topic 7

• Conductive Pathway of the Heart (until AVN)

  1. SAN:

  • The sinoatrial node (SAN) generates an electrical impulse that initiates a wave of depolarisation 

  1. Atria contract:

  • This causes atria to contract 

  1. AVN:

  • Depolarisation is carried to atrioventricular node (AVN) 
  • After a slight delay, the AVN is stimulated 
• Conductive Pathway of the Heart (from purkyne fibres)

  1. Purkyne Fibres:

  • The purkyne fibres conduct the impulses to the apex of the heart from the AVN

  1. Bundle of His:

  • The impulses spread upwards through the bundle of His into the ventricular walls

  1. Ventricles contract:

  • This causes the muscle to contract from the base upwards and blood is forced out of ventricles into the pulmonary artery and aorta 
• What is the AVN

  the only point that impulses can pass through the non-conducting layer between atria and ventricles 
• Why is there a non-conducting layer

  • Creates a delay between atria and ventricles contracting to allow all the blood to enter the ventricles and to prevent top-down ventricular contraction 
• Control of heart rate

  1. Receptors detect stimuli in the blood:

  Chemoreceptors:

  • Detect the concentration of oxygen in blood
  • The changes in pH result from carbon dioxide dissolved in the blood, forming carbonic acid

  Baroreceptors :

  • Changes in blood pressure

  1. These receptors are stimulated, generating impulses which are sent to the medulla oblongata 
  2. The cardiovascular control centre of the medulla oblongata changes the rate at which the SAN fires according to the signals
• Heart rate decreases

  • If blood pressure or oxygen concentration is high, the cardiovascular centre decreases the rate at which the SAN fires. 
  • The parasympathetic nervous system is activated
  • The parasympathetic neurons release the neurotransmitter Acetylcholine 
  • Acetylcholine  binds to receptors on SAN
  • This decreases the rate of SAN firing 
• Heart rate increases

  • If blood pressure or oxygen concentration is low, the cardiovascular centre increases the rate at which the SAN fires. 
  • The sympathetic nervous system is activated
  • The sympathetic neurons release the neurotransmitter Noradrenaline
  • Noradrenaline binds to receptors on SAN
  • This increases the rate of SAN firing 
• Inhalation

  1. The inspiratory centre in the ventilation centre in the medulla oblongata is stimulated
  2. Nerve impulses are sent to the intercostal muscles and diaphragm muscles. 
  3. External intercostal muscles contract. The rib cage moves up and out
  4. The diaphragm contracts and flattens
  5. This increases volume of lungs and decreases pressure so pressure inside is lower than pressure outside so air is drawn in.
  6. The volume of thorax increases
  7. The pressure inside the thorax decreases
• Exhalation

  1. As the lungs inflate, stretch receptors in the bronchioles are stimulated.
  2. These receptors send inhibitory impulses back to the ventilation centre.
  3. Impulses to the muscles stop and the muscles of the diagram and the intercostal muscles relax.
  4. Elastic recoil of the lungs and gravity acting on the ribs, exert pressure on the lungs and air leaves the lungs.
• ventillation centre

  1. Receptors detect stimuli in the blood:

  Chemoreceptors (chemical receptors): located in aortic and carotid bodies 

  • Detect the concentration of oxygen in blood
  • The changes in ph resulting from carbon dioxide dissolved in blood, forming carbonic acid

  Baroreceptors (pressure receptors): located in aortic and carotid bodies 

  • Changes in blood pressure

  1. These receptors are stimulated, generating impulses which are sent to the medulla oblongata 
  2. The ventilation centre of the medulla oblongata is responsible for changing the breathing rate according to these signals
• Changes in ventilation as exercise begins

  1. As exercise begins, impulses from the motor cortex act on the ventilation centre of the medulla oblongata.
  2. These impulses act more frequently on the intercostal and diaphragm muscles which causes the rate and strength of their contractions to increase 
  3. Effects of this:

  • Ventilation rate increases
  • Breathing rate and depth increases 
  • more oxygen enters the lungs and more carbon dioxide exhaled 
• Action of peptide hormones

  1. Hormone attaches to receptors on cell surface membrane of target cell
  2. This binding activates an enzyme inside of the cell surface membrane 
  3. The activated enzyme hydrolyses ATP and activates a second messenger inside the cell - This is the ‘second messenger model of action’ 
  4. Functional second messenger activates enzymes or transcription factors , resulting in the desired response. 
• Action of steroid hormone

  1. Steroid hormones are lipid soluble so they diffuse through the phospholipid bilayer of the cell surface membrane and enter the cell, binding to receptors inside. 
  2. The binding of the hormone to the receptor creates a hormone-receptor complex which acts as a transcription factor 
  3. It binds to the promoter region of the gene and attracts other transcription factors to bind to it, resulting in transcription and translation of the target gene 
• Hormonal regulation of body temperature

  Involves hormones:

  Thyroid hormone

  Thyroxine

  The gene codes for a protein that increases metabolic rate

  This generates more heat and increases body temperature
• Hormonal regulation during normal body temperatures

  • Thyroid hormone receptor binds to promoter region of gene 
  • The binding of the thyroid hormone at the promoter region prevents the binding of the transcription initiation complex
  • This causes the gene to be switched off so gene is not transcribed
  • Protein is not produced 
• Hormonal regulation during cold body temperatures

