Physiology

Planes of movement 

Saggital plane

• Lies vertically, dividing body left and right.
• Flexion, extension, dorsi-flexion and plantar-flexion occurs on this plane.

Frontal plane

• Lies vertically, divides body into front and back.
• Abduction, adduction occurs here.

Transverse plane 

• Lies horizontally, divides body into upper and lower parts.
• Horizontal flexion/extension and rotation occurs here.

Joints- hinge, pivot, gliding, ball and socket, condyloid.

• Origin: point of muscular attachment to stationary bone e.g. biceps brachii origin is scapula in a  bicep curl.
• Insertion: point of muscular attachment to a moveable bone, gets closet to origin during muscular contraction e.g. biceps brachii insertion is on radius during an arm curl.

Antagonistic muscle action

• Agonist: muscle responsible for movement at a joint (prime mover) e.g. biceps brachii in flexion.
• Antagonist: muscle opposing to provide a resistance for co-ordinated movement e.g triceps.
• Fixator: muscle stabilisng one part of the body whilst the other causes movement- rotator cuff.

Muscle contraction 

• Isotonic: muscle changes length either concentrically (shortens under tension) or eccentrically (lengthens producing tension).
• Isometric: muscle contracts but doesn't change length e.g. holding a free weight, handstand.

Ankle

• Hinge joint with the articulating bones: tibia, fibula and talus.
• Movement on the saggital plane: dorsi-flexion and plantar flexion.
• Dorsi-flexion agonist =tibialis anterior and plantar-flexion agonist =gastrocenemius/soleus.

Knee 

• Hinge joint with the articulating bones of femur and tibia.
• Movement on saggital plane: flexion and extension.
• Agonist for flexion: biceps femoris group and agonist for extension is rectus femoris group.

Hip

• Ball and socket joint with articulating bones: pelvic girdle and femur.
• Movement on saggital, frontal and transverse plane: flexion, extension, abduction, adduction.
• Flexion agonist- illopsoas and extension agonist-gluteus maximus.
• Abduction agonist-adductor longus and abduction agonist is gluteus medius.

Shoulder

• Ball and socket joint with articulating bones of humerus and scapula.
• Movement on saggital, frontal and transverse plane: flexion, extension, adduction, abduction, horizontal flexion/extension and medial/lateral rotation.
• Flexion agonist-anterior deltoid and extension agonist-posterior deltoid.
• Adduction agonist-lattisimus dorsi and abduction agonist-middle deltoid.

Elbow

• Hinge joint with articulating bones of humerus, radius and ulna.
• Movement on saggital plane: flexion agonist-biceps brachii, extension agonist- triceps brachii.

Wrist

• Condyloid joint with articulating bones of radius, ulna and carpals.
• Movement on saggital plane: flexion agonist- wrist flexors and extension agonist- wrist extensors.

The Motor Unit and Skeletal muscle contraction

• Motor unit is made up of motor neuron and its muscle fibres: carries nerve impulses frrom the brain/spinal chord to muscle fibres to cause muscular contraction.
• Relies on action potential to conduct the impulse as electrical charge goes down axon to motor-end plates through neuromuscular junction.
• Neurotransmitter needed for action potential to cross synaptic cleft.
• Motor unit creates an action potential that reaches a threshold charge, all muscle fibres will contract simulataneously with force but it if doesn't, no fibres contract= ALL OR NONE LAW.

Muscle fibres and exercise intensity 

• Strength of contraction depends on number/size of motor unit recruited by the brain.
• E.g. stronger contractions send impulses down more motor units.
• Small motor neurons stimulate few small muscle fibres so motor unit produces a small force over a long time, resisting fatigue.
• Large motor units stimulate many large muscle fibres to produce a fast/large force over a short period of time but fatigue's quickly.

Muscle fibre types

Type 1 Slow oxidative (SO)

• High myoglobin stores to process O2 in mitochondria.
• Small force due to low PC stores but high fatigue resistance e.g. long distance runner.
• Red in colour- high capillarly density so efficient O2 delivery.

Type 2a Fast Oxidative Glycolytic (FOG)

• Moderate mitochondria/myoglobin stores so moderate fatigue resistance.
• High PC stores so fast speed of contraction e.g. 800m or netball player.

Type 2b Fast Oxidative Glycolytic (FG)

• Low mitochondria/myoglobin stores so low resistance to fatigue.
• White- low capillary density so low O2 delivery e.g sprinter, long jump.
• Large PC stores so large force/rapid energy production.

Muscle fibre types and recovery rates 

• Sub-maximal aerobic work recruits type 1 as they contract intermittently, they recover and are available within 90 seconds.
• Aerobic training work-to-relief ratios will be 1:1 to maximise use of type 1.
• Aerobic training can be performed daily as it's low-intensity and increases blood-flow.
• Type 2b are recruited near muscle exhaustion/maximal efforts.
• Type 2b causes eccentric muscle damage: DOMS (24-48 hours later)
• Maximal weight training ratios are high 1:3 so get 3 mins of rest with few reps.
• Type 2b takes 4-10 days to fully recover.

ATP- Adenosine Triphosphate

• High-energy compound and only immediately available energy source for muscular contraction.
• ATP provides 2-3 secs of energy: ATPase stimulates bond to break causing an exothermic reaction for muscular contraction, forming ADP and one phosphate.
• ATP resynthesis: ADP + P + energy = ATP (endothermic reaction).

ATP-PC system

• High-intensity exercise after first 2secs of activity depletes ATP stores.
• ATP levels fall, ADP + P rises stimulating creatine kinase to breakdown PC.
• PC broken down anaerobically in sarcoplasm: for every 1 mole of PC broken= 1 mole of ATP.
• Coupled reaction as breakdown of PC releases 1 phosphate + energy to resynthesise ATP.
• PC stores are small and exhausted quickly e.g. 8-10 secs when doing anerobic work.
• Doesn't require oxygen and creates no by-products.
• e.g. 100m runner, shotput, javelin throw, weightlifter.

Glycolytic/Lactic acid system

• High intensity after first 10 ses of actibity exhausts PC stores/ATP falls= ADP + P rises.
• Anaerobic glycolysis: PFK catalyses breakdown of glycogen to glucose, makes pyruvate but provides 2 ATP for energy.
• If glucose levels fall, GPP converts glycogen into glucose to maintain its concentration.
• No O2 available to continue energy extraction from pyruvate: LDH released converting pyruvate to lactic acid (slows ATP resynthesis as it inhibts enzymes due to ph decline).
• Causes OBLA which can be inhibited by buffering capacity.
• Don't need to wait for O2 delivery but low energy yield and lactic acid made e.g. 200m sprint.

Aerobic system

• Aerobic glycolysis: PFK converts glucose into pyruvate in sarcoplasm= 2 moles of ATP.
• GPP converts glycogen into glucose. Co-enzyme A produces Acetyle CoA.
• Krebs cycle: Acetyl CoA + oxaloacetic acid= citric acid which is oxidised by reactions.
• CO2, H2 + energy resynthesise 2 moles of ATP in the matrix of the mitochondria.

