoid
• Antagonist- anterior deltoid
• Location- covers shoulder joint

• Agonist- middle deltoid
• Antagonist- latissimus dorsi
• Location- covers shoulder joint

• Agonist- latissimus dorsi
• Antagonist- middle deltoid
• Location- posterior trunk

• Agonist- pectoralis major
• Antagonist- trapezius
• Location- top of chest

• Agonist- trapezius
• Antagonist- pectoralis major
• Location- posterior trunk

• Agonist- teres minor & infraspinatus
• Antagonist- teres major & subscapularis
• Location- attaches back of scapula to humerus

• Agonist- teres major & subscapularis
• Antagonist- teres minor & infraspinatus
• Location-attaches side & front of scapula to humerus

• Agonist- rectus abdominis
• Antagonist- erector spinae group
• Location- middle of abdomen

• Agonist- erector spinae group
• Antagonistic- rectus abdominis
• Location- covers length of spine

• Agonist- external obliques
• Antagonist - internal obliques
• Location- lateral abdomen & lateral abdomen beneath external obliques

• Agonist- iliopsoas
• Antagonist- gluteus maximus
• Location- anterior pelvis

• Agonist- gluteus maximus
• Antagonist- iliopsoas
• Location- posterior pelvis

• Agonist- gluteus medius & minimus
• Antagonist- adductor group
• Location- lateral hip

• Agonist- adductor group
• Antagonist- gluteus medius & minimus
• Location- medial thigh

• Agonist- biceps femoris, senitendinosus, semimembranosus
• Antagonist- rectus femoris, vastus lateralis, vastus medialis, vastus intermedius.
• Location- posterior thigh

• Agonist- rectus femoris, vastus lateralis, vastus medialis, vastus intermedius
• Antagonist- biceps femoris, semitendinosus, semimembranosus.
• Location- anterior thigh

• Agonist- tibialis anterior
• Antagonistic- gastrocnemius & soleus
• Location- cover anterior tibia

• Agonist- gastrocnemius & soleus
• Antagonist- tibialis anterior
• Location- calf muscles

• Condyloid joint
• Articulating bones: radius, ulna, carpals

• Hinge joint
• Articulating bones: radius, ulna & humerus.

• Pivot joint
• Articulating bones: radius & ulna

• Ball & socket joint
• Articulating bones: scapula & humerus.

• Cartilaginous, pivot & gliding joint
• Articulating bones: vertebrae

• Ball & socket joint
• Articulating bones: pelvis & femur

• Hinge joint
• Articulating bones: femur & tibia

• Hinge joint
• Articulating bones: tibia, fibula & talus.

Made up of: supraspinatus, teres minor, infraspinatus & subscapularis. Stabilises shoulder joint to prevent larger muscles displacing head of humerus during physical activity.

Tension is developed in a muscle

Tension is developed while joint movement occurs.

Tension produced while muscle shortens. Causes joint movement.

Tension produced while muscle lengthens. Controls joint movement.

Tension produced while no movement occurs. Stops joint movement.

Long cylindrical muscle cell. Held together in bundles to make up an individual skeletal muscle.

Associated with aerobic exercise. Produces small amount of force over long period of time: high resistant to fatigue. Suited to endurance based activities.

Associated with anaerobic work. Produces large force over short period of time: low resistance to fatigue. Suited to power based activities.

More resistant to fatigue but generate slightly less force.

Greatest anaerobic capacity generates largest amount of force.

Small

Large

Large

Large

Moderate

Small

Large

Moderate

Small

High

Moderate

Low

Low

High

High

Low

High

High

High

Moderate

Low

• Reduction in muscle viscosity, improve efficiency of muscular contractions
• Greater speed & force of contractions, due to higher speed of nerve transmission
• Increased flexibility reduces risk of injury, due to increased extensibility of tendons & ligaments

• Increase speed of removal of lactic acid & carbon dioxide, that raise acidity levels, affect pain receptors due to oxygen rich blood
• Decreased risk of DOMS, muscle pain experienced 24-48 hrs after exercise due to microscopic tears in muscle fibres.

Occur through: inactive lifestyle, general wear & tear, natural ageing process or due to injury, either an acute impact or overuse & repetition

Low bone density & deterioration of bone tissue. Severely weakens & makes prone to fractures. Hip, spine, wrist most common. Older gen & women more at risk. Any sudden bump or fall would cause fracture.

