Unit 5 Scientific Article June 2015 Questions These are some possible questions that could come up from the material in the scientific article. There is some repetition of topics and so some questions will have similar answers. The number of marks, in brackets after the question, indicates the detail required by the answer. This is the number of relevant points I could think of for the answer, but there may be more that I have missed.

1) Para 2&3 (also mentioned in other paragraphs e.g. para 37 and 46) Is it ethical to allow the use of performance-enhancing drugs in sports? What are some of the issues we have to consider e.g. safety, costs, availability? Who is to blame if an athlete fails a drugs test? (minimum 4)

some of these issues are highlighted in the rest of the article. You should be able to produce arguments for both sides of this issue i.e. why should we allow athletes to use performance-enhancing drugs and why should they be banned?

2) Para 3 List three different classes of performance-enhancing drugs and describe briefly how they act to enhance athletic performance? (6) Any three from:

anabolic steroids build muscle mass stimulants e.g. caffeine increase heart rate to improve alertness

beta-2 agonists dilate airways, allowing more oxygen into lungs beta-blockers slow down heart rate and reduce trembling hormones and their releasing factors increase the effects of natural, endogenous hormones

narcotics allow athletes to ignore pain diuretics cause excess urination to eliminate drug traces in the urine

3) Para 6 How do anabolic steroids (steroid hormones) have an effect on cells? (5)

hydrophobic/lipophilic

cross the cell membrane

bind to a receptor protein

complex acts as a transcription factor

binds to DNA/increases gene transcription

4) Para 7 Beta-blockers are drugs that block the action of the sympathetic nervous system on the heart. Describe how the resting heartbeat is coordinated within the heart. What would be the effect of an athlete using beta-blockers? (10)

SAN node

atrial wall

causes/depolarises atria

atria contract/atrial systole

(depolarisation reaches) AV node

delay (to allow atrial contraction)

excitation passes along Purkinje fibres/bundle of His

ventricular contraction/systole

diastole/relaxation

(beta-blockers) slow down heart rate; relax the athlete

5) Para 14 what are the functions of tendons and ligaments? How are their structures/properties related to their functions? Why might steroid injections weaken the ligaments or muscles? (9)

tendons join muscle to bones

inelastic

large amounts of collagen

function: do not stretch/transmit force of muscle contraction to skeleton

ligaments join bones to bones more elastic

collagen and elastic fibres

function: stretch to allow a range of bone movements

injections might weaken the fibre snap under tension/when pulled/stretched

6) Para 15 If you were to analyse a muscle sample from a weight-lifter or a judo competitor, what type of muscle fibres do you think would be more prominent? Why? What are the properties of these types of fibres? (5)

fast-twitch/glycolytic fibres

useful for fast, powerful muscle contractions (in judo etc)

glycolytic (if not mentioned already)

low levels of myoglobin

less blood capillaries

7) Para 17 anticholinergic agents block the action of acetylcholine. Describe the how acetylcholine is involved in synaptic transmission of nerve impulses. How might anticholinergic agents interfere with the normal function of acetylcholine? (10)

neurotransmitter

released from pre-synaptic neuron/synaptic bulb/knob

by exocytosis

diffuses across synaptic cleft/gap

binds to post-synaptic receptors/neuroreceptors

causes sodium channels to open

(anticholinergics) block binding of acetylcholine to receptor

may bind to the receptor themselves

may bind to acetylcholine and prevent it binding

may cause increased acetylcholinesterase activity

8) Para 18 Beta-2 agonists cause hyperpolarisation of smooth muscle cell membranes. How might they achieve this? (3)

bind to receptor protein (on membrane surface)

cause opening of potassium channels

cause opening of chloride channels

9) Para 19 the haematocrit is the proportion of red blood cells in a blood sample. Why might a high haematocrit be dangerous for an athlete? (2)

may cause increased blood clotting

resulting in stroke/heart attack etc

10) Para 19 the production of recombinant human erythropoietin is currently being investigated using transgenic sheep. The human erythropoietin will be secreted into the sheeps milk and purified. Explain how such an animal could be produced. (9)

isolate gene for human erythropoietin

using restriction enzymes

place into a vector

virus/liposomes/microinjection/plasmid

insert gene into zygote/fertilised egg of sheep

use of promoter to ensure gene expression

use of marker gene to select cells containing vector

embryo implanted into uterus

of surrogate ewe/adult female sheep

11) Para 21 With reference to the structure of skeletal muscle, in what way could anabolic steroids affect muscle so as to promote muscle growth? (3)

idea of increasing synthesis of muscle proteins

e.g. myosin, actin, tropomyosin, troponin

by changing gene expression

12) Para 21 Describe how anabolic steroids could lead to changes in protein synthesis (7)