• ETC: H2 atoms carried along cristae of mitochondria by NAD/FAD, splitting into H+ and electrons, the H2 ions are then oxidised and removed as water.
• Pairs of H2 electrons carried by NAD release energy to resynthesise 30 ATP and FAD makes 4 moles of ATP= 34 ATP.
• Energy yield of 38 ATP so highly efficient for long-duration low-intensity e.g. running, cycling.

Aerobic system and FFAs

• Endurance athletes want to reserve glycogen stores for higher-intensity sections.
• Betaoxidation: fats can be metabolised aerobically as FFAs: lipase converts triglycerides into FFAs and glycerol.
• FFAs converted into Acetyl CoA- follow same path through Kreb's cycle and ETC.
• FFAs produce more Acetyle and more energy but need more O2 to metabolise so activity intensity must remain low.

Energy continuum 

• Relative contribution of each system to overall energy production, depends on intensity/duration.
• ATP/PC predominant for very high-intensity (2-10secs): makes up 99% of energy for ATP resynthesis.
• Glycolytic system predominant for high-intensity (10secs-3mins): makes up 60-90% energy for ATP resynthesis.
• Aerobic system predominant for low-moderate intensity (+3mins): makes up 99% energy for ATP resynthesis.

Intermittent exericise

• When intensity alternates during intervals between work and relief or during breaks of play.
• Threshold is point at which the predominant system moves to another system.
• ATP-PC/glycolytic threshold: sprint to catch ball then regaining possession for 1min.
• Glycolytic/aerobic threshold: jog to half way after a try is scored.

Recovery periods 

• PC stores replenish quick so timeouts are essential.
• O2 in myoglobin can be relinked within 3 mins of rest/low intensity.
• Prolonged high-intensity bouts cause OBLA but with sufficient relief/O2, it can be removed.
• During intermittent exercise, lactic acid fluctuates so replenish w/glycogen or water.

Fitness level

• High VO2 max/aerobic capacity= efficient CV system so can perform at high intensity.
• High buffering capacity so muscles are flushed of lactate and oxygenated.
• Can use FFAs to conserve stores of glycogen so increases duration of performance.

Additional factors affecting contribution of systems

• Position: midfielder will use glycolytic mostly whereas goalkeeper will use ATP/PC.
• Tactics: man on man marking will raise intensity so needs more aerobic energy.
• Competition level: easy match will be lower intensity so use aerobic more.
• Game structure: field games are longer so use aerobic more, courts use anaerobic more.

Cardiovascular system 

• Heart is a dual pump working in 2 circuits: pulmonary carrying deoxygenated blood to lungs and oxygenated blood to the heart and systemic carrying oxygenated blood to body and deoxygenated back to the heart.
• Left side of cardiac muscle contracts with more force to circulate O2 blood from lungs through systemic circuit to body.
• Right side contracts to circulate deoxygenated blood from body through pulmonary circuit to lungs.

Path of blood through the heart

• Left side: O2 blood at lungs- pulmonary vein- left atria- bicuspid valve- left ventricle- aorta- muscles and organs.
• Right side: deO2 blood from body- vena cava- right atrium- tricuspid valve- right ventricle- pulmonary artery- deO2 blood to lungs.

The Conduction system 

• 1- SA NODE: pacemaker in right atrial wall generates impulse to make atrial walls contract.
• 2- AV NODE: delays impulse for 0.1 secs to allow atria to stop contracting, relaying impulse to Bundle of His.
• 3- BUNDLE OF HIS: splits impulse into 2 to distribute into each separate ventricle.
• 4- BUNDLE BRANCHES: carry impulse to the base of each ventricle.
• 5- PURKINJE FIBRES: distribute impulse through ventricle, making them contract.
• Atria and ventricle relax and re-fill with blood= one heartbeat.

The Cardiac cycle 

• 1 Cardiac cycle is one heartbeat and has 2 phases: cardiac diastole and then systole.
• Diastole- atria/ventricles relax, AV Valves open and blood passively enters.
• Atrial systole- force remaining blood into ventricles.
• Ventricular systole- increase pressure to close AV valves to prevent backflow into atria and SL valves open as blood leaves ventricles into aorta/pulmonary artery.

Heart rate, stroke volume and cardiac output

Heart rate

• N.o of cardiac cycles per minute (average 72bpm).
• Lower it is, the more efficient the cardiac muscle (bradycardia is below 60bpm).
• Increases during sub-max exercise but can plateau once O2 supply meets demand.

Stroke volume

• Volume of blood ejected out of the left ventricle per contraction (average 70ml at rest).
• Depends on: venous return (greater it is, more volume of blood in ventricles to eject) and ventricular elasticity/contractility (greater the stretch of muscle fibres, greater force of contraction which raises SV).
• SV increased during exercise due to increased venous return- more blood filling ventricles.
• Starling's Law: incresed volume of blood returning to heart results in an increased end-diastolic volume in ventricles so greater stretch on ventricle walls- more blood ejected.

Cardiac output 

• Volume of blood ejected out of the left ventricle per minute (HR x SV) resting is 5l/min.
• Due to cardiac hypertrophy, cardiac muscle's more efficient as more blood can be ejected so HR can reduce.

Heart rate regulation

• Brain can cause HR to increase/decrease due to cardiac control: CCC in medulla receives info from sensory nerves and sends direction through motor nerves to change HR.
• Increase in HR: sympathetic nervous system releases adrenaline/noradrenaline sends stimulation to SA node via cardiac nerve.
• Decrease in HR: parasympathetic nervous system inhibits this via vagus nerve.
• Neural control: chemoreceptors, proprioceptors and baroreceptors.
• Intrinsic control: temperature changes and venous return.
• Hormonal control: adrenaline/noradrenaline released from adrenal glands increase force of ventricular contraction (and SV) and speed of impulse through the heart (and HR).

The Vascular system 

• Ensures O2/nutrients are delivered to respiring cells for energy/wastre removal.

Arteries/Arterioles

• Transport O2 blood away from heart to body: main artery is the aorta.
• Arteries have a large layer of smooth muscle to smooth pulsating blood flow, arterioles large layer of smooth muscle let vessels vasodilate/constrict to regulate blood flow.
• Arterioles have a ring of smooth muscle at pre-capillary sphincters to control blood flow through capillary bed by dilating/constricting.

Capillaries

• Bring blood into contact w/muscle and organ cells for gaseous exchange.
• Diffues O2 into body and intakes CO2 from body to be carried bacl to the heart.
• High capillary density in muscles: permeable walls/once cell thick so allow gaseous exchange.

Veins/venules

• Transport deoxygenated blood from body towards the heart: main one is vena cava.
• Small layer of smooth muscle to venodilate/constrict to maintain slow blood flow to heart.
• One-way pocket valves to prevent back-flow of blood in the wrong direction.