Inactivity, serious injury leading to sedentary lifestyle or immobility.

Best defence is build strong & healthy bones. Bone has peak bone density a high one minimises risk. High impact, resistance & strength & weight bearing activities have positive effect & long term reduced risk.

Injuries in children common cause its weak. Injuries fractures caused by sudden force through bone in competitive, contact or impact sports. Also result from overuse by repetitive practice of specific skill.

Most result from impact injuries e.g sprains or dislocations. Also due to inflammatory or degenerative conditions.

Degenerative. Loss of articular cartilage at ends of bones. Affects large weight bearing joints. friction between bones can lead to bone spurs. Causes pain, swelling & reduced motion in joints.

Small projections of bone form around joints due to damage to surface. Limit movement & cause pain in joint.

Major injury to joint & being overweight

Increases areobic capacity, manages weight & reduces body fat so reduces mechanical strain on joints. Also improves joint stability & joint mobility is maintained or even improved.

Deeper joints most stable. More & stronger ligaments mean greater stability but make them prone to stretching or even snapping. Good muscle tone also improves.

Strengthens articular cartilage, ligaments & surrounding muscles. No exercise ligaments shorten & become less elastic, muscle tone lost& will shorten & reduce flexibility. Reduce synovial fluid being produced but impact & contact sport can lead to injury.

Skeletal muscle for posture, trunk area. Greater muscle tone in muscles around trunk mean better posture & core stability. Prevents excess pressure on lumbar spine which causes lower back pain.

Controls body weight, less strain on muscles & joints, easier to maintain alignment. Strength/Swiss ball training increases postural muscles. Improve alignment of spine & minimises risk of lower back pain.

Body moves in straight or curved line all parts moving same distance in same direction at same speed.

Body or part of body moves in a circle or part of a circle about a particular point called axis of rotation.

Combination of linear & angular motion.

Performer in toboggan travelling straight down the hill.

Female gymnast doing circles

Approach run of javelin thrower.

Push or pull that alters or tends to alter the state of motion of the body.

• Causes body at rest to move
• Causes moving body to change direction, accelerate or decelerate
• Changes an objects shape

Ball will remain still until footballer kicks it.

Goalkeeper saves a goal & therefore pushes the ball in a opposite direction.

Footballer will apply large force to the ground when running to accelerate.

If goal scored net will make ball decelerate

Where a players boot meets a ball it'll slightly deform

Reluctance of a body to change its state of motion

Rate of change of velocity

Body remains in a state of rest unless acted upon by external forces.

When a force acts on an object the rate in change of momentum is proportional to size of force & takes place in direction in which force acts.

For every action there's an equal & opposite reaction.

Amount of material of which it's made.

Point at which body is balanced in all directions

• Position of centre of mass
• Position of line of gravity
• Size of area of support

How difficult it is to disturb a body from a balanced position

Line extending from centre of mass directly down to the ground

Line of action of the force passes through the body's centre of mass. Known as direct force.

Line of action of force passes outside body's centre of mass. Known as eccentric force.

With oxygen

Without oxygen

Heart, vascular & respiratory systems

Ability to supply & use oxygen to provide energy for prolonged periods. Limited by efficiency of aerobic systems.

Blood depleted of oxygen

Blood saturated with oxygen

Takes in O2 and removes co2 in lungs.

Receives blood from lungs & acting as double pump forces blood around vascular system to lungs & to body tissues/muscles.

Blood & blood vessels which transport & direct O2/co2 to & from lungs heart & body.

Thoracic cavity underneath ribs in chest.

Consists of 2 pumps separated by septum. Pumps consist of atrium & ventricle which make up 4 chambers of the heart.

Upper, low pressure chambers. Collect & store blood before pumping it into ventricles. Muscular walks relatively thin.

Lower high pressure chambers. Generate force/ pressure to pump blood to whole body. Walls thick as greater force needs greater contraction. Left ventricle thicker as pumps to whole body.

• Control forward direction of blood flow through heart
• Prevent back flow of blood within heart chambers

• Separate atria from ventricles.
• Right- tricuspid
• Left- bicuspid

• Right-pulmonary, exits right ventricle to pulmonary artery.
• Left- aortic- exits left ventricle to aorta.

