METABOLISM + EXERCISE

What are the immediate effects of exercise on the body

• increased heart rate - increased secretion of adrenaline that stimulates the sympathetic nervous system

• vasodilation of arterioles - greater blood flow to skeletal muscles + signalled by nitrous oxide from endothelium

• increased stroke volume - more blood leaves left ventricle per beat

• increased breathing rate - increased ventilation —> increased conc. gradient so more O2 diffuses in and CO2 diffuses out

• increased breathing depth - electrical impulses sent to intercostal muscles + diaphragm —> contract more forcibly

• reduced blood flow to digestive system 

What are the long term effects of exercise on the circulatory system

• increased VO2 max

• increased stroke volume

• increased heart size - hypertrophy ( increased cardiac muscle size) —> stronger contractions

• increased no. of RBCs - athlete’s have thicker (more viscous) blood as more dense

• decreased resting heart rate

what are the long term effects of exercise on the respiratory system

• increased breathing rate

• increased tidal volume (vol of air inhaled/exhaled at rest)

• increased vital capacity (max. volume of air exhaled after a deep breath in) - due to developed intercostal muscles + diaphragm

• increased density of capillaries in lungs - increased SA for gas exchange

what are the long term effects of exercise on the skeletal system

• increased efficiency in lipid metabolism in muscle fibres - conserves CBH stores in muscle cells

• increased capillary network surrounding muscle fibres

• increased vascularisation of muscles (inc. size/no. blood vessels that deliver to the skeletal muscles)

• increased myoglobin glycogen stores

• increased size/no. mitochondria

what is aerobic fitness

the ability of your heart and lungs to respond to the demands of aerobic exercise

how to achieve aerobic fitness

• 20 mins of aerobic exercise every day over a sustained period at 70% max. heart rate

factors that affect aerobic fitness

• age

• gender

• smoking

• diet

• alcohol consumption

• mindset/amount of exercise you do

• drug use

benefits of having good aerobic fitness

• stronger skeletal muscles

• decreases risk of type 2 diabetes

• lowers blood pressure

• improves mental health

• greater cardiovascular health - lowers risk of stroke/heart attack

What does F.I.T.T stand for

• frequency

• intensity

• time

• type of training

3 ways to measure the success of a training program?

1. larger VO2 max

2. lower resting heart rate

3. shorter recovery time

What does VO2 max mean?

the maximum rate that oxygen can be taken in and used

what’s the units of VO2 max

dm³ kg^-1 m^-1 / dm³ min^-1

EQ: Describe how VO2 max is measured (INDIRECT)

• graded exercise test e.g multilevel treadmill

• at 3 min intervals increase speed + incline of treadmill

• measure the O2 and CO2 concentration of inhaled and exhaled air

• VO2 max is when oxygen consumption remains steady whilst intensity of exercise increases

• continue until person is fatigued

What to do BEFORE assessing someone’s VO2 max

• person must consent

• carry out risk assessment to check for pre-existing medical conditions

• ensure all participants have had training on how to use equipment

what’s a DIRECT measure of VO2 max

• use a gas analyser

• measure ventilation rate and conc. of O2 and CO2 in the inhaled and exhaled air

PROS/CONS of direct measure

• more accurate data obtained

• BUT specific equipment needed

What are the methods of enhancing athletic performance

• erythropoietin

• blood doping

• steroids

• carbohydrate loading

How does erythropoietin enhance performance

Erythropoietin (EPO) is a hormone that stimulates RBC production

• inject body with recombinant erythropoietin

• more RBCs produced —> more haemoglobin —.> more O2 transported to muscles —> inc. rate of aerobic respiration

PROS / CONS of erythropoietin

PROS:

• more RBCs = more oxygen to muscles = more aerobic respiration

• good for endurance sports

CONS:

• too many RBCs can make blood more viscous = inc. risk of blood clots, heart attack + stroke

How does blood doping enhance performance

Artifically increasing no. of RBCs by injecting either your own blood (removed months before competition) or a donor’s

• extra blood = more RBCs = more haemoglobin = more O2 transported to muscles = more aerobic respiration

PROS:

•  increases VO2 max

• delays muscle fatigue - longer aerobic respiration

CONS:

• illegal

• more RBCs = thicker blood = inc. risk of blood clots/stroke

• greater heart strain - contract harder to pump thicker blood

what’s the structure of haemoglobin

• quaternary structure - 4 ppc

• haem group attached to centre of each ppc

• each haem group can carry 1 OXYGEN MOLECULE

What does association and dissociation mean?

• association/loading = binding of an O molecule to 1 haem group to form oxyhaemoglobin

• dissociation/unloading = release of an O molecule from a haem group

Describe and explain the shape of an oxygen dissociation curve

• SIGMOIDAL SHAPE:

•  

1. initially, there’s a small increase in partial pressure of O2, so a small increase in % saturation of Hb

2. there’s a larger increase in PO2 so a larger increase in % sat of Hb

3. there’s a smaller increase in PO2 so a smaller increase in & sat Hb

• at 0, all the Hb is bound to an O molecule

What is cooperative binding

• it’s hard for the 1st haem group to bind to oxygen as it’s hidden

• but after the 1st haem group binds with O, Hb undergoes a conformational change, so it’s easier for the 2nd and 3rd haem group to bind (haem groups become more exposed)

• hard for 4th haem group to bind as there’s a lower chance of O binding to that specific haem group (less likely to collide)