Venous return mechanisms 

• VR: return of blood to heart through the venules and veins back to the right atirum.
• 1- POCKET VALVES: one-way valves in veins prevent backflow of blood,
• 2- SMOOTH MUSCLE: venoconstricts to create venomotor tone- aids blood movement.
• 3- GRAVITY: helps blood from upper-body return to the heart.
• 4- MUSCLE PUMP: skeletal muscle contracts compressing veins to squeeze blood to heart.
• 5- RESPIRATORY PUMP: increasing the rate/depth of respiration promotes venous return/Q.
• Blood pooling: accumulation of blood in veins due to gravitational pull and lack of VR (active recovery can combat this to maintain muscle/respiratory pump to aid blood return to heart).

Vascular shunt mechanism

• Controls redistribution of blood-flow.
• Arterioles lead to capillary beds which bring blood in contact w/organ and muscle cells: blood flow into capillary beds is controlled by pre-capillary spinchters (constrict to limit/dilate to max).
• Capillaries are sites for gaseous exchange.
• Rest- higher % of Q distributed to organs but low % to muscles as arterioles to organs vasodilate whilst arterioles to muscles vasoconstrict to limit it.
• Pre-capillary spinchters dilate so more blood to organs but constrict to limit flow to muscle.
• During exercise, roles reverse e.g. arterioles dilate to maximise blood flow.

Vasomotor control

• Vascular shunt is controlled by VCC in medulla: when sensory info if received, it alters levels of stimulation sent to arterioles/pre-capillary spinchters.
• Vasomotor tone: smooth muscle in walls of arteries always in a state of constriction.
• VCC receives info from: chemo/baroreceptors and sympathetic nervous system is increased/decreased to alter level of constriction in arterioles/pre-capillary sphincters.

Respiratory system

• 2 main functions: pulmonary ventilation and gaseous exchange (internal/external respiration).
• CV provides the links for these processes by transporting deO2 blood to lungs to get O2.

Gas transport

• O2 carried in blood from alveoli to body tissues for aerobic energy: greater the efficiency to inspire, transport and utlise O2, greater the aerobic capacity.
• O2 can be transported in 2 ways: w/haemoglobin as oxyhaemoglobin or with blood plasma.
• CO2 must be transported to alveoli either by: dissolved in water as carbonic acid, carried as carbinohaemoglobin or dissolved in blood plasma.

Breathing rate 

• N.o of inspirations/expirations per minute (average is 12-15).
• Increases in proportion w/intensity but can plateu in sub-maximal steady state if supply meets demand for oxygen.

Tidal volume 

• Volume of air inspired/expired in one breath (average is 500ml).
• Of the 500ml, 350ml reaches alveoli for gaseous exchange and 150ml remains in airways.
• Short-shallow breaths runners have before they reach exhaustion.

Minute ventilation

• Volume of air inspired/expired per min (VE= TV x F).
• Increases in proportion with intensity whereby TV and F will both increase.
• During sub-max, VE can plateau as we reach a steady-state due to O2 supply meeting demand.
• Using an active recovery maintains VE providing the continued need for O2 for aerobic energy and removal of waste.

Mechanics of breathing 

Inspiration at rest

• Active process: 2 muscles contract to increase volume of thoracic cavity.
• External intercostals contract to lift rib cage/sternum up and out.
• Diaphragm contracts/flattens: volume increases in cavity whilst pressure decreases.
  
• Gases move from low to high so air rushes in.

Inspiration during exercise

• Extra muscles recruited for larger force of contraction: sternocleidomastoid/pectoralis minor.
• Greater up/outward movement of rib/sternum- increasing volume/decreases pressure in thoracic cavity so more air is inspired.

Expiration at rest

• Passive process: muscles relax into natural state to decrease volume of thoracic cavity.
• External intercostals relax- lower ribs/sternum down and in.
• Diaphragm relaxes, returning to dome shape; decresed volume and increased pressure.
• Air pushed out the lungs as gases move from high to low.

Expiration during exercise

• Becomes an active process: natural relaxation of muscles doesn't give enough force to expire fast enough for breathing rate to increase.
• Internal intercostals and rectus abdominis recruited: greater down/inward movement of ribs/sternum which decreases volume/increases pressure in thoracic cavity- more air expired.

Respiratory regulation

• Respiratory control: RCC receives info from sensory nerves, sending direction via motor nerves to change rate of respiratory muscle contraction.
• IC stimulates inspiratory muscles to contract at rest/during exercise.
• EC inactive at rest, but during exercise stimulates extra muscles to contract.

Respiratory regulation at rest

• IC responsible for rythmic breathing: stimulate muscles to contract via intercostal nerve to external intercostalsn and phrenic nerve to diaphragm.
• Thoracic cavity volume increases= lowers lung air pressure= 500ml inspired.
• Inspiratory muscles relax and passive expiration occurs, repeated 12-15 times per minute.
• EC inactive at rest due to natural relaxation of diaphragm and external intercostals.

Respiratory regulation during exercise 

• Breathing rate/depth increases to meet O2 demand/CO2 removal: sensory nerves relay info to RCC where EC and IC initiate response.
• RCC recives neural stimuli: thermoreceptors, baroreceptors and proprioceptors and chemo.
• Neural stimuli inform IC via phrenic nerve from medulla which increases stimulation of diaphragm/external intercostals to contract w/more force.
• IC recruits additional muscles to contract: greater force of contraction increased depth of inspiration.
• Baroreceptors inform EC on extent of lung inflation, it it's very stretched, stimulates additional expiratory muscles to contract- reduces volume and increases pressure- forced expiration.
• As intensity increases, both IC and EC control leads to increased breathing rate/decreased breathing depth to maximise efficient respiration.

Gaseous exchange 

• Blood around the alveoli from capillaries is deoxygenated so lots of CO2 but the air inspired into alveoli is oxygen-rich at sea level so low CO2; partial pressure of O2 and CO2 either side.
• Movement of gases done by diffusion: diffuse from area of high to low partial pressure.
• Difference between high to low pp= diffusion gradient, steeper it is, greater the rate of gaseous exchange (exercise steepens this).

External respiration (gaseous exchange at lungs)

• Exchange at lungs between deoxygenated blood in capillaries with O2 in alveoli.
• High ppO2 in alveoli to low pp capillary blood down diffusion gradient= oxyhaemoglobin at lung.
• High ppCO2 in capillaries to low ppCO2 in alveoli down diffusion gradient.

Internal respiration (gaseous exchange at tissues)

• Exchange at muscle cells between O2 blood and CO2 muscle cells.
• High ppO2 in capillary bed to low ppO2 in muscle; haemogblobin dissociates O2.
• High ppCO2 in muscle cells to low pp in capillary blood down diffusion gradient: waste removal through blood.

Gaseous exchange during exercise

External respiration

• Muscles use more O2 so make more CO2= deoxygenated blood at lungs has high ppCO2.
• O2 diffusion gradient steepens, O2 diffuses from high pO2 in alveoli to low pO2 capillary blood.
• CO2 diffusion gradient steepens, CO2 diffuses from high pCO2 capillary blood to low pCO2 in the alveoli.