Links to lungs

Deoxygenated blood from body to right atrium

Deoxygenated blood from right ventricle to lungs.

Oxygenated blood from lungs to left atrium

Oxygenated blood from left ventricle to whole body.

Left & right branches from aorta encircle supply heart muscle with oxygen & glucose.

Alongside coronary arteries drain deoxygenated blood directly back to right atrium via coronary sinus

Events of one heartbeat

Cardiac impulse initiated from SA node.

Impulse travels through left & right atrial walls causing both atria to contract. Ventricles insulated from atria & can't be stimulated.

Cardiac impulse reaches & activates AV node in right atrium, passes impulse down into bundle of HIS.

AV node helps delay impulse allowing contraction of atria to finish before ventricles begin to contract.

Bundle if HIS splits into left & right branches.

Spreads impulse down to bottom of heart & then up & around walls of both ventricles walls via a network of purkinje fibres causing both ventricles to contract.

The ventricles relax & it's then repeated with next cardiac impulse initiated from SA node

At rest 1 cycle lasts 0.8 secs & repeats 72 times a minute. 2 phases contraction & relaxation of heart muscle.

0.5 secs relaxation phase

0.3 secs contraction phase

Both atria fill with blood. AV valves closed.

Atrial blood pressure rises above ventricle pressure.

Rising blood forces AV valves open & blood passively passes into both ventricles. Semilunar valves closed.

Both atria contract, actively forcing the remaining atrial blood into both ventricles.

Semilunar valves remain closed.

Both ventricles contract increasing ventricular pressure.

Aortic and pulmonary valves forced open. AV valves close.

Bloo forced out into: aorta to body tissues/muscles (stroke volume) & pulmonary arteries to lungs.

Diastole of next cardiac cycle begins. SL valves close preventing back flow of blood from aorta and pulmonary arteries.

Resting heart rate below 60

Increase in size of heart muscle wall.

Number of times heart ventricles beat in one minute. Average 70-72 BPM. Maximal 220- age.

Indicates high level of endurance fitness. HR below 60 (bradycardia) is due to increase in stroke volume due to hypertrophy.

Amount of blood ejected from both ventricles in one beat. Determined by hearts ability to fill and empty at each beat.

• Amount of blood ejected from ventricles per minute. Average resting value 5L.
• Calculation: SVxHR=Q

Exercise performed at an intensity below an athletes maximal aerobic capacity.

When an athlete runs SV increases linearly as the running speed/intensity increases up to 40-60% of maximal running speed. After this it reaches a plateau as maximal SV values are reached. 40-60% values increase to 120-140ml per beat.

• Venous return-SV increases due to increase in blood returning to the heart.
• Ventricles ability to stretch further and enlarge

• Greater EDV provides greater stretch on heart walls
• Greater stretch increases force of ventricular systole.

• -increase above resting values before exercise starts.
• - increases as intensity increases
• - increases with intensity but slows prior to maximal values
• -decreases as intensity decreases
• -increases with intensity but reaches plateau
• -decreases rapidly immediately after exercise.

Increases directly in line with exercise intensity. Increases to supply the increased demand of oxygen to the working muscles.

Additional oxygen consumption during recovery above that usually required when at rest

Found in Medulla oblongata. Primarily responsible for maintaining the heart. Controlled by autonomic nervous system, under voluntary control & consists of sensory & motor nerves from either sympathetic or parasympathetic nervous system.

Nerves increase heart rate

Nerves decrease heart rate.

Stimulate muscle tissue causing motor movement.

Transmit information to central nervous system.

Sense organs that pick up stimuli which are relayed to the brain.

Either initiates sympathetic or parasympathetic nervous systems to stimulate SA node.

• -neural control
• -hormonal control
• -intrinsic control

• CCC stimulated by following sensory receptors:
• - proprioreceptors
• - chemoreceptors
• - baroreceptors

In muscles, tendons & joints. Inform CCC that movement activity has increased. Increases HR & SV

Sensitive to chemical changes in muscles, aorta & carotid arteries. Inform CCC lactic acid & co2 levels have increased & oxygen & PH levels have decreased. Increases HR.

