SNAB topic 7

• 7.1 Know the way in which muscles, tendons, the skeleton and ligaments interact

  to enable movement, including antagonistic muscle pairs, extensors and

  flexors.

  Tendons- non elastic tissue, muscle connected to bone

  Ligaments- elastic tissue that holds bones together and determines the amount of possible movement at a joint

  Muscles move the bone they are attached to, in their antagonistic pairs.

  1) The muscle contracts and pulls on the tendon 2) The tendon cannot stretch, so it pulls on the bone 3) The bone is moved

  Extensors straighten the joint, flexors bend the joint

  
• 7.2 Understand the process of contraction of skeletal muscle in terms of the sliding

  filament theory, including the role of actin, myosin, troponin, tropomyosin,

  calcium ions (Ca2+), ATP and ATPase.


  [Textbook pic shows ADP and Pi still attached to myosin head in the bottom left diagram, printing error]

  
• 7.2 [Muscle contraction explanation]

  1) Ca2+ bind to troponin

  2) troponin moves tropomyosin, revealing myosin head binding site

  3) Myosin head binds to binding site. Right now, ADP and Pi are both on the myosin head

  4) ADP and Pi are released.

  5)Head nods forward

  6) Actin filament slides towards centre of sarcomere

  7) ATP binds to myosin head, breaking the bridge between myosin/actin

  8) ATP is hydrolysed, causing energy to be released

  9) The head cocks back to its original position

  10) The head binds to the next binding site, and the process repeats
• 7.3 i) Understand the overall reaction of aerobic respiration as splitting of the

  respiratory substrate, to release carbon dioxide as a waste product and

  reuniting of hydrogen with atmospheric oxygen with the release of a large

  amount of energy.


  Overall reaction:

  C6H12O6 + 6O2-->6CO2 +6H2O

  
  

  (+ ATP)
• 7.3 ii) Understand that respiration is a many-stepped process with each step

  controlled and catalysed by a specific intracellular enzyme.

  Glycolysis

  
  

  Link reaction

  
  

  Kreb's cycle

  
  

  Oxidative phosphorylation
• 7.4 Understand the roles of glycolysis in aerobic and anaerobic respiration,

  including the phosphorylation of hexoses, the production of ATP, reduced

  coenzyme, pyruvate and lactate (details of intermediate stages and compounds are not required).


  Glycolysis produces:

  2 molecules of pyruvate

  2 (net) molecules of ATP

  2 molecules of NADH

  From one glucose molecule by phosphorylating and oxidising it.

  
  

  in anaerobic respiration the pyruvate is reduced into lactate with the help of NADH.
• 7.5 Understand the role of the link reaction and the Krebs cycle in the complete oxidation of glucose and formation of carbon dioxide (CO2), ATP, reduced NAD and reduced FAD (names of other compounds are not required) and why these steps take place in the mitochondria, unlike glycolysis which occurs in the cytoplasm.


  Link reaction:Pyruvate is bound to Coenzyme A.Producing acetyl coenzyme A-NADH is produced

  Krebs cycle:-Acetyl CoA enters the krebs cycle.-6 carbon compound is formed, which is decarboxylated and oxidised(CO2 + NADH released)

  -5 carbon compound is formed, which is decarboxylated and oxidised(CO2 + ATP + 2NADH + FADH2 released)

  -4 carbon compound is formed again

  
  

  Happens in mitochondria instead of cytoplasm•The mitochondria acts as a place where all the specific/necessary enzymes are localised.•This means that enzymes are contained and respiration happens quickeras thesubstrate does not need to diffuseacross cytoplasm to find the enzymes

  
• 7.6 Understand how ATP is synthesised by oxidative phosphorylation associated

  with the electron transport chain in mitochondria, including the role of

  chemiosmosis and ATP synthase.

  1) The NADH/FADH2 that has been made so far,releases hydrogen ions and electronsat the inner mitochondrial membrane.

  *FADH2 releases electrons only at the (middle) complex ii*NADH releases electrons at the first complex, complex i

  2)Electrons travel down the ETC,releasing energyused to pump H+ ions against the concentration gradient (through the three complexes), into the intermembrane space.

  3) H+ ions move back into the matrix through theATP synthaseprotein.

  4) Thisreleases energy, used by ATPase to synthesise ATPfrom ADP and Pi

  5)Oxygen is the final acceptor of electronsthat are in the matrix, forming H2O with H+ ions
• 7.7 Understand what happens to lactate after a period of anaerobic respiration in

  animals.