Internal respiration

• Muscle tissue's demand for O2 increases= waste produce increases.
• More intense= lower the pO2 and higher CO2.
• O2 diffusion gradient steepens, diffuses from high pO2 in capillary blood to low pO2 in muscle cell.
• CO2 diffusion gradient steepens, diffuses from high pCO2 in muscle cell to lower pCO2 in capillary blood.

Dissociation of oxygen from haemoglobin

• When ppO2 in the blood is high (capillaries), almost all of the haemoglobin will become saturated with oxygen.
• When ppO2 is low (i.e. capillaries supplying the tissues of the body), the haemoglobin will release it’s oxygen and thereby supply the cells of the tissue with oxygen for respiration.
• Oxyhaemoglobin dissociation curve: as intensity increases, pO2 lowers in muscle and more O2 dissociates from haemoglobin for diffusion.

The Bohr shift

• 3 other effects of exercise which increase O2 dissociation: temp, CO2, lactic and carbonic acid.
• These move the curve to the right, at any given pO2 for exercising muscle the saturation of oxyhaemoglobin is lower and so dissociation of O2 is greater (more O2 for aerobic energy).
• In recovery, curve shifts back to the left: haemoglobin saturated with normal levels of O2- allows greater association of O2 to haemoglobin in alveoli so blood can be oxygenated.

The recovery process

Excess post-exercise oxygen consumption (EPOC)

• Post-exercise: depletion of ATP/PC, myoglobin loses O2, glucose is depleted, lactic acid.
• EPOC is the amount of O2 our body consumes following a bout of exercise that is in excess of the pre-exercise oxygen consumption baseline level.
• O2 deficit is how much of your effort was anaerobic- depends on intensity/duration.
• Low-intensity: small O2 deficit as steady-state O2 consumption is met, little lactic acid made.
• High-intensity: large O2 deficit as O2 supply can't meet demand and OBLA occurs.

Fast alactacid component of recovery

• Accounts for 10% of EPOC: completed in 2-3 mins, 50% of PC resynthesised in 30secs as phosphagen is restored to rebuild bond to make ATP and PC.
• Uses an extra 1-4 litres of O2 to replenish myoglobin with O2: during exercise, O2 dissociates from haemoglobin in blood/myoglobin in muscle but EPOC resatures them with oxygen.

Slow alactacid component of recovery

• 5-8l of O2 required for: provision of energy to maintain VE, body temp, removal of lactate.
• Can take minutes up to hours depending on buffering capacity.
• Lactate is oxidised into CO2, H20, glucose/glycogen and protein (fuels for energy).
• Post-exercise, breathing remains elevated to increase O2/CO2 removal then decreases.

Removal of lactic acid/replenishment of glycogen

• Anaerobic/high-intensity: lactate accumulates in muscle, causing fatigue as they reach OBLA.
• Post-exercise: 50-70% oxidised in mitochondria and re-enters krebs/ETC for H20/CO2, 10% converts to glucose, some converted into protein and removed as sweat/urine.
• Removal of lactate relies on buffering capacity of blood: takes 1hr but can take up to 24hrs depending on intensity, volumes of lactate accumulated and recovery used.
• OBLA- the point at which you can start to build lactic acid: training increases time it takes.
• Delay OBLA: high lactate tolerance, high VO2 max e.g. athletes reach it at 75% VO2 max.

Implications of recovery on training

• 1-Warm up: aerobic energy systems so no lactate, early increase in O2 minimises O2 deficit.
• 2-Active recovery: flushes muscle w/O2 blood, removes lactate, reduces length of slow alactacid component of EPOC.
• 3-Cooling aids: Ice baths lower blood temp/metabolic rate and demand on slow lactacid phase.
• 4-Intensity of training: high-intensity increases ATP/PC capacity which boosts fast component of recovery/delays OBLA. Low-intensity: increases aerobic capacity/minimises lactic acid.
• 5-Work to relief ratios: 1:3 for ATP/PC resynthesis, glycolytic use 1:2 to increase lactate tolerance, for aerobic system use 1:1 to delay OBLA and promote adaptation. 
• 6-Strategies and tactics: timeouts allow 30secs for 50% of ATP/PC resynthesis, delay play by keeping ball to clear lactate, delay OBLA.
• 7-Nutrition: to maximise PC use creatine/protein to increase fast stage of recovery, to maximise glycogen carbo-load to maximise slow stage of recovery, bicarbonate to enhance buffering process and nitrates speed u recovery times.

Altitude 

• The height/elevation of an area above sea level (2000m), very humid.
• Takes 30days for it to have effects: lower ppO2 so stimulates EPO to make haemoglobin.

Effects of altitude on CV and Respiratory system 

• As altitude increases, barometric pressure/ppO2 decreases.
• At rest, ppO2 in deoxygenated capillary blood arriving is 40mmHg.
• At high altitude, rate of O2 diffusion decreases, reducing haemoglobin saturation= poor transport of O2 to muscle tissues for aerobic energy.
• 1- Breathing frequency increases to maintain O2 consumption.
• 2- Blood vol decreases, plasma volume decreases up to 25% to increase O2 transportation.
• 3- SV decreases in hours of altitude: increase HR to maintain and raise cardiac output.
• 4- Maximal Q, SV and HR decrease with altitude during max-intensity.
• Reduces aerobic capacity and VO2 max: for every 1000m above 1500m altitude, VO2 max drops by 8-11%= greater demand on anaerobic energy system for energy.

Acclimatisation 

• Process of gradual adaptation to a change in environment (lower pO2 at altitude).
• Altitude starts to have effect at 1500m and guidelines allow:
• 1: 3-5 days for low-altitude performance (1-2000m).
• 2: 1-2 weeks for moderate-altitude performance (2-3000m).
• 3: 2+ weeks for high altitude (3000m), have rest days to prevent hypoxia.
• 4: 4+ weeks for extreme altitude (5-5500m).

Benefits on CV and respiratory system

• Benefits last up to 6-8 weeks.
• Release of EPO increases within 3hrs: increases red blood cell production.
• Increased myoglobin= store more O2 and increased O2 carrying capacity.
• Delay OBLA: work for longer before reaching lactate threshold.
• Reduced incidence of hypoxia, headaches, breathlessness, lack of appetite, poor sleep.

Limitations of altitude training 

• Benefits lost within a few days at sea level.
• Time away from family- need a month for it to have benefits.
• Altitude sickness- nausea/light headed so won't feel like training initially= train low-intensity and will have to force haemoglobin production= low OBLA.

Exercise in the heat

• Thermoregulation:process of maintaining internal core temp, theremoreceptors detect changes.
• If temp rises, metabolic heat taken by blood to body's surface and released via sweat using vasodilation (can cause dehydration).
• Rate of heat loss via sweat is affected by humidity: if low, increases sweat, if high, decreases it.
• Rise in body temp can cause hyperthermia: due to prolonged exercise in heat/high humidity.
• For exercising athlete, redirection of blood to skin limits venous return and rising core temp alters function of enzyemes so affects rate of chemical reactions.

Effect of heat, humidity and body's thermoregulatory response on CV system

• 1: Dilation of arterioles/capillaries to skin causes increased blood pooling in limbs.
• 2: Decreased venous return, SV, Q leads to reduced O2 transport/more strain on CV system.