  • The body releases the hormone thyroxine 
  • Thyroxine binds to the thyroid hormone receptor 
  • The binding of thyroxine to thyroid hormone inhibits the thyroid hormone so it can no longer attach to the gene
  • This allows RNA polymerase to bind to the start of the gene and the gene is switched on
  • The gene can be transcribed 
  • The protein is produced in larger quantities, leading to an increase in body temperature 
• Erythropoietin (EPO)

  • It is a peptide hormone produced naturally by the kidneys 
  • It stimulates the formation of new red blood cells in the bone marrow
  • It can be produced synthetically using recombinant DNA technology
  • By injecting EPO, number of red blood cells increase
  • This causes oxygen carrying capacity to increase so more oxygen can be made available for aerobic respiration 
  • This leads to greater endurance 
  • It is a natural substance so it is difficult to test whether increased levels of EPO are natural or not 
• Testosterone:

  • It is a steroid hormone produced in the testes in males and in small amounts in males and females by the adrenal gland
  • Testosterone binds to androgen receptors on cell surface membrane of target tissue cells
  • The binding of testosterone modifies gene expression to alter the development of the cell 
  • They increase the rate of metabolic reactions such as protein synthesis in muscle cells, increasing the size and strength of muscles. 
  • This increases the strength, speed and stamina of the individual 
• Creatine

  • It is an amino acid-derived compound that is found naturally in meat and fish 
  • Creatine supplements increase the levels of creatine phosphate in muscles 
  • Creatine phosphate is a molecule that can supply ATP for muscle contraction. During intense activity, phosphocreatine donates phosphate to ADP to produce ATP.
• Creatine phosphate/phosphocreatine

  Phosphocreatine is a molecule that can supply ATP for muscle contraction 

  During intense activity, phosphocreatine donates a phosphate to ADP to produce ATP

  ATP is used in muscle contraction

  During periods of low activity, ATP can be used to phosphorylate creatine back to phosphocreatine. 
• Damage to articular cartilage:

  • The articular cartilage covering the surface of bones wears away so bones grind on each other, causing damage. 
  • This damage can lead to inflammation and a form of arthritis
• Patellar tendonitis:

  • Occurs when the kneecap (patella) does not glide smoothly across the femur due to damage of the articular cartilage on the femur 
• Bursae:

  • Fluid sacs that cushion the points of contact between bones, tendons and ligaments can swell up with extra fluid
  • Causes tenderness and inflammation 
• What is keyhole surgery?

  • A small video camera is inserted into the incision, along with specialised medical instruments with which to perform the surgery
  • Used for treating damaged cruciate ligament 
• Advantages of keyhole surgery:

  • Less invasive 
  • Less blood loss and scarring of skin
  • Less pain after surgery and quicker recovery 
  • Shorter hospital stay 
• What are prostheses?

  prostheses are artificial body parts designed to restore function or appearance
• Use of prostheses:

  • The damaged cartilage and bone is replaced by a metal device on both long bones to create a smooth surface for articulation
  • A plastic spacer is often inserted between the metal ends of the prosthesis to provide cushioning and reduce the impact on the knee
• Where is the SAN located?

  right atrium
• P wave

  depolarisation of the atria, leading to atrial contraction (atrial systole)
• PR interval

  the time taken for the impulses to be conducted from the SAN across the atria to the ventricles, through the AVN
• QRS complex

  the wave of depolarisation resulting in contraction of ventricles (ventricular systole)
• T wave

  repolarisation (recovery) of the ventricles during diastole
• Tidal Volume

  • amount of air breathed in and out during normal restful breathing
• Breathing rate

  • number of breaths per minute 
• • Ventilation rate
  • tidal volume * breathing rate
• Describe how SAN is involved in increasing heart rate as a result of increased level of activity

  cardiovascular control centre stimulates the accelerator nerve, which causes more stimulation of SAN

  more frequent waves of depolarisation initiated by SAN to atria

  leading to more contractions of atria
• effects of exercise on immunity

  moderate exercise increases the number and activity of natural killer cells

  release protein perforin which makes pores in the target cell membrane and causes apoptosis of the cell
• vigorous exercise and immunity

  the specific immune system is temporarily depressed / suppressed because the number of natural killer cells, phagocytes, b cells and t helper cells falls.

  Less t helper cells so less cytokines and less activated b cells so fewer antibodies produced

  inflammatory response occurs in muscles due to damage to muscle fibres by heavy exercise. Reduces number of cells available in non-specific immune system

  psychological stress = cortisol and adrenaline released due to stress also suppress immune system
• heat loss / decreased temperature

  thermoreceptors detect changes in temperature and send signals to the hypothalamus

  hypothalamus stimulates sweat glands to secrete sweat

  hypothalamus triggers vasoconstriction of the shunt vessels which causes the arterioles to dilate

  More blood flows closer to the surface and so more heat is lost by radiation

  hair erector muscles relax

  liver reduces metabolic rate

  no shivering
• heat gain / increased temperature

  inhibits sweat glands

  arterioles constrict and shunt vessels dilate.

  More blood flows through shunt vessels so away from surface of the skin so less energy is lost by radiation

  hair erector muscles contract

  skeletal muscles contract causing shivering