Sensitive to stretch within blood vessel walls, in aorta & in carotid arteries. Inform CCC blood pressure has increased. Decrease HR but neutralised due to demand for O2

Before & during exercise adrenaline released from adrenal glands into bloodstream stimulates SA node increase HR & strength of ventricular contraction in turn increases SV.

• - temperature increases, therefore increasing speed of nerve impulses, which increases HR.
• - venous return increases directly increases EDV & therefor SV & HR

• - temperature and HR decreases
• - venous return decreases therefore SV & HR decrease.

SV dependent upon venous return = any increase in VR means increase in SV & Q.

Take oxygenated blood away fro heart to tissues/muscles

Bring blood directly in contact with tissues where oxygen & CO2 are exchanged.

Take deoxygenated blood back towards the heart.

• - pocket valves
• - muscle pump
• - respiratory pump
• - smooth muscle
• - gravity

One way valves in veins prevent back flow of blood & direct blood towards the heart.

Veins situated between skeletal muscles, when contracting & relaxing help squeeze blood back towards heart.

Dying exercise breathing deepens causes pressure changes in thorax & abdomen. Increase pressure in abdomen squeezes large veins in that area helping force blood back towards heart.

Contraction & relaxation of smooth muscle in middle layer of vein walls also helps push blood through veins and towards heart.

Blood for upper body is aided by gravity and it descends to heart.

VR requires force to push blood back towards heart. If insufficient pressure blood will sit in pocket valves in veins. Skeletal & respiratory pump needed during & after exercise to prevent.

• 15-20% to muscles
• 80-85% to body organs

• 80-85% working muscles
• Decrease % to body organs, blood to brain maintained, increase blood supply to skin during light work decrease as intensity increases.

Vasomotor control centre in medulla oblongata stimulates sympathetic nervous system to either vasodialate & vasoconstrict the pre capillary sphincters & arteriolis supplying muscles & organs. Receives information from chemoreceptors & baroreceptors.

VCC increases sympathetic stimulation which vasoconstricts the arteriols and pre capillary sphincters. Both decrease and distributes blood flow away from non essential capillaries of the organs.

VCC decreases sympathetic stimulation which vasodilates the arterioles and pre capillary sphincters. Both increase & distribute blood flow towards capillaries of working muscles.

Widening of arterial blood vessels

Narrowing of arterial blood vessels

• 97% transported within protein haemoglobin & packed with red blood cells as oxyhaemoglobin.
• 3% within blood plasma.

Each molecule can carry 4 molecules of O2. It'll combine with o2 when it's available & gives it up to tissues when needed.

Level of acidity. Low PH = High acidity & vice versa.

• 70%- Combines with water within red blood cells as carbonic acid
• 23%- combines with HB as carbahaemoglobin
• 7%- dissolved in plasma.

• -Prolongs duration of anaerobic and especially aerobic activity.
• -Delays anaerobic threshold
• - Increases possible intensity/work rate of activity.
• -Speeds up recovery during and after exercise.

Cigarette smoke contains carbon monoxide. HB has higher affinity to CO & so combines with it in preference to O². Reduces HBO² to lungs and therefore performers maximal O² uptake.

• Gradual increase in blood flow/Q due to VSM via:
• -Vasoconstriction of arteriloes/pre capillary spincters to organs decreasing blood flow to them & thereby increasing blood flow to working muscles.
• -Vasodilation of arterioles & Pre capillary sphincters increase blood flow to working muscles.
• -Increase temp causing more rapid increase in transport of enzymes. Decreases blood vicosity flow, increase dissociation of O² from haemoglobin in muscle tissues.
• -Decrease onset of OBLA.

• - Keeps metabolic activity elevated, gradually decreses HR and repiration
• - Maintains respiratory/muscle pumps (prevent blood pooling & maintain venous return)
• - Maintains blood flow to supply oxygen, maintaining BP
• -Keeps capillaries dilated to flush muscles with oxygenated blood, increases removal of blood & muscle lactic acid & CO²

contractive force of heart ventricles provides pressure to force blood through arteries. After leaving the heart this force is applied from the blood against the arterial blood vessel walls.

Pressure exerted by blood against the blood vessel walls. BP=  Equation = Q x resistance. any increase in Q leaving the heart will cause Bp to increase.