  Lactate decreases the blood pH, which affects enzyme activity & causes muscle fatigue.

  It can leave the cell, enter the blood and :•It can be oxidised back to pyruvate in the liver(which is then used in the krebs cycle to produce ATP). This causes oxygen debt, which is why we breathe faster during exercise

  •It can be converted into glucose by the liver, to be used for respiration/storage
• CORE PRACTICAL 16:

  Investigate rate of respiration.


  Equipment:•sodalime, dye, identical maggots, stopwatch, ruler/scale, gauze.

  •Three way tap, glass tubing, 1cm^3 diameter pipette and a test tube are all used in conjunction as the respirometer.• Syringe can be used to reset it.•A water bath can be used to control temperature

  u tube vs simple respirometer

  Method1) Set up tube with soda lima, gauze and cotton wool.2) Set up spirometer with delivery tube, bung and syringe joined.3) Mark starting point of dye4)Place 5g equal size maggots in tube, close bung5) Mark the position of the fluid on the pipette every minute for 20 minutes, record in table

  Control variablesSpecies of maggot, size of maggot, temperature and time

  Control:Plastic beads in another tube

  Calculation:

  Volume of oxygen= πr2 * distance dye travelled.• r is the radius of the pipette.Stats:Mean and standard deviation

  
• 7.8 i) Know the myogenic nature of cardiac muscle.

  Myogenic:it is able to initiate its own contraction
• 7.8ii) Understand how the normal electrical activity of the heart coordinates the

  heart beat, including the roles of the sinoatrial node (SAN), the atrioventricular

  node (AVN), the bundle of His and the Purkyne fibres.


  Depolarisation originates in theSAN.1) This spreads through the atria-->ATRIAL SYSTOLE

  •Depolarisation cannot spread directly to the ventricles because ofnon-conductive tissuebetween the atria and ventricles

  2) Depolarisation reachesAV node- this passes it into the conducting fibres: theBundle of Hisand then to the Purkyne Fibres.

  3) Ventricular systole occurs upwards from theapexof the heart, after a delay between the atrial systole.

  There is a delay so that the ventricles can fill up with blood.

  
• 7.8iii) Understand how the use of electrocardiograms (ECGs) can aid the diagnosis

  of cardiovascular disease (CVD) and other heart conditions.


  different shapes=different conditions

  
  

  (not sure if this is on spec but helps if u learn it)P wave=depolarisationof atriaQRS complex=depolarisationof ventriclesT wave=repolarisationof ventricles

  
• 7.9 i) Be able to calculate cardiac output.


  Cardiac output=stroke volume*heart rate
• CORE PRACTICAL 17:

  Investigate the effects of exercise on tidal volume, breathing rate, respiratory

  minute ventilation and oxygen consumption using data from spirometer traces.


  Equipment:SpirometerKymographNose clipSoda lime

  
  

  Method:

  1) Calibrate the spirometer2) Fill the spirometer with oxygen3) Attach mouthpiece to tube4) Place nose clip on subject5) Attach mouthpiece to mouth of subject6) Switch on recording apparatus

  Some air always remains in the lungs as residual air, to prevent alveolar walls from sticking together

  Tidal volume is the volume of each breath.Count number of breaths in 60 seconds for breathing rate OR just see how long one breath takes, and divide 60(s) by this time period

  Minute ventilation = tidal volume × rate of breathing
• 7.9 ii) (PART A) Understand how variations in cardiac output enable rapid delivery of oxygen to tissues and the removal of carbon dioxide from them, including how the heart rate is controlled and the roles of the cardiovascular control centre in the medulla

  oblongata.


  Heart rate is increased by:-Low pH/High CO2/Low O2detected bychemoreceptorsin carotid/aortic arteries-Stretch receptorsdetecting muscle movement-Adrenalinerelease-Decrease in blood pressure,detected by baroreceptors

  Heart rate is decreased by :-Increase in blood pressure-High blood O2/Low CO2/High pH

  Impulse direction to increase heart rate:

  Receptor detects stimuli, sends impulse->Cardiac control centre (medulla oblongata)-- ->Sympathetic nerve----->Neurotransmitter such as noradrenaline binds to SAN------> FASTER heartrate

  [OR, adrenaline/similar hormones bind to the SAN through the blood, increasing heartrate]

  Impulse direction to decrease heart rate:

  Receptor detects stimuli, sends impulse-->CCC in m.oblongata---->parasympathetic nerve------>acetylcholine binds to SAN------->SLOWER heartrate
• 7.9 ii) (PART B) Understand how variations in ventilation enables rapid delivery of oxygen to tissues and the removal of carbon dioxide from them, including how the ventilation rate is controlled and the roles of the ventilation centre in the medulla

  oblongata.