Effect of heat, humidity and body's thermoregulatory response on Respiratory system

• 1: Dehydration in temp above 32degrees= decreased vol of air for gaseous exchange/mucus.
• 2: Increased breathing frequency to maintain O2 consumption causes increased O2 cost.
• 3: High heat increases effects of pollutants: increased irritation of airways= coughing/asthma.

Effect on performance 

• Longer the event, greater the effect due to rise in metabolic rate associated w/high core temp.
• More elite= less impact due to physiological adaptations and heat acclimitisation.
• Pre comp: 7-14 days acclimitisation to increase tolerance, cooling aids to reduce core temp.
• During comp: pacing strategies, sweat-wicking clothes, hypotonic/isotonics.
• Post comp: cooling aids and rehydrate with isotonics to replace lost electrolytes.

Carbohydrates 

• Vital for: energy, cell division, active transport, formation of molecules.
• Accounts for 75% of energy requirements: glycogen is primary fuel for aerobic/anaerobic.
• Starches: stored in glycogen/liver as slow-release, maximise glycogen stores.
• Sugars: circulate in blood as glucose for fast-release (only 10%- can covert into body fat).

Proteins 

• Amino acids are essential for growth/repair of cells/tissues.
• Used to make haemoglobin, enzymes, antibodies, collagen or energy when low on carbs/fats.

Fats 

• Insulate nerves, form cell membranes, cushion organs, provide energy (higher yield than carbs)
• Provide essential fatty acids and fat-soluble vitamins (A, D and E).
• Saturated fatty acids should be limited to reduce risk of CV disease.
• Unsaturated should be the majority of intake to help improve recovery, reduce inflammation
• Omega 3s boost O2 delivery and improve endurance/recovery rates.

Minerals

• Essential inorganic nutrients to maintian healthy body functions: necessary for bone health, enzyme formation and breaking down food for energy.
• Calcium: bone/teeth health, muscle contraction, blood clotting and nerve transmission.
• Iron: formation of haemoglobin, enzyme reactions and immune system.
• Phosphorous: bone health and energy production (fish, nuts, dairy).

Vitamins

• Essential organic nutrients for healthy body functions: fat and water soluble.
• Fat soluble stored in body/fatty foods: A, B, E, K.
• Water-soluble aren't stored: C, B.

Fibre 

• Dietary fibre helps normal function of large intenstine, can reduce cholestrol and risk of diabetes/obesity by preventing constipation.

Water

• Accounts for 2/3 of bodyweight and is essential for chemical reactions/moving substances.
• e.g. blood plasma is 90% water and carries glucose for respiring muscles.
• Essential for hydration as dehydration can decrease plasma volume/make it more viscous.

Energy expenditure 

• Sum of BMR, thermic effect of food and energy expended during exercise.
• BMR: minimum amount of energy needed to sustain essential physiological functions.
• TEF: energy needed to eat, digest and absorb food.
• Metabolic equivalent values are used to show additional energy expenditures: body typically uses 1 kcal per kg of body mass per hour at rest e.g. sitting has a MET value of 1.

Energy intake: total amount of energy from food/drink consumed.

Energy balance: relationship between energy intake/expenditure, if they match you maintain weight, if intake is higher you gain weight and if intake is lower you lose weight.

Ergogenic aids

• Group of substances that can be manipulated to improve performance: PEDs.
  
• WADA lists prohibited/non-prohibited substances: Athlete Biological passport to monitor.

Pharmacological aids

Anabolic steroids

• Synthetic hormones resembling testosterone= protein synthesis for muscle growth.
• Quality/quantity of training increased as recovery speed improves.
• Increase in fat metabolism- power sports, rugby players, throwers, sprinters.
• Risks: aggression, liver/kidney damage, heart disease, decreased fertility/sperm count.

Erythropoietin (EPO)

• Natural hormone- produces red blood cells/haemoglobin to increase O2 carrying capacity.
• RhEPO can be supplemented to increase red blood cells (endurance performers).
• Faster EPOC, increases buffering capacity and increase lactate threshold.
• Risks: hyper-viscosity of blood, blood clots/heart failure, decreased natural EPO production.

Human growth hormone (HGH)

• Synthetic product copying natural growth hormone which declines w/age: supplementation increases protein synthesis, recovery/repair, glucose levels and trainng quaility.
• Risks: heart failure, enlarged intestines, diabetes, fat desposits, abnormal bone growth.

Physiological aids 

Blood doping

• Blood removed 4 weeks pre-event and re-injected 2-3 days before: body naturally replenishes lost blood so haemoglobin content is high (increasing O2 carrying capacity).
• Risks: transfusion reactions/infections (HIV), decreased cardiac output, heart failure.

Intermittent hypoxic training (IHT)

• Low ppo2: stimulates muscles to adapt, increases mitochondrial density/buffering capacity.
• Used by endurance athletes to acclimatise: wear mask during exercise interval.
• Risks: benefits lost when stopped, disrupt training pattern, dehydration.

Hypoxic tent 

• Recreates altitude conditions: air filter lowers ppO2 and you enter after training to recover.
• Increases haemoglobin, myoglobin, delays OBLA, no hypoxia.

Cooling aids- ice vest, cold towel, ice bath

Pre-event 

• Reduce core body temp to sustain intensity whilst reducing thermal strain/CV drift.
• Reduce over-heating, dehydration: used by endurance athletes in hot climates (for 10-30mins).

Injury treatment 

• Nerve endings numbed to reduce pain as arterioles vasoconstrict to reduce swelling/blood flow.
• Used after knocks/sprains/strains following PRICE procedure.

Post-event 

• Reduce DOMS: blood vessels vasoconstrict (removes waste) then dilate when you leave ice bath which flushes muscle-tissue with oxygenated blood flow.
• Risk: chest pain, ice burns, hide injuries, dangerous for those with heart conditions.

Amount, timing and consumption of meals 

Pre-event 

• 3 hours prior: slow-digesting carbs (complex/low GI to maximise glycogen stores) like oats.
• 1-2 hours prior: smaller fast-digesting carb (simple/high GI) to top up glucose like energy bar.
• Body may try to counter-act raised glucose= rebound hypoglycaemia (be cautionary).

During event

• Athletes performing for 1hour+ should consume fast-digesting carbs to maintain glucose/preserve muscle glycogen stores e.g. gels/bananas/drinks.

Post-event 

• Rapid post-exercise recovery aided by meal within 30mins: repeat at 2hr intervals for up to 6hrs post event.
• Moderate/fast-digesting carbs to promote faster recovery.

Amount, timing and consumption of meals for endurance training

Pre-event 

• 3 hours prior: slow-digesting carbs (complex/low GI to maximise glycogen stores) like oats.
• 1-2 hours prior: smaller fast-digesting carb (simple/high GI) to top up glucose like energy bar.
• Body may try to counter-act raised glucose= rebound hypoglycaemia (be cautionary).