Systolic blood pressure represents the highest arterial pressure & reflects ventricular systole.

Blood pressure represents lowest arterial pressure & represents ventricular diastole.

Friction of blood cells as the travel against blood vessel wall, termed viscosity. Arteriol blood vessels can vasodialate & vasoconstrict due to smooth muscle. Body can decrease Bp by dilating & increase Bp by constricting. This is how it regulates Bp. 

• Measured using a sphygmomanometer
• 1. wrap cuff round bent upper arm & inflate to 180mmHg, no sufficient pressure for blood to pass cuff. Stethoscope is placed over brachial artery
• 2.Air pressure released & pressure reading noted on first audible noise- Systolic pressure
• 3.Continue to release & note when sound disappears- Diastolic.

Increases in line with exercise intensity & ill plateau during sub-maximal exercise. May decrease gradually if sub-max intensity is prolonged.

Changes little during sub-max work, irrespective of intensity however during gross muscle activities localised muscular diastolic Bp may fall. May increase a little as exercise intensity reaches max levels.

Lifting heavy weights during strength training involves isometric work. Blood vessels are blocked by sustained static muscle contractions. Restricts blood flow through arterial & venous blood vessels & increases vascular resistance. Can cause an increase in both systolic and diastolic Bp as blood flow builds up behind this area of constriction. Resting Bp tends not to change after training some cases it may decrease.

This often occurs during isometric/resistance training. It's where the athlete attempts to breath out while the mouth, nose & glottis are closed. Not recommended for people already prescribed as hypertensive.

Systolic Bp decrease temporarily below pre exercise levels for up to 12 hours. Diastolic pressure also remains low often below normal resting levels. May have important application in promoting healthy lifestyle may help lower Bp as exercising regularly can reduce Bp.

• Mixed evidence. Most likely due to: CV adaptions, diet, smoking, weight & stress.
• -Resting Bp may reduce with endurance training
• -Resting Bp lowered in people already mild/moderate hypertension
• -Endurance training can reduce risk of high Bp
• -Bp changes little during sub-max work rate
• -Although resistance/isometric training significantly increases both systolic & diastolic Bp it doesn't increase resting Bp.
• -Little or no changes to those who are already max hypertensive.

Hypertension only present if high blood pressure prolonged. 160/95mmHg is commonly regarded as hypertension. Interrupts control system for maintaining a normal Bp if not treated can cause harmful effects. Generally supported exercise reduces risk & indirectly reduces Bp by reducing obesity & stress.

• -Increase workload on heart
• -Increase/accelerating atherosclerosis
• -Increasing/accelerating arteriosclerosis
• -Arterial damage increase risk of stroke & congestive heart failure.

Single largest cause of death in Western world. More likely when sedentary lifestyle is followed. Four CHD diseases show a cause & effect relation where the two blood vessel diseases can lead to the two heart related diseases.

Loss of elasticity, thickening/hardening of arteries, reduces efficiency to vasodialate/constrict therefore regulates Bp & VSM. Smoking accelerates hardening & narrowing process ahead of natural aging process. Younger you start earlier the process will start & blood clots 2-4 times more likely.

Form of arteriosclerosis involves changes in lining of arteries high levels of cholesterol & fat deposits accumulate within arterial walls forming fatty plaque, leading to progressive narrowing of the lumen which increases likelihood of blood clots. Restrict blood flow & lead to high Bp.

Partial blockage of coronary artery causing severe chest pain. Occurs when inadequate O²/Blood flow to heart muscle wall. Arteriosclerosis & Atherosclerosis in coronary arteries deprives areas of the heart of O²/blood. Can occur any time especially during exercise.

More severe/sudden or total restriction in O²/blood supply to part of heart muscle wall. Usually permanent damage more likely result of blood clots from larger coronary arteries that get stuck in smaller ones & plug them shut. Death can result.

CHD 2-3 times more likely in people with sedentary lifestyle. Inactivity is a major risk factor almost doubling risk of fatal heart attack. Lifelong involvement in physical activity will maintain significant protection against CHD.