hormones are hydrophobic/lipophilic

diffuse through cell membrane

bind to steroid hormone receptors in cytoplasm

steroid:receptor complex diffuses into the nucleus

binds DNA

acts as a transcription factor

changes gene expression

13) Para 21 What is atherosclerosis? What could be the consequences of developing this condition? (9)

hardening of the artery walls

due to accumulation of fats/cholesterol

following damage to the endothelium/lining of the artery

presence of macrophages/foam celss

inflammation

formation of an atheroma or plaque

narrowing of the lumen of the artery

increased blood pressure

risk of blood clotting

14) Para 24 SERMs are drug molecules that bind to the oestrogen steroid hormone receptor. What effects would this have in the cell? (2)

block the effects of oestrogen/stop oestrogen binding to the receptor

stop transcription of oestrogen-sensitive genes

15) Para 26 Describe how peptide hormones act on target cells (6)

hormones bind to a receptor on the cell surface membrane

(receptor is an) integral or transmembrane protein

hormone binding causes the receptor to become activated

causes production of a second messenger in the cytoplasm/changes to molecules in the cytoplasm

leads to activation of transcription factors in the nucleus

causes transcription of target genes

16) Para 29 Proteins such as recombinant human growth hormone can be made in large quantities using bacteria and simple genetic engineering techniques. Describe you would produce this recombinant protein in bacteria (7)

isolate the human gene/DNA for human growth hormone from human cells/DNA

using restriction enzymes/endonucleases

add to a plasmid/vector

using DNA ligase

add recombinant plasmid to bacterial cells/transform bacterial cells with the recombinant plasmid

grow bacterial cells (in a fermenter)

purify protein from bacterial cells/split open cells and extract the growth hormone

17) Para 30 What is homeostasis? If GH has the opposite action to insulin, with respect to glucose homeostasis, describe how the body can use these hormones in glucose homeostasis. (8)

homeostasis = maintenance of a constant internal environment

if blood glucose increases: insulin released

from pancreas (beta cells)/Islets of Langerhans

causes conversion of glucose to glycogen

in liver and muscle

if blood glucose decreases: GH released

(from anterior pituitary gland)

causes conversion of glycogen to glucose in the liver/muscle

18) Para 31 Describe how gene doping for insulin growth factor 1 could be carried out on human athletes. (4)

isolate the human insulin growth factor 1 gene/DNA

using restriction enzymes/endonucleases

use a vector/virus/injection

introduce DNA into athletes cells/body

19) Para 40 A mutation in the EPOR gene is thought to cause increased cell division in the blood cells that

will differentiate to form red blood cells. Describe the sequence of events that occurs when cells divide in this manner. How is this cell division usually controlled? (12)

DNA is replicated/copied

DNA/chromatin condenses/chromosomes become visible

nuclear envelope and nucleolus disappear

centrioles divide and migrate to opposite sides/poles of the cell

spindle fibres/microtubules are produced

microtubules attach to chromosomes/centromeres

chromosomes line up on the equator of the cell

sister chromatids are pulled apart (as microtubules contract/shorten)

nuclear envelope reforms

chromosomes decondense/chromatin forms

controlled by cyclins and cyclin-dependent kinases

form checkpoints for the cell cycle

20) Para 41 What is a fast-twitch muscle fibre? Why would the lack of a protein from fast-twitch muscle fibres be a disadvantage for sprinters? (10)

glycolytic fibre

function anaerobically

fatigue quickly

poor blood supply

low levels of myoglobin

few mitochondria

rich glycogen stores

high levels of creatine phosphate

many myofibrils

fast twitch muscle fibres are useful for powerful contractions over short periods of time

21) Para 47 Describe how it would be possible to use gene therapy to introduce an desirable allele of a gene for a muscle protein into one of the muscle cell. (4)

isolate the human gene/DNA for the muscle protein

using restriction enzymes/endonucleases

use a vector/virus/injection

introduce DNA into athletes cells/body

22) Para 47 describe how the muscle proteins work together to achieve contraction of the muscle. (9)

calcium ions bind to troponin

bind causes troponin to change shape

change in shape cause it to pull tropomyosin away from myosin-binding sites on actin fibres

myosin (heads) bind to actin/(actomyosin) cross-bridge formed

ADP and Pi are released from myosin head

myosin head changes position, pulling past the actin fibre

ATP binds myosin and allows release from actin fibre

ATP hydrolysed by myosin ATPase, producing ADP and Pi

returns myosin head to its original position

23) Para 50 What is the role of creatine in a muscle cell? Why would an athlete want to achieve higher creatine levels in their muscles? (6)

stored as creatine phsophate

allows production of ATP

from ADP

creatine transfers phosphate group to ADP

high levels of creatine will allow more creatine phosphate to be formed

allowing more ATP production