During event

• Athletes performing for 1hour+ should consume fast-digesting carbs to maintain glucose/preserve muscle glycogen stores e.g. gels/bananas/drinks.

Post-event 

• Rapid post-exercise recovery aided by meal within 30mins: repeat at 2hr intervals for up to 6hrs post event.
• Moderate/fast-digesting carbs to promote faster recovery.

Amount, timing and consumption of meals for strength training

• Increase muscle mass: 5-6 small meals per day, 30% lean protein and complex carbs.

Pre-training meal

• 30-1hr before equal quantities of fast-digesting carbs and protein- accessed during training.

Post-training meal

• Within 2hrs: fast-digesting carbs/protein to replace lost glycogen/boost protein synthesis.
• E.g. protein shakes as they're easily digestible. 

Glycogen (carbo) loading 

• Maximise glycogen stores in muscles/liver for endurance performers.
• 4 phases: glycogen depletion then tapering training before maximising carb stores.
• Benefits: larger fuel store for energy due to super-compensation, increase time to fatigue.
• Risks: hypoclycaemia, poor recovery, lethargy in depletion phase, injury.

Hydration 

• Losing 2% of bodyweight in sweat can cause 20% decrease in performance due to: decreased heat regulation, increased temp/blood viscosity/HR, fatigue, decreased cognitive function.
• Hypotonic: lower concentration of glucose than blood (4%), provides small amounts of glucose for energy (used for hydration without energy boost e.g. jockey/gymnast).
• Isotonic: equal concentration of glucose to blood (5-8%)-  runners, games players.
• Hypertonic: higher concentration of glucose to blood (15%), used post-exercise to maximise glycogen replenishment in recovery, or for ultra-distance athletes.

Creatine supplementation

• Produced naturally from amino acids, stored in muscle tissue as PC for high-intensity energy.
• Easy accessed as creatine monohydrate in tablet form- increase PC by 50% to train longer.
• Increase max explosive strength and extend ATP-PC system up to 11-12 seconds.
• Risks: initial weight gain from water retention, gastrointestinal issues, muscle cramps.

Caffeine

• Stimulant to heighten CNS/increase fat breakdown for energy to preserve glycogen stores.
• Aids endurance athletes as they can keep carb stores for energy to delay fatigue.
• Increase alertness, concentration/reaction time: legal under WADA.
• Risks: gastrointestinal issues, insomnia, anxiety, diuretic, irregular heart beat.

Bicarbonate- sodium bicarbonate/baking soda

• Alkaline substance- buffer to neutralise rise in blood acidity.
• During intense anaerobic activity, lactic acid induces fatigue: bicarbonate increases tolerance.
• 'Soda loeading': increases buffering capacity of blood/delays OBLA.
• Risks: gastointestinal issues, unpleasant taste= diarrhoea, bloating.

Nitrate

• Inorganic compounds: stored as nitrates and under low O2 conditions are converted into nitric oxide which helps vascular/metabolic control.
• Supplementing nitrates can dilate blood vessels, reduce bp and increase blood flow.
• Endurance athletes close to anaerobic threshold produce conditions needed to maximise effect of nitrate (5,000m).
• Risks: headaches, long-term effects unclear and possible carcinogenic risk.

Protein

• Aim to increase muscle mass/muscle growth and repair- good if not eating enough meat.
• Increased work for liver/kidneys if you take too much- increased risk of kidney damage.

Training

Training programme design

• Specific, progression, overload, variance, moderation, reversibility.
• Test to measure what intensity to train at and measure improvement.
• Warm up (pulse raiser, mobility, dynamic stretches), cool down (pulse-lowering,static stretch).

Periodisation

Cycles

• 1: Macro-cycle: long-term plan over 1yr to achieve a long-term goal, several meso-cycles.
• 2: Meso-cycle: mid-term plan over 4-16 weeks. Achieve mid-term goal (maintain fitness).
• 3: Micro-cycle: short-term plan over 1-3 weeks. Achieve short-term goal- split into sessions.
• Aim: reach physiological peak at correct time, avoid injury and realistic goals.

Training

Training programme design

• Specific, progression, overload, variance, moderation, reversibility.
• Test to measure what intensity to train at and measure improvement.
• Warm up (pulse raiser, mobility, dynamic stretches), cool down (pulse-lowering,static stretch).

Periodisation

Cycles

• 1: Macro-cycle: long-term plan over 1yr to achieve a long-term goal, several meso-cycles.
• 2: Meso-cycle: mid-term plan over 4-16 weeks. Achieve mid-term goal (maintain fitness).
• 3: Micro-cycle: short-term plan over 1-3 weeks. Achieve short-term goal- split into sessions.
• Aim: reach physiological peak at correct time, avoid injury and realistic goals.

Phases 

• Design of each meso-cycle depends on phase of training you're in.
• Preparatory phase 1: off-season doing conditioning work/aerobic trianing.
• Preparatory phase 2: pre-season, progressive overload, sport-specific training.
• Competive phase 3: training load reduces, strategies are the focus.
• Competitive phase 4: tapering 2-3 weeks pre-event to ensure full recovery.
• Transition phase: active rest/recovery. Low intensity aerobic work.

Tapering and peaking 

• Taper: reduction in volume of training pre-event (physically/mentally prepare so you peak).
• Time peak so that performer can benefit from removal of training-induced fatigue but without reversability having an effect.

Aerobic training

• Aerobic capacity: ability to inspire, transport and utilise O2 to perform sustained aerobic activity.
• Key component of this is VO2 max: max volume of O2 inspired and utilised per minute.

Affecting factors

• Physiological make up: greater the efficiency of respiratory/CV system the higher the VO2 max (strong respiratory/CV muscles, increased haemoglobin, capillarisation).
• Age: VO2 max declines 1% after 20s (lost elasticity in heart, blood vessels reduces efficiency).
• Gender: females have 15-30% lower VO2 max due to higher bodyfat, low haemoglobin/SV.
• Training: aerobic training increases it by 10-20% (higher myoglobin, respiratory muscles).

Evalutation

• Direct gas analysis: continuous exercise at progressive intensities to exhaustion.
• Cooper 12min run: can do large groups at once but not sport-specific.
• Queen's college step test: done for 3 mins and HR taken every 5secs for 15secs.
• NCF multi-stage fitness test: continous 20m shuttle run at progressive intensities to fatigue.

Training zones

• If intensity is too high, can fatigue/adapt anaerobically e.g. learn to tolerate lactate.
• HR training xone to monitor intensity to ensure correct type of structural adaptations.

Continuous training 

• Steady-state low/moderate intensity for prolonged time.
• Stressed aerobic system and slow-oxidative muscle fibres- aerobic adaptation.

HIIT (high-intensity interval training)

• Periods of work followed by periods of recovery: can manipulate variables.
• Work intensity: 80-95% of HR max for 5secs to 8mins.
• Recovery intensity: 40-50% of HR max, 1:1 work to relief ratio.
• Requires longer recovery periods than steady state.

Adaptations of aerobic training 

Respiratory system

• Stronger respiratory muscles= increased max lung vol and less respiratory fatigue.
• Increased SA of alveoli= increased external gaseous exchange.