• -Improve heart hypertrophy, pumping capacity & circulation; vascularisation; increase capacity/size of coronary circulation
• -Decrease blood fibrinogen, blood clotting & blood viscosity, improving blood flow to coronary circulation
• -Decrease blood lipids which can be deposited on arterial walls
• -Decrease LDL which are deposited on vessel walls
• -Increase HDH remove cholesterol from arterial walls
• -Lower Bp & reduce risk hypertension
• - Reduce obesity helps against hypertension & control diabetes
• -Alleviate tension/stress reducing hypertension
• Net effect- Reduce arterial damage/disease which in turn reduces risk of Angina/Heart attack

• -Stop smoking & improve diet stimulus to healthy lifestyle
• -Cessation of speeding reduces speeding up of arteriosclerosis
• -Proper diet reduces: obesity, blood diet, glucose, body fat.
• Summary- Physical activity & weight control offer greatest protection against CHD.

Intensity can be low but higher intensity exercise will provide further protection. WHO's & ACSM recommend individuals engage in adequate levels of physical activity throughout their lives.

• 1. Pulmonary ventilation- breathing of air in and out of lungs.
• 2. External respiration- exchange of oxygen & carbon dioxide between lungs and blood.
• 3. Internal respiration- Exchange of oxygen & carbon dioxide between blood and muscle tissues.

Breathing through noise has advantages of moistening, filtering & warming up air aided by ciliated mucus lining & blood capillaries within the walls of respiratory structure before it enters the lungs improves exchange of CO² & O². From noise & mouth air passes through pharynx, larynx & trachea.

Lobes are diversions of lungs right lung has 3 lobes left lung has 2 for the heart. Left & Right bronchi branch further forming bronchioles which branch into each lobe of the lungs. Bronchioles terminate into alveoli ducts, leading to alveoli sacs or grape-like clusters or tiny air sacs. Each individual air sac is called alveolus & is the actual site for gas exchange.

• -Form a vast surface area for gaseous exchange to take place.
• -Have a single-cell layer of epithelial cells, reducing the distance for gas exchange with:
• - Moist lining of water helping dissolve & exchange oxygen
• -Extensive network of narrow alveoli capillaries producing short diffusion path.

Doubled walled sacs in lungs consisting of 2 membranes filled with pleural fluid, reduces friction between lungs & ribs when breathing. Outer layer attaches to ribs & inner layer to lungs, ensures lungs move with chest as it expands & relaxes.

• -Muscles Actively constrict or passively relax to cause:
• -Movement of the ribs, sternum & abdomen which causes:
• -Thoracic cavity volume to increase or decrease which in turn causes:
• -Lung air pressure to increase or decrease which causes
• -Inspiration or Expiration - air breathed in or out

Volume of air inspired or expired per breath. Aprox 500ml at rest.

Number of breaths taken in one minute. Aprox 12-15 at rest.

Volume of air inspired/expired in one minute. Equation- TV x F=VE. Aprox 7.5L/min at rest.

respiration increase in line with intensity to supply increasing oxygen demands of working muscles. Both rate (F) & depth (TV) increase therefore increasing VE. TV & F increase at low intensity to increase VE but during maximal work only F increases as it's not efficient to increase TV towards maximal value due to time/effort it takes.

Exchange of gas namely O² and CO². Relies on diffusion. Diffusion is the movement of gases from an area of high pressure to an area of low pressure. Difference between the high & low pressures is called the diffusion gradient. Bigger the gradient the greater the diffusion & gaseous exchange that takes place.

PP of gas is the pressure it exerts within a mixture of gases. Gases always move from areas of high PP to areas of low PP.

• Inspiring air entering the alveoli in the lungs had a high PP of O² & a low PP of CO² compared with deoxygenated blood in the alveoli capillaries which has low PP of O² and high PP of CO². These two pressure gradients cause diffusion of:
• 1. Oxygen from alveoli into the blood of the capillaries to be transported back to the left atrium
• 2. Carbon dioxide from the capillary blood into the alveoli of the lungs where it is expired.

Red pigment in muscle that stores O².

Oxygenated blood is pumped around systemic circulation until it reaches the capillaries surrounding the body tissues/muscles. Capillary blood has high PP of O² and low PP of CO² compared to tissue muscle cells having used their oxygen for energy production & given of CO² as a by product. O² passed into the muscle cells is transferred from the haemoglobin in blood capillaries to the myoglobin within the muscle tissue, which both stores & transports the O² to the mitochondria where it's used for energy production.