  Ventilation rate is increased by:-High blood CO2/Low O2/Low pH detected bychemoreceptors-Impulses fromstretch receptors-Voluntary control

  How ventilation is controlled-->impulse from inspiratory centre is sent---->impulses tointercostal muscles/diaphragm muscles

  ------>contraction of muscles, volume of chest increases

  ---------->Air flows in

  ------>stretch receptorsin lungs detect capacity reaching, send impulse to expiratory centre

  ----> impulse sent to diaphragm/intercostal muscles, they relax and the volume of the chest decreases.-->Air flows out.

  How ventilation is affectedimpulse from stretch/chemorecepters->VCC inmedulla oblongata-->more frequent nerve impulsesto intercostal/diaphragm muscles--->ventilation rate increases----->blood pH returns to normal------->breathing rate returns to normal
• 7.10 i) Know the structure of a muscle fibre.

  Muscle fibre=muscle "cell" (it has multiple nuclei).

  Sarcolemma:The membrane around the fibre

  Transverse T-tubules:•These run close to the SR•Transmits an impulse from sarcolemma to sarcoplasmic reticulum

  Sarcoplasmic reticulum:•Stores calcium ions•Releases calcium ions to bind to troponin for contraction

  Sarcoplasm:•The cytoplasm of muscle fibres, contain many mitochondria and myofibrils

  Motor neurone/neuromuscular joint:•Releases acetylcholine that bind to the postsynaptic membrane at the joint.•This initiates depolarisation, and an impulse spreads to T-tubules.

  
• 7.10 ii) Understand the structural and physiological differences between fast and

  slow twitch muscle fibres.

  
• 7.11 i) Understand what is meant by negative feedback and positive feedback

  control.

  Negative feedback reduces the change from the norm to maintain the condition at the set point

  Positive feedback enhances the change from the norm

  
• 7.11 ii) Understand the principle of negative feedback in maintaining systems within

  narrow limits.

  e.g. decrease in testosterone stimulates pituitary gland to release hormones that stimulate the testes to synthesise testosterone

  
• 7.12 Understand homeostasis and its importance in maintaining the body in a state

  of dynamic equilibrium during exercise, including the role of the hypothalamus

  and the mechanisms of thermoregulation.


  The hypothalamus is like the thermostat, turning on the appropriate effectors to maintain the body temperature at the set point (37.5 degrees C)

  Lower temperature:reactions occur too slowly for body to remain activeHigher temperature:Enzymes will denature, a rise of just 5 degrees in core body temp. can befatal.

  Exercise can affect homeostasis

  •temperature increasesoverheating needs to be prevented•oxygen decreases/carbon dioxide increases:->increase in blood pH: can cause denaturing of enzymes

  •blood pressure increases, blood pressure needs to be maintained to meet the body's nutrient requirements

  •fluid/electrolytes decrease from sweating, can affect hydration

  
• 7.13 Understand the analysis and interpretation of data relating to possible

  disadvantages of exercising too much and exercising too little, recognising correlation and causal relationships.

  Exercising too much:•Wear and tear on joints• Suppression of the immune system

  data that might suggest this= T killer/macrophage cell count, likelihood of injury vs time spent exercising

  Exercising too little:•Increased risk of obesity,•Cardiovascular disease (CVD) and diabetes

  data that might suggest this= weight, BMI, energy intake/output
• 7.14 Understand how medical technology, including the use of keyhole surgery and

  prostheses, is enabling those with injuries and disabilities to participate in

  sports.

  Keyhole surgery:

  Recovery time is shorter, enables athletes to get back quicker

  Cheaper than open surgery

  
  

  Prosthesis:

  An artificial body part enabling regaining of appearance/functionality
• 7.15 Be able to discuss different ethical positions relating to whether the use of

  performance-enhancing substances by athletes is acceptable.

  Why PEDs may be unacceptable:-Unfair competition-Athletes may not know the risks-Disparity between those who have access and those who do not

  Why PEDs may be acceptable:-Athletes have autonomy over their own body-Athletes have the right to decide for themselves.-It may allow the disadvantaged to compete at a higher level e.g. lionel messi taking HGH to treat dwarfism
• 7.16 (PART A) Understand how genes can be switched on and off by DNA transcription factors

  including hormones.

  
• 7.16 (PART B) Understand how genes can become switched on and off by hormones.