Cardiovascular system

• Cardiac hypertrophy= increased SV, CO due to increased force of ventricular contraction.
• Increased elasticity of arteries= increased efficiency of vascular shunt, decreased resting bp.
• Increased blood plasma vol= lower blood viscosity, aiding venous return.
• Increased haemoglobin= increased O2 carrying capacity/gaseous exchange.
• Capillarisation= increased SA for blood flow/gaseous exchange.

Musculo-skeletal system

• Slow-oxidative fibres= more potential for aerobic energy.
• Increased mitochondria/myoglobin= increased storage/transport of O2.
• Increased stores of glycogen= increased aerobic energy fuels/duration of performance.

Metabolic function

• Increased activity of aerobic enzymes= increased metabolism of glycogen/triglycerides.
• Decreased fat mass= increased lean mass/breakdown of fats.
• Decreased insulin resistance= improved glucose tolerance.

Stength

• Static- force applied against a resistance without movement (isometric).
• Dynamic- force applied w/movement at a joint so muscles change length (e.g. power output).
• Maximum- ability to produce a maximal amount of force in a single muscle contraction.
• Explosive- ability to produce a max amount of force in one/several rapid muscular contractions.
• Strength endurace- ability to sustain repeated muscular contractions withstanding fatigue.

Affecting factors

• Cross-sectional area: greater it is, greater the strength and force produced.
• Fibre type: FOG provide greater strength over a shorter period of time (large motor units).
• Gender: males have higher muscle mass/cross-sectional area due to high testosterone.
• Age: strength decreases with age due to decline in efficiency of neuromuscular system.

How to test: hand grip strength dynamometer, ab curl test, vertical jump test.

Adaptations to strength training

Neural pathways

• Increased recruitment of motor units and type 2a and b fibres.
• Decreased inhibition of 'stretch reflex'- increased force of contraction from agonist.

Muscle + connective tissues

• Muscular hypertrophy and hyperlasia: increased force production.
• Increased bone density and mass so more calcium in ones and more joint stability.

Metabolic function

• Increased PC/glycogen stores so more energy for high-intensity activity.
• Increased muscle mass: increased calorie expenditure so more lean.
• Increased buffering capacity- can remove lactate easier/higher tolerance.

Flexibility 

• Static: ROM at a joint without movement.
• Static active: contract agonist to stretch the antagonist e.g. contract bicep to stretch tricep.
• Static passive: partner assists stretch by taking to end of ROM e.g. using band/partner.
• Dynamic: ROM at a joint whilst movement occurs at the joint e.g. arm circles by a swimmer.

Factors affecting flexibility

• Joint type: size/shape affects ROM e.g. ball and socket has greater flexibility than hinge.
• Surrounding tissues: greater the length/elasticity, the greater the ROM.
• Gender: females are more flexible than males (oestrogen hormones).
• Age: highest at childhood and declines with age (elasticity of connective tissue declines).

Developing flexibility 

• Static stretch: hold ROM for 10-30 secs in cool down.
• PNF: static passive, isometric contraction, static passive again but with more ROM (cool-down).
• Isometric stretch: can be active/passive e.g. wall-calf stretch.
• Ballistic stretch: use momentum to move to end of joint ROM.
• Dynamic stretch: warm-up, takes joint through full ROM with control over entry/exit.

Adaptations to flexibility 

• Allows better technique and faster/powerful contractions due to ability of joint to reach full ROM.
• 3-6 times per week for 6 weeks for long-term adaptations.

Structural adaptation

• Increased resting length: increased ROM at joint, muscle spindles adapt to new length and reduce the stretch reflex.
• Increased elasticity: increased static/dynamic flexibility, increased stretch of agonist and decreased inhibition from the antagonist.

Acute injuries 

• Occur suddenly/immediate onset e.g. collision with player, fall from horse.
• Signs/symptoms: sudden/severe pain, swelling, bruise, lack of movement or disfiguration.

Acute: Hard tissue-injuries 

Fractures

• Partial/complete break in bone due to excessive force that overcome's bones ability to flex, due to direct or indirect force.
• Compound (open): bone breaks through skin whereas simple (closed) doesn't break skin.
• Also: incomplete, greenstick, transverse, comminuted, impacted and avulsion.

Dislocation

• When one bone is displaced from another, out of its original position (direct/indirect force pushing joint past its extreme ROM).
• Subluxation (incomplete/partial) causes damage to ligaments that connect bone to bone.

Acute: soft-tissue injuries 

Contusion and haematoma 

• Contusion is tissue in which blood vessels have ruptured, most are minor (severe causes deep-tissue damage)
• Deep-tissue damage leads to a haematoma- localised congealed bleeding (ruptured vessels).

Sprain

• Damage (overstretch/tear) to ligaments connecting bone-bone and support a joint.
• Due to sudden twist, impact/fall pushing joint past its extreme ROM.
• 1st degree is overstretch of a few fibres, 2nd degree partial tear, 3rd degree detachment of ligament from bone and total rupture is a tear.

Strain

• Damage (overstretch/tear) to muscle fibres/tendon connecting muscle to bone due to overstretching too quickly or contracting muscle too quickly.
• Minor damage is grade 1, partial rupture is grade 2 and complete rupture is grade 3.

Abrasion 

• Superficial damage to skin due to scraping action against surface.
• If a laceration is caused, may need medical attention (have blood rules in sport).

Blisters

• Separation of layers of skin where a pocket of fluid forms due to friction.
• Preventable with right equipment/clothing or training load.

Concussion

• Traumatic brain injury resulting in disturbance of brain function caused by direct blow to head/other body parts causing rapid movement of the head.
• Blow accelerates brain against rough inner wall of skull and rebounds against other side= disruption in electrical proceses between neurones in brain (confused state).

Chronic injuries 

• Occur over a period of time/slowly developed due to repeated or continuous stress.
• Due to: sudden intensity/frequency/duration increase, inadequate prep, no recovery etc.

Chronic: Hard-tissue injuries 

Stress-fracture

• Tiny crack in surface of bone due to overuse (fatigue/insufficiency fracture).
• Pain subsides with rest, usually in lower body e.g. tibia. and in distance runners.
• Due to: overtraining, unfamiliar surfaces, and inappropriate equipment.

Chronic: Soft-tissue injuries

• Shin splints: repeated overuse of tibialis anterior and posterior, in running known as MTSS.
• Tendonitis: connects muscle to bone, is the deterioration of tendon's collagen in response to chronic overuse (repetitive movements without adequate rest e.g. tennis elbow or in achilles.

Injury prevention

Intrinsic risk factors 

Individual variables

• Previous injury: loss in connective tissue strength, decreased joint stability.
• Posture/allignment: small misalignment can cause joint to weaken/muscular imbalance.
• Age: bone tissues lose stength as connective tissues suffer overuse.
• Nutrition: protein for growth/repair of cells, carbs for energy, fats for protection, minerals.