Both internal and external increase during exercise in order to increase the supply of oxygen.

Informs us of amount of haemoglobin saturated with oxygen. Haemoglobin fully bound with oxygen is termed saturated or association whereas oxygen unloading from haemoglobin is called disassociation.

Higher the PP in oxygen, higher the % of oxygen saturation to haemoglobin. During exercise association needs to be made in the lungs so that blood can carry oxygen to the muscle capillaries so it can dissociate & upload the oxygen to the muscle tissue to provide energy for work.

Deoxygenated venous blood returning to lungs from right ventricle has higher PP of CO² & lower PP of O². Alveolar air has high PP of O² & low PP of CO². Increases diffusion gradient of both O² and CO² between alveoli-capillary membrane resulting in both quicker & greater amount to gaseous exchange. High PP of O² in alveoli & low PP of O² in capillaries ensures haemoglobin is almost fully saturated with O². O² & CO² will diffuse across until PP are equal.

• 4 factors that increase dissociation of oxygen from Hb in blood capillaries to the muscle tissue are:
• 1.Increase In blood & muscle temperature.
• 2.Decrease PP O² within muscle, increasing oxygen diffusion gradient
• 3.Increase PP of CO², increasing CO² diffusion gradient
• 4.Bohr effect - increase in acidity (lower PH)
• All these increase during exercise the effect is that working muscles:
• -Generate more heat when working
• -Use more O² to provide energy, lowering PP oxygen
• -Produce more CO² as by product
• -Increase lactic acid levels & muscle/ blood acidity
• This all therefor delays fatigue & increases possible intensity/duration of performance.

• 1.Anticipatory rise-prior to exercise in all 3 intensities due to release of hormones which stimulate RCC
• 2. Rapid rise in VE- Start of exercise due to neural stimulation of RCC by muscle & joint proprioceptors
• 3. Slower increase/Plateau- In Sub-Max exercise due to continued stimulation of RCC
• 4.Continued but slower increase- In VE towards max values due to continued stimulation of receptors
• 5. Rapid increase in VE- All 3 intensities when exercise stops
• 6. Slower decrease- Towards resting VE More intense the exercise the longer it takes to remove  by products.

Regulates pulmonary respiration located in Medulla Oblongata. Responds in conjunction with CCC & VCC.

Respiratory muscles under involuntary neural control. two areas inspiratory & expiratory centres, responsible fore stimulation of the respiratory muscle at rest & during exercise

• Inspiratory centre- Responsible for rhythmic cycle of inspiration & expiration to produce a respiratory rate of 12-15 breaths a minute:
• a) Inspiratory centre sends impulses to respiratory muscles via:
• -Phrenic nerves to diaphragm
• -Intercostal nerves to external intercostals.
• B) When stimulated these muscles contract, increasing the volume of the thoracic cavity causing inspiration.
• C) when the stimulation stops the muscles relax decreasing the volume of thoracic cavity causing expiration.
• 2. Expiratory centre - Inactive during quite/ resting breathing expiration is passive as a result of the relaxation of the diaphragm & external intercostals.

• Pulmonary ventilation increases during exercise increasing both depth & rate of breathing regulated by:
• 1. Inspiratory centre which:
• a) Increases stimulation of the diaphragm & external intercostals
• b) Stimulates additional inspiratory muscles for inspirations, increase force of contraction therefore depth of inspiration
• 2. Expiratory centre- Stimulates expiratory muscles internal intercostals, rectus abdominus & oblique's - causing forced expiration which reduces duration of inspiration.
• Inspiratory centre immediately stimulates inspiratory muscles to inspire.
• Net effect: Exercise intensity & rate of breathing increase, depth of breathing decreases.

• Chemoreceptors- from Medulla & carotid arteries send info to inspiratory centre on:
• a) Increase in PP of CO²
• b) Decrease in O² PP
• c) Decrease in Ph
• 2. Proprioceptors located in muscles & joints send info to inspiratory centre on motor movement of active/working muscles.
• 3. Thermoreceptors - Info to inspiratory centre on increase in body temperature
• 4. Baroreceptors - Located in lungs stretch receptors send info to expiratory centre on the extent of the lung inflation during inspiration. 