Difference between adult Hb and fetal Hb

fetal Hb has HIGHER AFFINITY FOR OXYGEN —> binds more readily to O2 and less willing to release it

• increases exchange of O2 from mum to fetus

• exchange of blood occurs in placenta by a counter current system that ensures they never mix

difference between adult Hb curve and fetal Hb curve

• fetal Hb curve is shifted more LEFT (not far left as O would only be released at really low PO2)

What does it mean if an O dissociation curve was shifted more RIGHT

• decreased affinity of Hb for oxygen

• more oxygen is released at low PO2

• so more oxygen is available for aerobic respiration

• so higher rate of aerobic respiration

structure of MYOGLOBIN

• only found in muscles

• made up of 1 ppc attached to 1 haem group

• so only binds to 1 oxygen molecule

function of myoglobin

• stores O2 in skeletal muscles

• HIGHER affinity for oxygen than Hb —> only releases O2 at really low PO2

What factors affect oxygen dissociation from respiratory pigments?

• temperature

• pH

• CO2

How does temperature affect O2 dissociation

• INCREASE temp = shifts RIGHT

• higher temp weakens association between O2 molecules and haem groups + disrupts H bonds in tertiary/quaternary structure

• affinity decreases

e.g during exercise, muscle temp inc

How does pH affect O2 dissociation

• DECREASE pH = shifts RIGHT

• decreased pH = increased H+ ion conc. = more binding to Hb to form more haemoglobinic acid that reduced affinity

How is CO2 transported in the blood

• dissolved in the blood plasma

• as hydrogen carbonate ions dissolved in plasma

• combines with NH2 groups on Hb to form carbaminohaemoglobin

Explain how haemoglobin acts as a buffer

1. CO2 reacts with water to form carbonic acid (H2CO3)

2. this reaction is catalysed by carbonic anhydrase

3. H2CO3 dissociates to form H+ and HCO3- (hydrogen carbonate/bicarbonate)

4. Due to an imbalance of charges, Cl- ions diffuse into RBC via CHLORIDE SHIFT

5. H+ ions combines with Hb to form haemoglobinic acid 

6. H+ ions also reduces the affinity of oxyhaemoglobin, HbO8, (that’s already present in the RBC) for oxygen, so O2 diffuses out of the RBC

What happens when the partial pressure of CO2 is low

• Hydrogen carbonate (HCO3-) ions diffuses back into the RBCS, whilst Cl- ions diffuses out

• HCO3- ions reacts with H+ ions to reform carbonic acid (H2CO3)

• H2CO3 is hydrolysed by carbonic anhydrase to form CO2 which diffuses out of the RBCs into the plasma

• CO2 is exhaled

types of muscle

1. cardiac - myogenic so contracts without external stimulation needed

2. smooth muscle - contains actin/myosin but not striated

3. skeletal - striated muscle

describe the ultrastructure of skeletal muscle

1. muscle fibre - long, cylindrical multinucleated cell

2. myofibril - rod-like structures running through the fibres, made up of sarcomeres

3. myofilaments - THICK = myosin, THIN = actin

4. sarcoplasmic reticulum = stores and releases Ca2+ ions needed for muscle contraction + contains T TUBULES that conduct the action potential into the muscle fibre

5. Sarcolemma = encloses the muscle fibre and separates it

what is a sarcomere

1 contractile unit of a myofibril

describe a sarcomere

• A band = DARK BAND that shows where the myosin is

• I band = LIGHT BAND = only ACTIN

• actin = THIN

• myosin = THICK

• H ZONE = area of just myosin

• M line = centre of H zone

• Z Disc = marks start and end of sarcomere

what are the proteins found in muscle fibres

• troponin - has a Ca2+ binding site

• tropomyosin - blocks the actin-myosin binding site

• actin

• myosin - tail and head (complementary to A/M binding site)

What is the sliding filament theory

• sarcolemma depolarises

• T tubules depolarises

• this causes Ca"2+ ion channels to open and Ca2+ ions diffuse out

• Ca2+ ions binds to the troponin which causes the tropomyosin to move

• this exposes the actin-myosin binding site on the actin molecules

• myosin heads binds complementary to the actin to form a cross bridge

• myosin head tilts backwards and ADP + Pi is released —> POWER STROKE

• ratchet mechanism as cross bridges break and reform as actin filaments slides forwards

• ATPase in myosin hydrolyses ATP to ADP + Pi to release the myosin head from the actin

• sarcomere shortens

What happens at a cholinergic synapse

1. ACTION POTENTIAL arrives at the presynaptic membrane causing the depolarisation of the motor neurone membrane

2. Ca2+ ion channels open and Ca2+ ions diffuses down the electrochemical gradient and into the synaptic knob

3. this stimulates acetyl choline containing vesicles to fuse with the presynaptic membrane

4. acetyl choline (ACH) molecules are released into the synaptic cleft by exocytosis

5. ACH diffuses across the synaptic cleft and binds to acetyl choline receptors on the post synaptic membrane

6. this causes Na+ ion channels to open and Na+ ions to diffuse down the electrochemical gradient and into the sarcolemma

7. sarcolemma gets depolarised

8. acetyl choline is broken down by acetylcholineesterase to acetase and choline to prevent permanent depolarisation

9. choline reabsorbed back into presynaptic membrane and reacts with acetyle coA to form ACH again

what happens at neuromuscular junction

What does EPOC mean

the increased volume of oxygen consumed after vigorous exercise