Training effects

• Poor prep: correct warm up/cool down, sleep, nutrition, reocvery, training.
• Inadequate fitness levels: if intensity/duration/frequency are too high can cause poor tech.
• Inappropriate flexibility: poor joint stability or lack of flexibility in connective tissues can limit ROM and lead to acute injuries or too much flexibility can cause dislocations.

Extrinsic risk factors 

Poor technique and training 

• Places excessive stress on muscles/tendons/ligaments which can deteriorate (tennis elbow).
• Coaches should use the correct technique, warm up/cool down for age/ability.
• Condition your neuromuscular system- power plates teach nerves/muscles to work together.

Incorrect equipment and clothing

• Should be age, stature and ability related. e.g. child can't use a full-size racket (Mini tennis).
• Shoulder/ankle straps to help stabilise joint or gum-shilds to reduce risk of injury.
• Technological fabrics can wick moisture, lightweat, padding and shock absorption.

Inappropriate intensity, duration and frequency of activity

• Principles of training must be followed when designing a training programme: progressive overload must be according to ability.
• Injuries can occur without adequate rest/too intense/high frequency.

Warm-up and cool down effectiveness

Warm up:

• Raise body temp- prepares you psychologically and physiologically (20+ mins).
• 3 distinct stages: pulse raiser, stretch/mobilisers, sport-specific drills to active neural pathways.
• Rise in temp increases enzyme activity, diffusion gradients an metabolic activity.
• Most effective connective tissue is warm/can cope with elastic/explosive strength (dynamic).

Cool down:

• Maintain HR and blood flow to flush muscle tissue w/O2 blood and remove waste (20-30mins).
• Several distinct stages: moderate-intensity to maintain HR and aid venous return, stretching exercises to reduce muscle tension and increase muscle relaxation.
• Flushes blood of lactate/toxins.
• During high-intensity events, active cool down is better as aerobic energy production is activated earlier and speed of lactic removal is increased.
• Low-intensity aerobic- passive recovery is better to return back to original temp.

Responding to injuries/medical conditions in sport 

Assessment using 'SALTAPS'

• 1: Stop the game and ask if the player is injured/observe injury.
• 2: Ask questions about the injury, where does it hurt?
• 3: Look for signs of bruising/swelling/bleeding.
• 4: Touch the injured area gently to identify painful regions.
• 5: Active moement of injured area without assistance.
• 6: Passive movement of injured area if they can, to full ROM.
• 7: Strength-testing (ask them to stand/put pressure on injured area).
• If at the look stage they show obvious injury signs, remove player.
• For the 'Touch, Active and Passive movement' need to be qualified.

Acute management using PRICE

• Acute soft-tissue injuries trigger inflammation, pain and bruising.
• Protection (stop play, splints, crutches), Rest (heal), Ice (10mins), Compression (tape) and Elevation (raise injury above heart level to reduce blood flow/swelling).

Recognising concussion using the six R's

• Recognise- know the sings/symptoms of concussion (player/parent or coach)
• Remove- immediately remove them from the field of play.
• Refer- refer to qualified healthcare professional who's trained in treatment/evaluation.
• Rest- must rest till symptom free (supervised for first 24 hours)
• Recovery- fully recover/symptom free (adults 1 week, u18s 2 weeks before authorised return)
• Return-  must be symtpom free, written authorisation and complete a GRTP (graduated return to play)

Rehabilitation

• Early stage: gentle exercises encouraging damaged tissue to heal.
• Mid stage: progressive loading of connective tissue/bone to develop strength.
• Late stage: functional exercise/drills to ensure your body is ready to return.

Treatment methods

Stretching

• Acute phase: no streching in first 3 days of injury, PRICE.
• Mid phase: 2 weeks of heat therapy and static/passive stretches.
• Later phase: for 2 more weeks ROM/strength focused on. PNF to increase ROM.
• Long-term: increase ROM/strength of connective tissue. Active/dynamic stretching.

Hypoxic tents

• Low levels of O2 so recreates altitude: increases haemoglobin and myoglobin (fitness).

Hyperbaric chambers 

• More O2 in haemoglobin and more dissolved in blood plasma= more O2 to muscle tissues.
• Tissues heal quicker when oxygenated: chamber is 100% pure O2.
• Reduces swelling and increases white blood cell production: fight infection at injury site.

Massage

• Sports massage- deep muscle therapy to realign connective tissue fibres/flush toxins.
• Good for soft-tissue injuries and injury prevention by increasing flexibility/mobility at joint.
• Sports massage can: move fluid to encourage healing, stretch tissues, break down scar tissue, reduce pain.
• Can be used on soft-tissue injuries like tendon ruptures, open wounds, or contusions.

Anti-inflammatory drugs

• Non-steroid anti inflammatory drugs (aspirin) treat acute injuries (inhibit inflammation).
• Side effects- heartburn, nausea, diarrhoea.
• Long-term use for chronic injuries should be monitored (possible stroke, heart attack).f

Cold, heat and contrast therapies 

• Cold therapy reduces metabolic rate/nerve impulse speed and vasocontricts vessels to decrease blood flow and DOMS (e.g. cyrotherapy for acute injuries).
• PRICE method for actue soft-tissue injuries, cold water immersion (10mins), cryokinetics (ice then rehab exercise), cryostretching (cold application and stretch).
• Heat therapy reduces muscle tension, vasodilates vessels and increases blood flow, mainly for chronic/later stage acute injuries.
• Heat pack, hot towels and warm water immersion and stretching increases connective tissue elasticity during rehab.
• Contrast: hot and cold to increase blood flow and decrease pain. e.g. immerse body up to shoulder post-exercise.
• Applying cold vasoconstricts blood vessels and heat makes them vasodilate, increasing flow.

Physiotherapy

• Can consist of: mobilisation of joints/tissues, electrotherapy, exercise therapy to strengthen muscles, massage, posture/alignment training.
• 1st phase: pain relief, ice therapy, shoulder sling.
• 2nd phase: tailored exercises to maintain rotator cuff muscle strength.
• 3rd phase: restore normal ROM, muscle length and tension w/mobilisation/stretching.
  

Surgery

• Sports injury related surgical procedures include repair of damaged soft-tissue, realignment of bones and repositioning of joints.
• 1. Knee alignment surgery e.g. ACL reconstruction after rupture.
• 2. Shoulder stabilisation e.g. after repeated dislocations (throwing athletes).
• 3. Meniscal tear surgery e.g. cartilage tear in knee (meniscus is resurfaced).
• Arthroscopy: keyhole- small incision made, minimise damage to tissues and repair cartilage.
• Open surgery: incision to open a joint to repair/reconstruct damaged structures.

Treatment of common injuries

• Fractures: PRISE, immobilisation, meds, surgery if severe.
• Dislocations: medical attention, surgery, immobilisation, PRICE, meds, surgery.
• Sprain: PRICE, immobilisation, meds, strength exercises, surgery if 3rd degree detachment.
• Torn cartilage: PRICE, medical attention, sugery, meds.
• Exercise induced muscle damage: caused by eccentric exercise (downhill run, plyometrics)- combat with adequate warm-up, cold therapy, massage, meds, stretching.