Exposure to high altitude has significant effects on performance. at high altitude PP O² is significantly reduced. Decreases efficiency of respiratory process & consequently negates performance.

Anything that improves performance

Main rationale of altitude training is that the body adapts by increasing release of EPO, Stimulates increase in red blood cells and increases capillerisation. Primarily vascular adaption. Upon return to sea level this increases VO² max & this increases aerobic based performance.

Most research shows performing at high altitude doesn't have many positive effects on performance at sea level. If a performer is competing at a high altitude acclimatisation is essential or inspiratory muscle training in a 4-6 week block will help overcome huge increase in respiratory effect.

• - Increase Alveoli, increases surface area for diffusion
• -Increases elasticity of respiratory structures
• -Increases longevity of respiratory structure of efficiency

• -Increase efficiency/economy of respiratory muscle, reduces O² cost of respiratory muscles, reducing respiratory fatigue.
• -Increase in strength, power & endurance of respiratory muscles.

• - Lung volumes & capillaries change little
• -TV can increase during max exercise
• -Respiratory frequency decreases at rest/sub max activity but can increase during max work.
• -Max VE can significantly increase from around 120Lmin to 150Lmin after training.

• -Unchanged at rest & sub max exercise
• -Increased in pulmonary diffusion in maximal activity
• -Increased VO² diff at max activity

maximal oxygen consumption.

Start of anaerobic work.

• Net Effect- VO² max & lactate threshold increase.
• Main performance benefits are:
• -Areobic performance during higher/max work rate is increased & prolonged
• -More effect with aerobic endurance activity
• -Reduces effort in Sub max work so increases duration of performance
• - More efficient & healthy respiratory system. Promotes lifelong involvement.

Characterised by a reversible narrowing of airways with common symptoms of: hyperirritability of airways, coughing, wheezing, breathlessness or mucus production. Occurs in response to trigger or allergen

Measured by inhaling into spirometer & measuring exhaled volume of air. If individual improves their expiratory volumes after inhaling bronchodilator treatments they're considered asthmatic.

major trigger is drying of respiratory airways normally due to water loss from the airway surfaces causing an inflammatory response & triggering constriction of airways. Bronchoconstriction often brought on shortly after exercise. Link between exercise & asthmatic symptoms is termed exercise induced asthma (EIA). Other common allergies including asthma are: Exhaust fumes, air pollutants, dust, hair & pollen. EIA is particularly high in cold whether sports as cold air is dryer than warm air.

• -Normally treated by inhaled medication - Bronchodilators which are reliever medication that relax muscles around airways taken before exercise or in response to symptoms
• -Corticosteroids preventer medication which supress chronic inflammation & improve pre exercise lung function. Reduce sensitivity of airways structures.

• -Warm up at least 10-30 minutes at 50-60% max HR provides refractory period for up to 2 hour after which exercise is possible without triggering EIA
• -Dietary modification, reduce salt, increase fish oils & vitamins C & E. Also shown to help reduce inflammatory response to EIA.
• - Caffeine also Bronchodilator but IOC limit is 12mg/ml.

Increased respiratory effort is major principle symptom of breathlessness. Strong relationship between strength of respiratory muscles & sense of respiratory effort. IMT can't cure asthma but has shown to increase air floe & alleviate breathlessness. For competitive athletes it's a non pharmacological approach & may be their only option. IMT reduces use of medication & improves quality of life. 'POWERbreath' is available on prescription shows IMT well established drug free method of managing asthma. stop conditions that trigger in first place. Restrain from endurance training & avoid exercising in cold whether.

• -Impairs natural development in teenagers
• -Impairs lung function & diffusion rates
• -Increased damage & likelihood of respiratory diseases, infection & symptoms below:
• -Asthma
• -Irritates/damages respiratory structures: Cilia, alveoli, bronchioles, trachea & larynx
• -Narrows/constricts respiratory airways
• -Emphysema (decreases elasticity of respiratory structures)
• -COPD ( Chronic obstructive pulmonary disease)
• Cancers of respiratory structures
• -Shortness of breath, coughing, wheezing & mucus/phlegm in the lungs.

Decreases efficiency of the respiratory system to take in & supply O² to out working muscles. Works against positive long term adaptations from involvement in physical activity. Mostly effects endurance based exercise, especially high intensity max activity but reduces respiratory health in general.